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Med Surg > Exam 3 > Flashcards

Exam 3 Flashcards

1
Q

Signs and symptoms of anemia

A

Palpitations
Fatigue
Weakness

Worse:
Pallor
*Chest pain
*Dyspnea
*Increased RR
*Increased HR
(Anemia is serious when RR and HR need to compensate)

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2
Q

What is included with a CBC with differential?

A

RBC
Hemoglobin
Hematocrit

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3
Q

Normal values for hemoglobin

A

Males: 14-17
Females: 12 to 15

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4
Q

Normal values for hematocrit

A

Men: 41-50
Women: 36-48

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5
Q

What do iron tests look for?

A

Ferritin
Serum iron
(To diagnose anemia)

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6
Q

What does a reticulocyte count do?

A

Reflects bone marrow activity when diagnosing anemia

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7
Q

What things are looked at when testing for anemia?

A

RBC
Hemoglobin
Hematocrit
Iron studies
Reticulocyte count
Folic acid
Cobalamin (vitamin B12)
Bilirubin
Blood type and screen

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8
Q

Level of hemoglobin when a blood transfusion is needed?

A

7

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9
Q

What causes iron deficiency anemia?

A

Inadequate intake of iron, malabsorption, blood loss or hemolysis

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10
Q

Characteristics of RBCs with iron deficiency anemia

A

Microcytic, Hypochroic
(Small and pale RBCs)

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11
Q

Symptoms of iron deficiency anemia

A

Pallor = most common symptom
Glossitis (shiny, red, beefy tongue) = 2nd most common
HA, paresthesias, burning sensation of tongue

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12
Q

Treatment of iron deficiency anemia

A

Dietary or iron supplements
*Dietary intake:
- dark leafy greens
- red meat (esp organ meats)
- iron fortified foods

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13
Q

How can you prevent oral iron from staining pt’s teeth?

A

Have them drink it through a straw

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14
Q

What causes megaloblastic anemias?
Two types of megaloblastic anemias

A

A problem with DNA synthesis:
- cobalamin deficiency
- folic acid deficiency

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15
Q

Difference between cobalamin deficiency anemia and pernicious anemia

A

Low B12 causes DNA synthesis to be impaired because without it, folic acid cannot get into cell (low B12 = low folic acid absorption)

Without intrinsic factor, cobalamin cobalamin cannot get into cell (low intrinsic factor = low B12 absorption) *does not have neuromuscular symptoms

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16
Q

Causes of cobalamin deficiency anemia

A

Autoimmune
Surgical removal of parts of stomach
Vegan/vegetarian diets
Excessive alcohol use
Smoking
Long term H2 blocker / PPI use

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17
Q

Symptoms of cobalamin deficiency anemia

A

Jaundice
Glossitis
Fatigue
Weakness
N/V
Abdominal pain
Neuromuscular symptoms such as paresthesias of hands/feet, gait disturbances

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18
Q

Interventions for cobalamin deficiency

A

Vitamin B12 (oral for pts with proper absorption only)
Dietary counseling: animal proteins, dairy, eggs, fortified cereals

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19
Q

Causes of chronic anemia disease

A

Chronic inflammation
Autoimmune disorders
Infectious disease
Malignancy
HF
(Immune issue (cytokines) can’t put iron into storage)

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20
Q

*What is aplastic anemia?

A

*Decline in all cells due to bone marrow depression *(pantocytopenia)

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21
Q

Treatment of aplastic anemia

A

*Remove or treat cause if known
Immunosuppressive meds
Colony stimulating factors
Hematopoietic stem cell transplantation

Nursing interventions:
- prevent complications due to bleeding risk and infection

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22
Q

Acquired causes of hemolytic anemia

A

Destruction of RBC that is faster than production of RBCs
- Physical destruction such as DIC
- Antibodies produced against RBCs
- Infectious

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23
Q

Most common symptom of hemolytic anemia why?

A

Juandice
Because increased bilirubin which is a byproduct of hemolysis

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24
Q

Treatment for hemolytic anemia

A

IV fluids to protect the kidneys
Transfusion
Steroids
(Removal of the cause is the ultimate goal)

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25
Q

Causes of intrinsic hemolytic anemia

A

*Tissue hypoxia: PAIN
Sickle cell
Chronic fatal hereditary disease
Normal Hb replaced with Hb S

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26
Q

Treatment for intrinsic hemolytic anemia

A

Prevent sickle cell crisis
Opioids for tissue hypoxia
Hydrate pt
Prevent infections and treat them promptly

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27
Q

Why does polycythemia cause circulation impairment?

