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CV487 > Class 10: Pain & Alterations in Hematological Function > Flashcards

Class 10: Pain & Alterations in Hematological Function Flashcards

1
Q

Nociceptors are..

A

Free nerve endings in the afferent PNS

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2
Q

3 portions of the nervous system responsible for sensation, perception and pain response

A

-Afferent pathways, interpretive pathways and interpretive centers

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3
Q

Afferent pathways are.. & stimuli goes..

A

-Where nociceptors live in the PNS
-Stimuli go to the dorsal horn then to the CNS

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4
Q

Interpretive centers include the..

A

Brainstem, midbrain diencephalon and the cortex

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5
Q

Efferent pathways do what and stimuli goes where?

A

-Respond to pain
-CNS to dorsal horn and then to the spinal cord

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6
Q

Pain can be…

A

Emotional, spiritual or cultural

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7
Q

Phases of nociception

A

-Pain transduction, transmission, perception and modulation

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8
Q

Slide 8&9

A
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9
Q

Glutamate is a…

A

Excitatory neurotransmitter that has a role with chronic pain

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10
Q

Substance P is…

A

A tachykinin released from afferent fibers during inflammation
-Co-exists with glutamate

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11
Q

Histamine does what?

A

Evokes the release of substance P and plays a role in neurogenic inflammation and leads to vasodilation

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12
Q

Prostaglandins cause…

A

-Increased vascular permeability, neutrophil, chemotaxis and pain by direct effects on nerves
-NSAIDS and ASA inhibit cyclooxygenase (COX) which produces prostaglandins

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13
Q

Bradykinin causes and acts with…

A

Vasodilation, acts with prostaglandins

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14
Q

-a-delta fibers are…

A

Large and myelinated, transmit sharp localize fast pain sensations such as a burn, prick on the skin or a fracture

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15
Q

-c-fibers are…

A

-More plentiful but are small and unmyelinated, located in the muscle, tendons, organs and the skin
-Transmit a dull ache/burning sensation

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16
Q

Reticular and limbic system…

A

Receive pain stimuli

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17
Q

Initial acute pain…

A

Induces a sympathetic response, over time it causes a behavioural response

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18
Q

Slide 10,11&12

A
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19
Q

Neurophysiological pain

A

-Nociceptive pain includes somatic (skin, muscle, bone) & visceral (intestine, liver, stomach)
-Neuropathic (non-nociceptive) includes central pain (lesion in brain or spinal cord) & peripheral pain (lesion in PNS)

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20
Q

Neurogenic pain

A

-Neuralgia (pain in the distribution of a nerve)
-Constant pain is either sympathetically independent or sympathetically dependent

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21
Q

Temporal pain (time related, duration)

A

-Acute pain; somatic
-Visceral pain; chronic

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22
Q

Nociceptive pain is blank, whearas neuropathic pain is…

A

-Normal processing of a stimulus
-Abnormal processing

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23
Q

Somatic pain is in the…

A

-Joints & muscles that begin with a-delta then leads to c-alpha fibers

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24
Q

Visceral pain is transmitted with…

A

C-fibers and can radiate

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25
Q

Slide 16-18

A
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26
Q

Composition of blood

A

Plasma, albumin & globulins

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27
Q

Cellular components of blood

A

-Erythrocytes, leukocytes & platelets

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28
Q

Leukocytes

A

-Granulocytes (neutrophil, eosinophils, basophils & mast cells)
-Agranulocytes (phagocytes or immunocytes) (lymphocytes)

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29
Q

Albumin regulates…

A

Water, and when there is too little, fluid moves to the extracellular space. This decreases oncotic pressure and fluid moves into the extravascular space

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30
Q

Albumin is given to…

A

Move fluid into the intravascular space

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31
Q

The first thing to increase when there is an infection is what?

A

Neutrophils

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32
Q

How to test for mast cells test

A

CRP protein which indicates inflammation

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33
Q

Lymphocytes are and do what?

