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NSG 322 Med Surge I > Exam 4 > Flashcards

Exam 4 Flashcards

1
Q

hematopoiesis

A
  • blood cell production
  • occurs within the bone marrow: produces RBCs, WBCs, and platelets
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2
Q

what are nondifferentiated immature blood cells in the bone marrow called?

A

stem cells

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3
Q

why might the body make more RBCs?

A

loss of blood, anemia, need more O2

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4
Q

how much of our blood does plasma constitute?

A

55% of blood

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5
Q

what is plasma composed of?

A

primarily of water but also contains proteins, electrolytes, gases, nutrients, and waster products

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6
Q

serum plasma

A

refers to plasma minus its clotting factors ~ has everything to do with hydration

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7
Q

how much of our blood do blood cells constitute?

A

45%

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8
Q

erythrocytes

A

RBCs ~ oxygen transportation

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9
Q

leukocytes

A

WBCs ~ protection from infection

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10
Q

thrombocytes

A

platelets ~ promote coagulation

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11
Q

normal platelet count

A

150-450

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12
Q

what does hematocrit show?

A

hydration status

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13
Q

if you give fluids, what will H&H be like?

A

low

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14
Q

erythropoiesis

A
  • making RBCs
  • stimulated by hypoxia
  • controlled by erythropoietin (created by kidneys)
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15
Q

what do reticulocytes do?

A

mature into RBCs and are a good indication of production rates

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16
Q

what does hemolysis do?

A

removes abnormal, defective, damaged, and old RBCs from circulation

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17
Q

if someone is in kidney failure, what can we expect?

A

them to be anemia

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18
Q

two types of leukocytes

A
  • granulocytes
  • agranulocytes (have to do with immunity)
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19
Q

types of granulocytes

A
  • neutrophils (most common)
  • eosinophils
  • basophils
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20
Q

types of agranulocytes

A
  • lymphocytes
  • monocytes
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21
Q

why would neutrophils be increased?

A

due to bacterial infection

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22
Q

neutrophils

A
  • primary function is phagocytosis
  • primary phagocytic cells involved in acute inflammatory response
  • mature neutrophil is segmented (“seg”)
  • immature neutrophils are called bands
  • first site of infection
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23
Q

an increase in percent of bands is called what?

A

a shift to the left, meaning bone marrow is releasing less-mature cells into circulation in response to a site of injury (increased in acute infection and inflammation)

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24
Q

life-span of neutrophils

A

2-14 days

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25
Q

eosinophils

A
  • have a reduced ability for phagocytosis compared with neutrophils
  • granules contain histamine
  • engulf antigen-antibody complexes formed during an allergic response
  • defend against parasites
  • found in large numbers in lungs and GI tract
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26
Q

basophils

A
  • limited role in phagocytosis
  • have cytoplasmic granules that contain heparin, serotonin, and histamine
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27
Q

lymphocytes

A

form the basis of cellular and humoral immune response

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28
Q

two subtypes of lymphocytes

A

B cells and T cells

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29
Q

if there is a dysfunction in B and T cells, what can that mean?

A

lost ability of immune system

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30
Q

monocytes

A
  • potent phagocytic cells
  • second type of cell to arrive at site of injury ~ try to clean things up
  • when they migrate into tissue, they become macrophages
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31
Q

macrophages

A

monocytes that have migrated to tissue

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32
Q

where are macrophages stores?

A
  • in spleen, lymph nodes, tonsils, and liver
  • when damage, infection, or injury triggers a response, the monocytes leave their primary location and travel through blood stream to enter other tissues and organs
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33
Q

what would happen if we removed someone’s spleen?

A

they would be immunocompromised

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34
Q

what are thrombocytes regulated by?

A

thrombopoietin

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35
Q

hemostasis

A

the arrest of bleeding

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36
Q

vascular response of hemostasis

A
  • immediate local vasoconstrictive response of injured blood vessels
  • reduces leakage of blood
  • gives time for platelet response and plasma clotting factors to be triggered
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37
Q

platelet plug formation of hemostasis

A
  • activated by exposure to interstitial collagen from the injured blood vessel
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38
Q

plasma clotting factors of hemostasis

A
  • form a visible fibrin clot on the platelet plug ~ scab
  • always present in circulation in inactive forms
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39
Q

two pathways of clotting

A
  • intrinsic pathway is activated by collagen exposure
  • extrinsic pathway is initiated when tissue factor or tissue thromboplastin is released from injured tissue
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40
Q

thrombin

A

most powerful enzyme in the coagulation process because it converts fibrinogen to fibrin

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41
Q

lysis of clot

A

anticoagulation, the reverse of clotting, helps keep blood fluid

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42
Q

what two means does anticoagulation occur by?

