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NURSING 210 > Test 4 > Flashcards

Test 4 Flashcards

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1
Q

Risk factors for RA

A

-Women between 40-60 years
-Family history
-Smokers
-Possible Genetic link

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2
Q

RA extra-articular manifestations

A

fever, fatigue, anemia, lymph node enlargement, Raynaud’s phenomenon and Sjogren’s syndrome(dry eyes/mucus membranes), skin and mucosal manifestations

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3
Q

RA treatment

A

no cure, treat/relieve manifestations, balance rest & exercise, PT and suppression of inflammatory processes

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4
Q

RA diagnostic tests

A

-rheumatoid factors
-sed rate
-CBC & infectious process/anemia
-asp. of sinovial fluid
-xray (shows demineralization/progression)
-c-reactive protein (will be elevated and shows inflammation)
-ANA & C3&C4 (shows complement levels)

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5
Q

RA pharmacologic therapies

A

-salisalates (aspirin)
-NSAIDS anti-inflamm.
-DEMARDS (disease modifying anti-rheumatic drugs)
-immune modulators
-TNF blockers (tumor necrosis blockers)

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6
Q

RA surgeries/procedures

A

-synovectomy
-arthrodesis
-arthroplasty
-plasmapheresis total lymphoid irradiation

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7
Q

Diagnostic criteria for RA

A

(4 of the following)
-morning stiffness lasting 1hr for 6 weeks
-arthritis w/ swelling of effusion of 3 or more joints lasting 6 weeks
-arthritis of the wrist, knuckles & PIP joints for 6 weeks
-symmetrical arthritis
-rheumatoid nodules
-positive rheumatoid factor(blood test)
-characteristic xray changes of RA

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8
Q

what is systemic lupus erythematosus?

A

a chronic inflammatory connective tissue disease that affects almost all body systems. Caused by deposition of antigen-antibody complexes in connective tissues

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9
Q

Lupus risk factors

A

-more women than men 9:1
-women of childbearing age
-drug-induced lupus– resolves when medication is discontinues
-need to be in remission for at least 6 months before becoming pregnant

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10
Q

lupus manifestations

A

butterfly rash, inflamm. of lungs, splenomegaly, arthritis in joints, glomerulonephritis, anti-nuclear antibodies, neurological damage, anemia, thrombocytopenia

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11
Q

lupus diagnostic tests

A

-complement levels (C4 will be low)
-H&H low (anemia)
-ANA would be positive
-sed rate would be high

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12
Q

lupus pharmacologic therapy– mild/remittent

A

little or no therapy

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13
Q

lupus pharmacologic therapy–skin/arrhythmic manifestations

A

antimalarial drugs
(plaquenil)

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14
Q

lupus pharmacologic therapy–severe& life threatening menifestations

A

corticosteroid therapy in high doses
-40-60mg prednisone daily
-taper as rapidly as the disease allows

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15
Q

lupus pharmacologic therapy

A

immunosuppressants, NSAIDS, steroids, DHEA (mild male hormone therapy that helps treat mild to moderate lupus symptoms)

client at risk for infection

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16
Q

lupus clinical therapy

A

-topical steroids
-avoid estrogens
-complementary therapies (exacerbation linked to stress & stress reducing techniques)

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17
Q

Nursing process for lupus

A

watch lungs, BUN&creatinine, look at heart, med. education, avoid the sun

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18
Q

how long do RBC’s live?

A

last about 90-120 days

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19
Q

if there is not enough O2 in the body what do they kidneys do?

A

release erythropoeitin and signals the bone marrow to produce more RBCs

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20
Q

what do B12 and folic acid do?

A

help make and develop healthy RBCs

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21
Q

anemia prevalence in the elderly?

