Advanced Med-Surg Exam 1 9.23.08

Front 1

What protects the body from foreign invasion?

Back 1

the immune system

Front 2

The protein make-up on cells is ____?

What effect does this have on transplants?

Back 2

inherited

The closer a relative is to you, the better they are to give you their organs

Front 3

HLA = ?.
What is HLA used for?
How many HLA's?

Back 3

HLA = human leukocyte antigens.
HLA is used to match organ donors.
40 major ones, and many more minor ones.

Front 4

What is the protein make-up on cells called?

Back 4

HLA or human leukocyte antigens.

Front 5

What does the immune system do to anything non-self?

Back 5

Recognizes self from non-self and destroys that which is non-self.

Front 6

Since the immune system destroys anything non-self, what must be done when pt has transplant?

Back 6

Immune response must be suppressed.

Front 7

Why does the immune system remember foreign antigens?

Back 7

So that it can mount a swifter, more effective response the next time it is exposed to an antigen

Front 8

What are the 3 processes needed for immunity?

Back 8

-Inflammation
-Antibody (humoral) mediated immunity
-Cell mediated immunity

Front 9

What are the 3 ways that immunity happens?

Back 9

-Exposure through day-to-day life.
-Active immunity
-Passive immunity

Front 10

2 ways active immunity can happen?

Back 10

-Natural Active (best)
-Artificial Active (may or may not be lifelong)

Front 11

Passive immunity lasts how long?

Back 11

Not very long. Protection is immediate and short-term.

Front 12

What are the 2 ways that passive immunity can happen?

Back 12

-Natural passive breast feeding
-Artificial passive gamma globulin.

Front 13

What is artificial passive gamma globulin?

Back 13

-1 way passive immunity happens
-antibodies are prod by someone else & then injected into other person's body.

Front 14

What are the 2 basic categories of immunity?

Back 14

-Non-specific or Innate Immune response, also called natural
-Specific or Adaptive Immune response

Front 15

What is an example of artificial active immunity?
1. PPD
2. Hepatitis B immune globulin
3. Tetanus booster
4. Influenza vaccine
5. Both 3 and 4

Back 15

Both 3 and 4

Front 16

An elderly client asks the nurse why she has developed herpes zoster. The best response by the nurse is:
1. This skin thins as you age
2. Your immunity to chicken pox decreases with age
3. Immune system function declines with age

Back 16

3. Immune system function declines with age

Front 17

Which of the following might prevent the development of autoimmune dzs?
1. regular exercise
2. 81 mg of ASA a day
3. Diet rich in antioxidants

Back 17

3. Diet rich in antioxidants

Front 18

Which of the following assessment findings is most indicative of an altered immune system in a client?
1. T101
2. BP 200/98
3. Macular rash over most of body
4. White patches in mouth

Back 18

White patches in mouth: bc indicates yeast infection that is extremely rare in someone w/ normal immune system

Front 19

What indicates that an infection is probably viral?

Back 19

Increased lymphocyte count.

Front 20

A client is allergic to penicillin. An order for which of the following should be questioned?
1. Ceftriazone
2. Metronidazole
3. Azithromycin
Doxycycline

Back 20

Ceftriazone

Front 21

The nurse believes a client is suffering an acute rxn to an antibiotic. The nurse should first:
1. Assess client’s respiratory status
2. Take the client’s BP

Back 21

Assess client’s respiratory status

Front 22

What are the 4 organs of the immune system?

Back 22

·Bone marrow
·Thymus
·Lymph nodes and spleen
·Mucosa associated lymphoid tissue
- MM surfaces of the body

Front 23

3 functions of potassium?

Back 23

-controls intracellular osmotic pressure: OP is what keeps things where they need to be.
-regulates acid-base balance
-maintains neuro/muscular function via the Na/K pump

Front 24

What is the txment for hypokalemia?

Back 24

-K+ supplements, oral or parental

Front 25

4 things should know about K+ parental administration?

Back 25

–Maximum amount-5-10 mEq/hr
–May need cardiac monitoring: bc hypokalemia interferes w/ cardiac
–Can not be given SQ, IM or IVP
–Should check renal function first

Front 26

8 reasons for hyperkalemia?

Back 26

–Renal failure
–Crushing injuries/burns
–Excessive K in IVs/potassium containing foods
–Addison’s disease
–MI
–Hemorrhage/shock
–Blood transfusions(Whole blood/packed cells):
–Uncontrolled diabetes

Front 27

How can crushing injuries/burns cz hyperkalemia?

Back 27

damages cell & czs K+ to leave cell.

Front 28

9 czs of hypokalemia?

Back 28

–Diuretic therapy
–Excessive use of digitalis/steroids
–Gastric losses via wound drainage/NG suction
–Vomiting/diarrhea
–Infusions of K free IV fluids
–Cushing syndrome
–Renal disease
–Water intoxication
–NPO status

Front 29

How can Cushing's syndrome cz hypokalemia?

Back 29

Have too much aldosterone bc dz process is releasing too much aldosterone and holding on to Na while losing K.

Front 30

What is renal dz more likely to cz than hypokalemia?

Back 30

Hyperkalemia

Front 31

How can water intoxication cz hypokalemia?

Back 31

K+ is still there but now excess fluid.

Front 32

What is a normal BUN?

Back 32

7 -17

Front 33

3 K+ containing foods?

Back 33

green leafy veggies, tomatoes, bananas

Front 34

How can bld transfusions cz hyperkalemia?

Back 34

citrate in bld products is high in K+

Front 35

5 signs of hypokalemia?

Back 35

-Muscle weakness/decrease reflexes
-Abdominal distension, flatulence progressing to paralytic ileus
- Dysrhythmias-PVCs initially
- Ventricular fibrillation
- EKG changes

Front 36

What is a common/early symptom of hypokalemia?

Back 36

Muscle weakness/decreased reflexes

Front 37

How can Addison's dz cz hyperkalemia?

Back 37

Addison's dz is a problem w/ too little aldosterone.

Front 38

What organ regulates potassium within the body & how?

Back 38

Kidneys: 80% of K+ is removed 4m body this way
- aldosterone: retains Na and gets rid of K.
- Na/K pump: Na is removed 4m inside of cell for every K+ that is placed inside cell.

Front 39

Assessment findings for a client w/ hyponatremia includes which of the following?
1. Constipation & paralytic ileus
2. Watery diarrhea w/ abdominal cramping
3. Muscle cramping & spescity
4. Tachypnea and diminished breath sounds

Back 39

2. Watery diarrhea w/ abdominal cramping

Front 40

Normal Na+ level?

Back 40

normal is 135 - 145

Front 41

Normal K+ level?

Back 41

3.5 – 4.5

Front 42

Normal pH?

Back 42

7.35 - 7.45

Front 43

Normal CO2 level?

Back 43

35 - 45

Front 44

Normal Mg level?

Back 44

1.5 – 2.5

Front 45

Normal Hct level?

Back 45

35% - 45%

Front 46

Normal Ca+ level?

Back 46

8.5 – 10.5

Front 47

How can uncontrolled diabetes cz hyperkalemia?

Back 47

become DKA so K goes up bc it moves 4m ICF to ECF.

Front 48

7 s/s of hyperkalemia?

Back 48

- Muscle spasticity progressing to flaccid paralysis
- Diarrhea/nausea
- Cardiac manifestations
- bradycardia
- hypotension
- Ventricular fibrillation
- EKG changes

Front 49

Why would someone have diarrhea/nausea w/ hyperkalemia?

Back 49

bc body is trying to correct K+ problem

Front 50

Na+ loss is usually a ____ prob.

Back 50

water prob not a Na+ prob.

Front 51

What is Na+ level in the body controlled by?

Back 51

-aldosterone
-osmolality/osmolarity
-renin mechanism: depends on perfusion of kidney whether it is excreted or not

Front 52

Na+ functions to?

Back 52

-regulate the osmotic pressure
-control neuromuscular function via Na/K pump
-acid-base balance

Front 53

What is hyponatremia?

Back 53

A decrease in the amount of Na in relation to the amount of water

Front 54

5 czs of hyponatremia?

Back 54

-H20 intoxication
-dilutional hyponatremia
-SIADH
-true hyponatremia
-starvation hyponatremia

Front 55

How can water intoxication cz hyponatremia?

Back 55

drink too much water and don’t get rid of it, psych cond where always drinking water, sweating a lot but only replace with water and no electrolyte drinks, infant in swim classes bc swallow too much water

Front 56

What is dilutional hyponatremia?

Back 56

person has retained large amt of fluid due to their dz process, ex: CHF (most common), ppl who are on dialysis which czs them to lose fluid

Front 57

What is SIADH & how does it cz hyponatremia?

Back 57

syndrome of inappropriate ADH, ADH stops diuresis, are secreting too much ADH hormone, holding on to fluid, Na level goes down

Front 58

What is true hyponatremia?

Back 58

person w/ diarrhea loses Na

Front 59

What is starvation hyponatremia?

Back 59

NG suction takes out GI Na+ but not being irrigated w/ normal saline.

Front 60

5 s/s of hyponatremia?

Back 60

- Change in CNS level-maybe be decreased (apathy/lassitude) or increased (irritability)
- N/D-abd.cramping
- Weight gain and edema: if retaining too much fluid
- Hypotension or hypertension
- Decreased skin turgor

Front 61

Txment for hyponatremia?

Back 61

·Depends on the cause:
-for increased water-restrict fluids
-for Na loss-give sodium: would probably just start with normal saline
-for malnutrition-improve nutrition

Front 62

Nursing responsibilities for hyponatremia?

Back 62

- Maintain accurate intake and output records
- Weigh patient:
- Obtain vital signs
- Regulate IV fluids
- Be alert to CNS changes

Front 63

What is hypernatremia?

Back 63

- Condition that occurs when water losses exceed sodium losses or when water intake is inadequate

Front 64

Czs of hypernatremia?

Back 64

-excessive water losses
-increased sodium intake

Front 65

S/S of hypernatremia?

Back 65

-changes in CNS level-maybe increased or decreased
-dry sticky mucous membranes -flushed skin
-oliguria
-restlessness, confusion
-edema (if hypervolemia is present)
-muscle twitching to muscle weakness/decreased DTR

Front 66

Txment of hypernatremia?