A

Increased volume and viscosity

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28
Q

What is primary polycythemia?

A

*Polycythemia Vera (have splenomegaly and hepatomegaly) that causes increase of RBC

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29
Q

What causes secondary polycythemia?

A

Too many RBC usually hypoxia driven
(High altitude, COPD, CHF)

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30
Q

S/S of polycythemia

A

Ruddy face and hands
HTN
*HCT >55
Pruritus
Splenomegaly
Paresthesias

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31
Q

major complications of polycythemia

A

Clots: CVA, MI, CHF

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32
Q

Treatment for polycythemia

A

Periodic phlebotomy (goal = <45%)
Hydration
Myelosuppression agents
Low dose aspirin (to help prevent clots due to slow moving blood)

Nursing indications:
- Strict I&O
- prevent thrombus formation

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33
Q

Symptoms of an infusion reaction

A

Febrile: sudden chills, fever, headache, flushing (reacting to donor’s WBC, making antibodies, most common)

Allergic: urticaria, dyspnea, anxiety, wheezing (reacting to donor blood)

Hemolytic: low back, chest, or flank pain Tachycardia, tachypnea (breaking up of RBC b/c of mismatched blood types)

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34
Q

Actions to take if pt is having a transfusion reaction

A

Stop blood
Maintain IV saline

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35
Q

What is an elevated BP?

A

120-129 and <80

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36
Q

What is HTN stage 1?

A

130-139 or 80-89

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37
Q

What is HTN stage 2?

A

> 140 or >90

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38
Q

How does epinephrine influence BP?

A

Increases HR and contractibility = increased CO

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39
Q

How does norepinephrine influence BP?

A

Activates A1, A2, B1 & B2 & dopamine receptors

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40
Q

How does aldosterone influence BP?

A

Retains Na+ and water = raises blood volume & CO

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41
Q

How does ADH influence BP?

A

Increases ECF - reabsorbs water in kidneys and increases blood volume = increased CO & BP

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42
Q

Nonmodifiable risk factors for HTN

A

Age
Gender
Ethnicity
Family history
Socioeconomic status

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43
Q

Modifiable risk factors for HTN

A

Obesity
Sedentary lifestyle
Alcohol use
Tobacco use
Diabetes
Elevated serum lipids
Excess dietary sodium
Stress
Socioeconomic status

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44
Q

*Major organs affected by HTN

A

Heart (CAD, MI, LVH)
Brain (TIA, CVA, HTN encephalopathy)
PVD (aortic aneurysm, aortic dissection)
Kidney (CKD)
Eyes (damage to retina/arterioles)

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45
Q

Dietary recommendations for HTN

A

DASH diet
- Fruits, veggies
- fat- free or low-fat dairy
- whole grains
- fish, poultry, beans
- seeds and nuts

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46
Q

Sodium and alcohol intake recommendations for HTN

A

1500-2300 mg of salt/day

Men: 2 drinks/day. Women: 1 drink/day

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47
Q

Exercise recommendations for HTN

A

30 min x 5 days - goal of 150 min/week
With muscle-strengthening 2x/week

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48
Q

Classes of HTN drugs:

A

AAABCDD
ACEs
ARBs
Alpha 1 receptor blockers
Beta blockers
CCBs
Diuretics
Direct vasodilators

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49
Q

How do diuretics help HTN?

