disorders of blood and blood supply post

reduced blood flow causes

injury/hemorrhage, limited coagulation, reduced blood volume (dehydration), reduced cardiac output, occlusion

arteriosclerosis

thickening, loss of elasticity, calcification of arterial walls, plaque buildup, endothelial cells are damaged

atherosclerosis complications

aneurysm, stroke/TIA, MI/heart failure, legs, mesenteric claudication, renal failure

arteriosclerosis/atherosclerosis diagnosis

checking pulses in extremities, laboratory workup (hyperlipidemia, diabetes), treadmill test with echocardiography, ankle-brachial index (ABI), ultrasonography, angiography

arteriosclerosis/atherosclerosis treatment

lifestyle changes, medications, surgery to open occluded arteries, angioplasty, endarterectomy, stents

chronic venous insufficiency (CVI)

most common cause of chronic venous disease, veins unable to return adequate blood to heart

CVI causes

DVT, varicose veins

CVI patho

low pressure in venous system, squeezing of skeletal muscles surrounding veins, stretching of veins, rupture of valves and clot formation

CVI common complications/associated conditions

leg ulcers, varicose veins, DVT

CVI diagnosis

assessment of symptoms and triggers, ultrasound, venography, D-dimer test

CVI treatment

preventive measures, sclerotherapy, radio frequency, laser ablation, anticoagulants, filter in inferior vena cava to trap emboli

peripheral artery disease

plaque build up in the major arteries that supply blood to the legs, numbness, pain, infection can occur, intermittent claudication

hemodynamics of shock

the forces the heart has to respond to in order to maintain blood flow through the cardiovascular system and supply oxygen to all tissues

factors influencing circulation of shock

blood volume, systemic vascular tone, heart rate, force of contraction, blood pressure and vascular resistance affect blood flow

hypovolemic shock (hemorrhagic shock) patho

rapid or excessive loss of significant amount of whole blood, hemodynamic instability, compensatory mechanisms

hypovolemic shock clinical manifestations

hypotension, orthostatic/postural hypotension, rapid breathing, severe SOB, sudden, rapid heartbeat (tachycardia), loss of consciousness, weak pulse, sweating, pale skin, cold hands or feet, urinating less than normal or not at all

hypovolemic shock diagnosis

complete blood count, serum electrolyte concentrations, blood glucose level, arterial blood gas, prothrombin time and partial thromboplastin time, hemoglobin and hematocrit, serum lactate concentration and arterial pH

hypovolemic shock treatment

maximize oxygen, prevent further fluid loss, replace lost fluids, basic life support, cardiac monitoring, central venous line, control of bleeding, plasma expanders, pharmacoptherapy

cardiogenic shock

heart unable to circulate adequate amount of blood

cardiogenic shock patho

loss of myocardial function and contractility, number one cause of myocardial infarction

cardiogenic shock clinical manifestations

cyanosis with cool skin and mottled extremities; rapid and faint peripheral pulses; low pulse pressure, tachycardia; low and distant heart sounds; peripheral edema and jugular distension; crackles in lungs

cardiogenic shock treatment

patent airway maintenance, fluid resuscitation (unless pulmonary edema), pharmacologic therapy

distributive shock

impaired distribution of blood flow due to extensive vasodilation and loss of vascular tone

distributive shock patho

anaphylaxis, adrenal insufficiency, drug reactions, hepatic insufficiency, systemic inflammatory response syndrome

anaphylactic shock patho

antibody IgE, histamine and other substances of anaphylaxis, increased vascular permeability and bronchoconstriction

anaphylactic shock triggers

drugs, foods, and proteins; animal or insect venoms; latex; heavy metal poisoning; exercise and exposure to cold temperature

anaphylactic shock clinical manifestations

stridor; tachycardia; dyspnea, wheezing, coughing; edema; laryngospasm, bronchoconstriction; angioedema, urticaria, pruitus, hives; gastrointestinal cramps; hypotension

anaphylactic shock treatment

epinephrine, patent airway, beta agonists, intravenous fluid expanders, vasopressors

anaphylactic shock diagnosis

shock, respiratory symptoms, possible manifestations of anaphylaxis

septic shock

organ dysfunction caused by dysregulated host reposonse to infection

septic shock qSOFA diagnostic criteria

patient in ICU, respiratory rate >= 22/min, altered mentation, systolic blood pressure