A
  • antithrombins: interfere with thrombin
  • fibrinolysis: process that results in dissolution of the fibrin clot
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43
Q

function of the speeln

A
  • filtration
  • immunologic
  • storage
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44
Q

what does lymph system help with?

A
  • F/E movement
  • protein and fat from the GI tract and certain hormones are returned to circulatory system
  • returns excess interstitial fluid to the blood to prevent or reduce edema
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45
Q

what does too much interstitial fluid or reduced absorption lead to?

A

lymphedema

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46
Q

what do lymph nodes indicate?

A

infection

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47
Q

primary function of lymph nodes

A

filtration of pathogens and foreign particles carried by lymph fluid

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48
Q

what does the liver do for the lymph system?

A
  • functions as a filter
  • produces all procoagulants essential to hemostasis and blood coagulation
  • stores excess iron
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49
Q

thrombocytopenia

A
  • reduction of platelets
  • results in abnormal hemostasis = prolonged or spontaneous bleeding
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50
Q

causes of thrombocytopenia

A
  • inherited
  • acquired
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51
Q

acquired types of thrombocytopenia

A
  • immune thrombocytopenia purpura (ITP)
  • thrombotic thrombocytopenia purpura (TTP)
  • heparin-induced thrombocytopenia (HIT)
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52
Q

most common acquired thrombocytopenia

A

ITP

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53
Q

ITP

A
  • syndrome of abnormal destruction of circulating platelets
  • autoimmune disease
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54
Q

manifestations of ITP

A
  • chronic in adults
  • gradual onset with transient remissions
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55
Q

TTP

A
  • an uncommon syndrome with a variety of features that are not always present
  • associated with enhanced aggregation of platelets that form into microthrombi ~ like in DIC
  • caused by plasma enzyme deficiency
  • idiopathic or from drug toxicities
  • medical emergency! bleeding and clotting occur simultaneously
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56
Q

HIT

A
  • associated with increased use of heparin ~ creates positive feedback loop which can result in clots
  • life-threatening
  • platelet destruction and vascular endothelial injury
  • develops 5-10 days after heparin therapy is started
  • clots while on heparin
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57
Q

major clinical problems with HIT

A
  • venous thrombosis
  • arterial thrombosis
  • DVT and PE
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58
Q

clinical manifestations of thrombocytopenia

A
  • patients are often asymptomatic
  • most common symptoms is mucosal or cutaneous bleeding - think GUMS and HANG-NAIL
  • petechiae (microhemorrhages)
  • purpura (bruise form numerous petichiae)
  • ecchymoses (larger lesions from hemorrhage)
  • prolonged bleeding after routine procedures
  • hemorrhage
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59
Q

how will platelet counts look in thrombocytopenia?

A
  • prolonged bleeding < 50,000
  • hemorrhage < 20,000
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60
Q

what kind of drug should pts. avoid with thrombocytopenia?

A

aspirin and other medications that affect platelet function or production

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61
Q

in ITP, when is therapy initiated?

A

if platelets are < 30,000

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62
Q

how do we treat ITP?

A
  • corticosteroids
  • high dose of IVIG and anti-Rh (competes with antiplatelet antibodies for macrophage receptors in the spleen
  • rituximab
  • splenectomy (an enlarged spleen sequesters and destroys platelets, resulting in less available in circulation
  • platelet transfusions (indicated for platelet counts < 10,000 or if bleeding is anticipated before a procedure
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63
Q

how do we treat TTP?

A
  • first treat underlying disorder or remove cause
  • plasmapheresis is used to aggressively reverse platelet consumption
  • rituximab
  • other immunosuppressants
  • splenectomy
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64
Q

how do we treat HIT?

A
  • permanently stop all heparin including heparin flushes
  • start pt. on direct thrombin inhibitor
  • start coumadin
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65
Q

causes of anemia

A
  • deficiency in the number of erythrocytes (RBCs)
  • quantity of Hgb
  • volume of packs RBCs (Hct)
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66
Q

what is used to determine the severity of anemia?