A

Promote urinary excretion of Na+ and water = lowers circulating blood volume

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50
Q

How to measure for orthostatic hypotension

A

Measure BP supine, sitting, and then standing with 1-2 min between position changes

Positive if:
- Decrease of 20 or more in SBP
- Decrease in 10 or more in DBP
- HR increase of 20 bpm or more

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51
Q

BP measurement for hypertensive crisis

A

> 180 and/or >120

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52
Q

Causes of hypertensive crisis

A

Hx of HTN, non adherent or under medicated
Cocaine, amphetamines, PCP, LSD
- leading to seizures, CVA, encephalopathy or MI

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53
Q

Issues that cause target organ damage and need to be treated IMMEDIATELY

A

Encephalopathy
Intracranial or subarachnoid hemorrhage
HF, MI
Renal failure
Dissecting aortic aneurysm
Retinopathy

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54
Q

Symptoms of encephalopathy

A

HA, N/V, seizures, confusion, coma

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55
Q

Nonmidifiable risk factors for atherosclerosis

A

Age
Gender if <75 (> 75 y/o = equal risk)
Ethnicity (AA = > risk)
Family history
Genetic predisposition

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56
Q

Modifiable risk factors for atherosclerosis

A

Elevated serum lipids
Hypertension (>130/80)
Obesity (BMI >30)
Diabetes
Metabolic syndrome

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57
Q

Goal for cholesterol levels

A

<200 mg/dL

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58
Q

Goal for triglyceride level

A

Males <135
Females <160

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59
Q

Goal for LDL level

A

<130 mg/dL

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60
Q

Goal for HDL level

A

Female: >55
Male: >45

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61
Q

Parameters for metabolic syndrome

A

3 of the following:
1 - central obesity (women >35 in, men >40 in)
2 - fasting blood glucose >100 or prior T2DM Ex
3 - BP >130 / >85, or on drug tx
4 - triglycerides >150 mg/dL
5 - HDL <50 women, <40 men or on drug tx

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62
Q

What do you ask when a patient says they have chest pain?

A

PQRST:
Precipitating events
Quality of pain
Radiation of pain
Severity of pain (pain scale)
Timing (how long does it last, how often?)

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63
Q

Difference between stable and unstable angina

A

Stable - intermittent CP with exertion in familiar pattern (same pattern of onset, duration, and intensity)

Unstable - new onset, occurs at rest, lasts >15 min

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64
Q

What is prinzmetal’s angina?

A

*Spasm of major coronary artery

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65
Q

What is silent ischemia

A

No symptoms, associated with diabetic neuropathy

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66
Q

What should you teach pts with chronic stable angina?

A

Stop activity
Rest
Nitroglycerin (take 1 wait 5 min - up to 3 doses)
If pain still there after 15 min, call 911
And chew 2-4 baby aspirin

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67
Q

Nursing goals for chronic stable angina

A

Reduce O2 demand and/or increase O2 supply to:
*Optimize myocardial perfusion
- relieve pain

Immediate and appropriate treatment
Preservation of heart muscle if MI is suspected

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68
Q

*Nursing actions for chronic stable angina

A

Position upright, apply O2
Assess: VS, heart and breath sounds
Continuous ECG monitor (telemetry)
- Sometimes 12 lead ECG
Troponin levels
Provide support and reduce anxiety
Pain relief - nitroglycerin, IV opioid if needed
Obtain labs - cardiac bio markers
Obtain chest x ray

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69
Q

What should troponin levels be without heart damage?

A

<0.03

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70
Q

What is coronary angiography? And what is it used for?

A

Cardiac catheterization to visualize blockages in arteries and diagnose

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71
Q

What is percutaneous coronary intervention?

A

Opens blockages and fixes them:
- balloon angioplasty
- stent

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72
Q

What cause unstable angina?

A

Partial occlusion of coronary artery:
- UA - may have ECG change; troponin normal
- NSTEMI - ECG changes w/o ST elevation; troponin elevated

Total occlusion of coronary artery:
- STEMI - ECG changes w/ ST elevation; troponin elevated

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73
Q

Atypical symptoms of MI or angina in women

A

Chest pain, but not always
Pain or pressure in lower chest, upper abdomen, or upper back
Fainting
Indigestion
Extreme fatigue

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74
Q

BP requirements for nitroglycerin

A

SBP >100
If <100, don’t give, need to call provider

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75
Q

What should you teach pt about nitroglycerin and knowing if it’s still working when they take it at home?

A

Should tingle when they place it under their tongue

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76
Q

What plays a major role in development of atherosclerosis?

