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NUR 141 > 2.2 Cardiovascular Vascular > Flashcards

2.2 Cardiovascular Vascular Flashcards

1
Q

anemia

A

↓ RBCs &/or ↓ hemoglobin

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2
Q

anemia defined

A

Results in reduced oxygen-carrying capacity of blood

Incidence increases with aging, not always a clear cause

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3
Q

anemia S/S

A

S/S depend on degree & if onset is gradual or acute and are RT tissue hypoxia
S/S: ↑HR, ↑R, angina, fatigue, SOB, pallor, HA, dizziness

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4
Q

anemia causes?

A

Causes:
Decreased RBC production or impaired HgB synthesis
-Altered Hgb synthesis: iron deficiency, chronic inflammation
-Altered DNA synthesis: B12 or folic acid deficiency
-Bone marrow failure

Increased RBC loss/destruction

  • Acute or chronic blood loss (loss of volume, cells, & components)
  • Increased hemolysis
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5
Q

Nutritional anemias

IRON DEFICIENCY

A

IRON DEFICIENCY: most common, Fe supply inadequate
↓# RBCs, microcytic (small), hypochromic (pale), malformed RBCs
Can be due to chronic blood loss, inadequate intake/absorption, or increased needs

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6
Q

Nutritional anemias

IRON DEFICIENCY S/S

A

S/S: spoon-shaped nails, cheilosis (corners of the mouth become inflamed, which can lead to cracking and pain at the corners of the mouth), smooth, sore tongue, pica (craving) + common anemia S/S

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7
Q

Nutritional anemias VITAMIN B12

A

VITAMIN B12 DEFICIENCY: B12 animal sources

  • PERNICIOUS ANEMIA (B12 deficiency): unable to absorb due to lack of intrinsic factor secreted by gastric mucosa
  • Other absorption problems (gastric bypass, ETOH, chronic gastritis)
  • Dietary deficiency in vegans

RBCs large (macrocytic), misshapen, thin membranes, short-lived & fragile

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8
Q

Nutritional anemias VITAMIN B12 S/S

A

S/S: pallor, slight jaundice, weakness, diarrhea, sore beefy red tongue, also neuro symptoms with deficiency

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9
Q

Nutritional anemias FOLIC ACID

A

FOLIC ACID DEFICIENCY: green, leafy vegs, fruits, cereals and meats, intestinal absorption,
RBCS: megaloblastic cells (lg, immature)
Inadequate intake: in chronically undernourished, elderly
Impaired metabolism: ETOH suppresses folate metabolism, some meds (chemo drugs)
Impaired absorption: celiac, med-related
Increased needs: pregnancy, dialysis, hemolytic anemias

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10
Q

Nutritional anemias FOLIC ACID S/S

A

S/S: gradual onset of pallor, weakness, glossitis (looks like B12 deficiency, but NO NEURO symptoms)

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11
Q

Assessment (megaloblastic anemia):

A

Tissue hypoxia causes the symptoms

Clinical S/S: (depend on severity of anemia)

  • Beefy red tongue, sore
  • Anorexia, nausea, vomiting
  • Abd pain
  • Weakness
  • Tachycardia
  • Ataxia
  • Muscle weakness
  • B12 only: Neuro: paresthesias; (hands/feet) gait ataxia; impaired thought
  • Impaired thought processes (confusion to dementia).
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12
Q

Assessment (megaloblastic anemia):
Labs
Treatment

A

Labs:
Cobalamin, folate levels, Hgb/Hct, MCV, test for IF antibodies,
Treatment:
Supplements (cobalamin can’t be oral if IF deficiency – give IM)

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13
Q

Polycythemia

A

Increased production of RBCs.

Impaired circulation due to increased blood viscosity.

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14
Q

Polycythemia 2 Type

A

2 Types:

Polycythemia Vera: Chronic chromosomal mutation with ↑RBCs, WBCs and platelets uncommon (HCT >55%)

Secondary Polycythemia:
Hypoxia driven - ↑ oxygen demand (high altitudes, smoking, COPD) = ↑EPO (erythropoietin) most common
Hypoxia independent- malignant or benign tumors

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15
Q

Assessment of polycythemia

A

HTN: HA, dizziness, vision & hearing changes
Venous stasis: plethora (ruddy color), itching of fingers/toes
Retinal engorgement
Hypermetabolism: weight loss, night sweats
Altered mental status: drowsiness, delirium
Splenomegaly (primary only)
GI bleeding
Intermittent claudication
thrombosis

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16
Q

Teaching management of polycythemia

Primary Polycythemia

A 
Primary Polycythemia Vera (not preventable).
Perform phlebotomy (500ml)
Monitor I & O -hydration
Prevent stasis & DVT exercise, ASA
Meds (leukemia risk)
17
Q

Teaching management of polycythemia

Secondary polycythemia

A 
Secondary polycythemia
Controlling chronic pulmonary disease
Smoking cessation
Avoid high altitudes. 
Monitor I & O, hydration
Prevent stasis & DVT
18
Q

Peripheral Arterial Disease Pathophysiology

A

Pathophysiology
Progressive thickening of walls, narrowing lumen, and ↓elasticity of the arteries of the neck, abdomen, and extremities.
Atherosclerosis is major cause
4 to 5 times the risk of dying from MI/stroke.
Strongly RT other CVD

19
Q

Peripheral Arterial Disease PAD Risk Factors

A 
PAD Risk Factors
4 most significant factors:
Cigarette smoking
Hyperlipidemia
Hypertension
Diabetes
Other risks:
Obesity
Hypertriglyceridemia
Hyperuricemia
Family history
Sedentary lifestyle
Stress
20
Q

Intermittent claudication

A

Ischemic muscle ache or pain precipitated by exercise which resolves within 10 minutes or less with rest and is reproducible.(lactic acid)

Progresses slowly causing atrophy of the skin and underlying muscles.