A

Hgb levels

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67
Q

normal Hgb levels in men and women

A

men: 13.8 - 17.2
women: 12.1 to 15.1

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68
Q

clinical manifestations of anemia

A
  • pallor
  • jaundice
  • pruritus
  • tachycardia due to CO being maintained by increasing the HR and SV
  • fatigue
  • imbalanced nutrition
  • ineffective self-health management
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69
Q

goal of anemia therapy

A

correcting the cause

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70
Q

acute interventions for anemia

A
  • blood or blood product transfusions
  • drug therapy such as erythropoietin and vitamins
  • volume replacement
  • dietary and lifestyle changes
  • O2 therapy
  • prevent falls and injuries
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71
Q

what is common in older adults with anemia?

A

nutritional deficiencies ~ S/S may go unrecognized or may be mistaken for normal aging changes

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72
Q

what do we always give blood with?

A

NS

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73
Q

life span of RBC

A

120 days

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74
Q

iron-deficiency anemia

A
  • one of the most common chronic hematologic disorders
  • iron is present in all RBCs as heme in hemoglobin
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75
Q

where does iron absorption occur?

A

in the duodenum ~ diseases of surgery that alter, destroy, or remove the absorption surface can cause anemia

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76
Q

where does blood loss most commonly occur in iron-deficiency anemia?

A

GI and GU systems

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77
Q

what else contributes to iron-deficiency anemia?

A

pregnancy

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78
Q

clinical manifestations of iron-deficiency anemia

A
  • pallor is most common
  • glossitis
  • cheilitis
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79
Q

how do we treat iron-deficiency anemia?

A
  • treat underlying disease causing reduced intake or absorption of iron
  • replace iron
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80
Q

how is iron best absorbed?

A

as ferrous sulfate in an acidic environment

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81
Q

side effects of taking iron?

A

heartburn, constipation, diarrhea, black stools

82
Q

why would we give parenteral iron?

A
  • indicated for malabsorption, oral iron intolerance, need for iron beyond normal limits, poor patient compliance
  • IV or IM ~ IM may stain skin
  • hospital or infusion center
83
Q

when do we check iron levels are starting therapy and how long until it returns to normal levels?

A

check again in 1 month, won’t return to normal for 3 months

84
Q

thalassemia

A
  • a group of diseases involving inadequate production of normal Hgb ~ decreased erythrocyte production
  • common in ethnic groups near the mediterranean sea and equatorial or near-equatorial regions
  • genetic problem with globulin protein
85
Q

megaloblastic anemia

A
  • group of disorders caused by impaired DNA synthesis
  • presence of megaloblasts
  • majority result from deficiency in cobalamin (vit. B12) and folic acid
86
Q

what is required for cobalamin absorption?

A

intrinsic factor (IF)

87
Q

what is cobalamin deficiency most commonly caused by?

A

pernicious anemia which is caused by an absence of IF

88
Q

clinical manifestations of cobalamin deficiency

A
  • sore tongue
  • anorexia
  • N/V and abdominal pain
  • weakness
  • paresthesias of feet and hands
  • decreased vibratory and position senses
  • ataxia
  • muscle weakness
  • impaired though process
89
Q

how do we treat cobalamin deficiency?

A

parenteral or intranasal administration

90
Q

how does folic acid deficiency differ from cobalamin deficiency?

A

clinical manifestations are similar, but absence of neurologic problems

91
Q

normal serum folate levels

A

3-25 mg/mL

92
Q

how do we treat folic acid deficiency?

A
  • replacement therapy ~ 1 mg per day PO
  • eating foods with large amounts of folic acid
93
Q

aplastic anemia

A
  • pancytopenia ~ decrease in all blood cell types
  • hypocellular bone marrow
  • bone marrow made out of plastic, not working
94
Q

2 major types of aplastic anemia

A
  • congenital: chromosomal alterations
  • acquired: results from exposure to ionizing radiation, chemical agents, viral and bacterial infection
95
Q

clinical manifestations of aplastic anemia

A
  • symptoms caused by suppression of any or all bone marrow elements
  • fatigue, dyspnea
  • cardiovascular and cerebral responses
  • neutropenia
96
Q

how do we treat aplastic anemia?

