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Med Surg Block 3 > Test 1 > Flashcards

Test 1 Flashcards

1
Q

Normal Hemostasis

A
  • involves the vascular endothelium, platelets, and coagulation factors.
  • function together to stop hemorrhage and repair vascular injury.
  • disruption of any component may result in bleeding or thrombotic disorder
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2
Q

Thrombocytopenia can be ________ or ________

A
  • inherited

- Aquired

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3
Q

Acquired thrombocytopenia types (theres 3 of them)

A

Immune thrombocytopenia purpura (ITP)
Thrombotic thrombocytopenia purpura (TTP)
Heparin-induced thrombocytopenia (HIT)

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4
Q

Immune Thrombocytopenic Purpura (ITP)

What do you know about it??

A
  • most common acquired thrombocytopenia
  • syndrome of abnormal destruction of circulating platelets
  • primarily an autoimmune disease
  • body decides platelets are foreign and attacks/destroys
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5
Q

Thrombotic Thrombocytopenic Purpura (TTP)

What do you know about it??

A
  • uncommon syndrome
  • almost always associated with hemolytic-uremic syndrome (body is attacking all blood cells. MEDICAL EMERGENCIES)
  • associated with enhanced aggregation of platelets that form microthrombi
  • medical emergency- bleeding and clotting occur simultaneously
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6
Q

What is Thrombocytopenia

A

lack of platelets. not enough of them or getting destroyed in blood stream or in spleen and liver.

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7
Q

what is the lifespan of a platelet

A

5-6 days

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8
Q

Normal platelet range

A

150,000-450,000

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9
Q

Heparin-induced Thrombocytopenia (HIT)

A

platelet destruction and vascular endothelial injury are the two major responses to an immune-mediated response to heparin.

  • Associated with increased use of heparin
  • Life-threatening
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10
Q

Two major responses to an immune-mediated response to heparin

A

Platelet destruction

Vascular endothelial injury

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11
Q

Additional complications of Heparin induced Thrombocytopenia (HIT)

A

may include arterial vascular infarcts resulting in skin necrosis, stroke, and end-organ damage (e.g., kidneys).

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12
Q

Why are symptoms of bleeding rare with HIT

A

the platelet count rarely drops below 60,000/μL.

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13
Q

Clinical manifestations of Thrombocytopenia

A
  • Patients are often asymptomatic.
  • Most common symptom is mucosal or *cutaneous bleeding.
  • Petechiae – microhemorrhages
  • Purpura – bruise from numerous petechiae
  • Ecchymoses – larger lesions from hemorrhage
  • Prolonged bleeding after routine procedures.
  • Hemmorhage
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14
Q

Petechiae

A

small, flat, pinpoint, red or reddish-brown microhemorrhages. When the platelet count is low, RBCs may leak out of the blood vessels and into the skin to cause petechiae.

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15
Q

Purpura

A

When petechiae are numerous, the resulting reddish skin bruise is called purpura.

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16
Q

ecchymoses

A

Larger purplish lesions caused by hemorrhage. Ecchymoses may be flat or raised; pain and tenderness sometimes are present

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17
Q

With thrombocytopenia- internal bleeding may manifest as

A

weakness, fainting, dizziness, tachycardia, abdominal pain, or hypotension.

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18
Q

Diagnostic Studies for Thrombocytopenia

A 
↓ Platelet count (platelet count less than 150,000)
---Prolonged bleeding < 50,000/μL 
---Hemorrhage ↓ 20,000/μL 
Peripheral blood smear
Medical history
Clinical examination
Lab parameter comparisons
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19
Q

When are platelet transfusions recommended

A

not recommended until the count is below 10,000/μL (10 × 109/L) unless the patient is actively bleeding

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20
Q

Thrombocytopenia and collaborative care

A

Based on etiology of the disorder.
Removal or treatment of the underlying cause or disorder.
Avoid aspirin and other medications that affect platelet function or production.

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21
Q

Immune Thrombocytopenic Purpura (ITP) Collaborative Care

A 
Corticosteroids --FIRST LINE DEFENSE
High dose of IVIG and anti Rh (D)
Rituximab
Splenectomy-
Romiplostim (Nplate )
Aminocaproic acid (Amicar) 
Platelet Transfusion
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22
Q

(ITP) when is IVIG and anti-Rho used.

A

in the patient who is unresponsive to corticosteroids or splenectomy or for whom splenectomy is not an option. They compete with antiplatelet antibodies for macrophage receptors in the spleen

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23
Q

(ITP) Rituximab

A

reduces the immune recognition of platelets.

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24
Q

(ITP) Romiplostim (Nplate)

A

used for patients with chronic ITP who have not had success with other treatments. It increases platelet production.

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25
Q

(ITP) Aminocaproic acid (Amicar)

A

antifibrinolytic agent used for severe bleeding.

