Class 10: Pain & Alterations in Hematological Function Flashcards
1
Q
Nociceptors are..
A
Free nerve endings in the afferent PNS
2
Q
3 portions of the nervous system responsible for sensation, perception and pain response
A
-Afferent pathways, interpretive pathways and interpretive centers
3
Q
Afferent pathways are.. & stimuli goes..
A
-Where nociceptors live in the PNS
-Stimuli go to the dorsal horn then to the CNS
4
Q
Interpretive centers include the..
A
Brainstem, midbrain diencephalon and the cortex
5
Q
Efferent pathways do what and stimuli goes where?
A
-Respond to pain
-CNS to dorsal horn and then to the spinal cord
6
Q
Pain can be…
A
Emotional, spiritual or cultural
7
Q
Phases of nociception
A
-Pain transduction, transmission, perception and modulation
8
Q
Slide 8&9
A
9
Q
Glutamate is a…
A
Excitatory neurotransmitter that has a role with chronic pain
10
Q
Substance P is…
A
A tachykinin released from afferent fibers during inflammation
-Co-exists with glutamate
11
Q
Histamine does what?
A
Evokes the release of substance P and plays a role in neurogenic inflammation and leads to vasodilation
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
13
Q
Bradykinin causes and acts with…
A
Vasodilation, acts with prostaglandins
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
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
16
Q
Reticular and limbic system…
A
Receive pain stimuli
17
Q
Initial acute pain…
A
Induces a sympathetic response, over time it causes a behavioural response
18
Q
Slide 10,11&12
A
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)
20
Q
Neurogenic pain
A
-Neuralgia (pain in the distribution of a nerve)
-Constant pain is either sympathetically independent or sympathetically dependent
21
Q
Temporal pain (time related, duration)
A
-Acute pain; somatic
-Visceral pain; chronic
22
Q
Nociceptive pain is blank, whearas neuropathic pain is…
A
-Normal processing of a stimulus
-Abnormal processing
23
Q
Somatic pain is in the…
A
-Joints & muscles that begin with a-delta then leads to c-alpha fibers
24
Q
Visceral pain is transmitted with…
A
C-fibers and can radiate
25
Slide 16-18
26
Composition of blood
Plasma, albumin & globulins
27
Cellular components of blood
-Erythrocytes, leukocytes & platelets
28
Leukocytes
-Granulocytes (neutrophil, eosinophils, basophils & mast cells)
-Agranulocytes (phagocytes or immunocytes) (lymphocytes)
29
Albumin regulates...
Water, and when there is too little, fluid moves to the extracellular space. This decreases oncotic pressure and fluid moves into the extravascular space
30
Albumin is given to...
Move fluid into the intravascular space
31
The first thing to increase when there is an infection is what?
Neutrophils
32
How to test for mast cells test
CRP protein which indicates inflammation
33
Lymphocytes are and do what?
-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
34
T-cells come from the...
Thymus (form mature T-lymphocytes)
35
Think of lymph nodes as...
Check stops to identify viruses
36
Primary lymphoid organs
Thymus, bone marrow, spleen and lymph nodes
37
The spleen does what
-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
38
Platelets induce what
Vasoconstriction, the clotting cascade and the repair process (fibrinolysis)
39
Virchow's triad
Hemostasis, hypercoagulability and endothelial damage
40
Manifestations of altered platelet function
-Spontaneous petechiae and purpura (thrombocytopenia; low platelets)
-Bleeding from GI tract, GU tract, pulmonary mucosa and gums
41
Petchiae is blank than purpura
Smaller
42
Systemic disorders that affect platelet function
-Chronic renal failure, liver disease, cardiopulmonary bypass surgery, severe iron or folate deficiency, and antiplatelet antibodies associated with autoimmune disorders
Hematological disorders
43
Petechiae develops when...
Platelets are less than 50
44
If platelets are less than 20 then...