A
  • identify and remove all causative agents
  • provide supportive care
  • prevent infection
  • prevent hemorrhage
97
Q

anemia caused by blood loss

A
  • acute blood loss occurs as a result of sudden hemorrhage
  • the sources of chronic blood loss are similar to those of iron-deficiency anemia
98
Q

clinical manifestation of acute blood loss

A
  • caused by body’s attempts to maintain adequate blood volume and meet oxygen requirements
  • tired, falls, tachycardia
99
Q

how do diagnostic studies look with acute blood loss?

A
  • since it is sudden, values may seem normal or high for 2-3 days
  • once plasma volume is replaced, low RBC concentrations become evident
100
Q

how do we treat acute blood loss?

A
  • replace BV to prevent shock
  • identifying source of hemorrhage and stopping blood loss
  • providing supplemental iron
101
Q

chronic blood loss sources

A
  • bleeding ulcer
  • hemorrhoids
  • menstrual and postmenopausal blood loss
102
Q

how do we manage chronic blood loss?

A
  • identify the source
  • stopping the bleeding
  • providing supplemental iron
103
Q

hemolytic anemia

A

destruction of hemolysis of RBCs at a rate that exceeds production

104
Q

manifestations of hemolytic anemia

A
  • general manifestations of anemia
  • jaundice
  • enlargement of spleen and liver
105
Q

major focus of treatment in hemolytic anemia

A

maintenance of renal function is a major focus of treatment

106
Q

sickle cell disease

A
  • group of inherited, autosomal recessive disorders
  • characterized by the presence of an abnormal form of Hgb in the RBC
  • predominant in african americans
  • severe, painful, acute exacerbation of sickling causes a vaso-occlusive crisis
107
Q

how do we unstick sickle cells?

A

give more fluids

108
Q

in sickle cell disease, what can severe capillary hypoxia lead to?

A

tissue necrosis

109
Q

in sickle cell disease, what can be a result of severe O2 depletion?

A

life-threatening shock

110
Q

clinical manifestations of sickle cell disease

A
  • typical patient is asymptomatic except during sickling episodes
  • pain from tissue hypoxia and damage
  • pallor of mucous membranes
  • jaundice from hemolysis ~ prone to gallstones
111
Q

major complication of sickle cell disease

A

infection since the function of the spleen becomes compromised from sickled RBCs, pneumococcal pneumonia is most common

112
Q

what can severe infection in sickle cell crisis lead to?

A

aplastic crisis which can lead to shutdown of RBC production

113
Q

what do we want to teach pts. in sickle cell disease?

A
  • avoid high altitudes
  • maintain adequate fluid intake
  • treat infection promptly
  • avoid crisis
114
Q

acquired hemolytic anemia

A

hemolysis of RBCs is caused by four categories of extrinsic factors: macroangiopathic (physical trauma), microangiopathic, antibody reactions, infectious agents and toxins

115
Q

maroangiopathic destruction

A
  • physical destruction of RBCs results from exertion of extreme force on cells
  • hemolysis, extracorporeal circulation used in cardiopulmonary bypass, prosthetic heart valves, abnormal vessels
116
Q

microangiopathic destruction

A
  • results from fragmentation of the cells as the try to pass by abnormal arterial or venous microcirculation
  • RBCs are sheared as they try to pass by excessive platelet aggregation or fibrin polymer formation ~ seen in TTP and DIC
117
Q

two mechanisms involved in destruction from antibodies

A
  • isoimmune reactions : blood donor reactions
  • autoimmune reaction: antibodies develop against own RBCs
118
Q

how do infectious agents cause hemolysis?

A
  • invade RBCs and destroy its contents
  • release hemolytic substances
  • generate an antigen-antibody reaction
119
Q

how do we treat acquired hemolytic anemia?

A
  • supportive care until the causative agent can be eliminated or made less injurious
  • emergency preparedness: hydration, electrolyte replacement, corticosteroids, blood products, splenectomy
120
Q

cancer

A
  • group of diseases characterized by uncontrolled and unregulated growth of cells
  • higher incidence in men than women
  • second most common cause of death in U.S. after heart disease
  • leading cause of death in people 40-79 years of age
121
Q

two major dysfunctions in the process of cancer development

A
  1. defective cell proliferation (growth)
  2. defective cell differentiation
122
Q

what happens with cancer cells?