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26
Q

(ITP) Platelet transfusions

A

used to increase platelet counts in life-threatening hemorrhage. It is never used prophylactically because of antibody formation. It is indicated for platelet count < 10,000/μL or if bleeding is anticipated before a procedure.

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27
Q

Collaborative Care for Thrombocytopenia Purpura (TTP)

A 
Identification and treatment of cause.
Untreated TTP usually results in irreversible renal failure and death.
Plasmapheresis 
Corticsteroids may be added.
Immunosuppressants 
Splenectomy
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28
Q

Heparin-Induced Thrombocytopenia (HIT) collaborative care

A

Permanently stop all heparin including heparin flushes.
—-Note clearly on medical record.
Start patient on a direct thrombin inhibitor.
Start Coumadin when platelet count reaches 150,000/μL.
- For Severe Clotting : Plasmapheresis, Protamine sulfate, Thrombolytic agents, surgery to remove clots

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29
Q

What is protamine sulfate used for

A

The antidote to heparin

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30
Q

Collaborative care for acquired thrombocytopenia from decreased platelet Production.

A

Often caused by another underlying condition or the therapy used to treat another problem.
Corticosteroids if precipitating factor unknown.
Platelet transfusion

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31
Q

Thrombocytopenia nursing assessment

Subjective data

A

Past Health History – recent hemorrhage, cancer, anemia, chemotherapy
Medications – chemotherapy, heparin, thiazide diuretics, digoxin, herbs including garlic and ginseng.
Functional Health Patterns – family history of bleeding, GI bleed, coffee ground emesis, menorrhagia.

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32
Q

Thrombocytopenia nursing assessment

objective data

A

Fever, lethargy, bleeding, splenomegaly, abdominal distention
Lab data - Possible diagnostic findings include platelet count <150,000/μL, prolonged bleeding time, decreased Hct and Hgb, normal or increased megakaryocytes in bone marrow examination.

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33
Q

Thrombocytopenia - NURSING DX

A

Impaired oral mucous membrane r/t low platelet counts and/or effects of pathologic conditions and treatment
Risk for bleeding r/t decreased platelets
Deficient knowledge r/t lack of information regarding the disease process and treatment

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34
Q

Overall goals for patient with thrombocytopenia

A

have no gross or occult bleeding
maintain vascular integrity
manage home care to prevent any complications related to an increased risk for bleeding.

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35
Q

Health Promotion for thrombocytopenia

A

Discourage excessive use of OTC medications, especially aspirin products. Many medications contain aspirin as an ingredient. Aspirin reduces platelet adhesiveness, thus contributing to bleeding. Encourage patients to seek prompt treatment for any symptoms of bleeding. Vigilant nursing care for patients receiving cancer chemotherapy drugs

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36
Q

Thrombocytopenia- Nursing implementaion

A

*Acute intervention
Prevent or control hemorrhage.
Avoid IM injections.
If subcutaneous injection is unavoidable, use small-gauge needles and application of pressure or ice packs after.
Teach self-care measures to reduce risks that could cause bleeding.
Closely monitor the platelet count, coagulation studies, Hgb, and Hct.
Manage blood loss from excessive menstrual bleeding.
–Count pads.
–Use hormones to suppress menses.
Administer platelet transfusions.

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37
Q

What is Anemia

A

Anemia is deficiency in the number of erythrocytes (RBCs), the quantity or quality of hemoglobin, and/or the volume of packed RBCs (hematocrit).

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38
Q

Clinical manifestations of Anemia

A
  • Caused by the body’s response to tissue hypoxia

- Hemoglobin (Hgb) levels are used to determine the severity of anemia

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39
Q

Mild anemia

A

Mild states of anemia (Hb 10 to 12 g/dL) - may exist without causing symptoms. If symptoms develop, it is because the patient has an underlying disease or is experiencing a compensatory response to heavy exercise. Symptoms include palpitations, dyspnea, and mild fatigue.

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40
Q

Moderate anemia

A

moderate anemia (Hb 6 to 10 g/dL), cardiopulmonary symptoms are increased. The patient may experience them while resting, as well as with activity.

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41
Q

Severe anemia

A

severe anemia (Hb less than 6 g/dL), the patient has many clinical manifestations involving multiple body systems.

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42
Q

Integumentary Manifestations of Anemia

A

Pallor
–↓ Hemoglobin
–↓ Blood flow to the skin
Jaundice
–↑ Concentration of serum bilirubin. caused by destruction of RBC. will see in sclera and urine
Pruritus
–↑ Serum and skin bile salt concentrations

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43
Q

Cardiopulmonary manifestations of Anemia

A

Result from additional attempts by heart and lungs to provide adequate O2 to the tissues

Cardiac output maintained by increasing the heart rate and stroke volume

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44
Q

What are the two pathways to clotting

A
  • Intrinsic pathway- thru body process. Stimulated by extrinsic pathway
  • Extrinsic pathway
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45
Q

Hemoglobin

Hematocrit

A

hbg-physical count

HCT- percentage. how much blood is RBS’s. Should be 3X hbg.

