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NURS 487 > pain and hema > Flashcards

pain and hema Flashcards

1
Q

nociceptors

A

Processing harmful stimuli in anormal functioning nervous system is called nociception
Nociceptors or pain receptors are free nerve endings in the afferent peripheral nervous system stimulated = pain
3 portions of the nervous system that are responsible for the sensation, perception, and response to pain:
Afferent pathways
Interpretive centers
Efferent pathways

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2
Q

4 phases of nociception

A

Pain transduction
Pain transmission
Pain perception
Modulation

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3
Q

stimuli for skin

A 
pricking
cutting
crushing
burning
freezing
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4
Q

stimuli for GI tract

A

engorged or inflamed mucosa, distention or spasm of smooth muscle, traction on mesenteric attachment

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5
Q

stimuli for skeletal muscle

A

ischemia, injuries of connective tissue sheaths, necrosis, hemorrhage, prolonged contraction, injection of irritating solutions

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6
Q

stimuli for joints s

A

synovial membrane inflammation

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7
Q

stimuli for arteries

A

piercing, inflammation

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8
Q

stimuli for head

A

traction, inflammation, or displacement of arteries, meningeal structures and sinuses, prolonged muscle contraction

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9
Q

stimuli for heart

A

ischemia and inflammation

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10
Q

stimuli for bone

A

periosteal injury, fractures, tumor, inflammation

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11
Q

goals of pain assessment

A

To describe the patient’s sensory, affective, behavioral, cognitive, and sociocultural pain experience for the purpose of implementing pain management techniques
To identify the patient’s goal for therapy and resources and strategies for effective self-management

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12
Q

sensory-descriminative component of pain assessment

A

Pattern of pain
Area of pain
Intensity of pain
Nature of pain

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13
Q

other things to look at with pain assessment

A

Motivational-Affective, Behavioral, Cognitive-Evaluative, and Sociocultural Components

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14
Q

categories of pain

A 
neurophysiological pain
neurogenic pain 
temporal pain 
regional pain 
etiologic pain
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15
Q

neurophysiologic pain

A

A. Nociceptive pain
1. Somatic (e.g., skin, muscle, bone)
2. Visceral (e.g., intestine, liver, stomach)
B. Neuropathic (non-nociceptive)
1. Central pain (lesion in brain or spinal cord)
2. Peripheral pain (lesion in PNS)

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16
Q

neurogenic pain

A

A. Neuralgia (pain in the distribution of a nerve)
B. Constant
1. Sympathetically independent
2. Sympathetically dependent

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17
Q

temporal pain (time related, duration)

A

A. Acute pain
1. Somatic
2. Visceral
B. Chronic

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18
Q

regional pain

A 
A. Abdominal pain 
B. Chest pain 
C. Headache 
D. Low back pain 
E. Orofacial pain 
F. Pelvic pain
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19
Q

etiologic pain

A 
A. Cancer pain 
B. Dental pain 
C. Inflammatory pain 
D. Ischemic pain 
E. Vascular pain
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20
Q

causes of acute pain in peds

A 
Medical procedures
Surgical procedures
Medical treatments
Injury
Infection
Exacerbation of arthritis, sickle cell disease, cancer
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21
Q

pain intensity for peds

A

Defined as behavioral measures, physiological measures, and measures of self-report
Address domain of pain intensity
Based on age of the child

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22
Q

young infant response to pain

A

Generalized body response of rigidity or thrashing, possibly with local reflex withdrawal of stimulated area
Loud crying
Facial expression of pain (brows lowered and drawn together, eyes tightly closed, mouth open and squarish)
No association demonstrated between approaching stimulus and subsequent pain

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23
Q

older infant response to pain

A

Localized body response with deliberate withdrawal of stimulated area
Loud crying
Facial expression of pain or anger
Physical resistance, especially pushing the stimulus away after it is applied

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24
Q

young child response to pain

A

Loud crying, screaming
Verbal expressions such as “Ow,” “Ouch,” “It hurts”
Thrashing of arms and legs
Attempts to push stimulus away before it is applied
Lack of cooperation; need for physical restraint
Requests for termination of procedure
Clinging to parent, nurse, or other significant person
Requests for emotional support, such as hugs or other forms of physical comfort
Becoming restless and irritable with continuing pain
Behaviours occurring in anticipation of actual painful procedure

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25
Q

school-aged child response to pain

A

May see all behaviours of young child, especially during actual painful procedure, but less in anticipatory period
Stalling behaviour, such as “Wait a minute” or “I’m not ready”
Muscular rigidity, such as clenched fists, white knuckles, gritted teeth, contracted limbs, body stiffness, closed eyes, wrinkled forehead

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26
Q

adolescent response to pain

A

Less vocal protest
More verbal expressions, such as “It hurts” or “You’re hurting me”
Increased muscle tension and body control

27
Q

composition of blood

A

Plasma
Albumin
Globulins

28
Q

cellular components of blood

A

Erythrocytes
Leukocytes
Granulocytes (neutrophil, eosinophils, basophils, mast cells
Agranulocytes (phagocytes or immunocytes)
Platelets