A

bone marrows ability decreases and in an event they cant quickly compensate with new RBCs. This impacts cognition, mobility and increased depression

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22
Q

nutritional anemia

A

anemia based on the lack of certain nutritional elements in the diet

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23
Q

hemolytic anemia

A

inherited disorder of the RBC membrane (breaking of RBCs)

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24
Q

aplastic anemia

A

hypoproliferative (not making any RBCs)

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25
Q

iron deficiency anemia

A

MOST COMMON
from lack of iron intake, acute bleeding, alcoholism, pregnancy and GI malabsorption. Iron stores are depleted first followed by hemoglobin stores

Iron helps carry O2= impairment of O2 delivery

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26
Q

what is feratin?

A

a supplement that holds onto the iron

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27
Q

frank blood & occult blood

A

frank blood= bright red
occult blood= in the body/stool & black

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28
Q

iron deficiency anemia clinical manifestations

A

cheilosis (cracking of lips), pale, fatigue, possible dyspnea, tachy, brittle hair&nails, smooth red tongue

in children: poor motor and emotional cognition

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29
Q

iron deficiency anemia treatment

A

increase vit. C & protein (iron), control chronic bleding, iron supplements

  • take iron 1 hour before meals on an empty stomach, and do not drink with milk
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30
Q

what to give if overloaded with iron?

A

deferoximine- binds with iron and removes it from the system

s/s: N/V/D

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31
Q

what do the cells of someone with iron deficiency anemia look like?

A

small, pale cells

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32
Q

what do the cells of someone with vit. B12 deficiency anemia look like?

A

very large RBCs

33
Q

why is vit.B12 important?

A

essential for DNA synthesis and nuclear maturation which leads to normal RBC maturation and division. – helps make DNA

34
Q

causes of vit.B12 deficiency anemia?

A

malnutrition (alcoholics & strict vegans), lack of intrinsic factor and underproduction of hydrochloric acid in the stomach (long term use of H-2 receptor blockers and PPIs)

35
Q

what is pernicious anemia?

A

when there is a lack of intrinsic factor and thus decreases the absorption of B12 in the intestines. IF is made in the stomach.

36
Q

vit.B12 deficiency anemia clinical manifeststions

A

**numbness and tingling of extremities (paresthesia), red beefy smooth tongue(glossitis)- in pernicious

hypoxemia, pallor, jaundice, poor balance, anorexia, nausea, dementia, depression

37
Q

vit.B12 deficiency anemia treatment

A

cyanocobalamin(IM B12), increase PO intake of B12 in food, and PO B12 supplements

38
Q

what do folic acid deficiency anemia cells looks like?

A

Big RBC’s (megaloblastic)

39
Q

Why is folic acids role in the body?

A

it is required for DNA synthesis and RBC maturation

40
Q

Foods high in folic acid

A

fruits, seafood, liver, whole grains and beans

41
Q

risk factors of folic acid deficiency anemia?

A

celiac, chrons, alcoholics, people on anticonvulsants

42
Q

treatment of folic acid deficiency anemia

A

PO folic acid, stop alcohol consumption and beef up diet in high folic acid foods

43
Q

MCV low: microcytic cells

A

hemoglobin problem- need iron

44
Q

MCV normal

A

Good RBC’s but not enough- not a nutrition issue- blood loss

45
Q

MCV high: macrocytic

A

DNA problem- B12 and folic acid

46
Q

4 types of hemolytic anemia

A

thalassemia, acquired hemolytic anemia, glucose-6 phasphate dehydrogenase anemia and sickle cell anemia

47
Q

thalassemia cause

A

recessive gene(must inherit the defective gene by both parents) most common in asians, mediterranians and africans

48
Q

what do RBCs look like in thalassemia?

