2.2 Cardiovascular, vascular Flashcards

1
Q

Anemia

A

Abnormally low # of circulating RBCs, decreased Hgb concentration or both
R/T acute/chronic blood loss, inadequate RBC production or increase in RBC destruction
May affect all major organ systems depending on severity
Risk increases with age
Categorized by cause

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2
Q

Anemia Pathophysiology

A

Decreased oxygen carrying capacity of blood r/t deficiency of RBCs or Hgb = tissue hypoxia
Manifestations depend on severity, how quickly it develops, other factors

S/Sx develop as RBC & Hgb continue to decrease

Blood redistribution to vital organs & lack of Hgb = pallor of skin, MM, conjunctiva, nailbeds

Tissue oxygenation decreases = HR & RR increases trying to increase cardiac output & tissue perfusion

Rapid Blood Loss

  • Blood volume rapidly decreases which decreases oxygen carrying capacity of blood
  • Tachycardia, tachypnea, skin pale cool & clammy, poss signs of circ shock
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3
Q

Pathophysiologic Mechanisms of Anemia

Decreased RBC Production

A

Decreased RBC Production

Altered Hgb Synthesis

  • Iron Deficiency
  • Thalassemias
  • Chronic inflammation

Altered DNA Synthesis
-Vit B12 or Folic Acid malabsorption or deficiency

Bone Marrow Failure

  • Aplastic Anemia
  • Red Cell Aplasia
  • Myeloproliferative leukemias
  • Cancer Metastasis, lymphoma
  • Chronic Infection, inflammation, physical & emotional fatigue
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4
Q

Pathophysiologic Mechanisms of Anemia

Increased RBC Loss or Destruction

A

Increased RBC Loss or Destruction

Acute or Chronic Blood Loss

  • Hemorrhage or trauma
  • Chronic GI bleeding, menorrhagia

Increased Hemolysis

  • Hereditary Cell membrane disorder
  • Defective Hgb=sickle cell dx or trait
  • PK deficiency
  • Immune mechanisms/disorders
  • Splenomegaly
  • Infection
  • Erythrocyte trauma (d/t CABG)
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5
Q

Nutritional Anemias

Iron Deficiency Anemia

A

Iron Deficiency Anemia

  • Most common type of anemia
  • Supply of iron is inadequate to make Hgb
  • Results in fewer number of RBCs
  • Usually caused by excessive iron loss d/t chronic bleeding
  • Inadequate diet or malabsorption may also be cause

Manifestations:

  • Chronic iron deficiency
  • Brittle, spoon shaped nails
  • Cheilosis (cracks at corner of mouth)
  • Smooth, sore tongue
  • Pica(person eats things not usually considered food)
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6
Q

Nutritional Anemias

Vitamin B 12 Anemia

A

Inadequate B12 is consumed or poorly absorbed from GI tract

  • Pernicious Anemia = failure to absorb dietary B12
  • Malabsorption
  • Dietary factors (vegans)

Manifestations:

  • Pallor
  • Slight jaundice
  • Weakness
  • Smooth, sore beefy red tongue
  • Diarrhea
  • Neurologic symptoms
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7
Q

Nutritional Anemias

Folic Acid Deficiency

A

Folic Acid Deficiency

Folic Acid: green leafy veggies, fruit, cereal, meats & absorbed in intestines

Caused by:
-Inadequate Dietary Intake
Older adults, alcoholics, TPN
-Increased Metabolic Requirements
Pregnant, Infants/Teens, HD, hemolytic anemia
-Folic Acid Malabsorption & Impaired Metabolism
Celiac sprue, Chemo agents, Alcoholism

Manifestations:

  • Pallor
  • Progressive weakness & fatigue
  • SOB, Heart palpitations
  • Similar to B12
  • Glossitis, cheilosis, diarrhea but NO Neuro S/Sx
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8
Q

Anemia Diagnostics

A
Diagnostics
CBC
Iron Level
Serum Ferritin
Schilling Test
Cobalamin
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9
Q

Anemia Medications

A
Medications
Dependent on cause
Iron replacement
-Black stools/constipation
Cobalamin
Folic Acid
Dietary modifications
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10
Q

Polycythemia

A

Polycythemia

Excess of RBCs characterized by Hct > 55%
Impaired circulation due to increased blood viscosity
Primary Polycythemia (Polycythemia Vera)
-Uncommon, cause unknown
-Overproduction of RBCs, WBCs, platelets
-Mostly affects men of Euro Jewish ancestry btw 40-70

Secondary Polycythemia

  • More Common
  • Increased # of RBC d/t excess EPO secretion or prolonged hypoxia
  • Usually develops as response to chronic hypoxia
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11
Q

Polycythemia Manifestations

A

Increased Blood Volume & Viscosity = Manifestations

HTN common = HA, dizziness, vision & hearing disruptions

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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12
Q

Management of Polycythemia

Primary Polycythemia Vera

A
Primary Polycythemia Vera 
Perform phlebotomy (500ml)
Monitor I & O -hydration
Prevent stasis & DVT exercise, ASA
Meds (leukemia risk)
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13
Q

Management of Polycythemia

Secondary Polycythemia

A
Secondary Polycythemia
Controlling chronic pulmonary disease
Smoking cessation
Avoid high altitudes 
Monitor I & O, hydration
Prevent stasis & DVT
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14
Q

Venous Thrombosis

A

Blood clot forms on wall of vein, accompanied by inflammation of vein wall & some degree of obstructed venous blood flow
Superficial or deep veins

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15
Q

Venous Thrombosis Factors Associated

A
Factors Associated:
Immobilization
Surgery
Cancer
Trauma
Pregnancy & Delivery
Hormone Therapy
Coagulation Disorders
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16
Q