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46
Q

Anemia- Subjective Data

A

Subjective data include important health information including recent blood loss, trauma, chronic liver disease, GI ulcers, medications, recent surgeries and dietary history. Also includes Functional Health Patterns including
Family history of anemia
Nutritional-metabolic history of nausea, vomiting, weight loss, dysphagia, dyspepsia.
Elimination – hematuria, GI bleed,
Activity-exercise including fatigue muscle weakness, hemoptysis and shortness of breath
Cognitive-perceptual including headache, painful tongue, pruritis,
Sexuality-reproductive including menorrhagia, and pregnancy

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47
Q

Anemia- objective data

A

Objective Data includes:
General – lethargy, sensitivity to cold
Integumentary – pale skin and mucous membranes, icteric sclera (jaundice), spoon shaped finger nails, petechiae
Respiratory – tachypnea, shortness of breath
Cardiovascular – tachycardia, systolic murmur, dysrhythmias, postural hypotension, widened pulse pressure, claudication (pain and/or cramping in the lower leg due to inadequate blood flow to the muscles), and ankle edema.
Gastrointestinal – glossitis (beefy red tongue), anorexia
Neurologic – headache, irritabilit
Diagnostic findings – Low RBC, Hb, ferritin, folate, cobalamine, positive guaiac.

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48
Q

Nursing diagnosis for anemia

A
  • Fatigue
  • Imbalanced nutrition: Less than body requirements
  • Ineffective self-health management
  • Assume normal activities of daily living
  • Maintain adequate nutrition
  • Develop no complications related to anemia
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49
Q

Iron Deficiency Anemia

A
  • One of the most common chronic hematologic disorders
  • Iron is present in all RBCs as heme in hemoglobin and in a stored form.
  • Heme accounts for two-thirds of the body’s iron
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50
Q

What is erythropoiesis

A

Production of red blood cells

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51
Q

Normal Hemoglobin range

A

16-18

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52
Q

Normal RBC range

A

4.3-6.0

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53
Q

Causes of Iron Deficiency anemia

A
  1. Inadequate dietary intake. Only 5-10 percent of ingested Iron is absorbed.
  2. Malabsorption. Iron is absorbed in duodenum disease or SX that effect this area can cause anemia.
  3. blood loss. 2ml whole blood contains 1 mg of iron.
  4. Hemolysis
  5. pregnancy contributes to this condition
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54
Q

Clinical manifestations of Iron deficiency

A

General manifestations of anemia
Pallor is the most common finding.
Glossitis is the second most common.(Inflammation of the tongue)
Cheilitis (Inflammation of the lips)

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55
Q

Glossitis

A

inflammation of the tongue

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56
Q

Cheilitis

A

inflammation of the lips

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57
Q

Diagnostic studies for iron deficiency anemia

A 
Laboratory findings (Hgb, Hct, MCV, MCH, MCHC, reticulocytes, serum iron, TIBC, bilirubin, platelets)
Stool guaiac test
Endoscopy 
Colonoscopy 
Bone marrow biopsy
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58
Q

Drug therapy for Iron Deficiency Anemia

A 
Oral iron (Inexpensive,
Convenient )
Factors to consider:
Enteric-coated or sustained-release capsules are counterproductive. Wont be absorbed!!!!! IV or IM needed
Daily dose is 150 to 200 mg.
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59
Q
  1. Ferrous sulfate

2. Ferrous gluconate

A

For Iron deficiency anemia

  1. used for best absorption
  2. used for patients with sulfide/sulfate reactions
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60
Q

who is at risk for iron defieciency

A 
Premenopausal women
Pregnant women
Persons from low socioeconomic backgrounds
Older adults
Individuals experiencing blood loss
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61
Q

Megaloblastic Anemias

A

caused by impaired DNA synthesis with presence of Megaloblasts.
RESULT OF deficiency of B12 or folic acid.

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62
Q

Cobalamin deficiency

A
  • Intrinsic factor deficiency. cobalamin (B12) not absorbed without intrinsic factor
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63
Q

Etiology of Cobalamin deficiency (B12)

A

Most commonly caused by pernicious anemia

  • caused by an absence of IF
  • Insidious onset
  • Begins in middle age or later
  • Predominant in Scandinavians and African Americans
  • or from GI surgery, disease in Gi tract, chronic alcoholics, strict vegetarians, long term users of proton pump inhibitors or histamine receptor blockers
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64
Q

Clinical manifestations of cobalamin deficiency

A

General manifestations of anemia develop slowly due to tissue hypoxia.
Gastrointestinal manifestations: (Sore tongue, anorexia, nausea, vomiting, & abdominal pain)
Neuromuscular manifestations:
(Weakness, paresthesias of feet & hands, ↓ vibratory and position senses, ataxia, muscle weakness, and impaired thought processes)

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65
Q

Diagnostic Studies for cobalamin deficiency

A
  • Macrocytic RBCs have abnormal shapes and fragile cell membranes.
  • Serum cobalamin levels are decreased.
  • Normal serum folate levels and low cobalamin levels suggest megaloblastic anemia is due to cobalamin deficiency.
  • Upper GI endoscopy with biopsy of gastric mucosa
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66
Q

Cobalamin deficiency treatment

A

Parenteral or intranasal administration of cobalamin is the treatment of choice.
Patients will die in 1-3 years without treatment.
This anemia can be reversed with ongoing treatment but long-standing neuromuscular complications may not be reversible.