A

they have no regard for cell boundaries ~ grow on top of one another on top of or between normal cells

123
Q

bacteriostatic

A

slows down, stops

124
Q

two genes that can be affected by mutation

A
  • protooncogenes: regulate normal cellular processes such as promoting growth
  • tumor suppressor genes: suppress growth
125
Q

protooncogenes

A
  • genetic locks that keep cells functioning normally
  • mutations that alter their expression can activate them to function as oncogenes
126
Q

what do mutations do with tumor suppressor genes?

A

they make them inactive ~ results in loss of suppression of tumor growth

127
Q

when is screening recommended if a close family member had cancer?

A

10 years before that family member had it

128
Q

carcinogens

A
  • cancer-causing agents capable of producing cell alterations
  • many are detoxified by protective enzymes and are harmlessly excreted
  • failure of protective mechanisms allows them to enter cell’s nucleus and alter DNA
  • can be chemical, radiation, or viral
129
Q

what type of cancer is UV radiation associated with?

A

melanoma (worst cancer) and squamous and basal (most benign) cell carcinoma ~ sunlight is main source of UV exposure

130
Q

what is the length of the latent period associated with?

A

mitotic rate of tissue of origin and environmental factors

131
Q

what do lymphocytes do in cancer?

A

continually check cell surface antigens and detect and destroy abnormal cells

132
Q

what do oncofetal antigens help with?

A

monitor therapy and look for reoccurance

133
Q

stages of cancer

A

o: cancer in situ
I: tumor limited to tissue of origin; localized tumor growth
II: limited local spread
III: extensive local and regional spread
IV: metastasis

134
Q

TNM cancer classification

A

T = tumor size and invasiveness
N = spread to lymph nodes
M = metastasis

135
Q

can stage classification be changed?

A

no, not once established

136
Q

osteomyelitis

A

severe infection of bone, bone marrow, and surrounding soft tissue

137
Q

how long does acute osteomyelitis last?

A

infection of < 1 month in duration

138
Q

clinical manifestations of acute osteomyelitis

A
  • pain that worsens with activity; is unrelieved by rest
  • swelling, tenderness, warmth
  • restricted movement
  • fever, night sweats, chills, restlessness, nausea, malaise, drainage
139
Q

how long does chronic osteomyelitis last?

A

infection lasting > 1 month or has failed to respond to initial antibiotic treatment

140
Q

how does chronic osteomyelitis present and what might the pt. need to be taken home on?

A

continuous and persistent or process of exacerbations and remissions ~ wound pump to deliver antibiotics

141
Q

clinical manifestations of chronic osteomyelitis

A
  • systemic manifestations reduced
  • local signs are more common: pain, swelling, warmth
142
Q

how do we care for acute osteomyelitis?

A
  • aggressive, prolonged IV antibiotic therapy
  • cultures or bone biopsy
  • surgical debridement and decompression
143
Q

how long are antibiotics given and for how long in acute osteomyelitis?

A
  • 4-6 weeks or longer
  • via CVAD
144
Q

how do we care for chronic osteomyelitis?

A
  • surgical removal
  • extended use of antibiotics
  • acrylic bead chains containing antibiotics
  • intermittent or constant antibiotic irrigation of bone
  • casts or braces
  • wound vac
  • muscle flaps, skin grafts, bone grafts
  • amputation
145
Q

persons at risk for osteomyelitis are usually what?

A
  • immunocompromised
  • have diabetes, orthopedic prosthetic devices, vascular insufficiencies
146
Q

what can lengthy antibiotic therapy cause?

A

overgrowth of candida albicans and clostridium difficile

147
Q

osteoporosis

A
  • chronic, progressive metabolic bone disease marked by low bone mass and deterioration of bone tissue
  • leads to increased bone fragility
  • known as the “silent thief”
148
Q

why is osteoporosis more common in women?

A
  • lower calcium intake
  • less bone mass
  • bone resorption begins earlier and becomes more rapid at menopause
  • pregnancy and breastfeeding
  • longevity
149
Q

screening guidelines for osteoporosis

A
  • initial bone density test in women over 65
  • repeat 15 years if normal
  • earlier and more frequent if high risk
150
Q

how can we best prevent osteoporosis?

