Exam 5 module 9 Flashcards by Taylor Roney

S/S of anemia

Fatigue
Increased HR
Pallor
Low hemoglobin and hematocrit

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Patho for Iron deficiency

Low HgB/Hct
Low Ferritin

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Causes of Iron deficiency

Nutritional (vegan/chron’s)
High demand (pregnancy/growth)
Lack of absorption (gi issues)
Chronic blood loss

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Patho of sickle cell anemia

Autosomal recessive pattern
RBC abnormal shape
Triggered by stress, illness w/ hypoxia

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Affects of sickle cell anemia

Blockage of vessels
Ischemic pain

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Aplastic anemia patho

Damaged stem cells
Decreased production by bone marrow

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Causes of aplastic anemia

Radiation and chemotherapy
Exposure to toxins
Some autoimmune disorders
Viral infections

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S/S of aplastic anemia

(BMS)
Fatigue
Infection
Bleeding/bruising

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Vitamin B12 deficiency causes

Diet
Alcohol consumption
Lack of intrinsic factor
GI issues
Crohn’s disease
Bacterial growth

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Pernicious anemia

Lack of intrinsic factor associated with VB12 deficiency

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S/S of VB12 anemia (unique)

Neurological: peripheral tingling, ataxia, dementia/behavior changes

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Nomocytic anemia types

Aplastic
(Low count, normal appearance)

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Microcytic anemia types

Iron deficiency
Thalassemia
(Low count, small RBC)

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Macrocytic anemia types

B12/pernicious
Folate deficiency
(Low count, large size)

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Blood transfusion reactions: Acute hemolytic

(Acute allergy)
ABO incompatibility
Hemoglobinuria (RBC’s in urine)
Acute renal failure
DIC
Death

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Disseminated intravascular coagulation (DIC)

Blood clots excessively formed in the body’s vessels, using all of the clotting factors

Leaves no clotting factors to stop bleeding in other parts of the body.

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Blood transfusion reactions: Febrile reactions

Leukocyte incompatibility
WBC’s from donor aren’t removed.

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Polycythemia vera

Cancerous condition of blood cells
Over production of RBS, WBH and PLatelets

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Complications of Polycythemia vera

Excess RBC = thick blood
Clots, splenomegaly, trapped RBC

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S/S of polycythemia vera

Blurred/double vision,
Shortness of breath
Headache
Itching
Flushed skin
Fatigue
Excessive sweating

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Thalassemia

Genetic condition » reduced hemoglobin
(Autosomal recessive
Alpha Or Beta (depending on cells effected)

S/S of Thalassemia

Mild to severe anemia
Fatigue
Splenomegaly
Bone problems
Jaundice
Dark Urine

Von willebrand Disease

Lack of protein to help platelets stick together (von Willebrand factor)
Autosomal dominant

S/S of Von Willebrand

Nosebleeds
Heavy periods
Bleeding after dental procedures

Active Compensatory Mechanisms

Sympathetic Nervous System to maintain BP ADH reabsorbs fluid RAAS » angiotensin II » vasoconstriction, aldosterone reabsorbs sodium

Active compensatory mechanism goals

Increase HR and Cardiac Output peripheral vasoconstriction ADH secretion RAAS activation Decreased urine output

Stop the bleeding (Hemostasis) Mechanism

Platelet activation- Vasoconstriction with platelet plug formation Coagulation system activated - strong fibrin clot Reticulocyte count - Bone marrow responding, release of immature RBCs

Stop the bleeding mechanism goals

Vasoconstriction at bleeding site Platelet activation at injury/bleeding Coagulation system activated Fibrin clot Increased reticulocyte

ANP/BNP function

Decreases renin, angiotensin II and aldosterone Increases GFR

Goals of ANP/BNP

Vasodilation Decrease BP Decrease BP

Atrial Fibrillation

Always irregular Trembling atrium No P-wave Potential clotting in atrium Potential stroke

Causes of atrial fibrillation

Coronary artery disease Congestive heart failure Surgery

Preload

Amount of stretch in left ventricle at the end of diastole.

Causes of decreased preload

Sepsis, hemorrhage, dehydration decreased venous return.

Afterload

Force or resistance that the left ventricle must pump against to expel blood into the aorta.

Causes of increased afterload

Increase in Congestive heart failure, atherosclerosis and hypertension

Contractility

Strength of the contraction

Peripheral artery disease

Atherosclerosis in some blood vessels= likely atherosclerosis in all vessels Plaque created over time by deposit of fatty materials Narrowing of arteries Risk of occlusion ( Ischemia)

S/S of peripheral artery disease

Intermittent Claudication (lower extremity pain) Pale, cool skin Weak or absent pulses Ulceration or sores

Hypertension: contributing factors

High peripheral vascular resistance Increased cardiac output RAAS system activation

S/S of hypertension

Silent killer Asymptomatic until organ failure

Coronary artery disease

Damage to vessels from high pressure, plaque builds up and leads to blockage

results of coronary artery disease

Angina, MI, Heart failure, Pulmonary edema

Left ventricular hypertrophy

LV enlarges due to being overworked Lead to heart failure

Raynaud’s disease

Vasospasm of the arterioles of hands or feet: cycles of vasodilation and vasoconstriction

Risk factors for Raynaud’s disease

Stress, autoimmune diseases, cold climates

S/S of Raynaud’s disease

Painful, loss of sensation, white»Blue»red of fingers toes, nose and ears

Venous insufficiency

Damage to valves in veins of legs Impaired/stasis of blood flow Can leads to ulcers

Risk factors of venous insufficiency

Obesity Pregnancy Prolonged standing Varicose veins