Back 66

Depends on the cause:
-for decreased water-give water
-for increased sodium-give salt free solutions

Front 67

Nursing responsibilities for hypernatremia?

Back 67

-maintain accurate intake and output records
-be alert for CNS changes
-administer fluids as ordered

Front 68

6 czs of hypocalcemia?

Back 68

–Hypoparathyroidism especially after thyroid or parathyroid surgery/thyroid radiation
–Decreased absorption from the intestines
–Low Levels of vitamins D
–Inadequate calcium intake
–Renal disease
–Diarrhea/draining wounds

Front 69

How can thyroid or parathyroid surgery/thyroid radiation cz hyponatremia?

Back 69

parathyroid and thyroid gland regulates Ca) bc those glands are no longer there to regulate mvmt of Ca from bone to serum. Tell pt to notify doc if start to have tingling in hands/feet.

Front 70

S/S of hypocalcemia?

Back 70

·Parathesias( tingling) of nose, ears, fingertips, toes
·Tetany/seizures (tight, tense, muscles)
·Cardiac irregularities-prolonged QT interval
·Trousseau’s sign
·Chvostek’s sign
·Painful muscle spasms (Charley horse) seen early

Front 71

Trousseau’s sign?

Back 71

assoc w/ Ca disturbances, goes w/ thumb (T & T)

Front 72

Chvostek’s sign?

Back 72

assoc w/ Ca disturbances, goes w/ thumb (T & T)

Front 73

Txment of hypocalcemia?

Back 73

·IV calcium
·Po calcium
·Vitamin D supplements

Front 74

Nursing responsibilities for hypocalcemia?

Back 74

·Observe for changes in neuromuscular irritability
·Seizure precautions
·Decrease stimulation ( helps if on seizure precaution)
·Administer digitalis preps with caution (bc interferes w/ Ca as it moves back into heart cells)
·Have trach tray ready (after thyroid surgery): swelling could block airway
·Prevention of injuries (esp to bones)

Front 75

7 czs of hypercalcemia?

Back 75

–Primary hyperparathyroidism
–Multiple myeloma/metastatic cancer
–Vitamin D overdose
–Over use of aluminum hydroxide gel (calcium containing antacid)
–Paget’s disease
–Renal failure
–Prolonged bedrest/immobility

Front 76

How can multiple myeloma/metastatic cancer cz hypercalcemia?

Back 76

when cancer spreads into bone it pushes Ca out into serum & prolonged bed rest/immobility are two most common czs of hypercalcemia

Front 77

How can over use of aluminum hydroxide gel cz hypercalcemia?

Back 77

many contain Ca and other electrolytes

Front 78

What is Paget's dz?

Back 78

metabolic disorder of bone remodeling resulting in incr. resorption or loss of bone

Front 79

Txment of hyperkalemia?

Back 79

–Limit po intake
–Dialysis
–Take K out of IV fluids
–Correction of acidosis
–CA salts-(protection)
–Nursing responsibilities with Hyperkalemia
–Be alert to K values
–EKG changes
–Fresh blood transfusion
–IV glucose and insulin
–Kayexalate enema or po

Front 80

How does Kayexalate enema or po tx hyperkalemia?

Back 80

will pull out K from GI tract when enema comes out, if given po will cz diarrhea and K will be in diarrhea

Front 81

How does IV glucose and insulin tx hyperkalemia?

Back 81

glucose adds many other things that czs K to move back into cell. Insulin is given to prevent hyperglycemia

Front 82

S/S of hypercalcemia?

Back 82

·Lethargy leading to coma
·Anorexia/N and V/dehydration
·Constipation: no peristalsis
·Decreased QT intervals on EKG
·Renal stones: due to excess Ca in bldstream
·Pathological bone fractures: a piece of bone breaks w/ normal use
·Severe muscle weakness/decreased DTRs

Front 83

Txment of hypercalcemia?

Back 83

·Definitive treatment-remove the cause: ROM excercises, get them up, moving around
·Hydrate with NS: not getting rid of Ca but diluting it
·Oral phosphate
·Mithracin

Front 84

Nursing responsibilities for hypercalcemia?

Back 84

·Encourage mobility when possible
·Strain urine if kidney stones suspected
·Observe for CNS and musculoskeletal changes

Front 85

Normal phosphorous level?

Back 85

3.0 to 4.5 mEq/L

Front 86

What type of relationship do phosphorous & Ca have?

Back 86

have an inverse relationship. If one goes up the other goes down

Front 87

6 czs of hypophosphatemia?

Back 87

–Malnutrition/starvation
–Antacids-aluminum based and magnesium based
–Hyperparathyroidism: low phosphate, high calcium
–Hypercalcium
–Hyperalimentation
–Metastatic cancer: low phosphorus, high calcium

Front 88

Signs and symptoms of hypophosphatemia?

Back 88

·Decreased metabolic energy
·Decreased cardiac contractions resulting in decreased cardiac output (seen as decreased BP and pulse) : bc heart also doesn’t have any metabolic energy
·Rhabdomyolosis (muscle breakdown): have high levels of MM bands, (skeletal muscle) CK-MM can not be broken down by kidneys, so go into renal failure
·Muscle weakness: should be most concerned w/ weakness of respiratory muscles
·Pathological fractures
·CNS changes

Front 89

Txment for hypophosphatemia?

Back 89

·Oral phosphate agents
·Vitamin D supplement
·IV phosphorus
·Decreased intake of calcium rich foods

Front 90

About Hyperphosphatemia?

Back 90

·Usually tolerated fairly well
It is usually the calcium imbalance that causes the trouble

Front 91

Czs of hyperphosphatemia?

Back 91

·Renal insufficiency
·Increased intake of phosphorus
·Hypoparathyroidism

Front 92

When are probs w/ Mg usually seen?

Back 92

Problems with magnesium usually seen with potassium and calcium imbalances: usually seen with a K prob first and when not corrected by txment, will see if have Mg prob.

Front 93

Functions of Magnesium?

Back 93

–Activates many enzyme systems
–Has sedative effect on the CNS
–Facilitates transport of Na and K across the cell membrane

Front 94

Czs of hypomagnesium?

Back 94

–Impaired absorption (malnutrition/starvation)
–Too rapid excretion thru the kidneys
–Inadequate intake (must be ingested on a daily basis, body does not store)
–Citrate (blood products):
–Diuretic therapy
–Renal failure

Front 95

S/S of hypomagnesium?

Back 95

·Neuromuscular irritability-tingling, twitching, tetany
·Hallucination/agitation/personality changes
·Hypertension
·Positive chvostek’s sign/Trousseau’s sign
·Ventricular irritability-PVCs( premature ventricular contraction), VT, VF

Front 96

Txment for hypomagnesium?

Back 96

IM or IV magnesium sulfate
–Watch for symptoms of hypermagnesium: bc may have txed too much, may complain of a warm feeling, face may be flushed/hot
–IV rate not to exceed 150 mg/min
–Do not give in renal insufficiency (check creatinine)
–Watch for resp. depression or heart block: would indicate that are how in too high levels of Mg.
–Check deep tendon reflexes and RR: would be diminished if now too high
–Calcium gluconate is antagonist

Front 97

Czs of hypermagnesium?

Back 97

–Renal failure
–Excessive use of magnesium containing antacids
–Ingestion of cathartics (Epsom’ salts, MOM)
–Hyperalimentation

Front 98

6 S/S of hypermagnesium?

Back 98

·Diminished reflexes
·Resp depression
·Hypotension
·Flush, feeling of warmth, sweating
·Bradycardia
·Drowsiness

Front 99

Txment for Hypermagnesium?

Back 99

·Calcium gluconate
·Stop administering any magnesium
·Hydration
·dialysis

Front 100

S/S of hypomagnesium?

Back 100

·Neuromuscular irritability-tingling, twitching, tetany
·Hallucination/agitation/personality changes
·Hypertension
·Positive chvostek’s sign/Trousseau’s sign
·Ventricular irritability-PVCs( premature ventricular contraction), VT, VF

Front 101

The Calcium Train and its mystery passenger...

Back 101

·If you know the signs of hypocalcemia, hypercalcemia is the opposite
·Ca and Mg go together (the mystery passenger)
·Ca and Phosphorus go in opposite directions: low phosphorous = high Ca, and vice versa

Front 102

Cellular mitosis r/t pathophysiology of cancer?

Back 102

all cellular activities including reproduction follow an orderly series of events under the control of DNA.

Front 103

Normal cell division r/t pathophysiology of cancer?

Back 103

Normal cells divide only to meet the needs of the body and only in enough numbers to replace dying cells. Cancer cells are dividing and reproducing out of control. Chemotherapy targets rapidly dividing cells.

Front 104

Hypertrophy r/t pathophysiology of cancer?

Back 104

tissue that increases in size by increasing the size of each cell-ie, heart

Front 105

Hyperplasia r/t pathophysiology of cancer?

Back 105

tissue that increases in size by increasing the number of cells-ie skin flap

Front 106

Neoplasia r/t pathophysiology of cancer?

Back 106

cell growth that continues over and above what is needed for replacement

Front 107

What is cell cycle time?

Back 107

the time from mitosis of a cell to its mitosis into a daughter cell.

Front 108

Human cell cycle time varies from ___ to ____ days.

Back 108

1 to 5 days.

Front 109

3 normal types of cells that have a quick cell time?

Back 109

Bone marrow tissue, hair follicles and epithelial lining of the GI have a very quick cell cycle time. So chemotherapy affects these cells as well.

Front 110

What type of cell division do cancer cells have?

Back 110

Have rapid or continuous cell division

Front 111

Cancer cells do not respond to signals for?

Back 111

apoptosis (cells that die when they are supposed to)

Front 112

Cancer cells show ___ morphology

Back 112

Show aplastic morphology-no longer look like the parent cell

Front 113

What type of nuclei do cancer cells have?

Back 113

Have a large nuclei-cytoplasmic ratio

Front 114

What happens to cancer cells function?

Back 114

Lose some or all of their specialized function

Front 115

How do cancer cells adhere together?

Back 115

Adhere loosely together

Front 116

Migratory ability of cancer cells?

Back 116

Are able to migrate

Front 117

How do cancer cells grow?