A

-T-cells & B-cells
-T-cells are good for remembering bacteria and fighting them, killer cells, big dogs
-B-cells provide natural immunity, surveillance/bodyguards

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34
Q

T-cells come from the…

A

Thymus (form mature T-lymphocytes)

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35
Q

Think of lymph nodes as…

A

Check stops to identify viruses

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36
Q

Primary lymphoid organs

A

Thymus, bone marrow, spleen and lymph nodes

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37
Q

The spleen does what

A

-Gathers immune cells and acts as a blood reservoir
-If punctured/sliced then the patient enters the golden hour. This means they will bleed out within 1 hour

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38
Q

Platelets induce what

A

Vasoconstriction, the clotting cascade and the repair process (fibrinolysis)

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39
Q

Virchow’s triad

A

Hemostasis, hypercoagulability and endothelial damage

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40
Q

Manifestations of altered platelet function

A

-Spontaneous petechiae and purpura (thrombocytopenia; low platelets)
-Bleeding from GI tract, GU tract, pulmonary mucosa and gums

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41
Q

Petchiae is blank than purpura

A

Smaller

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42
Q

Systemic disorders that affect platelet function

A

-Chronic renal failure, liver disease, cardiopulmonary bypass surgery, severe iron or folate deficiency, and antiplatelet antibodies associated with autoimmune disorders
Hematological disorders

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43
Q

Petechiae develops when…

A

Platelets are less than 50

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44
Q

If platelets are less than 20 then…

A

The patient can bleed for no reason

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45
Q

Petechiae, purpura and ecchymosis are all…

A

Signs of bleeding

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46
Q

Heparin induced thrombocytopenia (HIT) is a..

A

-Immune-mediated, adverse drug reaction caused by IgG Antibodies that results in platelet consumption and a subsequent decrease in platelets
-Begins 5-10 days after it is administered

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47
Q

In HIT, monitor for…

A

platelet levels dropping & virchow’s triad

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48
Q

HIT develops because of a…

A

Previous tx of heparin (d/t cardiac issues), and in subsequent admissions patients are at risk for HIT

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49
Q

HIT manifestations

A

-Thrombocytopenia *, venous thrombosis resulting in DVT, arterial thrombosis of lower extremities leading to limb ischemia

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50
Q

Evaluation & tx of HIT

A

-HIT antibody teeter level & lab values
-Withdraw heparin and use alternative anticoagulants… NO COUMADIN

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51
Q

Coagulation disorders

A

-Impaired hemostasis
-Consumptive thrombohemorrhagic disorders

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52
Q

Impaired hemostasis

A

-Inability to promote coagulation and develop a stable fibrin clot
-Examples include Vitamin K deficiency and liver disease (usually associated with liver disease)

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53
Q

Consumptive thrombohemorrhagic disorders

A

Disseminated intravascular coagulation (DIC)

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54
Q

DIC

A

-Occurs in sepsis & maternity lesions
-Hospital-acquired condition
-Clots start to form and puts the pt at risk for simultaneous bleeding and clotting

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55
Q

Pathophysiology of DIC

A

Bleeding & clotting at the same time, body consumes platelets to plug up bleeds. Reduces circulating platelets and bleeding elsewhere occurs. Common in postpartum bleeds in small petite women that are prone to severe tearing.

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56
Q

DIC begins with

A

Damage to the vascular endothelium

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57
Q

Clots in DIC

A

-Fibrin clots are formed in vessels which blocks blood flow to organs and causes multiple organ failure

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58
Q

DIC etiology

A

Sepsis*, trauma, liver disease, malignancy, bacterial & viral infections, pregnancy complications, medical devices, hypoxia & low blood flow states

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59
Q

Slide 30

A
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60
Q

Rate of fibrinolysis in DIC is…

A

Diminished d/t the production of plasminogen which digests clots in addition to the production of pAi-1 which is plasmins natural inhibitor. Excessive plasmin causes bleeding

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61
Q

DIC + hemorrhage

A

Occurs secondary to high consumption of clotting factors and platelets which leads to thrombocytopenia

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62
Q

Clotting in DIC causes…

A

Backflow leading to hypoperfusion. Ischemia, infarction and necrosis ensue

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63
Q

Slide 33

A
64
Q

DIC manifestations

A

-Hemorrhage, shock & low BP, microvascular thrombosis that cannot be seen during organ failure
-Presentation of multisystem organ failure

65
Q

Slide 35

A
66
Q

DIC nursing assessment

A

-Diagnosed based on manifestations & labs (thrombocytopenia, prolonged clotting times & D-dimer)