A

*endothelial injury and inflammation

77
Q

Tests for markers of widespread endothelial damage in CV disease

A

C-reactive protein (CRP) - serum
- *Nonspecific marker of inflammation
(Linked with unstable plaques and oxidation of LDL cholesterol)

Microalbuminuria
- urine test

78
Q

Uses of beta blockers

79
Q

Actions of beta blockers

A
  • Block beta receptors in heart and peripheral blood vessels
  • Decrease HR
  • Decrease force of ventricular contraction
  • Reduce release of renin from kidneys
80
Q

Side effects of beta blockers

A

Bradycardia, heart block, hypotension, HF
Adverse effect on lipids
Bronchoconstriction if block Beta 2 receptors

81
Q

Antiplatelet therapy used for CAD

A

Aspirin
Clopidogrel (plavix)

82
Q

Actions of Antiplatelet therapy

A

Irreversibly inhibits platelet aggregation for life of platelets

83
Q

Use of Antiplatelet therapy

A

Prevent arterial clots, MI, ischemic CVA

84
Q

Side effects of Antiplatelet therapy

A

GI upset
Increases risk for GI bleed and hemorrhagic CVA
Effects last up to 7-10 days = d/c 1 week before surgery

85
Q

What do beta blockers end in?

86
Q

What do ACE inhibitors end in?

87
Q

Uses of ACE inhibitors

88
Q

Actions of ACE inhibitors

A
  • Block production / conversion of angiotensin I to angiotensin II
  • Reduces Afterload through vasodilation
  • Lipid neutral
89
Q

Side effects of ACE inhibitors

A

Cough (bradykinin in lungs)
Hyperkalemia (avoid salt substitutes)
Angioedema

90
Q

What do ARBs end in?

91
Q

Uses of ARBs?

92
Q

Actions of ARBs

A
  • Block action of angiotensin II receptor sites
  • Vasodilation and decrease in aldosterone
  • Increases renal excretion of Na and water
  • Lipid neutral
  • Renal and cardioprotective in hypertensive diabetic pts
93
Q

Side effects of ARBs

A

Cough
Hyperkalemia
Angioedema

94
Q

Examples of calcium channel blockers that lower HR

A

Verapamil (Calan)
Diltiazem (Cardizem)

95
Q

Actions of CCBs

A
  • Prevent Ca++ (a vasoconstrictor) from entering cells
  • Relax smooth muscle, causes vasodilation
  • Blocks SA node and AV node conduction which decelerates HR
96
Q

Side effects of CCBs

A

HF
Hypotension
Dyspnea
Weight gain
Edema of lower extremities
*Bradycardia
Dizziness

97
Q

Example of CCB that does not effect HR

A

Amlodipine (Norvasc) = SE of high HR

98
Q

What do alpha 1 receptor blockers end in?

99
Q

Action of alpha 1 receptor blockers

A
  • Lower BP through vasodilation by decreasing peripheral vascular resistance (relaxes smooth muscle)
  • Favorable effect on lipids
100
Q

Side effects of Alpha 1 receptor blockers and nursing interventions

A
  • Orthostatic dizziness/syncope
  • *Also used in BPH
  • *Watch for syncope with 1st dose = admin 1st dose at bedtime
101
Q

What are statins used for?

A

Lowering lipids

102
Q

Actions of statins

A
  • Increases # of LDL receptors on hepatocytes to allow for more removal of LDL
  • Lowers triglycerides and increases HDL cholesterol
103
Q

Side effects of statins

A

Monitor for liver damage and myopathy

104
Q

What is Niacin (Niaspan)?

A

A B vitamin used to lower lipids

105
Q

Action of Niacin (Niaspan)

A

Lower triglycerides and increase HDL (not to same degree as statins)

106
Q

Side effects of Niacin

A

*Flushing
Pruritus
GI side effects
Orthostatic hypotension
Hepatoxic

107
Q

What is fenofibrate (Tricor) used for?

A

Best at lowering triglycerides and increasing HDL

108
Q

Side effects of fenofibrate (Tricor)

A

GI complaints (b/c works through GI tract)

109
Q

What is Ezetimibe (Zetia)?

A

Bile acid sequestrant used to decrease cholesterol absorption in small intestine (GI complaints)

110
Q

Definition of heart failure

A

Clinical syndrome with current or prior S/S caused by a structural/functional cardiac abnormality

With at least one of the following:
- Elevated Natriuretic peptide levels (BNP)
- Symptoms of congestion

111
Q

Classification of Heart Failure by Ejection Fraction

A

HF with reduced EF: LVEF <40%

HF with preserved EF: LVEF >50%

112
Q

How is HF classified?