A
  • regular weight-bearing exercise
151
Q

what age do we reach our peak bone mass?

A

by age 20

152
Q

osteoblasts

A

deposit bone

153
Q

osteoclasts

A

resorb bone

154
Q

what happens in osteoporosis with resorption and deposition?

A

bone resorption exceeds bone deposition

155
Q

clinical manifestations of osteoporosis

A
  • occurs commonly in spine, hips, and wrists
  • back pain
  • spontaneous fractures
  • gradual loss of height
  • kyphosis or “dowager’s hump”
156
Q

what do T-scores test for?

A

bone density

157
Q

t-score between +1 and -1 is

A

normal bone density

158
Q

t-score between -1 and -2.5 is

A

osteopenia

159
Q

t-score -2.5 or lower is

A

osteoporosis

160
Q

recommended calcium intake

A
  • 1,000 mg/day for women ages 19-50 and men ages 19-70
  • 1,200 mg/day for women 51 years or older and men 71 years or older
161
Q

good sources of calcium

A

milk, yogurt, turnip greens, cottage cheese, ice cream, sardines, spinach

162
Q

what vitamin is necessary for calcium absorption/function?

A

vitamin D

163
Q

radicular pain

A

irritation of nerve root

164
Q

referred pain

A

source of pain is another location

165
Q

why is back pain common in the lumbar region?

A

lumbar region:
- bears most of body weight
- contains nerve roots
- has poor biomechanical structure

166
Q

ideal BMI

A

18.5-24.9

167
Q

what should we teach pts. with lower back pain?

A
  • sleep in a side-lying position with knees and hips bent
  • sleep on back with a lift under knees and legs or with 10-inch pillow under knees to flex hips and knees
  • prevent lower back from straining forward by placing a foot on a step or stool during prolonged standing
  • use a lumbar roll or pillow for sitting
  • exercise 15 minutes in the morning and evenings regularly
  • carry light items close to body
  • use local heat and cold application
  • maintain appropriate body weight
168
Q

multiple nerve root (cauda equina) compression

A
  • severe low back pain, weakness
  • bowel and bladder incontinence
  • medical emergency
169
Q

when do most pts. heal from intervertebral disc disease?

A

within 6 months with good back-strengthening exercises

170
Q

when is surgery indicated in intervertebral disc disease?

A
  • conservative treatment fails
  • radiculopathy worsens
  • loss of bowel or bladder control
  • constant pain
  • persistent neurologic deficit
171
Q

what mechanism can we use after spinal disc surgery?

A

log rolling, spinal precautions

172
Q

what can we expect after spinal surgery?

A
  • potential for CSF leakage
  • monitor for and report severe headache or leakage of CSF
  • clear or slightly yellow drainage on dressing
    • for glucose
173
Q

osteoarthritis

A
  • slowly progressive noninflammatory disorder of the diarthrodial joints
  • gradual loss of articular cartilage
  • formation of osteophytes ~ bone chunks, extra bone that builds up
174
Q

risk factors of OA

A
  • age
  • decreased estrogen at menopause
  • obesity
  • anterior cruciate ligament injury
  • frequent kneeling and stooping
175
Q

what can help prevent OA?

A

regular exercise

176
Q

is inflammation common in OA?

A

no, it is just bone broken down and rebuilding

177
Q

what is the distinction between OA and RA?

A

systemic manifestations are NOT present in OA

178
Q

clinical manifestations of OA

A
  • joint pain that worsens with joint use
  • pain may be referred to groin, buttock, or outside of thigh or knee
  • early morning stiffness usually resolves within 30 minutes
  • crepitation
  • asymmetrical
  • deformity at DIP and PIP joint
179
Q

what kind of interventions are the basis for OA management?

A

nondrug: balance rest and activity, avoid prolonged standing, kneeling, or squatting, assistive devices

180
Q

what is critical when trying to prevent OA?

A

weight reduction

181
Q

rheumatoid arthritis

A
  • chronic, systemic autoimmune disease
  • inflammation of connective tissue in diarthrodial (synovial) joints
  • periods of remission and exacerbation - SPELLS
  • three times as many women as men
  • antigen triggers formation of abnormal IgG
  • autoantibodies develop against abnormal IgG (rheumatoid factor)
  • T helper cells (CD4) are activated
  • edges are being shaved off and bones are falling on top of each other
182
Q

in RA, what can increase the risk in patients who are genetically predisposed?