The patient can bleed for no reason
45
Petechiae, purpura and ecchymosis are all...
Signs of bleeding
46
Heparin induced thrombocytopenia (HIT) is 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
47
In HIT, monitor for...
platelet levels dropping & virchow's triad
48
HIT develops because of a...
Previous tx of heparin (d/t cardiac issues), and in subsequent admissions patients are at risk for HIT
49
HIT manifestations
-Thrombocytopenia *, venous thrombosis resulting in DVT, arterial thrombosis of lower extremities leading to limb ischemia
50
Evaluation & tx of HIT
-HIT antibody teeter level & lab values
-Withdraw heparin and use alternative anticoagulants... NO COUMADIN
51
Coagulation disorders
-Impaired hemostasis
-Consumptive thrombohemorrhagic disorders
52
Impaired hemostasis
-Inability to promote coagulation and develop a stable fibrin clot
-Examples include Vitamin K deficiency and liver disease (usually associated with liver disease)
53
Consumptive thrombohemorrhagic disorders
Disseminated intravascular coagulation (DIC)
54
DIC
-Occurs in sepsis & maternity lesions
-Hospital-acquired condition
-Clots start to form and puts the pt at risk for simultaneous bleeding and clotting
55
Pathophysiology of DIC
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.
56
DIC begins with
Damage to the vascular endothelium
57
Clots in DIC
-Fibrin clots are formed in vessels which blocks blood flow to organs and causes multiple organ failure
58
DIC etiology
Sepsis*, trauma, liver disease, malignancy, bacterial & viral infections, pregnancy complications, medical devices, hypoxia & low blood flow states
59
Slide 30
60
Rate of fibrinolysis in DIC is...
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
61
DIC + hemorrhage
Occurs secondary to high consumption of clotting factors and platelets which leads to thrombocytopenia
62
Clotting in DIC causes...
Backflow leading to hypoperfusion. Ischemia, infarction and necrosis ensue
63
Slide 33
64
DIC manifestations
-Hemorrhage, shock & low BP, microvascular thrombosis that cannot be seen during organ failure
-Presentation of multisystem organ failure
65
Slide 35
66
DIC nursing assessment
-Diagnosed based on manifestations & labs (thrombocytopenia, prolonged clotting times & D-dimer)
67
Tx of DIC
-Treat underlying cause, control ongoing thrombosis, maintain organ function
68
Hematological conditions
Anemia, polycythemias and alterations in leukocyte function
69
Anemia
Insufficient volume of erythrocytes
70
Classifications of anemia
Cause & changes that affect size, shape or substance of the erythrocyte
71
Causes of anemia
-aProduction, blood Loss, increased erythrocyte destruction
-Combination of all Three
72
Slide 39
73
Types of anemia
Macrocytic-normochromic anemia, pernicious anemia & folate deficiency anemia
74
Pernicious anemia
-Gastritis/PUD can lead to pernicious anemia (H. pylori)
-Develops slowly and it is often too late when tx is sought
75
Pathophysiology of pernicious anemia
-Absence of intrinsic factor that inhibits vitamin B12 which is needed for maturation & synthesis of RBC
76
Etiology of pernicious anemia
-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
Manifestations of pernicious anemia
-Develops slowly
-Early manifestations: Infections, aMood, and GI, cardiac & kidney ailments
78
Progressing symptoms of pernicious anemia
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
Microcytic-hypochromic anemia
-Small erythrocytes that contain reduced amounts of hemoglobin
-Iron deficiency anemia
80
Siderblastic anemia
-Insufficient iron uptake that results in abnormal hemoglobin synthesis
-Acquired, hereditary, and reversible
81
Normocytic-normochromic anemia
-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
Normocytic-normochromic anemia presents as...