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67
Q

Types of megaloblastic anemias

A 
Cobalamin deficiency (b12)
Folic Acid deficiency
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68
Q

Folic Acid Deficiency

A
  • cause of megaloblastic anemia
  • Folic acid is required for DNA synthesis, RBC formation and maturation
  • Clinical manifestations are similar to those of cobalamin deficiency, but absence of neurologic problems differentiates them
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69
Q

Common causes of Folic Acid deficiecny

A 
Dietary deficiency
Malabsorption syndromes
Increased requirement 
**Alcohol abuse and anorexia 
**Loss during hemodialysis

** specific to this anemia

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70
Q

DX and treatment for folic acid deficicnecy

A 
Serum folate level is low.
Serum cobalamin level is normal.
Treated by replacement therapy
Usual dose is 1 mg per day by mouth.
Encourage patient to eat foods with large amounts of folic acid.
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71
Q

Management of Megaloblastic anemias

A

Early detection and treatment
Ensure safety (Diminished sensations to heat and pain from neurologic impairment)
Focus on compliance with treatment
Regular screening for gastric cancer

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72
Q

At an outpatient clinic, K.L.’s 78-year-old grandma is found to have a Hgb of 8.7 g/dL (87 g/L) and a Hct of 35%. Based on the most common cause of these findings in the older adult, the nurse collects information regarding

A. a history of jaundice and black tarry stools.
B. a 3-day diet recall of the foods the patient has eaten.
C. any drugs that have depressed the function of the bone marrow.
D. a history of any chronic diseases such as cancer or renal disease.

A

Answer: D
Rationale: Anemia in the older adult population is commonly caused by co-morbid conditions such as cancer or renal disease.

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73
Q

What is blood composition

A

55% plasma (water, protein, stuff)

45% is blood cells (Erythrocytes, leucocytes, platelets)

74
Q

Primary function of erythrocytes

A

gas transport. Maintain acid/base balance. MOVE THAT O2!

75
Q

Lifespan of erythrocyte

A

120 days

76
Q

Primary function of thrombocyte

A

forming platelet plug during the initial clotting process.

77
Q

Lifespan of thrombocyte

A

5-9 days

78
Q

Blood transfusion

Acute response

A
  • Stop the Transfusion

- Stay with patient

79
Q

Blood Transfusion

Circulatory Overload

A

-slow rate of infusion
-place client in upright position
-notify physician
0administer O2, diuretics, and morphine sulfate
- monitor for dysrhythmias

80
Q

Transfusion related Acute Lung injury (TRALI)

A

Sudden development of non cariogenic pulmonary edema.

  • 6-12 hours post transfusion up to 72 hours after.
  • leading cause of transfusion related death
81
Q

What to know about transfusions

A
  • Proper pt identification and blood matching by 2 RNS
  • consent prior to administration
  • only give NS with blood NOTHING in same line.
  • start slow
  • finish in under 4 hours
  • follow policy
82
Q

Symptoms get worse as the day progresses with ____ ____

A

myasthenia gravis

83
Q

Myasthenia Gravis is

A

Autoimmune disease of the neuromuscular junction.
-Fluctuating weakness of certain skeletal muscle groups.
-

84
Q

Which muscles does myasthenia gravis primarily effect

A

Central ones -chest, face, mask

85
Q

When is the onset for myasthenia gravis

A

MEN: 50-70 years
WOMEN: during childbearing age

86
Q

Etiology of Myasthenia Gravis

A

AUTOIMMUE. antibodies attack Each. Decreased ACh prevents stimulation of skeletal muscle. Smooth and cardiac muscle not effected

87
Q

MG effects movement of

A

the body, diaphragm and intercostal muscles.

-usually effects face and neck first

88
Q

Patients become symptomatic once the number of ACh is reduced to

A

approx 30% of normal

89
Q

S/S of myasthenia Gravis

A

Specific muscle weakness.
Fluctuating weakness of skeletal muscles.
Affects muscles of eye, eyelids, chewing, swallowing, speaking, and breathing.
Course of disease – Variable.

90
Q

What can trigger or make MS worse.