A

Based on how the pt can function in their life

113
Q

Symptoms of left sided heart failure

A

Fatigue, anxiety, weakness
Restlessness, acute confusion
S3, S4 heart sounds
Pulses alterans (weak, strong)
Angina, palpitations, tachycardia
Dyspnea (orthopnea, exertional dyspnea, PND)
Dry, hacking cough
Crackles or wheezes
Frothy, pink-tinged sputum
Oliguria/Nocturia

114
Q

Symptoms of right sided heart failure

A

Fatigue, anxiety
Tachycardia
JVD
Weight gain (most reliable indicator of fluid gain/loss)
GI bloating
Nausea, anorexia
Ascites
Hepatomegaly
Spleenomegaly
Edema - pedal, scrotal, sacrum

115
Q

What is HFrEF?

A

Left sided heart failure with reduced EF (systolic failure)

Inability to pump blood effectively

116
Q

What is HFpEF?

A

Left sided heart failure with preserved EF (diastolic failure)

LV is stiff/noncompliant
Ventricles do not relax during filling

117
Q

What are the counterregulatory mechanisms for heart failure?

A

Natriuretic peptides:
- ANP (atrial natriuretic peptide)
- BNP (b-type natriuretic peptide)

118
Q

What do the natriuretic peptides do to counter-regulate heart failure?

A

Made and released by heart muscle in response to increased blood volume in heart

  • Lead to: diuresis, vasodilation, and lower BP
    (counteract effects of SNS and RAAS)
119
Q

Impaired gas exchange due to HF is related to:

A

Alveolar-capillary perfusion changes

120
Q

Nursing actions for impaired gas exchange with HF

A

Assess RR and work of breathing
Auscultate lung sounds q4hr
Monitor ABGs
O2 therapy (keep O2 sat >92)
Administer IV morphine sulfate
Semi-fowlers position

121
Q

What is impaired cardiac output from heart failure related to?

A

Altered SV (contractibility, preload, Afterload)

122
Q

Nursing interventions for impaired cardiac output with heart failure

A

Monitor AP, BP, pulses, lung and heart sounds, JVD, UOP, weight, and ECG (telemetry)

ACE inhibitors to reduce Afterload (elevated pressure in vessels)
Digoxin (Lanoxin) to increase contractility

Sodium restricted diet (to reduce preload)
Diuretics (to reduce preload)

123
Q

Fluid imbalance with HF is related to:

A

Retention of sodium and water

124
Q

Nursing interventions for fluid imbalance from heart failure

A

Ensure patent IV
Administer rapid acting diuretics
Fluid restriction if severe
Monitor for hypokalemia and treat
Limit to 1500-2300 mg sodium intake
*Weigh daily
Monitor I&O (Strict and accurate) *Report if <30 mL/hr
Monitor serum sodium and potassium

125
Q

What is activity intolerance from heart failure related to?

A

Imbalance between O2 supply and demand secondary to cardiac insufficiency and pulmonary congestion

126
Q

nursing actions for activity intolerance from HF

A

Alternate rest with activity
Monitor response to activity
Collaborate with OT/PT
Reduce anxiety
Evaluate support system
Patient teaching:
- energy conserving behaviors
- increase gradually
- avoid extreme heat and cold
- rest after exertion
- exercise training (cardiac rehab)

127
Q

What do diuretics do for pts with HF?

A

Reduce edema, pulmonary venous pressure, and preload
Promote Na+ and water excretion (loop and thiazide)
Monitor potassium levels (*hypokalemia)

128
Q

Type of diuretic and Action of furosemide (lasix)

A

Loop diuretic

Blocks Na+ and water reabsorption in loop of Henle
Decreases preload and pulmonary congestion

129
Q

Side effects of furosemide (Lasix)

A

Excessive urination & dehydration
Hypokalemia, hyponatremia
Ototoxicity (transient deafness) *with rapid IV admin
Orthostatic hypotension

130
Q

Push rate for furosemide (Lasix)

A

10-20 mg/min

131
Q

Type of diuretic and action of hydrochlorothiazide (HydroDIURIL)

A

Thiazide

Blocks Na, Cl, and water reabsorption in distal convoluted tubule

132
Q

Side effects of hydrochlorothiazide (HydroDIURIL)

A

Orthostatic hypotension
Hypokalemia
Hyponatremia

133
Q

Type of diuretic and action of spironolactone (Aldactone)

A

Aldosterone antagonist

Block sodium-potassium exchange mechanism in distal tubule - prevents reabsorption and *Retains potassium

134
Q

Side effects of spironolactone (Aldactone)

A

Hyperkalemia

135
Q

Nursing actions for spironolactone (Aldactone)

A

Monitor and report weight gain
Avoid salt substitutes and foods high in K+

136
Q

Routes for administering potassium chloride?