67
Q

Tx of DIC

A

-Treat underlying cause, control ongoing thrombosis, maintain organ function

68
Q

Hematological conditions

A

Anemia, polycythemias and alterations in leukocyte function

69
Q

Anemia

A

Insufficient volume of erythrocytes

70
Q

Classifications of anemia

A

Cause & changes that affect size, shape or substance of the erythrocyte

71
Q

Causes of anemia

A

-aProduction, blood Loss, increased erythrocyte destruction
-Combination of all Three

72
Q

Slide 39

A
73
Q

Types of anemia

A

Macrocytic-normochromic anemia, pernicious anemia & folate deficiency anemia

74
Q

Pernicious anemia

A

-Gastritis/PUD can lead to pernicious anemia (H. pylori)
-Develops slowly and it is often too late when tx is sought

75
Q

Pathophysiology of pernicious anemia

A

-Absence of intrinsic factor that inhibits vitamin B12 which is needed for maturation & synthesis of RBC

76
Q

Etiology of pernicious anemia

A

-Results from autoimmune gastritis leading to deficiency of all secretions of the stomach including HCL, pepsin, and intrinsic factor
-May be secondary to previous H. pylori infection

77
Q

Manifestations of pernicious anemia

A

-Develops slowly
-Early manifestations: Infections, aMood, and GI, cardiac & kidney ailments

78
Q

Progressing symptoms of pernicious anemia

A

When hemoglobin reaches 70-80; weakness, fatigue, paresthesia of feet & fingers, aGait, decreased apetite, abdominal pain, weight loss, red beefy tongue (glossitis), lemon colored skin, enlarged liver and right sided HF

79
Q

Microcytic-hypochromic anemia

A

-Small erythrocytes that contain reduced amounts of hemoglobin
-Iron deficiency anemia

80
Q

Siderblastic anemia

A

-Insufficient iron uptake that results in abnormal hemoglobin synthesis
-Acquired, hereditary, and reversible

81
Q

Normocytic-normochromic anemia

A

-Depletion of T-cells
-Aplastic anemia; body stops producing new blood cells (look at growth plates to differentiate from idiopathic thrombocytopenia)
-Insufficient erythropoiesis is likely autoimmune in nature

82
Q

Normocytic-normochromic anemia presents as…

A

Pancytopenia or may present as only one deficiency (ITP or RBC’s)

83
Q

Pancytopenia

A

Reduced WBC, RBC & platelets

84
Q

Manifestations of normocytic-normochromic anemia

A

-Hypoxemia, pallor, GIB, prolonged bleeding, menorrhagia, purpura, peresthesias, and weakness with fever & dyspnea
-Diminished leukocytes may result in increased frequency and prolonged infections

85
Q

Other types of anemia

A

-Post hemorrhagic, hemolytic, and chronic inflammation anemia

86
Q

Polcythemia

A

Excessive RBC production causing a hypercoaguable state

87
Q

Types of polcythemia

A

Relative & absolute AKA polcythemia vera

88
Q

Polycythemia vera

A

-Abnormal proliferation of bone marrow stem cells with subsequent self-destructive expansion of RBCs
-Etiology is unknown

89
Q

Polycythemia + hereditary hemochromatosis

A

-Autosomal recessive disorder
-Characterized by GI iron absorption with subsequent tissue iron deposition

90
Q

Polycythemia + hereditary hemochromatosis manifestations

A

-Fatigue, fever, malaise, abdominal pain, arthralgia’s and impotence
-Clinical findings of hepatomegaly, cardiomegaly, aLiver enzymes, bronzed skin, and diabetes

91
Q

Slide 48

A
92
Q

Myeloid gives…

A

Lineage to neutrophils & basophils

93
Q

Blast cells are..

A

Immature

94
Q

Anything ending in cyte is a..

A

Mature cell

95
Q

In pancytopenia..

A

Cells lose the ability to mature

96
Q

Leukocytes (WBC) mnemonic (most abundant to least)

A

-Never (neutrophils)
-Let (lymphocytes)
-Monkeys (monocytes)
-Eat (Eosinophils)
-Bananas (Basophils)

97
Q

Lymphocytes are…

A

B&T cells

98
Q

Basophils release..