Delayed healing of wounds of lower extremities

Amputation of extremity with gangrene.

21
Q

Management PAD Diagnostic testing

A

Diagnostic testing

Doppler Ultrasound
Angiography to detect the location and extent of the disease process.
MRA is alternative to angiography(no dye)

22
Q

Management PAD

Treatment

A 
Treatment
Smoking cessation
Medications:
Antiplatelet agents: Aspirin, Plavix, Ticlid
Ace inhibitors
Trental, Pletal
23
Q

Management PAD Risk factor

A

Risk factor modification:
control DM, HTN, wt
Exercise therapy
Surgical therapy

24
Q

Nursing Implications for PAD

A

Assess pulses, pain, color, temperature & capillary refill. (R) Establishes baseline assessment data.

Position extremities dependent- (R) promotes arterial flow, increases perfusion, decreases pain.

Teach exercise benefits: (R) promotes collateral circulation to ischemic tissues & slows atherosclerosis. Teach rest when claudication begins with extremity dependent & resume when pain subsides.

Keep extremities warm- socks, slippers, light blankets NO heating pads. – (R) promotes circulation & prevents vasoconstriction.

Encourage position changes & ROM exercises- (R) ↓ pressure, ↑ circulation, ↓ tissue ischemia. ROM prevents muscle atrophy

25
Q

Nonatherosclerotic PAD

Buerger’s Disease

A

Buerger’s Disease: (Thromboangitis Obliterans)

  • Thrombosis & fibrosis occur inside the vessel →ischemia.
  • Nonatherosclerotic, autoimmune?
  • Segmental: isolated UE, LE, single leg, foot, or hand
  • Inflammatory cells invade artery wall, thrombus formation & vasospasm = impaired flow, intermittent with remissions
  • Progressive disease leads to scarring & collateral involvement
26
Q

Nonatherosclerotic PAD
Buerger’s Disease
S/S
Treatment

A

S/S: pain, skin changes over time, ↓ distal pulses, ulcers
Incidence: smokers, men< 40

TX: Smoking cessation, foot care, prevent vasoconstriction, exercise, meds for symptomatic relief, surgery (sympathectomy, bypass grafts, amputation)

27
Q

Nonatherosclerotic PAD

Raynaud’s

A

Raynaud’s :
Episodic vasospastic disorder of small cutaneous arteries of fingers and toes .
“disease”- no identifiable cause
“phenomenon”- secondary to disease or exposure

Can be RT trauma and pressure to fingertips in typists, pianists, and those using in handheld vibrating equipment.
Common in young women 15-45 years.

28
Q

Nursing assessment Raynaud’s

A

Fingers, toes, ears, and nose change colors (blue, white, red)
Patient describes coldness, numbness, followed by throbbing, aching, tingling and swelling.
Episodes lasts minutes to hours.
Precipitated by cold, emotional upsets, caffeine, and tobacco use
Skin becomes thickened and nails brittle over time

29
Q

Raynaud’s management

A

Diagnosis : persistent symptoms, HX

Treatment
PREVENTION:
-Keep warm, wear gloves
-Avoid injury
-Increase perfusion –swinging hands
-Smoking cessation
-Stress management

MEDICATION

  • Calcium channel blockers (nifedipine(Procardia)
  • Vasodilators
  • Alpha blockers
30
Q

Chronic Venous Insufficiency:

A

One-way valves in the veins are damaged = retrograde flow, pooling, and swelling

31
Q

Chronic Venous Insufficiency: Causes

A

Causes: incompetent valves in the legs, pressure in the vein ↑and forces fluid & RBCs into the tissue → edema and hemosiderosis (brownish discoloration)
Ulcerations RT complex inflammatory & circulatory factors

32
Q

Chronic Venous Insufficiency: S/S

A 
S/S:
Brawny, brownish, leathery fragile skin
Cyanosis if dependent
Persistent edema in LEs
Stasis dermatitis-itching with standing
Ulcers above medial malleolus
Pain ↑ if dependent
Recurrent ulcerations & cellulitis
33
Q

Care of venous vascular disease

A

COMPRESSION: essential
Ace wraps, ,custom-fitted compression stockings, SCD, Unna boot

Moist environment wound dressings

Nutritional evaluation & education

Education: avoid trauma, skin care, compression stockings

Activity: avoid prolonged standing/sitting or crossing legs, elevate to reduce edema, avoid constrictive clothing, avoid trauma, ambulation if indicated

Comparison of arterial and venous ulcers: (table 32-6 pg 1004 Lemone)

34
Q

Arterial vs. Venous PVD

Arterial disease

A 
Arterial disease
pulses: dim or absent
Cap refill: > 3 sec
Ulcers:
toes, foot, lateral malleolus
Round, smooth margins
Minimal drainage
Eschar, pale pink granulation
Pain: intermittent claudication, rest pain
Skin: rubor, pale elevated
Thin, shiny, taunt, hairless
Cooler gradient down leg
Thick toenails
35
Q

Arterial vs. Venous PVD

Venous disease

A 
Venous disease
pulses: +
Cap refill <3 sec
Ulcers: 
Near medial malleolus
Irregular shape
Mod to copious drainage
Yellow slough, dark red granulation
Pain: dull ache, heaviness
Skin: brown discoloration
Thick, hardened, indurated
    Warm 
    Itchy

NUR 141 (48 decks)

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