A

Oral
IVPB
**NEVER IVP

(*IV infusion rate not to exceed 10 mE/hr)

137
Q

Side effects of potassium chloride

A

Hyperkalemia
GI - abdominal discomfort, N/V, diarrhea

138
Q

What class does digoxin (Lanoxin) belong to?

A

Cardiac glycosides

139
Q

Actions of digoxin (Lanoxin)

A
  • Increases contractility and CO (*INOTROPIC effect)
  • Decreases AV contraction (chronotropic effect) which decreases HR
140
Q

Nursing actions for giving digoxin (Lanoxin)

A

*Take apical HR for 1 minute before administering
* If HR <60 or >120, withhold (instruct pt hot to take their own pulse)
- Monitor for therapeutic levels = *0.5-2.0 ng/mL
- Teach pt to report S/S of toxicity and hypokalemia

141
Q

Symptoms of digitalis toxicity

A

GI symptoms: N/V, anorexia
Cardiac: palpitations, irregular pulse
Visual changes: blurred vision, halos or rings of light around objects
Neurologic: HA

142
Q

What is heparin used for?

A

Anticoagulant
Used for risk for and actual DVT/VTE

143
Q

Antidote for heparin

A

Protamine sulfate

144
Q

Nursing actions for heparin

A

Monitor for HIT
APTT or PTT blood test q6hrs
Normal range = 30-40 sec, **want therapeutic: 1.5-2 times the normal range

145
Q

What is Enoxaparin (Lovenox)?

A

Low Molecular Weight Heparin

146
Q

Nursing actions for LMWH

A

No monitoring required
SC in abdomen = best place to administer

147
Q

Action of Warfarin (Coumadin)

A

Inhibits synthesis of vitamin K clotting factors
(Slow onset: about 72 hrs)
** Prevents clot formation or extension, but *Has no effect on existing clots

148
Q

Antidote for warfarin

149
Q

Nursing actions for warfarin

A

*PT and INR blood tests
Pt takes for 3-6 months
*Teach pt to maintain consistent intake of foods high in vitamin k, do not eliminate them

150
Q

Oral anticoagulants

A

Dabigatran (Pradaxa)
Apixaban (Elliquis)
Rivaroxiban (Xarelto)

151
Q

Pt teaching for oral anticoagulants

A

S/S of bleeding
Tell all providers on anticoagulant
Avoid ASA containing drugs
Use electric razor
Medic alert bracelet
Don’t massage injection sites

152
Q

Conservative teaching for varicose veins

A

Elevation - rest with limb > heart
Elastic - compression stockings
Exercises - leg-strengthening

Weight loss

153
Q

Classic symptoms of PAD

A

1- *Intermittent claudication (Pain)
2- Paresthesia in toes/feet
3 - Paralysis
Thin, shiny, dry, scaly, taut skin, thick toenails
Loss of hair on lower legs
4- Diminished or absent lower Pulses
5 - Elevation Pallor, dependent rubor
Muscle atrophy
6- Cold extremity

Pain at rest as disease progresses

154
Q

*Drug therapy for PAD

A

Aspirin
Clopidogrel (Plavix)
Statins

155
Q

Drug therapy for intermittent claudication

A

*Cilostazol (Pletal)

156
Q

Function of Cilostazol (Pletal)

A

For intermittent claudication
- Inhibits platelet aggregation
- Increases vasodilation and blood flow
- Decreases pain

157
Q

Side effects of Cilostazol (Pletal)

158
Q

Complications of PAD

A

Atrophy of skin and underlying muscles
Delayed wound healing
Wound infection
*Critical limb ischemia (stages 3 & 4)

159
Q

What is critical limb ischemia?