Back 117

Grow by invasion: of tissue around where they are started

Front 118

Cancer cells are not ___ inhibited.

Back 118

contact inhibited. Means they continue to divide even when touched on all surface areas by other cells.

Front 119

Chromosomes r/t cancer cells?

Back 119

Are aneuploid-gain or lose chromosomes: may have more or less than the normal 23

Front 120

What do cancer cells require a lot of ?

Back 120

Requires a large amt of energy.so pt look emaciated (cachexic) may need supplemental milkshakes, may not want to be around certain smells

Front 121

How do cancer cells metastasize by extension into surrounding tissues?

Back 121

tumors secrete enzymes that open up areas of surrounding tissues. Pressure as the tumor incr in size forces tumor cells to invade new territory.

Front 122

Ways that cancer spreads/metastasizes?

Back 122

Extension into surrounding tissues
Blood vessel penetration
Release of tumor cells
Invasion by
–A. Local seeding
–B. Blood borne metastasis
–C. Lymphatic spread

Front 123

How does cancer spread by bld vessel penetration?

Back 123

enzymes make large pores in client's bld vessels allowing tumors to enter bld.

Front 124

How does cancer spread by release of tumor cells?

Back 124

bc tumor cells are loosely held together, clumps of cells break off of primary tumor into bld vessels for transport.

Front 125

How do cancer cells spread by invasion via local seeding?

Back 125

Local seeding is the shedding of cancer cells in local area of primarY tumor. ex: ovarian cancer cells spill into peritoneal cavity.

Front 126

How do cancer cells spread by invasion via bloodborne metastasis?

Back 126

Most common. Tumor cell release into bld. clumps of cancer cells become trapped in capillaries, damaging capillary wall & allow cancer cells to enter surrounding tissue.

Front 127

How do cancer cells spread by invasion via lypmphatic spread?

Back 127

more lymph nodes involved, poorer pts prognosis bc spreads faster when in lymph nodes. r/t #, structure, & loc of lymph nodes & vessels.

Front 128

What should you know about the degree of malignancy (grading) r/t cancer?

Back 128

The lower the number, the better the prognosis.

Front 129

What should you know about extent (staging) r/t cancer?

Back 129

The lower the number, the better the prognosis.

Front 130

Explain TNM classification.

Back 130

T-anatomic size of the primary tumor
N-the extent of lymph node involvement
M-the presence or absence of metastasis

Front 131

Why do we use TNM classification?

Back 131

Improves communication to all members of the health care team
Assists in developing treatment protocol
Used to evaluate the treatment plan
Helps to determine prognosis
Used for research and statistical purposes

Front 132

7 factors that contribute to the development of cancer?

Back 132

-Age
-Genetic heritage
-Immunologic factors
-Drugs & chemicals
-Radiation
-Viruses

Front 133

How can age attribute to the development of cancer?

Back 133

bc immune system is weaker & have been exposed to cancer agents longer

Front 134

How can genetic heritage contribute to the development of cancer?

Back 134

some cancers have certain genetic linkage

Front 135

How can immunologic factors contribute to the development of cancer?

Back 135

decr immune systems more likely to develop certain cancers

Front 136

Cancer prevention?

Back 136

Avoid known carcinogens: smoking,
Modify risky behaviors: eat diets low in fat, smoking, drinking, chewing tobacco, broccoli helps decr risk of colon cancer.
Remove at risk tissue: ex: polyps during colonoscopy
Chemoprevention: put on after 1st dose of radiation to prevent further cancer
Screen: prostate exam, mammograms
Gene therapy

Front 137

How dx cancer?

Back 137

History: should give us a baseline, what s/s this person should have
Physical exam
Radiologic studies
Endoscopy: gives us a biopsy, this will tell definitively what cancer person has
Diagnostic tests

Front 138

What diagnostic tests can be done r/t cancer?

Back 138

–Cytology studies: pap smear
–CBC
PSA prostate specific antigen, CEA (for colon cancer) carcinogenic-embryonic antigen: These are tumor markers, which tell how well txment is working.

Front 139

7 warning signs of cancer?

Back 139

Change in Bowel/bladder habits: bld in stool or urine needs to be investigated, if stool become pencil or ribbon-thin (bc of tumor in colon)
A sore that does not heal
Unusual bleeding or discharge
Thickening or lump in the breast or elsewhere
Indigestion or difficulty swallowing
Obvious change in a wart or mole
Nagging cough or hoarseness

Front 140

Which groups of patients are at greatest risk for developing cancer based on poor health practices? Check all that apply.
A. Patients that smoke
B. Patients that have multiple sexual partners
C. Patients with a college education
D. Patients that are only children
E. Patients that consume large amounts of alcohol

Back 140

A. Patients that smoke
B. Patients that have multiple sexual partners
E. Patients that consume large amounts of alcohol

Front 141

What is radiation therapy?

Back 141

the movement of energy through a space or medium. Therapy is based on the concept that rapidly reproducing malignant cells are more sensitive to radiation than normal cells

Front 142

Goals for cancer txment?

Back 142

-Prophylaxis
-Diagnosis
-Cure
-Control
-Palliative-relief of symptoms
-Determination of therapy effectiveness
-reconstruction

Front 143

How long must a pt be cancer free to be termed 'cured'?

Back 143

if person is cancer free for 5 yrs, say they are cured of it. Exceptions: testicular cancer if cancer free for 2 yrs are cured, & certain types of breast cancer aren’t cured unless cancer free for 15- 20 yrs

Front 144

What 3 things should HC workers remember when caring for pt receiving radiation esp when radiation is inserted into body cavity?

Back 144

-Time-limit the amount of time in close proximity to the patient: about 30 min every 8 hrs
-Distance-increase the distance from the radiation source
-Shield-use lead barriers

Front 145

Factors that influence side effects (from radiation)?

Back 145

-Body site irradiated:
-Dose of radiation given: bigger the dose, the more side effects
-Extent of body treated: bigger the site, the more side effects
-Method of radiation

Front 146

If pt is receiving radiation and has a mark on their skin, what should you do?

Back 146

Don't erase the mark! It tells doc where to focus radiation.

Front 147

What is thrombocytopenia?

Back 147

Low platelet count

Front 148

What is the primary goal for pts that have pain r/t their cancer?

Back 148

Comfort

Front 149

Why do pts receiving chemotherapy also lose their hair & have stomatitis?

Back 149

Bc hair follicles & GI cells are also rapidly dividing cells.

Front 150

What are the 3 principles that guide protecting the hc workers 4m radiation exposure?

Back 150

-Time
-Distance
-Shield

Front 151

What are 3 reasons why a pt receiving chemotherapy gets constipated?

Back 151

-Narcotics
-Lack of food/fluid
-Decr. activity level

Front 152

What system is affected by the administration of the chemotherapy agent, Adriamycin?

Back 152

Cardiovascular

Front 153

Which pt has a better prognosis - a cancer pt w/ T2N2M1 or a pt w/ a T5N4M8?

Back 153

T2N2M1

Front 154

What is neutropenia?

Back 154

Low WBC count

Front 155

If a pt has a platelet cnt of 33,000, what nursing considerations should be taken?

Back 155

bleeding precautions

Front 156

What are the 2 types of immune response?

Back 156

• Non-specific or Innate aka natural
• Specific or Adaptive Immune Response

Front 157

When is natural immunity present?

Back 157

-Present at birth
- Immediate but short term response
-Have 4m birth to death

Front 158

Natural immunity is ___ to the invader...

Back 158

Natural immunity is non-specific to the invader, no memory.
-Always acts the same, regardless of the organism

Front 159

Components of natural immunity?

Back 159

-skin & mucous membranes
-WBC (neutrophils,bands,eosinophils,
basophils,monocytes,complement,
interferons

Front 160

What makes complement?

Back 160

the immune system

Front 161

What makes interferons?

Back 161

cells make when exposed to viruses

Front 162

What does natural immunity start that helps rid the body of harmful organisms & aid healing?

Back 162

Natural immunity starts tissue actions
that helps rid the body of harmful organisms & aid healing

Front 163

When does specific/adaptive immune mount a response?

Back 163

mounts a response when the innate immune response fails/when not sufficient.

Front 164

What does the specific/adaptive immune response do when encountering antigens?

Back 164

Recognizes & takes action against specific foreign antigens

Front 165

What does the specific/adaptive immune response fight?

Back 165

Fights viruses, fungus, foreign tissue such as transplanted organs, cancers

Front 166

Why does the specific/adaptive immune response have memory?

Back 166

so that subsequent responses are more rapid and intense.

Front 167

2 types of immunity w/in specific/adaptive immune response?

Back 167

-Cell mediated immunity
-Antibody mediated immunity

Front 168

Subjective data that you want to assess regarding immune system?

Back 168

-family history
-infection history
-allergy history
-social, sexual history
-Pets

Front 169

What type of WBC's have the most important role in cell mediated immunity?

Back 169

T lymphocytes

Front 170

Where do T lymphocytes come from?

Back 170

from the bone marrow & mature in the thymus.

Front 171

What do T lymphocytes respond to?

Back 171

respond to specific antigens & make T lymphocytes specifically to fight a certain antigen

Front 172

What to T4 lymphocytes do?

Back 172

T4 lymphocytes (CD4 cells) regulate T cell function & turn on the B-lymphocytes.

Front 173

How many T4 cells do you have compared to T8 cells?

Back 173

Normally have twice as many T4 cells as T8 cells. In HIV is the opposite.

Front 174

What do T8 cells (suppressor cells) do?

Back 174

modify the immune response. If many T8 cells = bad bc suppressing immune system.

Front 175

What do memory T cells do?

Back 175

allow the system to remember the antigen.

Front 176

What is the type of WBC that has the most helpful role w/ antibody mediated immunity?

Back 176

B lymphocytes

Front 177

Where are B lympocytes from?

Back 177

from marrow & lymphoid tissue

Front 178

B lymphocytes become ___ cells...

Back 178

become plasma cells which produce antibodies.
immunoglobulins = antibodies
gamma globulin = old antibodies

Front 179

When does IGM appear regarding infection?

Back 179

IGM appears 2-8 days post inf, will disappear, Will check this to see if pt has had a recent inf, within a couple wks

Front 180

When does IGG appear regarding infection?

Back 180

appears 1 week after IGM & remains for years. (lifetime)

Front 181

When does IGE appear?

