Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
152 Cards in this Set
- Front
- Back
|
Neutrophil
|
Granulocyte
Chief phagocyte- inflammatory response |
|
|
Eosinophil
|
Granulocyte
Engulf complexes formed from allergic responses & defend against parasites |
|
|
Basophil
|
Granulocyte
Releases heparin, histamine, serotonin |
|
|
Lymphocyte
|
Agranulocyte
T& B cells Immune response |
|
|
Monocyte
|
Agranulocyte
Potent phagocyte Becomes macrophages in tissue Ingests & Processes antigens for lymphocyte recognition |
|
|
5 steps of hemostasis
|
1) Vasospasm
2) Platelet plug 3) Clotting cascade 4) Blood clot forms 5) Blood clot dissolves |
|
|
Anemia
|
Decreased # of RBC's
or Decrease in Hgb content Caused by: Blood loss Impaired RBC production Increased RBC destruction |
|
|
Normocytic normochromic anemia
|
Normal size normal color RBCs
D.T. Posthemorrhagic anemia Anemia of chronic disease |
|
|
Macrocytic normochromic anemia
|
Large size normal color
Pernicious anemia (Vit B12 deficit) |
|
|
Microcytic Hypochromic anemia
|
Small size pale color RBCs
Iron deficiency anemia |
|
|
Posthemorrhagic anemia
|
Normocytic Normochromic
D.T. Acute or chronic loss of blood Acute: Trauma or surgical complications Chronic: Bleeding ulcer or tumor, menstral blood loss More often considered an iron deficiency anemia (anemia d.t. depletion of Fe stores) Fatal if loss exceeds 2000ml |
|
|
Anemia of chronic diseases
|
Normocytic Normochromic
D.T. decreased production of RBCs Decreased life span of RBCs Impaired Fe metabolism Some causes: Decreased EPO production secondary to renal disease Myelosuppression secondary to chemo Autoimmune diseases |
|
|
Pernicious anemia
|
Macrocytic Normochromic
Slow development Loss of parietal cells that make intrinsic factor or lack of vit B12 in diet Associated with: Autoimmune dysfunction Heavy alcohol consumption Complete or partial gastrectomy Intestinal disease |
|
|
Iron deficiency anemia
|
Microcytic Hypochromic
Most common type Fe demand exceeds what is available Either lack of intake, chronic bleeding, or Fe not utilized effectively Results in decreased Hgb synth |
|
|
Polycythemia
|
Excessive RBC's
Relative: dehydration Absolute: Primary=> Mutation in marrow stem cells Secondary=> Increased EPO secondary to chronic hypoxia or tumors that secrete EPO ex. high altitudes, smoking, resp disease, renal tumor |
|
|
Effects of Polycythemia
|
Long term effects:
Increased blood volume + viscosity Congestion of liver + spleen Clotting Thrombus formation |
|
|
Leukemia S/S's
|
A group of malignant neoplastic disorders of blood, bone marrow, lymph, and spleen
R.T. abnormal immature cells: Anemia, infection, hemorrhage, dyspnea, fatigue, bone/joint pain, fever, epistaxis, lymphadenopathy, increased WBC count |
|
|
Multiple Myeloma
|
Cancer of the plasma cells
Increased production of abnormal plasma cells in the bone marrow= decreased production of RBC Neoplastic plasma cells destroy bone Hallmark= BENCE JONES protein in urine High plasma cell count in blood Increased Ca+ lvls from bone destruction |
|
|
Lymphoma
|
Cancer of lymphocytes
2 types: Hodgkins Non-Hodgkins |
|
|
Hodgkins Lymphoma
|
Malignant disorder of lymph nodes
Abnormally giant multi nucleated cells in lymph nodes (Reed Sternberg cells) Occurs age 15-35 or >50 |
|
|
Non Hodgkins Lymphoma
|
Includes all lymphomas except Hodgkins
B- cell lymphomas make up 90% Poor prognosis Affects older adults Lymphoid tissue cells become abnormal and crowd out normal cells |
|
|
Thrombocytopenia
|
Decreased # of platelets
Can lead to spontaneous bleeding Mostly acquired, some congenital: Viral infections, myelosuppresive drugs, autoimmune disorders |