A

Chronic ischemic leg pain at rest
Tissue necrosis
Arterial ulcers

160
Q

Most serious complications of PAD

A

No healing arterial ulcers
Gangrene
May result in amputation!

161
Q

What is acute arterial occlusion?
What causes it?

A

An emergency!
Sudden occlusion of an artery D/T:
- Post-op vascular surgery (thrombus)
- A fib, heart valve disease, or infection (embolic)

162
Q

How to assess for acute arterial occlusion? and how to diagnose

A

Assess 6 P’s
- Pain
- Paralysis
- Pulses
- Perishingly cold
- Pallor
- Paresthesia
To diagnose: look at clinical presentation, echocardiogram, arteriogram

163
Q

Treatment for acute arterial occlusion

A

Early intervention is essential to saving affected limb (*within 6-8 hrs)
Thrombectomy
Anticoagulant therapy
Thrombolytic therapy
Tissue plasmin activator (TPA) IV infusion

Long term anticoagulation if at increased risk for another embolism

164
Q

What is compartment syndrome?

A

Big symptom = Pain that is out of proportion
Caused by pain and swelling in compartment that causes pressure on nerves and vessels

165
Q

What is buerger’s disease?

A

Inflammatory disorder that results in clotting/thrombus formation (acute phase) and tissue ischemia/fibrosis (chronic phase)

166
Q

Risk factors for buerger’s disease

A

Smoking/marijuana use
Males 20-45 yrs

167
Q

Assessment for buerger’s disease

A

Pain (claudication) in foot arch
Reddish blue color
Absent distal pulses
Ulceration
Gangrene

168
Q

What causes raynauds?

A

Vasospastic in small cutaneous arteries of extremities with intermittent, localized vasoconstriction

169
Q

Post-op nursing actions for vascular procedure or surgery

A

Frequently monitor NV checks and vitals
Monitor for potential complications:
*Graft occlusion (emergency) = acute arterial occlusion. Treatment = thrombectomy
*Compartment syndrome. Treatment = faciotomy

170
Q

Treatment for a leg with critical limb ischemia

A

Bypass surgery

171
Q

Non-modifiable risk factors for stroke

A

Age *Risk doubles each decade after 55
Gender (more common in men, more women die)
Ethnicity/race (AA)
Heredity/family history

172
Q

Modifiable risk factors for stroke

A

*HTN
*Smoking
Obesity
*Atrial fibrillation
*Diabetes
*Drug and alcohol abuse

Lack of exercise
Poor diet

Heart disease
Serum cholesterol
Sleep apnea
Metabolic syndrome

173
Q

Types of medications use to prevent CVAs

A

Antiplatelet meds
Antiplatelet agents
Cholesterol meds

174
Q

Interventions for CVA prevention

A

Can clip or coil aneurysms

175
Q

Major types of strokes

A

Thrombotic stroke (caused by atherosclerosis)
Embolic stroke (clot has brakes off & moves to cerebral artery)
Hemorrhagic stroke (injured vessel, aneurism, arterio/venous malformation from birth, etc.)

176
Q

How can you determine whether someone is having an ischemic vs. hemorrhagic stroke?

A

CT scan
*Need to know when their symptoms started

177
Q

Where do most ischemic strokes occur?

A

Middle cerebral artery

178
Q

What is a transient ischemic attack?

A

*Transient neurologic dysfunction with same S/S as CVA *caused by brief interruption of blood flow without infarction of brain
Occurs before a thrombotic stroke

179
Q

How long does a transient ischemic attack typically last? And what is the common cause?

A

< 1 hr
Carotid stenosis

180
Q

Which side of brain? Difficulty with language/ articulating words

181
Q

Which side of brain? Difficulty comprehending language

182
Q

Which side of brain? Short attention span/impulsive

183
Q

Which side of brain? Difficulty with spatial/perceptual ability

184
Q

Which side of brain? Difficulty with concept of time

185
Q

Which side of brain? Prone to anxiety and depression

186
Q

Which side of brain? Cautious/carries out tasks slowly

187
Q

What is receptive aphasia?

A

Loss of comprehension (Wernicke/sensory)

188
Q

What is expressive aphasia?

A

Loss of production of language
(Brock/motor)

Med Surg (12 decks)

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