Pancytopenia or may present as only one deficiency (ITP or RBC’s)
83
Pancytopenia
Reduced WBC, RBC & platelets
84
Manifestations of normocytic-normochromic anemia
-Hypoxemia, pallor, GIB, prolonged bleeding, menorrhagia, purpura, peresthesias, and weakness with fever & dyspnea
-Diminished leukocytes may result in increased frequency and prolonged infections
85
Other types of anemia
-Post hemorrhagic, hemolytic, and chronic inflammation anemia
86
Polcythemia
Excessive RBC production causing a hypercoaguable state
87
Types of polcythemia
Relative & absolute AKA polcythemia vera
88
Polycythemia vera
-Abnormal proliferation of bone marrow stem cells with subsequent self-destructive expansion of RBCs
-Etiology is unknown
89
Polycythemia + hereditary hemochromatosis
-Autosomal recessive disorder
-Characterized by GI iron absorption with subsequent tissue iron deposition
90
Polycythemia + hereditary hemochromatosis manifestations
-Fatigue, fever, malaise, abdominal pain, arthralgia's and impotence
-Clinical findings of hepatomegaly, cardiomegaly, aLiver enzymes, bronzed skin, and diabetes
91
Slide 48
92
Myeloid gives...
Lineage to neutrophils & basophils
93
Blast cells are..
Immature
94
Anything ending in cyte is a..
Mature cell
95
In pancytopenia..
Cells lose the ability to mature
96
Leukocytes (WBC) mnemonic (most abundant to least)
-Never (neutrophils)
-Let (lymphocytes)
-Monkeys (monocytes)
-Eat (Eosinophils)
-Bananas (Basophils)
97
Lymphocytes are...
B&T cells
98
Basophils release..
Histamine (occurs with anaphylaxis)
99
Leukocytosis
Increase in leukocytes
100
Leukopenia
Decrease in leukocytes
101
Granulocyte & monocyte alterations + increased levels are d/t..
-Infection
-Myeloproliferative disorders that increase stem cell production in bone marrow (polycythemia vera & chronic myeloid leukemia)
102
Granulocyte & monocyte alterations + decreased levels are d/t..
-Infectious processes that deplete the supply
-Disorders that supress marrow function
103
Alterations in granulocyte and monocyte function + neutrophilia
Neutrophilia (numerous); early stages of infection/inflammation
104
Alterations in granulocyte and monocyte function + neutropenia (reduced)
Hypoplastic of aplastic anemia, megablastic anemias, leukemia, HIV & Epstein-Barr Virus (EBV)
105
Alterations in granulocyte and monocyte function + easoniophilia
Asthma, hay fever or drug interaction
106
Alterations in granulocyte and monocyte function + eosinopenia
Cushing's disease, shock, surgery, burns, trauma or mental distress
107
Basophilia
Immediate inflammatory response and hypersensitivity, myeloid metaplasia and Chronic Myelgenous Leukemia (CML)
108
Basopenia
Hyperthyroidism, acute infection or long term steroid use
109
Lymphocytosis
Viral infections like EBV
110
Lymphocytopenia
Associated with HF & HIV
111
Slide 51
112
Band neutrophils
Immature neutrophils that appear when there is an additional infection that needs to be identified (ie. Catheter + UTI)
113
Myelodysplastic syndrome (MDS)
-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
Manifestations of myelodysplastic syndrome (MDS)
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
Myelo= & dysplastic =
-Myelo = myeloid
-Dysplastic = abnormal
116
Myelodysplastic syndrome (MDS) + leukemia
-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
Clinical manifestations of MDS are r/t...
-Immature myeloid blast cells (remember myeloid lineage gives rise to RBC, PLT, WBC)
118
MDS + fever & frequent infection manifestations are d/t
A lack of mature WBC
119
MDS + east bruising & bleeding is d/t...