A

Histamine (occurs with anaphylaxis)

99
Q

Leukocytosis

A

Increase in leukocytes

100
Q

Leukopenia

A

Decrease in leukocytes

101
Q

Granulocyte & monocyte alterations + increased levels are d/t..

A

-Infection
-Myeloproliferative disorders that increase stem cell production in bone marrow (polycythemia vera & chronic myeloid leukemia)

102
Q

Granulocyte & monocyte alterations + decreased levels are d/t..

A

-Infectious processes that deplete the supply
-Disorders that supress marrow function

103
Q

Alterations in granulocyte and monocyte function + neutrophilia

A

Neutrophilia (numerous); early stages of infection/inflammation

104
Q

Alterations in granulocyte and monocyte function + neutropenia (reduced)

A

Hypoplastic of aplastic anemia, megablastic anemias, leukemia, HIV & Epstein-Barr Virus (EBV)

105
Q

Alterations in granulocyte and monocyte function + easoniophilia

A

Asthma, hay fever or drug interaction

106
Q

Alterations in granulocyte and monocyte function + eosinopenia

A

Cushing’s disease, shock, surgery, burns, trauma or mental distress

107
Q

Basophilia

A

Immediate inflammatory response and hypersensitivity, myeloid metaplasia and Chronic Myelgenous Leukemia (CML)

108
Q

Basopenia

A

Hyperthyroidism, acute infection or long term steroid use

109
Q

Lymphocytosis

A

Viral infections like EBV

110
Q

Lymphocytopenia

A

Associated with HF & HIV

111
Q

Slide 51

A
112
Q

Band neutrophils

A

Immature neutrophils that appear when there is an additional infection that needs to be identified (ie. Catheter + UTI)

113
Q

Myelodysplastic syndrome (MDS)

A

-Group of diseases in which the bone marrow doesn’t make enough healthy mature blood cells
-Myeloid blast cells do not work properly and build up in the bone marrow and the blood

114
Q

Manifestations of myelodysplastic syndrome (MDS)

A

Fever, fatigue, frequent infections, easy bruising and bleeding, paleness, SOB, general feeling of discomfort or illness, abdominal discomfort or a feeling of fullness if the spleen or liver is enlarged

115
Q

Myelo= & dysplastic =

A

-Myelo = myeloid
-Dysplastic = abnormal

116
Q

Myelodysplastic syndrome (MDS) + leukemia

A

-Sometimes referred to as a pre-leukemia (pre-AML) BUT these cells are NOT dividing rapidly like in leukemia
-Abnormal cell has to acquire a second mutation to turn into leukemia (rare)

117
Q

Clinical manifestations of MDS are r/t…

A

-Immature myeloid blast cells (remember myeloid lineage gives rise to RBC, PLT, WBC)

118
Q

MDS + fever & frequent infection manifestations are d/t

A

A lack of mature WBC

119
Q

MDS + east bruising & bleeding is d/t…

A

A lack of mature PLT

120
Q

MDS + paleness, SOB, general feeling of discomfort or illness is d/t

A

A lack of mature RBC

121
Q

MDS + S&S d/t spleen and liver enlargement is r/t

A

The spleen and liver trying to compensate for the lack of mature cells in the circulation
Its hyperactivity & enlargement causes abdominal discomfort and a feeling of “fullness”

122
Q

Leukemia is a…

A

-Malignant disorder of the blood
-Uncontrolled proliferation of malignant leukocytes causing overcrowding in the bone marrow and decreased production and function of hematopoietic cells

123
Q

Acute leukemia

A

-Characterized by undifferentiated or immature cells called blast cells
-Onset is abrupt, rapid and has a short survival

124
Q

Chronic leukemia

A

-Cell is mature but does not function
-Onset is gradual and survival is longer

125
Q

Blast buildup + leukemia

A

Blast cells overcrowd bone marrow which prevents fighting off an infection

126
Q

Origin of leukemia

A

Myeloid or lymphoid

127
Q

Lymphoid origin of leukemia

A

-Overproduction of B-cells/T-cells
-Includes acute lymphocytic (ALL) & chronic lymphocytic (CLL)

128
Q

Myeloid origin of leukemia

A

-Overproduction of granulocytes/monocytes
-Includes acute myelogenous (AML) & chronic myelogenous (CML)

129
Q

Fever + acute leukaemic phase

A

-It is usually too late and they are septic. To prevent this, closely monitor temperature. Survival is more likely in chronic leukemia

130
Q

Pancytopenia

A

-Associated when leukemia blasts take over the marrow and cause cellular proliferation
-Characterized in aplastic anemia
-Reduction in all cellular components of the blood
-Patients may become immunocompromised (fevers are very serious!)