A

Bright sunlight, extreme temperatures
Surgery, illness, trauma
Immunization
Emotional stress
Menstruation, prgnancy
Intercurrent illness (eg, viral infection)
Medication – Antibiotics, Lithium, Beta-blockers, Statins

91
Q

Myasthenic Crisis

A

Acute exacerbation of muscle weakness
Triggered by infection, surgery, trauma, emotional distress, or drug overdose
Can result in aspiration and respiratory distress.

92
Q

Diagnosis of MG

A 
History and Physical Examination
EMG – Electromyogram
Tensilon Test
Atropine &amp; Resuscitation equipment
Differentiate from Cholinergic crisis.
Anti–acetylcholine receptor (AChR) antibody test 
Others – Chest X ray, CT scan
93
Q

Collaborative care of MG

A 
History and Physical Examination
EMG – Electromyogram
Tensilon Test
--Atropine &amp; Resuscitation equipment
--Differentiate from Cholinergic crisis.
Anti–acetylcholine receptor (AChR) antibody test 
Others – Chest X ray, CT scan
94
Q

use of EMG for MG test

A

EMG first thing checked. may show decreased response to repeated stimulation of the hand muscle indicating muscle fatigue.
-needle into each end of the muscle to look for conduction problem

95
Q

Tension test for MG

A
  • Only confirmatory test
  • administration of anti cholinesterase agent called Edrophonium chloride. Patient will temporarily improve if they have MG.
  • -this test can cause INTENSE cholinergic reaction.
96
Q

Clinical manifestations of cholinergic crisis

A

abdominal cramps, n/v/d, increased salivation & tearing, increased bronchial recreations, sweating, mitosis, hypertension, and increased weakness of specific muscles.

97
Q

Treatments for MG

A

Anticholinesterase- MESTINON(PYRIDOSTIGMINE) must take every 6 hrs right before food.

CORTICOSTEROIDS- for acute reactions. PREDNISONE.

Immunosuppressants- AZATHIOPRINE, to suppress immune response.

PLASMAPHERESIS- removed circulating AChR antibodies to decrease symptoms.

IVIG- decreases production of antibodies

Thymectomy- thymus produces AChR.

98
Q

Nursing DX for MG

A 
Ineffective airway clearance
Impaired Verbal communication
Activity intolerance
Disturbed body image
Potential for Aspiration
Potential for respiratory arrest
Discharge Teaching
99
Q

MG nursing implementation

A

Maintain airway.
Monitor speech and swallowing ability and prevent aspiration.
Encourage sitting up while eating.
Plan nursing care to provide adequate rest in between.
Monitor for Myasthenic and Cholinergic crisis.
Patient Education.

100
Q

What is Multiple Sclerosis

A

Disease of the brain that effects the communication of the brain.
-Chronic, progressive, degenerative disorder of CNS characterized by demyelination of the nerve fibers

101
Q

ONSET of MS

Who gets it?

A

Onset between 20 and 50 years of age.
Women are affected 2-3 times more than men.
More prevalent in temperate climates of Northern US, Canada and Europe.

102
Q

Etiology and patho of MS

A

Cause is unknown.

Related to infectious, immunologic, and genetic factors

Infection, smoking, physical injury, emotional stress, excessive fatigue, pregnancy, and a poorer state of health

103
Q

Patho process in MS

A

Chronic processes in MS -Demyelination, -Gliosis in the CNS.

An autoimmune process by activated T cells – disruption of BBB – antigen/antibody reaction – demyelination – axon damage – glial scar formation

104
Q

What is the onset of MS like

A

Onset of the disease is often insidious and gradual, with vague symptoms occurring intermittently over months or years.

105
Q

Clinical manifestations of MS

A

motor, sensory, cerebellar, and emotional problems

  • Vague symptoms occur intermittently over months and years.
  • Disease may not be diagnosed until long after onset of the first symptom.
  • Chronic, progressive deterioration in some.
  • Remissions and exacerbations in others.
106
Q

Four Primary patterns of MS

A
  1. Relapsing/Remitting. (clearly defined relapses with full recovery)
  2. Primary-progressive (slowly worsening neurological symptoms with no remissions)
  3. Secondary-progressive (initial relapsing-remitting initial course followed by progression with or without occasional relapses, minor remissions.)
  4. Progression-relapsing: (Progressive from onset with clear acute relapses, with or without full recovery.) instead of getting better will get worse and stay at certain point, then will get worse and stay…….ect
107
Q

Common manifestations of MS

A

Motor problems
Sensory problems
Cerebellar problems
Emotional problems

108
Q

motor manifestations of MS

A

Weakness or paralysis of limbs, trunk, and head
Diplopia
Scanning speech
Spasticity of muscles

109
Q

Sensory manifestations of MS

A 
Numbness and tingling
Blurred vision, Scotomas
Vertigo and tinnitus
↓ hearing
Chronic neuropathic pain
Lhermitte’s sign &amp; Radicular pain
110
Q

Lhermitte’s sign

A

a transient sensory symptom described as an electric shock radiating down the spine or into the limbs with flexion of the neck

111
Q

Cerebellar manifestations of MS

A 
Nystagmus
Ataxia
Dysarthria
Dysphagia
Fatigue
112
Q

How does MD effect bowl and bladder

A

Constipation

Spastic bladder- Small capacity for urine results in incontinence.
Flaccid bladder- Large capacity for urine and no sensation to urinate

113
Q

How will MS effect that sex drive?