septic shock treatment

perfusion restored with intravenous fluids, vasopressors, O2 support, broad-spectrum antibiotics, infection source control

septic shock monitored hourly in ICU

central venous pressure, pulmonary capillary wedge pressure, or central venous oxygen saturation; pulse oximetry; arterial blood gases; blood glucose, lactate, and electrolyte levels, renal function

neurogenic shock

caused by blockage of sympathetic nervous system outflow to intrathoracic sympathetic chain

neurogenic shock risk factors

spinal cord injuries above T6; brain injury; barbiturate overdose; hypoglycemia; medications; severe pain; spinal anesthesia; vasomotor center depression

neurogenic shock spinal shock

loss of reflex function below spinal cord injury level; resolves gradually over 4 weeks

neurogenic shock hypovolemic shock

associated with tachycardia

neurogenic shock clinical manifestations

triad of systolic hypotension, bradycardia, hypothermia; bradycardia and vascular dilation; hypoperfusion of organs; flaccid paralysis below level of injury; poiliothermia; priapism

neurogenic shock treatment

fluid replenishment; vasopressors; stabilization of spine and neck; airway patency; oxygen therapy; corticosteroids; atropine

obstructive shock

obstruction of blood flow to body’s organs; diagnosed when acute circulatory failure occurs; rare condition

obstructive shock causes

pulmonary embolism; cardiac tamponade; tension pneumothorax

obstructive shock clinical manifestations

disturbances of consciousness; oliguria; hypotension; tachycardia; decreased cardiac function and circulatory failure

obstructive shock treatment

pneumothorax- decrease chest tension or pressure in heart; needle thoracotomy and pericardiocentesis for pericardial effusion or cardiac tamponade

pulmonary emboli- surgical removal of block; thrombolytic agents

anemia classification

decreased production of erythrocytes; reduced survival time of erythrocytes; loss of erythrocytes (acute or chronic blood loss); functional changes in structure of erythrocytes

anemia laboratory tests

classify anemia, identify cause or risk for anemia

patho of anemia

nutritional deficits (macrocytic anemia: vitamin B12 and folic acid; iron deficiancy anemia and thalassemia: iron); reduced stem cells (aplastic anemia); medications and radiation; anemia of chronic disease; chronic or acute erythrocyte loss through blood loss; functional changes in the structure of erythrocytes

anemia clinical manifestations

reduction in ability of RBC to carry oxygen; increased respirations; pallor; cyanosis; headache, dizziness; tachycardia; fatigue most common clinical manifestation; muscle weakness

anemia diagnosis

medical history; blood tests (complete blood count \[CBC\]); identification of genetic causes

anemia treatment

blood transfusion (if blood loss); replacement of iron and vitamin B12 as needed; education

anemia nutritional deficiency

lack of iron and vitamin B12 affect cell maturation

anemia nutritional deficiency types and causes

iron deficiency anemia; cobalamin deficiency; folic acid deficiency

anemia nutritional deficiency treatment

supplementation (nutritional deficiency); administration of red blood cells; pharmacologic agents

hemolysis of red blood cells (RBCs)

physical trauma and stress to RBC; disruption in hemoglobin formation; immune-mediated process

sickle cell disease

cluster of autosomal recessive disorders; hemoglobin sickle or crescent in shape; genetic mutation

patho of sickle cell

hemoglobin cannot bind oxygen effectively; RBC collapses into sickle shape when oxygen released; RBC clump together and obstruct blood flow; RBC lifespan 10-20 days (as compared to 120 days); chronic inflammation

sickle cell clinical manifestations

hypoxia; tissue ischemia

sickle cell treatment

prevention, screening; supportive care; disease-modifying strategies; curative procedures; genetic analysis, prenatal counseling

thalassemia

group of autosomal recessive diseases that affect production of hemoglobin; increased incidence in individuals from mediterranean and Asia

thalassemia cause

defect in production of one or more globin chains

thalassemia clinical manifestations

defects at birth; growth retardation and cognitive deficits; jaundice

aplastic anemia

decrease in all cell populations produced by bone marrow; erythrocytes, leukocytes, platelets; body stops producing enough new blood cells

aplastic anemia causes

genetic, viral exposure, drugs or toxins, immune-mediated attack on bone marrow

aplastic anemia diagnosis

decreased: WBCs, platelets, RBCs, reduced hemoglobin; normocytic normochromic

hemolytic anmeia treatment

determination of severity; hematocrit and hemoglobin levels monitored; blood transfusion; considerations for sickle cell disease