Back 181

prod instead of IGM & IGG in allergies. Will be produced if have hay fever allergies, asthma, etc.

Front 182

What does IGA do?

Back 182

protect MM surface 4m invasion, only in breast milk. Infants breast-fed have fewer food allergies & GI probs.

Front 183

What are IGM,IGG,IGE, & IGA?

Back 183

B lymphocytes which become plasma cells which produce antibodies. Antibodies bind to foreign antigen & inactivate it.

Front 184

What do B memory cells do?

Back 184

allow the system to remember the antigen.

Front 185

How can we test for immunity?

Back 185

by looking for an antibody titer to a specific antigen.

Front 186

What is antibody mediated immunity responsible for?

Back 186

responsible for immunity 4m dz either through exposure to the dz or immunization.

Front 187

Why are you immunocompromised as one ages?

Back 187

-skin thins
-thymus shrinks in size
-lymphocytes "forget" as they age
-incr in autoimmune disorders

Front 188

Why is there an incr in autoimmune disorders as you age?

Back 188

-tissues deteriorate & may be viewed as non-self
-oxygen free radicals steal ions 4m the cells so they look different to the immune system: antioxidants help!

Front 189

Etiology of some immune system dzs?
(which occur sporadically)

Back 189

-women affected more than men
-acquire a virus, which specifically attacks the immune system
-family history
-sometimes bacteria looks like our tissue & the body attacks itself
*strep looks like heart valve tissue
*coxsackle virus looks like islet cells of the pancreas

Front 190

Immune status at birth?

Back 190

•Immunocompromised at birth, worse if infant is premature
-Get IGG antibodies thru the placenta (IGG can go thru placenta, IGM cannot)
-Get IGA if breastfed
-Acquire adaptive immunity as child is exposed to antigens

Front 191

Maintaining a healthy immune system?

Back 191

-sleep,nutrition,laughter,stress mgmt
-Massage, certain herbs stimulate the immune system
-breastfeeding,delay solid foods
-early exposure to some antigens may decr risk of developing allergy (cats/dogs)

Front 192

How can breastfeeding/delay of solid foods (4/6 months) help w/ immune system?

Back 192

the longer solid food/unknown proteins are delayed, the less chance of food allergies

Front 193

Objective data assessment for immune system function?

Back 193

-VS esp temp
-skin & MM
-Lymph nodes:body tries to sequester infs here, may be enlarged
-eyes,nose,facial features: red eye,runny nose, mouth breather
-respiratory system
-GI: food probs may cz diarrhea
-neurological:HIV can cz neurological manifestations early on

Front 194

7 diagnostic tests for immune system functioning?

Back 194

-CBC w/ differential
-CD4
-ESR
-C-reactive protein
-Complement
-Protein/immuneo electrophoresis
-Allergy testing (RAST, skin tests)

Front 195

What does a CBC w/ differential test for?

Back 195

-Neutrophils, called segs or granulocytes, mature WBC, 60-70%
-Bands incr w/ bacterial inf (1-5%), Left shift
-Monocytes, become macrophages (turn on B & T cells) in tissue
-Basophils, release substances that cz infl
-Eosinophils
-Lymphocytes

Front 196

Basophils incr when?
(CBC w/ differential)

Back 196

elevated when there is an allergic process

Front 197

Eosinophils incr when?
(CBC w/ differential)

Back 197

incr w/ parasitic inf, ppl w/ allergies

Front 198

Lymphocytes incr when?
(CBC w/ differential)

Back 198

incr w/ viral inf (38%), Right shift

Front 199

About CD4,CD8 diagnostic test?

Back 199

normal bw 500-1,000
-normally twice as many CD4 than CD8

Front 200

About ESR diagnostic test?

Back 200

Erythrocyte Sedimentation Rate
-anytime there is an infl rxn going on in body, ESR will be elevated.

Front 201

About C-reactive protein diagnostic test?

Back 201

will be elevated w/ infl response

Front 202

About complement diagnostic test?

Back 202

allows immune system to communicate w/ itself, when it falls, indication of exacerbation of chronic probs.

Front 203

Dx of Type I hypersensitivity rxns?

Back 203

-clinical S/S
-Pt history
-skin testing
-RAST

Front 204

Prevention of Type I hypersensitivity rxns?

Back 204

•Education
-Breastfeeding,medic alert bracesting kits,avoid exposure,clothing
•Exercise caution when at risk drugs are being given
- meds available,keep under supervision
•Check allergies,be aware of cross sensitivities
•Desensitization
•Avoidance of known triggers

Front 205

Type V hypersensitivity reaction - stimulatory?

Back 205

•Inappropriate stimulation of a cell by an autoantibody
•Grave's dz, hyperthyroidism

Front 206

Hgb values?

Back 206

Think developmental age -
Female: 12
Male: 14

Front 207

Ways to minimize skin damage to site where radiation is directed?

Back 207

-Avoid sun exposure, trauma to the skin, adhesive tape
-Use caution with soaps: must be gentle/mild
-No bath salts, perfumes, ointments or lotions
-No heat lamps, heating pads, ice packs
-Wear soft, cotton lightweight clothing
-May have medicated ointment prescribed

Front 208

Other Side Effects of radiation?

Back 208

-Hair loss
-Altered taste sensation
-fatigue

Front 209

What is Internal Radiation-Brachytherapy?

Back 209

the use of high energy radioactive sources placed into or directly on the body to treat a disease. Most commonly in oral cavity or vagina for cervical cancer.

Front 210

General Precautions to Internal Radiation?

Back 210

-Private room
-Radioactive sign on the door
-Wear film badge: tells you how much radiation you’ve been exposed to
-Encourage self care
-Rotate care givers
-Limit visitors
-Precautions if implant is dislodged

Front 211

Which of the following nursing interventions would you implement in the client with a cervical radiation implant in place? Check all that apply.
A. Use of a lead apron for shielding when providing client care
B. Limit visitors to 30 minute per day
C. Implement strict isolation protocol
D. Insert a foley catheter

Back 211

A. Use of a lead apron for shielding when providing client care
B. Limit visitors to 30 minute per day
D. Insert a foley catheter

Front 212

Chemotherapy agents affect?

Back 212

rapidly dividing cells (malignant cells)

Front 213

Routes of chemotherapy administration?

Back 213

-Oral
-IM
-IV
-Intracavity
-Intraperitoneal
-Intrathecal: via the spine
-Intrapleural: via the pleural space
-Intravesical: into the bladder
-Topical
-Intraarterial

Front 214

When is a vascular access device used?

Back 214

-Used if peripheral access is not available-PICC lines may be used
-Used for long term therapy
-Used when the vascular system needs to be accessed often
-Patient’s preference

Front 215

What is a tunnel catheter?

Back 215

-type of vascular access device
-pt has port under skin where needle goes, med goes into superior vena cava & into heart

Front 216

Advantages of tunnel catheter?

Back 216

1 advantage is cannot see under skin, can get wet, swim, etc. Advantage 2: if organism gets into a good immune system can get rid of it while org still in tube

Front 217

What is a Groshanq or Hickman catheter?

Back 217

-type of vascular access device
-tube hangs out of chest

Front 218

Disadvantages of Groshanq or HIckman catheter?

Back 218

Disadvantages: can’t get wet, if organism gets in will go straight to bldstream. decided by pt’s preference on whether they want to be stuck every time have chemo

Front 219

Safety Precautions for the Nurse/patient regarding chemo?

Back 219

-Follow OSHA guidelines
-Obtain special training
-Educate the patient

Front 220

Nursing actions for IV infiltration?
(chemo)

Back 220

-Follow hospital policy
-Stop infusion
-Apply ice/apply heat
-Administer antidote
-Prevent by checking IV patency first

Front 221

Which of the following interventions represents the best nursing actions should an extravasations of a vesicant (something irritating to skin) occur? (infiltration of a chemotherapy agent)
A. The infusion of the drug should be stopped and a new site chosen for administration
B. The site should be treated with appropriate antidote and observed for 3 to 4 weeks.
C. A plastic surgeon should be consulted immediately
D. Emergency medical care, including corticosteroids and epinephrine, should be administered immediately

Back 221

A. The infusion of the drug should be stopped and a new site chosen for administration

Front 222

4 side effects of chemo?

Back 222

-bone marrow depression
-neutropenia
-anemia
-thrombocytopenia

Front 223

What is bone marrow depression?

Back 223

a decrease in the number of circulating blood cells (both RBC and WBC and platelets)

Front 224

What is neutropenia?

Back 224

decrease in number of WBC. Patient will need neutropenic precautions (reverse isolation

Front 225

What is anemia?

Back 225

decrease in number of RBCs

Front 226

What is thrombocytopenia?

Back 226

decrease in number of platelets

Front 227

Chemotherapy has a cumulative effect so?

Back 227

it will take a little while before pt starts to feel bad.

Front 228

Nursing care of the immunosuppressed patient (low WBC)?

Back 228

-Good handwashing: so that we don’t take germs into room
-Prevent exposure to people with known infections
-Meticulous aseptic technique
-Careful observation for infection: bc WBC count is so low, may not respond to inf like a normal person would
-Possibly reverse isolation
-Neutropenic precautions-no flowers, fresh fruits, fresh vegetables (could bring in organisms) etc.

Front 229

You are the charge nurse in an oncology unit. A client with a low white blood cell count is placed in protective isolation. Which staff member should you assign to provide care for this client, under the supervision of an experienced oncology RN?
A. An LPN who has floated from the same day surgery unit
B. An RN from the float pool who usually works on the surgical unit
C. An LPN with 2 years of experience on the oncology unit
D. An RN who transferred recently from the ED

Back 229

C. An LPN with 2 years of experience on the oncology unit

Front 230

Nursing Care for a patient with Anemia (low RBCs)?

Back 230

-Observe for S and S of anemia-fatigue, hypoxia, hypotension, tachycardia, anxiety
-Plan rest periods
-Assist patient with activities
-Administer oxygen: RBC count low, won’t be getting enough O2
-Administer blood transfusions
-Promote good hygiene

Front 231

A 40 year old client is referred to a hematologist with a tentative diagnosis of acute myelogenous leukemia (AML). The client’s only complaint is fatigue. Which of the following diagnostic tests would the nurse expect to be ordered first?
A. Liver function studies
B. Uric acid
C. Lumbar puncture
D. Bone marrow biospy : would tell if pt has enough RBC’s

Back 231

D. Bone marrow biospy : would tell if pt has enough RBC’s

Front 232

What is the nurses biggest concern when caring for a pt w/ thrombocytopenia?