A 
---Sexual dysfunction can occur in MS. 
Erectile dysfunction
Decreased libido
Difficulty with orgasmic response
Painful intercourse
Decreased lubrication
114
Q

Cognitive Manifestations of MS

A

Difficulty with:
Short-term memory attention,
Attention, Information processing, Planning,
Visual perception, Word finding

115
Q

Emotional effects of MS

A

Anger
Depression
Euphoria (not as common)

116
Q

Diagnostic tests for MS

A

No definitive diagnostic test for MS. DX of exclusion.

Based on history, clinical manifestations.
MRI (to see scaring lesions. need progressed damage to see)
CT Scan
CSF analysis (can look for antibodies)
Delayed evoked potential response (nerve test)

117
Q

Immunosuppressive Therapy for MS

A 
Drug therapy used to slow the progression of  disease.
(steroids used to slow down first)
Immunosuppressants (2nd)
Immunomodulators, and
Adrenocorticotropic hormone.
For active and aggressive  MS 
IV natalizumab (Tysabri)
118
Q

Drugs for MS in addition to immunosuppressants……..

A

Muscle relaxants (for spacicity

CNS stimulants – Modafinil, Methylphenidate, Amantadine- used to treat fatigue

Anticholinergics - used to treat bladder symptoms

Tricyclic antidepressants and antiseizure drugs- for chronic pain syndromes

Selective potassium channel blocker (Dalfampridine) used to improve nerve conduction in damaged nerve segments

119
Q

Non Pharm Interventions for MS

A

Surgery

Dorsal column electrical stimulation

Intrathecal baclofen pump

Physical, speech and water therapy

120
Q

Subjective data for MS

A

Viral infections or vaccinations
Residence in cold or temperate climates
Physical and emotional stress
Medications – Adherence to corticosteroids, immunosuppressants, immunomodulators, cholinergics, anticholenergics.
Elimination problems
Weight loss, dysphagia
Muscle weakness or fatigue, tingling or numbness, muscle spasms
Blurred or lost vision, diplopia, vertigo, tinnitus
Decreased libido, impotence
Anger, depression, euphoria, isolation

121
Q

Objective data for MS

A

General: Apathy, inattentiveness
Skin: Pressure ulcers
Neuro: Scanning speech, tremor, Nystagmus, Ataxia, Spasticity, Hyperreflexia, ↓ hearing
Musculoskeletal: Muscular weakness, Paresis, Paralysis, Foot dragging, Dysarthria

122
Q

what are serial 7’s

A

When you have patient start at 7 and continue adding 7 to each number. 7,14,21,28,35, act

123
Q

Nursing DX for MS

A

Impaired physical mobility related to muscle weakness or paralysis and muscle spasticity.

Impaired urinary elimination related to sensorimotor deficits.

Ineffective self-health management related to knowledge deficit regarding management of MS.

124
Q

Overall goals for patient with MS

A 
The overall goals include:
Maximize neuromuscular function.
Maintain independence in activities of daily living for as long as possible. 
Manage disabling fatigue.
Optimize psychosocial well-being.
Adjust to the illness.
↓ factors that precipitate exacerbations
125
Q

Nursing implementation with MS

A

Help patient identify triggers and develop ways to avoid or minimize them.

Assist patient in dealing with anxiety and grief caused by diagnosis.

During acute exacerbation, prevent major complications of immobility. (prevent ulcers, DVT, aspirations, res and urinary infections)

Focus teaching on building general resistance to illness - Avoid fatigue, extremes of hot and cold, exposure to infection

126
Q

What to teach a patient with MS

A 
Good balance of exercise and rest
Minimize caffeine intake
Nutritious, well-balanced meals
Increase roughage, 
Treatment regimen
Management of medications
Bladder control – anticholinergics, self catheterization
Bowel problems – constipation.
National MS Society
127
Q

Expected outcomes for patient with MS

A

Maintain or improve muscle strength and mobility.

Use assistive devices appropriately for ambulation and mobility.

Maintain urinary continence.
Make decisions about lifestyle modifications to manage MS.

128
Q

Most important to know about MS. SUMMARY

A

A chronic, progressive, degenerative disorder of the CNS.
Segmental demyelination of nerve fibers of the brain and spinal cord.
Pathological processes: chronic inflammation, demyelination, gliosis in the CNS.
Common manifestations of MS - motor, sensory, cerebellar, and emotional problems.
No definitive diagnosis; history + MRI + CSF
No cure. Medications to limit symptoms.