A lack of mature PLT
120
MDS + paleness, SOB, general feeling of discomfort or illness is d/t
A lack of mature RBC
121
MDS + S&S d/t spleen and liver enlargement is r/t
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
Leukemia is 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
Acute leukemia
-Characterized by undifferentiated or immature cells called blast cells
-Onset is abrupt, rapid and has a short survival
124
Chronic leukemia
-Cell is mature but does not function
-Onset is gradual and survival is longer
125
Blast buildup + leukemia
Blast cells overcrowd bone marrow which prevents fighting off an infection
126
Origin of leukemia
Myeloid or lymphoid
127
Lymphoid origin of leukemia
-Overproduction of B-cells/T-cells
-Includes acute lymphocytic (ALL) & chronic lymphocytic (CLL)
128
Myeloid origin of leukemia
-Overproduction of granulocytes/monocytes
-Includes acute myelogenous (AML) & chronic myelogenous (CML)
129
Fever + acute leukaemic phase
-It is usually too late and they are septic. To prevent this, closely monitor temperature. Survival is more likely in chronic leukemia
130
Pancytopenia
-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
Priorities in pancytopenia
-Priorities include oxygenation and dysfunction in immunity
-Monitor for bleeding, SOB & fever
132
Alterations in the lymphatic system
-Lymphadenopathy; enlarged lymph nodes likely as a result of an infectious process or mass
133
Erythrocytes
Most abundant cells of the blood, responsible for tissue oxygenation
134
Slide 60-65
135
Diagnostic evaluation of hemolytic disease of the newborn + prenatal
-Maternal blood type & Rh factor
-Indirect Coomb's test
-Amniocentesis
136
Indirect Coomb's test is used...
To determine the presence of Rh sensitization
137
Amniocentesis is used to...
Determine the amount of bilirubin by-products indicating the severity of hemolytic activity (can be done as early as 26 weeks)
138
Diagnostic evaluation of hemolytic disease in the newborn + intrapartum
-Observation of amniotic fluid after the membrane rupture
-Straw-colored fluid indicates a mild disease
-Golden fluid indicates a severe fetal disease
139
Diagnostic evaluation of hemolytic disease in the newborn + postnatal
Direct Coomb's blood test, a positive result demonstrates Rh antibodies in the fetal blood
140
Manifestations of hemolytic disease in the newborn
-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
Tx of jaundice
Feed the baby so it passes the bilirubin
142
Slide 70&71
143
Generalized rashes are usually d/t
Systemic exposures or illnesses
144
Systemic exposures/illnesses causing generalized rashes
-Drug eruptions, viral illnesses, toxin-mediated processes and immune-mediated conditions
-Typically result in something else
145
Specialized features of localized rashes
Show part of a generalized rash and may help determine the etiology
146
Sequnce of a rash
-Where did it start?
-How did it spread and over what time?
-How has it evolved over time?
-Does it fluctuate?
147
Generalized itch indicates
-Infectious diseases, allergies, liver disease with jaundice and medication reactions
148
Localized itch etiology
Skin irritation from an insect bite or sting
149
Difference between a generalized & localized itch
Distribution & timing
150
Causes of localized or generalized itch
Chemical irritation (poison ivy), environment (drying, sunburn), hives (localized to general) and parasites (lice-body, head & pubic)
151
S&S associated with pruritis
-Fever, cough, conjunctivitis, runny nose, sore throat, tongue changes (strawberry)
-Pain, weakness
-Abdominal pain, N/V, diarrhea, dizziness, headache and swollen extremities
152
Branches involved in rashes that suggest particular etiologies
-Palms & soles
-Lower extremeties
-Mouth and/or tongue
-Eyes
153
Common etiologies: Palms & soles
-Hand-foot-mouth disease
-Scabies, atopic dermatitis, and allergic rashes
154
Common etiologies of oral rashes
Candidiases, hand-foot-mouth disease, varicella, scarlet fever, measles, Kawasaki syndrome and Steven Johnson Syndrome
155
Common viral causes of conjunctiva
Measles, rubella & varicella
156
Common bacterial etiologies of conjunctiva
Rocky mountain spotted fever & meningococcal infection
157
Slide 86-88
Be able to identify a picture of each one