29
Q

structure of lymphoid organs

A 
Primary lymphoid organs
Thymus and bone marrow
Spleen
Golden hour to rupture
Lymph nodes
30
Q

function of platelets

A

Contribute to regulation of blood flow in a damaged site by inducing vasoconstriction
Initiate platelet-to-platelet interactions resulting in a platelet plug to stop further bleeding
Activate the coagulation (or clotting) cascade to stabilize the plug
Initiate repair processes including clot retraction and clot dissolution (fibrinolysis)

31
Q

damage to the vessel initiates a process of platelet activation

A

Adhesion to damaged vascular wall
Secretion of chemicals that simulate changes in platelet shape and biochemistry
Aggregation of platelet to wall and platelet to platelet

32
Q

clinical manifestations of platelet dysfunction

A

Spontaneous petechiae and purpura

Bleeding from GI tract, GU tract, pulmonary mucosa and gums

33
Q

systemic disorders that affect platelet function

A 
Chronic renal failure
Liver disease
Cardiopulmonary bypass surgery
Severe deficiencies of iron or folate
Antiplatelet antibodies associated with autoimmune disorders
Hematological disorders
34
Q

heparin induced thrombocytopenia

A

Occurs primarily with IV heparin but there is a small incidence associated with LMWH
Immune-mediated, adverse drug reaction caused by IgG Antibodies
Increased platelet consumption and decrease in platelet count
BEGINS 5-10 DAYS after administration of heparin

35
Q

clinical manifestations of HIT

A

Thrombocytopenia *
Watch the trends in the blood work!!!
Venous thrombosis resulting in DVT and PE
Arterial thrombosis leading to limb ischemia

36
Q

evaluation and treatment for HIT

A

Clinical observations
Lab values
Withdraw heparin and use alternative anticoagulants NO COUMADIN

37
Q

impaired hemostasis

A

Inability to promote coagulation and develop stable fibrin clot
Usually associated with liver disease
Examples include Vitamin K deficiency and liver disease

38
Q

consumptive thrombohemorrhagic disorders

A

Disseminated intravascular coagulation

39
Q

Disseminated Intravascular Coagulation(DIC)

A

Acquired syndrome (a cause) that activates systemic coagulation
Damage to the vascular endothelium
Fibrin clots are formed in medium and small vessels
Blocks blood flow to organs multiple organ failure
Consumption of platelets and clotting factors that Leads to bleeding

40
Q

Disseminated Intravascular CoagulationEtiology

A 
Sepsis*
Malignancy
Infections (bacterial and viral
Intravascular hemolysis
Transfusion reactions
Drug induced hemolysis
Pregnancy complications
Eclampsia or preeclampsia
Placental abruption
Amniotic fluid embolism
Trauma 
Head injury
Burns
Tissue necrosis (Necrotizing fasciitis)
Liver disease
Obstructive jaundice
Prosthetic devices
Medical devices
Hypoxia and low blood flow states
Arterial hypotension secondary to shock
Cardiopulmonary arrest
41
Q

patho of DIC

A

Vascular damage  clotting cascade is activated to repair and protect
Tissue factor is released by the endothelium
Stimulation of cells such as inflammatory cytokines
Proinflammatory cytokines and platelet activating factor responsible for manifestations of DIC
Tissue factor binds to factor VII which converts prothrombin to thrombin and forms fibrin clots
Rate of fibrinolysis is diminished in DIC
Plasminogen plasmin that digests clots but pAi-1 (natural inhibitor to plasmin) is produced during DIC
These patients are at risk for severe bleeding EMERGENCY!!!
Hemorrhage occurs secondary to high consumption of clotting factors and platelets which leads to thrombocytopenia
Clots block blood flow  leads to hypoperfusion ischemia, infarction and necrosis

42
Q

clinical manifestations of DIC

A

Symptoms related to hemorrhage or thrombosis
Presents:
Rapid development of hemorrhage
Shock and low blood pressure
Microvascular thrombosis that cannot be seen leading to organ failure

Presentation of multisystem failure

43
Q

nursing assessment for DIC

A

Prompt recognition of symptoms
Diagnosis based on clinical manifestations and combination of laboratory tests
Thrombocytopenia and prolonged clotting times and D-dimer

44
Q

treatment of DIC

A

Treat underlying cause
Control ongoing thrombosis
Maintain organ function

45
Q

hematological conditions

A

Anemia’s
Polycythemias
Alterations in Leukocyte Function

46
Q

anemia

A 
Too few erythrocytes or insufficient volume of erythrocytes in blood
Classified 2 Ways:
Cause
Altered Production
Blood Loss
Increased Erythrocyte Destruction
Combination of all Three
Changes that affect the size, shape, or substance of the erythrocyte
47
Q

macrocytic-normochromic anemia

A

Characterized by large stem cells in the bone marrow that mature into erythrocytes that are unusually large in size, thickness, and voluvme
Result of ineffective DNA synthesis caused by deficiencies of Vitamin B12 (cobalamin) or folate (folic acid)
Defective erythrocytes die prematurely (eryptosis)