Back 232

need to be concerned about pt having bleeding issues

Front 233

Nursing care of a patient with thrombocytopenia (low platelets)?

Back 233

-Observe for S and S of bleeding-petechiae, bruising, bleeding gums, hematuria
-Observe for bleeding into the brain-headache, change in LOC, restlessness
-Administer platelet transfusion
-Encourage use of soft toothbrush, avoid razors, stool softeners, no aspirin: bc blood thinner

Front 234

A 67 year old client who is receiving chemotherapy for lung cancer is admitted to the hospital with thrombocytopenia. While you are taking the admission history, the client makes these statements. Which statement is of most concern?
“I’ve noticed that I bruise more easily since the chemotherapy started.”
“My bowel movements are soft and dark brown in color.”
“I take one aspirin every morning because of my history of angina.”
“My appetite has decreased since the chemotherapy started.”

Back 234

“I take one aspirin every morning because of my history of angina.”

Front 235

A client who is receiving chemotherapy for breast cancer develops bone marrow suppression. Which of the following instructions should a nurse include in the client’s discharge teaching plan?
A. Avoid people who have recently received vaccines
B. Avoid activities that may cause bleeding
C. Wash hands frequently
D. Increase intake of fresh fruits and vegetables
E. Avoid crowded places such as the shopping mall
F. Treat a sore throat with over the counter products

Back 235

B. Avoid activities that may cause bleeding
C. Wash hands frequently
E. Avoid crowded places such as the shopping mall

Front 236

Adverse effects of Chemo-stomatitis/mucositis?

Back 236

Frequent assessments of the oral cavity
Treatment
–Mouth care with mild baking soda, Magic mouthwash (Avoid commerical mouthwash)
–Nystatin swish and swallow (or swish and spit)
–Viscous lidocaine
–Soft toothbrush, no floss
–Lubricant to the lips
–Avoid hot spicy food
–Good fluid intake

Front 237

Adverse effects of chemo-pharyngitis?

Back 237

Same as for stomatitis

Front 238

Adverse Effects of Chemo-Anorexia?

Back 238

Anorexia may be due to:
–Effect of chemo on hunger center in the thalmus
–Nausea and vomiting
–Stomatitis
Patient may need enteral feedings or TPN
Offer small, frequent, high caloric feedings
Minimize food odors
Ask the patient what he likes

Front 239

Adverse effects of Chemo-nausea and vomiting?

Back 239

-Occurs due to the effect of the chemo on the emesis center in the thalamus. The drugs are emetogenic (vomiting inducing)
Offer small, frequent feedings
Dietary counseling
Cold bland foods
Antiemetic meds-give liberally. Work best when given 30-60 minutes before eating

Front 240

Adverse effects of Chemo-alopecia?

Back 240

-not all chemo agents affect hair follicle, so not everyone will lose their hair.
-A visible sign of the disease
-Hair may fall out in clumps or break off at the scalp
-Have wig made and ready before hair falls out
-Avoid frequent shampooing, hair brushing
-Should not color or dye hair or get permanents at this time
-Is temporary-new hair starts to grow back in one month after chemo stopped

Front 241

Which of the following nursing actions can be taken for a patient who has developed stomatitis secondary to chemotherapy? Check all that apply.
A. Use Listerine Q day
B. Use a soft toothbrush
C. Offer cold/bland foods
D. Obtain an order for nystatin swish and swallow

Back 241

B. Use a soft toothbrush
C. Offer cold/bland foods
D. Obtain an order for nystatin swish and swallow

Front 242

Name 2 chemo agents that are nephrotoxic?

Back 242

-Cytoxan
-methrotrexate

Front 243

What should you do for nephrotoxic chemo agents?

Back 243

-Monitor BUN and creatinine
-Encourage increased oral intake-maintains hydration
-Observe for signs of hemorrhagic cystitis-dysuria, hematuria

Front 244

What chemo agent is toxic to the pulmonary system?

Back 244

Bleomycin

Front 245

What should you monitor when pt is on chemo agent toxic to pulmonary system?

Back 245

-These agents have a cumulative effect on the pulmonary system.
-Observe for pneumonia, CHF, SOB, coughing: for 6 months after chemo done

Front 246

What chemo agent is toxic to cardiovascular system?

Back 246

Adriamycin (solution is red)

Front 247

What should you monitor when pt is receiving chemo agent toxic to cardiovascular system?

Back 247

-have a cumulative effect on the cardiovascular system
-Observe for signs of CHF: for 6 mo after last txment
-Obtain a baseline EKG

Front 248

What chemo agent is toxic to reproductive system? (teratogenic)

Back 248

-methotrexate

Front 249

What can pt on chemo agent that is toxic to reproductive agent can do?

Back 249

-Sperm banking: before txment to prevent birth defects.
-Birth control

Front 250

Chemo agent toxicity for hepatic system?

Back 250

-Problem with chemo agents that are metabolized by the liver
-Monitor liver function test

Front 251

3 step analgesic ladder?

Back 251

–Non-narcotic
–Weak narcotic
–Strong narcotic

Front 252

Nursing care-comfort r/t pain in cancer pt?

Back 252

-Must control the patient’s pain
-Three step analgesic ladder
-Concerns about addiction
-Administer meds around the clock: so pt doesn’t have to worry about peaks and valleys of pain meds
-Adjuvant therapy

Front 253

Why is nutrition a major challenge for cancer pts?

Back 253

–Growing cancer needs energy
–Chemo/radiation causing n/v, stomatitis
–Patient is losing weight-upsets families

Front 254

Nursing care - nutrition r/t cancer pt?

Back 254

-Give foods with high caloric value
-Give nutritional supplements
-Give small, frequent feedings
-Obtain a dietary consult
-Determine patient’s likes and dislikes
-Consider tube feeding/TPN

Front 255

Why is constipation a prob for cancer pts?

Back 255

Constipation is a problem due to:
-narcotics: bc slows down peristalsis
-decreased fluid intake
-lack of activity

Front 256

Nursing Interventions r/t elimination in the cancer pt?

Back 256

-increase roughage in diet
-adequate fluid intake
-laxatives, stool softeners
-enemas
-prevention

Front 257

What is superior vena cava syndrome?
(SVCS)

Back 257

-oncological emergency
-–A disorder of venous congestion caused by obstruction of venous drainage in the upper thorax either by a primary tumor or a secondary tumor

Front 258

S/S of superior vena cava syndrome (SVCS)?

Back 258

-slow and progressive
-SOB, headache, visual disturbances,facial edema

Front 259

What is spinal cord compression?

Back 259

-oncological emergency
-tumor presses on spine
–A disorder caused by direct pressure on the spinal cord with compromised vascular supply to the area leading to spinal cord infarct or veretebral collapse.

Front 260

S/S of spinal cord compression?

Back 260

depend on the site of compression
Early will be localized back pain and weakness in lower ext

Front 261

What is Pericardial effusion/cardiac tamponade?

Back 261

An increased accumulation of fluid in the cardiac sac due to the tumor invasion or pericardial thickening after radiation

Front 262

Hypercalcemia r/t the cancer pt?

Back 262

-the most common oncological emergency
Occurs in 10-20% of all cancer patients
Signs and symptoms-may manifest as pathological fracture

Front 263

What is tumor lysis syndrome?

Back 263

The destruction of large numbers of tumor cells is happening quicker than the elimination of them. This results in electrolyte imbalances. Bc cell breaks apart and K+ comes out of cell.
Can be prevented with good hydration
Treat-the electrolyte imbalance
A sign that the chemo is working

Front 264

Psychological needs of the pt/family?

Back 264

-Do not forget this.
-Talk to patient and family
-Try to follow their wishes
-Keep them informed
-Get outside help, i.e.hospice

Front 265

3 other oncologic emergencies?

Back 265

-SIADH
-DIC
-Septic Shock

Front 266

What are hypersensitivity rxns?

Back 266

-the immune system gone bad
-excessive rxns, inappropriate sites, inappropriate organ involvement

Front 267

Type I hypersensitivity rxn?

Back 267

Immediate or Anaphylactic (IGE mediated)

Front 268

Type II hypersensitivity rxn?

Back 268

antibody mediated - antigen - antibody rxn which destroys cells (cytotoxic)

Front 269

Type III hypersensitivity rxn?

Back 269

antigen-antibody rxn which czs infl (immune complex)

Front 270

Type IV hypersensitivity rxn?

Back 270

T lymphocytes destroy antigens

Front 271

Type V hypersensitivity rxns?

Back 271

stimulatory, autoantibodies that mimic the hormone itself

Front 272

Txment of Type I hypersensitivity rxns?

Back 272

-airway, BP
- tx severe rxns w/ epinephrine soln 1/1000 (given IV or IM if no venous access)
-opposes the action of histamine
-Anti-histamines, sedating (benadryl), non-sedating (claritin, etc)
·Corticosteroids, topical, inhaled, PO, IM,IV (prednisone etc)
·Bronchodilators, aminophylline, albuterol
·Mast cell inhibitors, cromolyn
·Leukotriene receptor antagonists, montelukast (Singular)

Front 273

Etiology of Type II Hypersensitivity Reaction?

Back 273

Binding of IGG or IGM antibody to an antigen on the surface of a cell resulting in cell death

Front 274

Ex of Type II hypersensitivity rxn?

Back 274

- Blood transfusion reaction- antigens on the RBC or WBC are attacked by circulating antibodies present in the individual
- Can involve RBC (hemolytic) or WBC (febrile), plasma protein allergy (allergic), Graft versus host disease (bone marrow transplants), delayed (7-14 days post transfusion

Front 275

S/S of Type II hypersensitivity rxn?

Back 275

·Signs and symptoms (generally occur in first 30 minutes after starting transfusion)
chills, fever, back pain, renal damage can occur

Front 276

Txment of Type II hypersensitivity rxn?