131
Q

Priorities in pancytopenia

A

-Priorities include oxygenation and dysfunction in immunity
-Monitor for bleeding, SOB & fever

132
Q

Alterations in the lymphatic system

A

-Lymphadenopathy; enlarged lymph nodes likely as a result of an infectious process or mass

133
Q

Erythrocytes

A

Most abundant cells of the blood, responsible for tissue oxygenation

134
Q

Slide 60-65

A
135
Q

Diagnostic evaluation of hemolytic disease of the newborn + prenatal

A

-Maternal blood type & Rh factor
-Indirect Coomb’s test
-Amniocentesis

136
Q

Indirect Coomb’s test is used…

A

To determine the presence of Rh sensitization

137
Q

Amniocentesis is used to…

A

Determine the amount of bilirubin by-products indicating the severity of hemolytic activity (can be done as early as 26 weeks)

138
Q

Diagnostic evaluation of hemolytic disease in the newborn + intrapartum

A

-Observation of amniotic fluid after the membrane rupture
-Straw-colored fluid indicates a mild disease
-Golden fluid indicates a severe fetal disease

139
Q

Diagnostic evaluation of hemolytic disease in the newborn + postnatal

A

Direct Coomb’s blood test, a positive result demonstrates Rh antibodies in the fetal blood

140
Q

Manifestations of hemolytic disease in the newborn

A

-Neonates with mild HDN may appear healthy or slightly pale, with slight enlargement of the liver or spleen
-Severe anemia: Pallor, splenomegaly, hepatomegaly, and CV failure +/- shock
-Hyperbilirubinemia (neonatal jaundice) leads to Kernicterus (caused by severe jaundice), cerebral damage and death

141
Q

Tx of jaundice

A

Feed the baby so it passes the bilirubin

142
Q

Slide 70&71

A
143
Q

Generalized rashes are usually d/t

A

Systemic exposures or illnesses

144
Q

Systemic exposures/illnesses causing generalized rashes

A

-Drug eruptions, viral illnesses, toxin-mediated processes and immune-mediated conditions
-Typically result in something else

145
Q

Specialized features of localized rashes

A

Show part of a generalized rash and may help determine the etiology

146
Q

Sequnce of a rash

A

-Where did it start?
-How did it spread and over what time?
-How has it evolved over time?
-Does it fluctuate?

147
Q

Generalized itch indicates

A

-Infectious diseases, allergies, liver disease with jaundice and medication reactions

148
Q

Localized itch etiology

A

Skin irritation from an insect bite or sting

149
Q

Difference between a generalized & localized itch

A

Distribution & timing

150
Q

Causes of localized or generalized itch

A

Chemical irritation (poison ivy), environment (drying, sunburn), hives (localized to general) and parasites (lice-body, head & pubic)

151
Q

S&S associated with pruritis

A

-Fever, cough, conjunctivitis, runny nose, sore throat, tongue changes (strawberry)
-Pain, weakness
-Abdominal pain, N/V, diarrhea, dizziness, headache and swollen extremities

152
Q

Branches involved in rashes that suggest particular etiologies

A

-Palms & soles
-Lower extremeties
-Mouth and/or tongue
-Eyes

153
Q

Common etiologies: Palms & soles

A

-Hand-foot-mouth disease
-Scabies, atopic dermatitis, and allergic rashes

154
Q

Common etiologies of oral rashes

A

Candidiases, hand-foot-mouth disease, varicella, scarlet fever, measles, Kawasaki syndrome and Steven Johnson Syndrome

155
Q

Common viral causes of conjunctiva

A

Measles, rubella & varicella

156
Q

Common bacterial etiologies of conjunctiva

A

Rocky mountain spotted fever & meningococcal infection

157
Q

Slide 86-88

A

Be able to identify a picture of each one

CV487 (15 decks)

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