129
Q

The 2 major neuropathologic findings in Parkinson disease

A
  1. degeneration of the Dopamine (DA) producing neurons loss of the substantia nigra of the midbrain
  2. the presence of Lewy bodies
130
Q

Parkinsons is

A

a disease of the basal ganglia characterized by:

bradykinesia, ↑ muscle tone(rigidity), Tremor at rest, Gait disturbance

131
Q

BRADYKINESIA

A

SLOW FOCUSED MOVEMENT

132
Q

Parkinsons disease is more common in……

A

MEN

133
Q

Cause of Parkinson’s disease is…..

A 
UNKNOWN
maybe related to: 
Genetic and Environmental factors.
Chemicals and certain medications.
Certain disease conditions
134
Q

Diagnosis of PD increases or decreases with age?

A

increases

135
Q

Parkinsons is caused by a lack of ______ in the brain

A

dopamine

136
Q

Pathologic process of Parkinson’s disease involves :

A

degeneration of dopamine-producing neurons in substantia nigra of the midbrain.

137
Q

Manifestation of Parkinson’s disease does not occur until:

A

80% of the neurons in the substantial nigra are lost

138
Q

Which area of the brain is targeted by Parkinson’s disease

A

The movement center of the brain (nigrostriatal fibers)

139
Q

The onset of Parkinson’s disease is:

A

gradual and insidious with ongoing progression

140
Q

What is the classic Triad of Parkinson’s disease

A

TREMOR
RIDGIDITY
BRADYKINESIA

141
Q

Parkinsons tremor can involve which areas of the body:

A

hand, diaphragm, tongue, lips, jaw

142
Q

Parkinsons Tremor- when is it most prominent?

A

More prominent at rest and is aggravated by emotional stress or ↑ concentration

143
Q

Who will notice Parkinson’s tremor first?

A

So minimal initially that only the patient may notice it

144
Q

Which disease has a tremor that can be described as pill rolling?

A

PARKINSON’S DISEASE

Described as pill rolling because thumb and forefinger appear to move in rotary fashion

145
Q

what is rigidity

A

Increased resistance to passive motion when limbs are moved through ROM

Rigidity is typified by a jerky quality when the joint is moved.

146
Q

Movements similar to intermittent catches in the movement of a cogwheel are associated with which disease

A

Parkinsons Disease

Rigidity

147
Q

What is Bradykinesia

A

Slowing down in initiation and execution of movement

148
Q

Bradykenesia is evident in PD patients when they have loss of :

A

automatic movements

ex: Blinking, Swinging of arms while walking, Drooling of saliva, Masked face/no expression, Stooped posture

149
Q

non-motor symptoms of Parkinson’s disease

A 
Depression
Anxiety
Fatigue
Pain
Constipation
Sleep problems
Short-term memory loss
150
Q

Appearance of a person with Parkinson’s disease

A

Blank facial expression

Forward tilt to posture

Slow, monotonous movements

Slurred speech

Tremor

short, shuffling gait

151
Q

what Symptoms increase as parkinsons disease progresses

A 
Motor symptoms 
Weakness
Akinesia
Neurologic problems (dementia)
Neuropsychiatric problems

Dementia increases in 70% of patients.

152
Q

dyskinesias

A

associated with motor symptoms of parkinsons.

Spontaneous, involuntary movements

153
Q

non motor complications of Parkinson’s disease

A

Impotence

Short-term memory impairment

Sleep problems
–Difficulty staying asleep, Restless sleep, Nightmares, Drowsiness during the day

dysphagia: malnutrition & aspiration

Orthostatic hypotension

154
Q

Diagnostic tests for PD

A

No specific tests for PD

Diagnosis is based on history and clinical features

155
Q

True or False. Having a patient focus on their tremors will help them control them

A

FALSE. Tremors get worse when they focus on them.

156
Q

Firm diagnosis of Parkinson’s disease can be made when

A

at least two of three characteristics of the classic triad (tremor, rigidity, and bradykinesia) are present

157
Q

what do antiparkinsonian drugs do

A

either:
Enhance or release supply of DA

OR
Antagonize or block the effects of overactive cholinergic neurons in the striatum

158
Q

what is the first drug used for parkinsons Disease

A

Levodopa with carbidopa (Sinemet) is often the first drug used

159
Q

What does Sinemet do?

A

Levadopa is a precursor of DA and crosses blood-brain barrier. It is converted to DA in the basal ganglia and Carbidopa inhibits an enzyme that breaks down levodopa before it reaches the brain.

Prolonged use can often result in dyskinesias and “off/on” periods when the medication will unpredictably start or stop working.

160
Q

What is the official diagnosis criteria for parkinsons Disease and when can it be done

A

Official diagnosis when levy bodies in the brain. Can only be done on a cadaver.