Back 276

- Stop transfusion, blood-to-blood bank, maintain NS infusion, call MD, and collect first voided urine

Front 277

Txment for Type II hypersensitivity rxn depends on?

Back 277

- Treatment depends on severity of reaction and cause
* resp, BP support in severe cases
* tylenol, antihistamines
* can modify transfusion to decrease chance of reaction in some cases (wash blood cells)

Front 278

Etiology of Type III hypersensitivity rxns?

Back 278

Antigen/antibody reaction in which the complex produced by this reaction is not cleared by the body and is deposited in the tissues producing an inflammatory reaction and subsequent tissue destruction (basis for autoimmune dzs)

Front 279

Ex of Type III Hypersensitivity Reactions?

Back 279

Autoimmune diseases such as Lupus, Rheumatoid arthritis, type 1 diabetes,

Front 280

Txment of Type III Hypersensitivity Reactions?

Back 280

- Supportive care, healthy lifestyle
- Immunosupressive drugs such as prednisone
- Other medications more disease specific

Front 281

Etiology of autoimmune dzs?

Back 281

- genetic component, female gender (lupus, RA), viral exposure, age, environment
·Includes a vast array of diseases that may involve a single tissue (type 1 diabetes) or multiple tissues (lupus)

Front 282

Pathophysiology of autoimmune dzs?

Back 282

- For some reason the body does not recognize self and destroys healthy tissues
* Inflammatory process, cell death can occur
- Disease process depends on tissue involved
* Type 1 diabetes, thyroid disease, Lupus, RA, Pernicious anemia, ITP, MS, etc

Front 283

Txment of autoimmune dzs?

Back 283

- depends on disease

Front 284

Etiology of Type IV hypersensitivity rxns?

Back 284

Involves cell mediated immunity where specific T lymphocytes are produced and destroy the antigen

Front 285

Ex of Type IV hypersensitivity rxns?

Back 285

contact dermatitis (poison ivy), tissue transplant rejection

Front 286

Txment for autoimmune disorders?

Back 286

immunosuppressive drugs

Front 287

3 types of tissue transplantation?

Back 287

- autografts- tissue from self
- allografts- tissue from same species
- xenografts- tissue from different species

Front 288

Criteria for tissue transplantation selection?

Back 288

- end stage organ failure
- age
- functional ability
- ability to comply with post-transplant regimen

Front 289

Donor criteria for tissue transplantation?

Back 289

- up to age 72
- organ donated not diseased
- negative HIV status
- has been liberalized to increase available organs
- Nursing responsibility
* One new patient is added to the wait list in US every 20 minutes and 7 people die daily waiting for transplantation

Front 290

Nursing responsibility r/t tissue transplantation?

Back 290

- MD communicates to family the status of the patient
- Family needs time to assimilate information
- Show compassion and support to family
- Offer the family the opportunity to consider donation
- Timing of the request is critical to the acceptance by the family

Front 291

Immunology & Transplantation?

Back 291

- T and B lymphocytes play a role in transplant rejection
- 2 major systems involved in an individual’s antigenic makeup
* HLA-human leukocyte antigens (100 antigens have been identified)
* ABO blood typing system

Front 292

About tissue typing & matching?

Back 292

·Numbers and types of tests needed varies by the type of tissue transplanted and the time frame possible for testing
- Bone marrow requires the closest matching

Front 293

Tests for tissue typing & matching?

Back 293

- ABO compatibility
- HLA testing
- MLC, mixed leukocyte culture
- T cell cross match

Front 294

What is the drug Cyclosporine (Neoral, Sandimmune) used for?

Back 294

-immunosuppressive therapy
-psoriasis
-RA

Front 295

Is Cyclosporine (Neoral, Sandimmune) toxic?

Back 295

Nephrotoxic, many drug interactions

Front 296

What can Cyclosporine (Neoral, Sandimmune) cz?

Back 296

Can cause hypertension, hyperkalemia, hyperglycemia( significant enough to take diabetes meds)

Front 297

SE of cyclosporine?

Back 297

SE-gingival hyperplasia, photosensitivity, hirsutism

Front 298

Nursing responsibility r/t cyclosporine?

Back 298

- Monitor for tremors, paresthesias
- Can cause seizures with high dose prednisone
- Avoid giving with grapefruit juice

Front 299

What can corticosteroids be used for?

Back 299

immunosuppressive therapy
-Used for many disorders, many side effects (usually if taken longer than 2 wks

Front 300

How can corticosteroids be given?

Back 300

Topical, PO, IM, IV, NS, MDI

Front 301

Nursing responsibilities r/t corticosteroids?

Back 301

- Sodium retention- edema, BP, low Na diet, weigh periodically
- Hyperglycemia- blood sugars
- Hyperlipidemia- Diet
- GI bleeding- with meals, monitor GI symptoms, stool guiac
- Cataracts: should have periodic eye exams
- Osteoporosis- regular exercise, calcium supplementation
- Growth delay in children
- Hypokalemia
- Masks signs of infection, delay wound healing
- Behavioral changes: mood disturbances, esp. if on high doses
- Vascular and skin fragility: bruise easily, skin tears more easily
- HPA axis suppression (taken long term = >2 weeks) MUST taper off meds, if stopped abruptly pt can die 4m acute suppression of the adrenal gland.
* should always wear a medic alert bracelet, education regarding administration, what to do if can’t be taken HPA = hypothalamus pituitary adrenal

Front 302

Nursing implications - transplants?

Back 302

·Emotional/physical preparation pre-op
·Education regarding medications, signs and symptoms of rejection, avoiding/treating infections
·Monitor for signs and symptoms of rejection
·At risk for other cancers
·Other issues covered under specific disorders

Front 303

Hyperacute organ rejection?

Back 303

* Within 48 hours of transplantation
* caused by antibodies-mediated response
* seen primarily with kidney transplants
* usually not reversible

Front 304

Acute organ rejection?

Back 304

* 1 week to 3 months post transplant
* humoral and cellular immune system
* treated with steroids and monoclonal antibodies

Front 305

Chronic organ rejection?

Back 305

* after 3 months
* cellular and antibody mediated response
* major unresolved problem as it is less responsive to medications
* Major cause of death after the first year post transplant

Front 306

Graft vs host dz?

Back 306

* seen in allogeneic bone marrow transplants
* donor’s cells recognize the recipient’s cells as foreign and attack them
* symptoms are seen in the liver, skin, and GI tract

Front 307

Antibody screening tests?

Back 307

( IGG, IGM, ANA, RF, ELISA, Western Blot)
·PCR (viral loads) PCR = polymerase chain reaction (looks for pieces of virus in person’s bld)
·Coombs test (direct and indirect)
·Tissue, blood compatibility tests
·Skin tests for disease exposure
- TB
- anergy (someone who’s immune system is so compromised that their immune system is no longer capable of launching an immune response

Front 308

Classification of Disorders of the Immune System?

Back 308

·Immunodeficiencies
- Primary (congenital, rare)
- Secondary (acquired) HIV
·Gammopathies (cancers), multiple myeloma
·Hypersensitivity reactions
Autoimmune diseases
·Induced immune deficiency
- Treat disease, prevent rejection

Front 309

Type I hypersensitivity reaction: anaphylactic?

Back 309

rxn can be local or systemic

Front 310

Ex of Type I hypersensitivity reaction: anaphylactic?

Back 310

allergic rhinitis, asthma, food and drug allergies,systemic anaphylaxis, atopic dermatitis

Front 311

What is Type I diabetes?

Back 311

genetic predisposition
autoimmune destruction of the islet of Langerhan cells of the pancreas
possible Viral association
Islet cell antibodies present
not an acute event- 80% of cells gone before symptoms are seen
true insulin deficiency

Front 312

What is Type II diabetes?

Back 312

have disease an average of 7 yrs prior to diagnosis, probably longer
insulin excess but insulin resistant: receptors that let insulin in no longer work. Pancreas still produces insulin and fatter you are, more insulin body produces.

Front 313

Significance of diabetes?

Back 313

-Leading cause of blindness, renal failure, amputation
-4th leading cause of death, major cause of premature disability
-Cardiovascular disease is leading cause of death in diabetics

Front 314

S/S of Type II diabetes?

Back 314

often none for many years
infections: bc of high glucose, prime opportunity for bacteria to grow
poor wound healing:
hypertension
dyslipidemia: high triglycerides/cholesterol
obesity

Front 315

Dx of Type II diabetes?

Back 315

FBS >125 FBS = fasting blood sugar
RBS 200 or > with symptoms (resting blood sugar)
OGTT 75 gm CHO
FPG >125 or 2 hr > 200

Front 316

Etiology/risk factors for Type II diabetes?

Back 316

-Overweight (BMI 25 to 30) or obese (BMI>30
-age
-inactivity
-race
-family history of diabetes
-GDM, macrosomic infants (over 8 lbs, 14 oz)

Front 317

Being overweight & type II diabetes?

Back 317

normal person needs 30-40 units of insulin/day, overweight/obese may need 70 or more
Central obesity worst (WC >40 inches in men, 35 inches in women)

Front 318

Age & Type II diabetes?

Back 318

Age (half of all DM in people older than 55)
18.4% of the elderly population has diabetes

Front 319

Inactivity & Type II diabetes?

Back 319

Sedentary lifestyle’s effect on CV system is equal to smoking 20 cigarettes per day

Front 320

Race & Type II diabetes?

Back 320

AA, Hispanics, Asian Americans, Pacific islanders: have higher incidence of type 2 than caucasians

Front 321

Pathophysiology of Type II diabetes?

Back 321

- insulin resistance
loose sensitivity of insulin receptors on the cell surface so glucose cannot get in
- increase in insulin output by the pancreas
Eventually patient develops insulin deficiency
- increase in glucose output by the liver: commonly happens at night
- Accompanied by other metabolic disorders that are associated with insulin resistance
Central obesity, hyper-triglyceridemia, atherosclerosis, hypertension (very common in assoc w/ T2 diabetes), PCO (polycystic ovarian) disease in women

Front 322

Prevention of Type II diabetes?

Back 322

weight control
avoid foods with a high glycemic index
regular exercise (150 minutes/week)
high fiber diet
FPG every 3 yrs starting at age 45
Age 30 for high risk groups esp AA and Hispanic
Age 30 with risk factors
Intervention with impaired glucose tolerance
FPG >110 <126, 2hr >140 <200 (fasting plasma glucose)
Patient with IGT who walked 30 minutes/day decreased the development of diabetes by 58%
Macrovascular disease actually starts during this period of time

Front 323

Goals of therapy for type II diabetics?