A

smoking

183
Q

stages of RA

A
  • stage I: no joint destruction
  • stage II: destruction in joint cartilage
  • stage III: extensive cartilage loss and possible deformity
  • stage IV: loss of joint function and formation of subcutaneous nodules
184
Q

clinical manifestations of RA

A
  • insidious
  • fatigue, anorexia, weight loss, generalized stiffness
  • symptoms occur symmetrically
  • often affects small joints, but larger joints and cervical spine may be involved
  • joint stiffness after inactivity ~ morning stiffness 60 minutes to several hours long
  • MCP and PIP joints swollen
  • tenosynovities
  • deformity and disability
  • walking disability
  • sjogren’s syndrome
  • felty syndrome
  • depression
185
Q

what laboratory studies are important in RA?

A
  • rheumatoid factor (RF)
  • ESR and c-reactive protein (CRP)
  • antinuclear antibody (ANA)
  • antibodies to citrullinated peptide (anti-CCP)
186
Q

how long do DMARDs take to have a therapeutic effect?

A

4-6 weeks; frequent monitoring is required

187
Q

since BRMs bind with TNFs, what should we check for?

A
  • TB test and chest x-ray
  • monitor for infection
  • avoid live vaccinations
188
Q

is prevention possible in RA?

A

no, early treatment to prevent further joint damage is

189
Q

what kind of exercises help with RA?

A
  • gentle ROM
  • aquatic exercises in warm water
190
Q

myofascial pain syndrome

A
  • chronic, musculoskeletal pain and tenderness in the chest, neck, shoulders, hips, lower back
  • referred pain to buttock, hand, head
  • can cause TMJ
  • pain within connective tissue of skeletal muscles
  • tender points
  • vague pain that is deep
191
Q

how can we treat myofascial pain?

A
  • “spray and stretch method”
  • topical patches
  • trigger point injections
  • massage, acupuncture
192
Q

fibromyalgia

A
  • chronic central pain syndrome
  • widespread, nonarticular musculoskeletal pain and fatigue
  • multiple tender points
  • might also have nonrestorative sleep, morning stiffness, IBS, anxiety
  • disorder involving abnormal CNS processing
193
Q

clinical manifestations of fibromyalgia

A
  • widespread burning pain
  • worsens and improves throughout day
  • trouble determining if pain is in muscles, joints, or soft tissues - VAGUE
  • head or facial pain
  • difficulty concentrating
  • feelings of being overwhelmed
  • migraine headaches
  • fatigue
  • paresthesia
  • RLS
  • depression and anxiety
  • stiffness
  • nonrefreshing sleep
  • IBS
  • difficulty swallowing
  • frequency of urination
  • difficult menstruation
194
Q

how do we diagnose fibromyalgia?

A
  • difficult to establish a definitive diagnosis
  • rule out
195
Q

it is fibromyalgia if what two criteria are met?

A
  • pain is experienced in 11/18 tender points
  • history of widespread pain noted for at least 3 months
196
Q

what do we want to teach patients in helping with fibromyalgia?

A
  • limit intake of sugar, caffeine, alcohol because they may be muscle irritants
  • vitamin and mineral supplements
  • relaxation strategies
  • psychologic counseling
197
Q

SEID

A
  • complex, multisystem disease in which exertion of any sort can adversely affect multiple organs
  • women more than men
198
Q

clinical manifestations of SEID

A
  • diagnosis requires three symptoms: profound fatigue lasting 6 months, post-exertional malaise, unrefreshing sleep; plus one of two: cognitive impairment, worsening of symptoms upon standing
  • insidious or intermittent episodes that become chronic
  • severe fatigue most common
199
Q

what other disorder is SEID similar to?

A

fibromyalgia ~ hard to distinguish

200
Q

how do we diagnose SEID?

A

rule out, diagnosis of exclusion

201
Q

what do we want to teach the patient who has SEID?

A
  • avoid total rest
  • strenuous exertion can exacerbate exhaustion
  • well-balanced diet
  • fiber intake
202
Q

who might we want to refer a pt. with SEID to?

A

behavioral therapy

NSG 322 Med Surge I (5 decks)

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