2 primary types:
Pernicious Anemia *
Folate Deficiency Anemia

48
Q

patho of pernicious anemia

A

Absence of intrinsic factor, a transporter required for gastric absorption of dietary Vitamin B 12, a vitamin essential for nuclear maturation and DNA synthesis in RBC
Result from autoimmune gastritis (gastric atrophy results from destruction of parietal and zymogenic cells) leads to deficiency of all secretions of the stomach, HCL, pepsin, and intrinsic factor
May be secondary to previous H. pylori infection

49
Q

clinical manifestations of pernicious anemia

A

Develops slowly
Early infections, mood swings, and GI, cardiac, and kidney ailments
When Hgb drops to 70-80 g/L patient may be weak, fatigue, paresthesia of feet and fingers, difficulty in walking, loss of appetite, abdominal pains, weight loss, tongue may become sore, smooth, and beefy red secondary to atrophic glossitis, skin may become sallow or “lemon yellow” due to pallor and icterus, enlarged liver, and rt sided heart failure

50
Q

microcytic-hypochromic anemia

A

Small erythrocytes that contain reduced amounts of hemoglobin
Iron Deficiency Anemia

51
Q

siderblastic anemia

A

Insufficient iron uptake, that results in abnormal hemoglobin synthesis
Acquired
Hereditary
Reversible

52
Q

normocytic-normochromic anemia

A

Aplastic
Insufficient erythropoiesis likely autoimmune in nature
Depletion of T-cells
Presents as pancytopenia or may present as only one deficiency (ITP or RBC’s)
Clinical manifestations: hypoxemia, pallor, and weakness with fever and dyspnea, bleeding in the GI tract, prolonged bleeding at other sites, menorrhagia, purpura, diminished leukocytes may result in progressive frequency and prolonged infections, paresthesias

53
Q

other types of anemia

A

Post Hemorrhagic
Hemolytic
Anemia of Chronic Inflammation

54
Q

polycythemia

A

Excessive red blood cell production

Two primary kinds;
Relative
Absolute aka Polycythemia Vera
abnormal proliferation of bone marrow stem cells with subsequent self-destructive expansion of red cells.
Etiology is unknown
Creates hypercoagulability
Hereditary Hemochromatosis
Autosomal recessive disorder
Characterized by GI iron absorption with subsequent tissue iron deposition
Symptoms such as fatigue, malaise, abdominal pain, arthralgia’s and impotence, and clinical findings of hepatomegaly, abnormal liver enzymes, bronzed skin, diabetes, and cardiomegaly

55
Q

mnemonic for white blood cells

A 
Never (Neutrophils)
Let (Lymphocytes)
Monkeys (Monocytes)
Eat (Eosinophils)
Bananas (Basophils)
(ordered most abundant to least abundant)
56
Q

leukocytosis

A

increase in leukocytes in the blood

57
Q

leukopenia

A

decrease in leukocytes in the blood

58
Q

granulocytes and monocyte alterations

A

Granulocyte and Monocyte Alterations:

  • Increased levels are due to a physiologic response to microbial invasion, or due to myeloproliferative disorders that increase stem cell proliferation in the bone marrow (polycythemia vera, chronic myeloid leukemia)
  • Decreased levels are due to infectious processes that deplete the supply or disorders that suppress marrow function
59
Q

Myelodysplastic Syndrome (MDS)

A

Group of diseases in which the bone marrow doesn’t make enough healthy mature blood cells
Immature myeloid blood cells, called blasts, do not work properly and build up in the bone marrow and the blood
Clinical Manifestations: fever, frequent infections, easy bruising and bleeding, fatigue, paleness, shortness of breath, general feeling of discomfort or illness, abdominal discomfort or a feeling of fullness if the spleen or liver is enlarged

60
Q

leukemia

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
Acute Leukemia
Characterized by undifferentiated or immature cells called blast cells
Onset is abrupt and rapid, short survival.
Chronic Leukemia
Cell is mature but does not function
Onset is gradual and survival is longer

61
Q

origin of leukemia

A 
lymphoid origin (overproduction of b-cells/t-cells) = acute lymphocytic (ALL), chronic lymphocytic (CLL)
meloid origin (overproduction of granulocytes/monocytes) = acute myelogenous (AML), chronic myelogenous (CML)
62
Q

origin of leukemia

A 
lymphoid origin (overproduction of b-cells/t-cells) = acute lymphocytic (ALL), chronic lymphocytic (CLL)
meloid origin (overproduction of granulocytes/monocytes) = acute myelogenous (AML), chronic myelogenous (CML)
63
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
Red blood cells, white blood cells and platelets
Priorities include oxygenation and dysfunction in immunity
Patients may become immunocompromised (Fevers are very serious!)

64
Q

lymphadenopathy

A

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

NURS 487 (8 decks)

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