A

pale color of RBCs

49
Q

thalassemia clinical manifestations

A

bronze skin, develops in first year of life, big bones due to bone marrow trying to grow more and more RBCs, splenomegaly

50
Q

thalassemia treatment

A

blood tx, too much iron is being stored in testes, pancreas, thyroid and heart so chelation is needed to get rid of the excess iron

51
Q

what should you do as the nurse for thalassemia

A

adm blood tx, 18G IV, encourage rest and recommend genetic counseling

52
Q

acquired hemolytic anemia labs and diagnostics

A

direct and indirect coombs test

53
Q

acquired hemolytic anemia treatment

A

steriod therapy for severe autoimmune, and stem cell transplant in aplastic anemia only, tx is same for both antibody and non-antibody types

54
Q

glucose 6 phosphate dehydrogenase anemia (most common)

A

X linked recessive disorder where men are effected and females are carriers. Most common in asians africans and mediterranians

55
Q

what can trigger glucose 6 phosphate dehydrogenase anemia

A

infections, drugs that increase oxidative stress, fava beans, ketoacidosis, moth balls and tonic water

56
Q

glucose 6 phosphate dehydrogenase anemia clinical manifestations

A

weakness, tachy, jaundice, pallor, and RUQ pain because thats where the liver and gallbladder are (possible gallstones)

57
Q

glucose 6 phosphate dehydrogenase anemia treatment

A

tx any infection quickly, avoid oxidant medication and foods (antimalarials, sulfonamides, nitrofurantoin and legumes), educate on food

58
Q

sickle cell anemia

A

inherited recessive disorder causing abnormal hemoglobin

59
Q

HgbS

A

linked to levels of O2 and stress

60
Q

HgbF

A

highest in infants

61
Q

RBCs of sickle cell anemia

A

sticky cells that clump up(hemolysis) and then occlude the capillaries

62
Q

complications of sickle cell anemia

A

anemia, and blood vessel occlusion- stroke, death, tissue ischemia and tissue death

63
Q

factors that cause sickling

A

cold, stress, physical exertion, infection, and illness that causes hypoxia, dehydration or acidosis

64
Q

what to give in a sickle cell crisis

A

keep hydrated, medicate with narcotics- could lead to aplastic anemia

65
Q

sickle cell anemia in pediatrics

A

leading cause of death, asymptomatic until 4-6 months(because of HgbF), prone to lung infections, high risk of stroke

66
Q

sickle cell anemia in pregnant women

A

more freq pain crises, more intense symptoms and higher risk of complications

67
Q

**sickle cell anemia treatment

A

blood tx(know when last one was), antibiotics prophalactically-hydroxyurea, increased HgbF- inhibits DNA synthesis and reduce pain crisis

68
Q

what is aloe immunization

A

an immune response to foreign antigens- happens with multiple blood transfusions

69
Q

aplastic anemia (hypoproliferative) cells

A

RBCs are normal size and color there just aren’t enough- decreased red, white and platelets

70
Q

aplastic anemia cause

A

is an immune response and not sure why it happens

71
Q

pancytopenia

A

if there is a decrease in WBCs, RBCs and platelets

72
Q

aplastic anemia treatment

A

immunosupressive therapy(prednisone), blood & platelet tx, bone marrow transplant(if cant be corrected) and splenectomy(last resort)

73
Q

aplastic anemia nursing

A

monitor labs, neutropenic prec., bleeding prec., monitor for infection and emotional support esp. for bone marrow biopsy

74
Q

testing for all anemias

A

-H&H will be LOW
-reticulocyte count
-MCV,MCH,MCHC (cell size)
-iron studies
-vit. B12
-folate
-bone marrow asp.

75
Q

hemophilia

A

inherited bleeding disorder, X linked genetic trait, females are more common

76
Q

two types of hemophilia

A

hemophilia A- factor 8 is deficient or defective
hemophilia B- factor 9 is deficient or defective

77
Q

clinical manifestations of hemophilia

A

1st sign is joint pain, muscle/nerve swelling, poor wound healing, tarry stools, prolonged bleeding, hemmorhage, hematuria

78
Q

what happens in severe hemophilia

A

you can just randomly spontaneously bleed out of nowhere

79
Q

hemophilia treatment

A

fresh frozen plasma, factor replacement therapy(may be everyday is severe), prophylaxis and glucocorticoids for joint pain and edema

NURSING 210 (5 decks)

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