Back 323

Pre-prandial blood glucose 70-130
nl<100
Post-prandial (2 hr) blood sugar <180 (nl <140)
Hemoglobin A1C <7% (in chronic hyperglycemia, levels go up) Used to monitor long-term control of blood sugar. Will tell you average bld glucose for last 2 months.
nl 4-6

Front 324

Txment of Type II diabetes r/t exercise?

Back 324

goal is 150-175 minutes a week
glucose available esp if on meds
cardiac evaluation prior to starting: bc many have underlying cardiovascular dz.
proper foot wear: always wear socks and inspect feet on daily basis
medic alert bracelet
stop smoking- CV disease
limited or no alcohol- calories, CV effect

Front 325

Txment of Type II diabetes r/t weight loss?

Back 325

250-500 calories less than needed/day
BMI 20-25 is goal
increase fiber 20-35 gm
even 10 lbs will improve control, make goals reasonable

Front 326

Txment of Type II diabetes r/t diet?

Back 326

Needs to see a dietician (especially newly diagnosed)
low Na if hypertensive
<30% calories from fat, unsaturated fats (get majority 4m plant sources)
Oily fish 2x week for omega three
20-30% calories from protein if normal renal function
40% calories complex carbohydrates, <130gms/day
Limit refined CHO, high glycemic index foods

Front 327

What does chromium picolinate do r/t Type II diabetes?

Back 327

decreases insulin and BS levels

Front 328

Oral Agents & Type II diabetes?

Back 328

started when lifestyle changes fail or when initial presentation warrants more aggressive management
Now have meds that work at different sites to improve glycemic control
2, 3,and even 4 meds may be used in combination

Front 329

What are the Sulfonylureas drugs for Type II diabetes?

Back 329

glipizide (Glucotrol and XL), glyburide (Diabeta, Micronase), micronized glyburide (Glynase Pres Tab), glimepiride (Amaryl)

Front 330

What do the Sulfonylureas drugs for Type II diabetes do?

Back 330

increase insulin secretion from pancreas
will cause weight gain
can cause hypoglycemia, cannot skip meals
avoid ETOH, decreases metabolism of drug
Sulfa allergy may preclude use

Front 331

What do meglitinide (Prandin), nateglinide (Starlix) do r/t Type II diabetes?

Back 331

increases insulin production by the pancreas
take before each meal
good for persons with erratic eating habits,
Elderly

Front 332

About acarbose (Precose), miglitol (Glyset) r/t Type II diabetes?

Back 332

interferes with absorption of CHO from duodenum, digested later in colon
problem is GI SE, flatus
SE decrease over time
not systemically absorbed
taken with first bite of each meal
cannot treat hypoglycemia with regular sugar
use lactose ex: milk

Front 333

About rosiglitazone (Avandia), pioglitazone(Actos) r/t Type II diabetes?

Back 333

increases insulin sensitivity at cell level by changing the cell membrane structure to increase insulin receptors
takes 2-4 weeks to see full effect: bc changes cell structure
can be hepatotoxic
monitor for S&S, LFT (liver function tests) monitored frequently bc can have liver probs
fertility may return
patient may gain weight
Some patients experience significant edema: report to doc if unusual pattern of weight gain.
Can precipitate or worsen heart failure due to fluid retention
Recent concern of association with increased risk of MI (Avandia)
rosiglitazone and glimepiride (Avandaryl)

Front 334

About metformin (Glucophage) r/t Type II diabetes?

Back 334

decreases glucose absorption by the gut
good for overweight, tend to lose weight
favorable effect on lipid profile, no hypoglycemia
side effects- flatus, diarrhea, decreases with time( if pt starts at lower dose then gradually increased, may help with side effects)
contraindicated with renal impairment
stop 48 hrs before any studies using dye, wait 48 to restart
can cause lactic acidosis (not in CHF, hypoxic states)
Contraindicated in liver disease, alcohol abuse

Front 335

New formations of metformin called?

Back 335

glyburide and glucophage (Glucovance)
Rosiglitazone and metformin (Avandamet)
glipizide and metformin (Metaglip)
Pioglitazone and metformin (Actoplus met)

Front 336

About Exenatide (Byetta) r/t Type II diabetes?

Back 336

New class of drugs, incretin mimetics
Can be used as monotherapy or with other oral agents
SC injection BID up to 60 minutes before the breakfast and evening meal
Comes in a pen, 5mcg or 10mcg per dose
New warning about pancreatitis (pts have died) if have abdominal pain tell doc

Front 337

Action of exenatide (Byetta)?

Back 337

Lowers postmeal and fasting glucose levels
Stimulates the pancreas to produce insulin
Slows food absorption
May cause weight loss
Can cause hypoglycemia

Front 338

About Sitagliptin (Januvia) r/t Type II diabetes?

Back 338

Inhibits the activity of enzymes that break down incretins which play a role in insulin synthesis and release from the pancreas
Adjunct to diet and exercise in type 2 diabetes
Can be monotherapy or with other oral agents
Given orally once daily

Front 339

About insulin (gen) r/t Type II diabetes

Back 339

indicated when BS cannot be controlled with oral agents (can combine oral agents) or during periods of stress such as infection
if an acute event may add SS only using short acting insulin
Combination of evening intermediate or long acting with daytime oral agent often used first: may give shot of Lantus at night, then oral agent during day.
split mix used commonly 70/30, 75/25, 50/50

Front 340

About Pramlintide (Symlin) r/t Type II diabetes?

Back 340

Injectible, SQ, before meals into abdomen or leg, rotate sites
Used with insulin or oral agents
Lowers blood sugar during the 3 hours after a meal
Slows absorption, decreases liver glucose, increases satiety
Risk is hypoglycemia
CANNOT be mixed with insulin
Stored like insulin
Vials 0.6mg/ml solution, given in micrograms
Also used for type 1 diabetics

Front 341

What is the BP goal in a Type II diabetic?

Back 341

-goal is BP <130/80 to preserve renal function
-want BP <125/75 if sign proteinuria already present

Front 342

The control of __ is more important than the control of BS in the prevention of renal deterioration?

Back 342

Control of BP more important than control of BS in preventing renal deterioration
ace inhibitors drugs of choice to preserve renal function (BB and diuretics neg effect on diabetes mgmt. Block sympathetic response, may stop person 4m knowing when BS is dangerously low.)

Front 343

What does a high glucose load do to the kidneys?

Back 343

stresses the kidneys

Front 344

What do ace inhibitors do the kidneys r/t Type II diabetes?

Back 344

Ace inhibitors (have protective effect on kidneys) lower the GFR (glomerular filtration rate) and normalize pressure within the nephrons
renal function, K must be monitored (& BUN, creatinine) (bc czs pt not to lose K)

Front 345

Ace inhibitor SE r/t Type II diabetes?

Back 345

SE is cough, edema (angioedema, can happen anywhere in body ex: lips, throat, etc, can stop respiration)

Front 346

Hyperlipidemia goal r/t Type II diabetes?

Back 346

goal is LDL <100, <70 with CAD (coronary artery dz)
HDL >40(men),>50(women)
TG <150

Front 347

Lifestyle changes r/t Type II diabetes & hyperlipidemia?

Back 347

most diabetics die of some type of cholesterol dz.
increase exercise
low fat diet
no smoking

Front 348

Meds for hyperlipidemia?

Back 348

HMG Co A reductase inhibitors (statins) statins are the gold standard for diabetics w/ hyperlipidemia
monitor for liver toxicity
myositis (type of muscle pain)
bile acid binding resins
gemfibrizil (TG) (good for lowering triglycerides)
niacin (may raise BS levels)
ASA (aspirin)daily if > 40 years of age or with risk factors unless have PUD.Tell not to take NSAIDS before contacting doc bc can negate good effects of aspirin

Front 349

Complications of hypoglycemia in Type II diabetes?

Back 349

<70 with or without symptoms, <80 with symptoms, <90 at bedtime or overnight: what most ppl consider hypoglycemia to be
too much insulin or not enough food

Front 350

S/S of hypoglycemia in Type II diabetic?

Back 350

increased sympathetic activity
decreased CNS glucose
pallor, diaphoresis, nervous, irritable, H/A, weak, shaky, diaphoresis

Front 351

Txment of hypoglycemia in Type II diabetic?

Back 351

check BS (nl LOC), if in doubt treat for hypogycemia
Check BS in 15 min, >80, snack if next meal >60 minutes
Give 15-20gms CHO
Glucagon (SC/IM, 1mg), IV D50 if severe (if pt losing consciousness)

Front 352

Prevention of hypoglycemia in Type II diabetic?

Back 352

eat at regular intervals
check BS
prepare for exercise
call if unable to eat (ex: sick and can’t keep food down after having taken insulin)
be aware that client may be taking drugs that may blunt the symptoms of hypoglycemia such as beta blockers

Front 353

How can hyperglycemia in Type II diabetic occur?

Back 353

Can occur when: not enough insulin, too much food, infection, stress, lack of exercise, drugs that increase blood sugar (steroids)

Front 354

S/S of hyperglycemia in Type II diabetic?

Back 354

weak, H/A, visual changes, weight loss, 3 classic symptoms: polyuria, polydipsia, polyphagia, N&V

Front 355

Txment of hyperglycemia in Type II diabetic?

Back 355

treat underlying cause
increase in antidiabetic medication (insulin, oral)
exercise
check urine for ketones (if BS >300)
always wrong answer if say check urine for sugar. Always check bld for sugar, urine for ketones.

Front 356

Mortality rate of HHNC?

Back 356

mortality 70% :bc usually doesn’t get dxed till late in elderly bc most elderly pts are sluggish, etc.
-complication of Type II diabetes

Front 357

Pathophysiology of HHNC?

Back 357

caused by deficiency of insulin but enough to prevent ketosis
persistent hyperglycemia causes osmotic diuresis with loss of water and electrolytes (always watch electrolytes w/ this syndrome)
dehydration and hypernatremia & hyperkalemia after Na normalizes (bc of severe dehydration) occur. pH usually normal
develops slowly and diagnosed late (elderly)

Front 358

What does HHNC stand for?