polycythemia vera

bone marrow disorder; too many RBCs produced; increased viscosity prevents blood from flowing efficiently, leading to end organ ischemia

polycythemia vera diagnosis

hematocrit over 70, increased platelets and WBCs, decreased iron count

polycythemia vera treatment

anticoagulation, therapeutic erythropheresis, chemotherapeutic approaches

myelogenous leukemia

neoplastic changes in myeloid cell line

lymphocytic leukemia

neoplastic changes in lymphoid cell line

acute leukemia

blocks in precursor hematopoietic cells

chronic leukemia

block in later stages of maturation and differentiation of hematopoietic cells

lymphoma

heterogeneous group of malignancies; originate in lymphatic system

multiple myeloma

proliferation of malignant plasma cells

multiple myeloma risk factors

toxin and hazardous chemical exposure, obesity, genetics

multiple myeloma clinical manifestations

anemia, pain, pathologic fractures, hypercalcemia, renal insufficiency or failure

multiple myeloma treatment

radiation and chemotherapy, stem-cell transplantation, treatments for anemia

leukopenia

reduced WBC

neutropenia

reduced neutrophils

lymphocytopenia

reduced lympocytes

thrombocytosis

excess platelets

thrombocytopenia

reduced platelets

transient ischemic attack (TIA)

temporary episode of neurologic dysfunction

TIA cause

focal brain, spinal cord, or retinal ischemia without acute infarcation

TIA etiology and pathophysiology

same as ischemic stroke, clot blocking blood supply to region of brain, atherosclerosis

TIA clinical manifestations

facial drooping; arm or leg weakness on one side of body; speech difficulty; sudden trouble seeing in one or both eyes; difficulty walking with dizziness; lack of balance or coordination; severe headache

TIA diagnosis and treatment

exclusion of conditions that mimic TIA; blood glucose and other blood tests; electrocardiography; noncontrast CT; MRI with diffusion-weighted imaging; CT angiography or magnetic resonance angiography; carotid doppler

ischemic and hemorrhagic stroke

interruption in blood supply to region of brain or bleeding of vessel resulting in brain tissue damage or infarction

ischemic: 87% hemorrhagic: 13

ischemic stroke etiology and patho

partial or complete occlusion of cerebral blood flow due to thrombus or embolus; atherosclerosis; cardiac disorders; thrombotic strokes

hemorrhagic stroke etiology and patho

bleeding into brain from burst blood vessel; subarachnoid hemorrhage; cerebral aneurysm; arteriovenous malformations (AVMs)

ischemic and hemorrhagic stroke clinical manifestations

sudden onset of focal neurologic deficit persisting for at least 24 hours due to reduction or occlusion of cerebral circulation or rupture of blood vessels

ischemic stroke treatment

restoration of blood flow and reducing area of infarction; penumbra: tissue surrounding infarction; supplemental oxygen; glycemic control; fibrinolytic therapy; antihypertensive therapy; aspirin 325 mg; hypothermia

hemorrhagic stroke treatment

osmotic diuretics; surgical evacuation; craniotomy with aneurysm clipping; endovascular therapy with coil embolization; delayed cerebral ischemia (DCI)

CAD (coronary artery disease) epidemiology

more than one in three adults in United States have one or more types of CVDs

CAD risk factors

modifiable, nonmodifiable, inflammation, other medical conditions

CAD prevention measures

ideal cardiovascular health

CAD diagnosis

presence of dysrhythmia (arrhythmia); blood tests; stress test; echocardiography; nuclear stress test (SPECT); coronary angiogram (coronary angiography or arteriography)

CAD treatment

lifestyle changes; hypertension management; lipid-lowering therapy (statins); anxiety management (counseling, support)

myocardial ischemia and infarction cell and tissue features

atherosclerosis-narrow coronary arteries; decreased blood flow; fracture in fibrous cap; superficial erosion of intima

disruption of coronary blood flow- imbalance among oxygen supply, demand, and consumption

reduced contractility of ischemic myocardial fibers; disruption in cardiac conduction system; ischemic cascade

myocardial ischemia and infarction stable angina

chronic form of ischemic heart disease (IHD); occurs with increased myocardial oxygen demand and reduced blood flow during exertion or emotional stress

myocardial ischemia and infarction stable angina clinical manifestations

related to exertion; resolve with rest or short-acting nitroglycerin