Venous Thrombosis Pathophysiology

A

Virchow’s Triad
Stasis of blood flow
Endothelial injury
Hypercoagulability

17
Q

Venous Thrombosis Manifestations

A

Dull, aching pain in affected extremity

Possible tenderness, warmth, erythema along vein

Cyanosis & edema in affected extremity

Chronic venous insufficiency

PE

18
Q

Venous Thrombosis Management Diagnostics

A

Diagnostics

Duplex Venous US
Plethysmography
MRI
Ascending Contrast Venography

19
Q

Venous Thrombosis Management Prophylaxis

A

Prophylaxis

Low molecular weight heparins

Oral

Elevate foot of bed, knees slightly flexed

Early mobilization & leg exercises

IPCs & TEDs

20
Q

Venous Thrombosis Management Medications

A

Medications

Thrombolytics

  • Streptokinase or tPA
  • May accelerate clot lysis & prevent damage to valves

Anticoagulants

  • Main treatment
  • Prevent clot extension
  • Enable body’s own lytic system to dissolve clot
  • Reduce risk of PE
  • Heparin infusion started calculated by aPTT
  • Warfarin may be started with heparin infusion
  • LMW Heparin used more frequently
21
Q

Peripheral Artery Disease (Arterial Insufficiency)

A

Atherosclerosis = ischemia of extremities (distal legs); Decreased sensation = Increased risk of injury

Risk Factors:
Age, males, heredity smoking, obesity, inactivity, HTN, hyperlipidemia, DM

22
Q

Peripheral Artery Disease (Arterial Insufficiency) Manifestations

A

Manifestations
Leg pain when walking relieved by rest (intermittent claudication)

Rest pain

Paresthesias

Diminished or absent peripheral pulses

Pallor with extremity elevation, dependent rubor when dependent

Thin, shiny, hairless skin; thickened toenails

Areas of discoloration or skin breakdown

23
Q

Peripheral Artery Disease (Arterial Insufficiency) Management Diagnostics

A
Diagnostics 
Stress Testing
Duplex Doppler US
Angiography
MRA
24
Q

Peripheral Artery Disease (Arterial Insufficiency) Management Medications

A

Medications

Platelet aggregate inhibitors (ASA, Plavix)

Pentoxifylline decreases blood viscosity

Vasodilators

25
Q

Peripheral Artery Disease (Arterial Insufficiency) Management Decrease Risk Factors

A

Decrease Risk Factors
Smoking Cessation

Control DM, HTN, Cholesterol levels, weight

Meticulous foot care

26
Q

Peripheral Artery Disease (Arterial Insufficiency) Management Revascularization

A

Revascularization

Bypass grafts to increase blood flow

27
Q

Buerger Disease (Thromboangiitis Obliterans)

A

Inflammatory cells infiltrate walls of small/midsize peripheral arteries

Thrombus formation & vasospasms occur = impaired blood flow

As disease progresses, vessels become scarred & fibrotic

Affects upper or lower extremities, usually leg or foot

Exacerbations & remissions, with each episode more severe & prolonged

Men under 40 who smoke

Smoking is most significant risk factor

28
Q

Buerger Disease Manifestations

A

Manifestations
Claudication & pain

Numbness or diminished sensation

Cool, pale, or cyanotic skin

Shiny, thin skin & white, malformed nails in affected extremities

Distal pulses difficult to locate or absent

Trophic changes to nailbeds

Ulceration & gangrene in later stages

Small, red, tender vascular cords in affected extremities

29
Q

Buerger Disease Diagnostics

A

Diagnostics
H&P
Doppler studies
Angiography/MRI

30
Q

Buerger Disease Management

A

Management
Smoking cessation

Regular exercise

Protect extremities from cold injury

Teach stress management

Medications

Surgical

31
Q

Raynaud Disease

A

Episodes of intense vasospasm in small arteries/arterioles of fingers

Disease: no identifiable cause

Phenomenon: secondary to disease or exposure

Young women between 20-40

Progressively worse over time

Triggers: emotional stress, exposure to cold

32
Q

Raynaud Disease Manifestations

A

Manifestations

Involves fingers and sometimes toes

Occurs intermittently
Blue =White = Red color changes

Numbness, stiffness, decreased sensation & aching pain

More frequent & prolonged over time

Fingertips thicken & nailbeds become brittle

33
Q

Raynaud Disease Diagnosis

A

Diagnosis

H&P

34
Q

Raynaud Disease Management

A

Management

Prevention by keeping hands warm

Avoid injury to hands

Swinging arms back & forth

Smoking cessation

Stress reduction

Medications

Vasodilators

Calcium Channel Blockers

Alpha Adrenergic Blockers

35
Q

Chronic Venous Insufficiency

A

Incompetent valves and increased venous pressure = vein dilation = blood cannot be pumped back to the heart = venous stasis

Decreased sensation, edema & hemosiderosis (brownish pigmentation) develop

Venous stasis ulcers develop

36
Q

Chronic Venous Insufficiency Manifestations

A

Manifestations
LE edema that worsens with standing

Itching, dull leg discomfort or pain increases with standing

Thin, shiny, atrophic skin

Cyanosis & brown skin pigmentation of lower leg/foot

Possible weeping dermatitis

Thick, fibrous subcutaneous tissue

Recurrent ulcerations of medial or anterior ankle

37
Q

Chronic Venous Insufficiency Management

A

Management
Elevate legs

Compression: Unna boot, TED, ACE wraps

Avoid constrictive clothing & crossing legs with sitting

Foot care: inspect daily
Avoid prolonged sitting or standing

Moist environment for wound care

Nutritional evaluation & education