Back 358

hyperglycemic hyperosmolar nonketotic coma/syndrome

Front 359

Etiology of HHNC?

Back 359

acute illness such as infection
meds (diuretics, corticosteroids)

Front 360

S/S of HHNC?

Back 360

polyuria, polydipsia
hypotension, tachycardia
profound dehydration (actually have neurological disturbance so don’t feel thirsty which is why have profound dehydration)
neurological changes

Front 361

Txment of HHNC?

Back 361

treat underlying cause ex: pneumonia underlying inf, meds, etc.
fluids, electrolytes, insulin

Front 362

Nursing concerns w/ HHNC?

Back 362

fluid balance
safety: bc of neurological changes
electrolyte imbalance
fluid overload
education: to prevent 4m happening again

Front 363

What type of complications are CVD & PVD? (Type II diabetes)

Back 363

macrovascular

Front 364

About the macrovascular compl of CVD & PVD r/t Type II diabetes?

Back 364

related to faulty metabolism
already discussed with hypertension and dyslipidemia
all diabetics should take ASA daily unless on anticoagulants or PUD
will have EKG done yearly, stress test as needed
may present atypically with an MI due to neuropathy (may not have classic symptoms of chest pain. May have back, jaw pain)

Front 365

In what type of diabetes are microvascular compl seen earlier?

Back 365

seen earlier in Type 1 but also occur in type 2

Front 366

What are microvascular compl in diabetics r/t?

Back 366

related to poor glucose control
glycosylated hemoglobin deposited in cell membrane causing inflammation and permanent changes in tissue. This is what czs disturbance in nerves, tissue & eyes.

Front 367

Retinopathy & the diabetic?

Back 367

leading cause of blindness in US
prevent with good glucose control
see ophthalmologist every year

Front 368

Neuropathy & the diabetic?

Back 368

decreased nerve conduction
may have pain and/or lack of sensation (numbness/tingling)
must examine feet daily and wear well fitting shoes and keep nails well trimmed
prompt treatment of any interruption in skin integrity
meds may be given to improve circulation

Front 369

Pain mgmt for neuropathy?

Back 369

often use antiepileptic meds such as neurontin
can also effect bladder (don’t know bladder is full), stomach (gastraparesis where stomach doesn’t empty), colon (can get mega colon), and sexual functioning

Front 370

How does nephropathy occur in the diabetic?

Back 370

increase glucose increases GFR which damages the nephrons over time
associated hypertension is also implicated in diabetic nephropathy
goal for BP with significant proteinuria is <125/75

Front 371

How can you prevent nephropathy in the diabetic?

Back 371

leading reason for dialysis and transplant
prevent with good control of BS, BP, no excessive protein in the diet

Front 372

What should urine be checked for w/ the diabetic r/t nephropathy?

Back 372

urine checked yearly for microalbuminuria
placed on ace inhibitor or ARB as soon as protein appears (bc this is beginning of renal deterioration) even if normotensive to lower GFR
these drugs can elevate K and decrease renal function so both must be monitored

Front 373

Nursing concerns for Type II diabetes?

Back 373

infection
injury (vision impaired, neuropathy)
tissue perfusion

Front 374

Education for the Type II diabetic?

Back 374

SBGM (self bld glucose monitoring), ketone checks if BG 250 or greater
diet
exercise
meds, glucose control, BP, chol, ASA, etc
sick day management
skin, foot care
eye exams
Immunizations(flu yearly, pneumococcal vaccine x1)
Antioxidants: eat brightly colored fruit & veggies
chromium picolinate: eat fresh fish
medic alert bracelet

Front 375

Etiology of Type I diabetes?

Back 375

genetic predisposition
autoimmune response
environmental factors
viruses, toxins
not an acute event
80% of cells gone for Sx to appear

Front 376

Prevention of Type I diabetes?

Back 376

evidence available that breast feeding decreases the risk of development
on the increase

Front 377

Pathophysiology of Type I diabetes?

Back 377

no insulin production by the beta cells
hyperglycemia which leads to glycosuria: excessive glucose loss thru kidneys bc pt has huge vol of fluid loss
osmotic diuresis leads to dehydration and electrolyte loss
glucose cannot enter cells for nutrition due to lack of insulin
fat used as fuel source with the development of ketone bodies which are acids
protein catabolism also takes place

Front 378

S/S of Type I diabetes?

Back 378

polyuria, polydipsia, polyphagia
weight loss
poor wound healing
infections such as UTI, yeast
may present in DKA
abdominal pain common presentation in children

Front 379

Nursing concerns for Type I diabetes?

Back 379

much the same as in Type 2 except you must take into consideration the age of the patient, developmental level and the effect the disease may have on children and adolescents
not overweight so diet for weight loss is not needed
actually will gain weight back that was lost when insulin started

Front 380

What are the 3 ultra-fast acting insulins?

Back 380

Insulin lispro (Humalog), insulin aspart (Novolog), insulin glulisine (Apidra)

Front 381

About ultra-fast acting insulins?

Back 381

onset <15 min peaks 1 hr, lasts 3-4 hrs
take when you sit down to eat (0-15 minutes before eating) so cannot give to pt unless tray is on floor or right in front of them. For kids usually give after eat to see how much kids eat.

Front 382

About Insulin glargine (Lantus), insulin detemir (Levemir)?

Back 382

never have a time when level goes up & then comes down. Stays at a plateau.
No peak, lasts 24 hours
Clear
Do not mix with any other insulin
Usually given at bedtime: only bc this is when studies were done. Doesn’t matter what time of day given as long as it’s given same time every day.

Front 383

Peak/lasts Humulin U?

Back 383

Peaks 8-20hrs, lasts 24-48 hrs

Front 384

Peak/lasts Humulin L, Novulin L, Iletin II Lente?

Back 384

Peak 6-18hrs, last 18-26 hrs

Front 385

Names of the Humalog mix 75/25, 50/50?

Back 385

Insulin lispro protamine and insulin lispro

Front 386

Etiology of DKA in Type I diabetes?

Back 386

infection, stress, too much food, not enough insulin, meds
-mortality rate about 10%

Front 387

S/S of DKA in Type I diabetes?

Back 387

dry, flushed skin, fruity breath odor, change in LOC
nausea, vomiting

Front 388

Txment & Prevention of DKA in Type I diabetes?

Back 388

Treatment - fluids, insulin, electrolytes, treat underlying cause
Prevention - education

Front 389

What is the Somoygi effect?

Back 389

-complication of Type I diabetes
-gluconeogenesis and glycogenolysis occurs during sleep due to hypoglycemia

Front 390

What is gluconeogenesis?

Back 390

the formation of glucose 4m excess amino acids, fats, or other noncarb sources.

Front 391

What is glycogenolysis?

Back 391

conversion of glycogen into glucose in the liver & muscles

Front 392

Gen info about the Somogyi effect?

Back 392

am BS high (BS high when wake up)
need to check BS at 2-3 am to identify (ask pt about dreams bc many pts have nightmares when BS is high)
treated by moving supper NPH to bedtime or give HS snack

Front 393

A healthy 32 year old man presents with herpes zoster (shingles) infection and the health care provider suggests a test for HIV. The client asks the nurse why this is necessary?
a.It is state law that we offer testing to everyone
b.Herpes zoster increases the transmission of HIV
c.Herpes zoster is a common infection seen in HIV positive individuals
d.This type of infection is not common in people with normal immune system function (seen in old ppl or ppl w/ compromised immune system)

Back 393

d.This type of infection is not common in people with normal immune system function (seen in old ppl or ppl w/ compromised immune system)

Front 394

Some factors that incr the risk of perinatal HIV transmission?

Back 394

high viral load, recent seroconversion, long labor, prolonged rupture of membranes, prematurity, etc.

Front 395

Prevention of perinatal HIV transmission?

Back 395

- offer antiretroviral therapy (AZT) from 10-12 weeks gestation to term, IV in labor, infant for 6 weeks
*if patient on meds no need to stop, may need to modify regimen
- offer Cesarean section
8if viral load undetectable and on drug therapy this is probably not indicated
- no invasive procedures
- infant washed immediately, discourage breastfeeding

Front 396

About AZT or zidovudine (RETROVIR)?

Back 396

-NUCLEOSIDE REVERSE TRANSCRIPTASE INHIBITOR
-- still a potent HIV drug
- CBC done frequently due to anemia : know that it czs anemia
oMay need drug therapy such as Procrit to counteract this side effect
- nausea a problem

Front 397

What should you monitor for when pt on NUCLEOSIDE REVERSE TRANSCRIPTASE INHIBITORS?

Back 397

- monitor for diarrhea, neuropathy (pts get numbness, tingling), pancreatitis: would have abdominal pain, N/V
- amylase, lipase done frequently
- must be taken on an empty stomach

Front 398

What drug cannot be used w/ AZT & why?

Back 398

D4T bc of bone marrow toxicity

Front 399

About hypersensitivity syndrome in nucleoside reverse transcriptase inhibitors?

Back 399

- 2-6 weeks after starting
- fever and rash, myalgia (joint aches), or GI symptoms: if have symptoms call doc right away.
- discontinue immediately
- do not EVER take again
- should not D/C and restart medication

Front 400

About non-nucleoside reverse transcriptase inhibitors (NNRTI's)

Back 400

·Potent in combination with NRTI or PI
·Resistance to one is resistance to all
·some drug interactions (lowers some drug levels)
rash which can be severe but is not an allergic reaction

Front 401

SE of NNRTI's?

Back 401

•side effects are rash, nausea, neuropathy and
•50% of patients will have disturbing dysphoria or nightmares which resolve with continued dosing. Dosed at night to reduce side effect.
•Teratogenic: czs birth defects
•Steven-Johnson’s syndrome: tell them to call doc if have rash.

Front 402

About protease inhibotors (PI)?

Back 402

·expensive
·resistance develops from missing doses
·high pill burden (improving)
·lipodystrophy( abnormal fat deposits, ex: chipmunk cheeks, men get gynecomastia, is disturbing to body image
·Hyperlipidemia: pancreatitis is side effect, hyperglycemia, and osteoporosis are side effects with long term use
·often used when VL is high or other drugs fail