161
Q

What is used to treat parkinsons disease when Sinemet no longer works

A

Bromocriptine (Parlodel)
Ropinirole (Requip)
Pramipexole (Mirapex)

they stimulate the DA receptors.

162
Q

Bromocriptine (Parlodel)

A

To treat PD
Monitor for dizziness due to orthostatic hypotension esp after the first dose and notify physician immediately if a severe headache develops that continues to get worse.

163
Q

Ropinirole (Requip)

A

to treat PD
Mild side effects include drowsiness, dizziness, flu like symptoms, nausea and dyskinesia. Inform physician if lower extremity edema, and diaphoresis, agitation, increased unusual body movements, increased coughing and nightmares

164
Q

Mirapex

A

to treat PD

165
Q

____ Inhibitors are used along with Sinemet to treat parkinsons disease

what other two types of drugs are used to treat PD

A

MAO-B inhibitors: blocks breakdown of Dopamine. Eg Rasagiline
LAST LINE OF DEFENSE

anticholinergic- decrease ACh. Have potent S/E. and dramatically increase effects (BENZTROPINE)

Antihistimines: anticholinergic effect. (DIPHENHYDRAMINE)

166
Q

what drug may be used to treat depression in a PD patient

A

Amitriptyline (Elavil)

167
Q

After 3-5 years of treatment PD patients experience episodes of hypo mobility. this is treated with

A

apomorphine (Apokyn)

Needs to be taken with an anticholinergic antiemetic drug – Trimethobenzamide (Tigan) to minimize severe nausea and vomiting.

168
Q

What is the only safe drug to use with apomorphine (spoken) for nausea?

A

Trimethobenzamide (Tigan).

when combined with Zofran will cause cardiac arrest.

169
Q

When is surgical Therapy for PD used?

A

Procedures aimed at relieving symptoms

Used in patients who are usually unresponsive to drug therapy or have developed severe motor complications

170
Q

What are the three categories of surgeries done for PD

A

Ablation Surgery

Deep brain stimulation (DBS):

Transplantation of fetal neural tissue into basal ganglia.

171
Q

What is ablation surgery

A

involves stereotactic destruction of areas in the thalamus (thalamotomy), globus pallidus (pallidotomy), and subthalamic nucleus (subthalamic nucleotomy).

172
Q

What is deep brain stimulation (DBS)

A

placing an electrode in thalamus, globus pallidus, or subthalamic nucleus and is connected to a generator placed in upper chest. The device is programmed to deliver specific current to targeted brain location. Unlike ablation procedures, DBS can be adjusted to control symptoms better and is reversible (the device can be removed).

173
Q

What is transplantation of fetal neural tissue into the basal ganglia used for?

A

PD.

surgical procedure that provides DA producing cells

174
Q

What are the nutritional needs for a PD patient

A

Provide food that is easily chewed and swallowed.

Adequate roughage

Cut food into bite-sized pieces.
Small frequent meals.

Don’t rush meal timings.

Supplementation with Vitamin B6

Protein in Evenings.

175
Q

Objective data for PD

A 
Blank faces, infrequent blinking
Seborrhea
Dandruff
Ankle edema
Postural hypotensionTremor at rest
“Pill rolling” 
Poor coordination
Subtle dementia
Cogwheel rigidity
Dysarthria
Bradykinesia
Contractures
Stooped posture
Shuffling gait
176
Q

nursing DX for Parkinson’s disease

A

Impaired physical mobility

Imbalanced nutrition: less than body requirements

Impaired swallowing

Impaired verbal communication

177
Q

Planning for patient with PD

A

Maximize neurologic function.

Maintain independence in activities of daily living (ADLs) for as long as possible.

Optimize psychosocial well-being.

178
Q

what should you focus teaching and nursing care on for a patient with PD

A

Maintenance of good health

Encouragement of independence

Avoidance of complications such as contractures and falls

Promote physical exercise and
a well-balanced diet

179
Q

Problems secondary to bradykinesia can be alleviated by

A

Consciously thinking about stepping over a line on the floor

Lifting toes when stepping

One step back and . . .
Two steps forward

180
Q

Expected outcomes for PD patient

A

Perform physical exercise.

Use assistive devices appropriately.

Maintain adequate nutritional intake.

Able to safely swallow food and fluid.

Able to communicate needs.
Able to interact with others.

181
Q

Summary of what you need ro know about PD

A

Neurological Disorder
Chronic and Progressive

Resting tremor, bradykinesia, rigidity and gait disturbances.

Degeneration of DA neurons – decreased DA and increased ACh.

Presence of Lewy bodies

Complications – Falls, Aspiration, Malnutrition

Treatment – Medications, Surgery, Deep brain stimulator

Patient Education and Caregiver strain

182
Q

Normal WBC

A

4000-10000

Med Surg Block 3 (4 decks)

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