|
|
DIC
|
Disseminated intravascular coagulopathy
Process of coagulation and fibrinolysis lose control Widespread clotting until TF runs out then bleeding occurs Results: Ischemia, impaired organ perfusion, end-organ damage Always secondary High mortality rate S/S's: Low BP, weak pulse, purpura, ecchymosis, petechiae, cyanosis, bleeding, hypoxemia, dyspnea, confusion, decreased LOC, seizure, oliguria, N+V, epistaxis, pain |
|
|
Atrophy
|
Decrease in size of tissue or organ D.T. decrease in:
Cell size or Number of cells Physiologic: Occurs in early development (thymus gland) Pathologic: Occurs from decreased workload, use, pressure, blood supply, nutrition, hormonal or nervous stimulation |
|
|
Hypertrophy
|
Increase in size of cells and organ that is affected
Results from increased workload on body part Common in skeletal muscle, heart + kidney Physiologic: heavy use of skeletal muscle Pathologic: hypertension causes heart to grow |
|
|
Hyperplasia
|
Increase in number of cells D.T. increased rate of cellular division
Occurs in cells capable of miotic division: Skin, intestines, glands Cannot occur in nerve, skeletal or cardiac muscles as these cells do not divide Physiologic: 1) Compensatory: allows certain organs to regenerate 2) Hormonal: Estrogen dependant organs (uterus + breast) Pathologic: Increase in # of cells D.T. high hormone lvls or growth factor |
|
|
Metaplasia
|
Reversable replacement of one mature cell by another
Usually D.T. chronic inflammation + irritation |
|
|
Dysplasia
|
Abnormal changes in size, shape, and organization of mature cells
Frequently found in cervix + resp tract |
|
|
4 common causes of edema
|
Increased cap membrane permeability
Decreased plasma oncotic pressure Increased hydrostatic pressure Lymphatic obstruction |
|
|
Fluid output
|
Kidneys:
Filter 180 L blood/day Produce 1200-1500 mL urine Skin: Regulated by SNS Sweat glands produce 500-600ml sweat/day Respiration: About 400 mL/day GI tract: In stool about 100-200mL/day |
|
|
Na+
|
Primary cation of ECF
135-145 mEq/L H20 balance by serum osmolarity Roles: H2O balance Nerve impulse transmission Regulation of ABG Chem rxns |
|
|
K+
|
Primary ICF cation
3.5-5.0 mEq/L Roles: Regs met. acts. needed for glycogen deposits in liver + skeletal muscle Transmission + conduction of nerve impulses normal cardiac conduction skeletal and smooth muscle contraction |
|
|
Ca++
|
4.5-5.5 mEq/L
Stored in bones mostly Binds with albumin when in plasma Bone/teeth formation, blood clotting, hormone secretion, cell membrane integrity, cardiac conduction, nerve impulse transmission, muscle contraction |
|
|
Cl-
|
95-108 mEq/L
Major ECF anion Reg'd by diet + kidneys |
|
|
PO4+
|
Phosphate
2.5-4.5 mEq/L Buffer anion in ICF ABG Healthy teeth + bones, neuromuscular acts. Reg'd by diet, renal excretion, intestinal absorption + PTH |
|
|
Mg++
|
Magnesium
1.5-2.5 mEq/L Cation Reg'd by diet, renal, PTH |
|
|
ABG normal findings
|
pH
7.35-745 PaCO2 35-45 HCO3- 22-26 |
|
|
Causes of constipation
|
Hypothyroidism
Opiates Aging Neurogenic disorders of large intestine Low residue diet Low activity level Mechanical or fxnal Constant suppression of stool Excessive antacid use |
|
|
Upper GI bleed
|
Esophagus, stomach, duodenum
D.T. Bleeding varices, peptic ulcers, Mallory-Weiss tear Hematemesis (coffee ground vomit) Melena (Black tarry stools) Hematochezia (Stool containing frank blood) |
|
|
Lower GI bleed
|
Jejunum, ileum, colon, rectum
D.T. polyps, inflammatory disease, cancer, hemorroids Hematochezia (Frank blood in stool) |
|
|
GERD
|
Gastroesophageal reflux disease
LES doesnt close properly, relaxes too much, or ineffective esophageal peristalsis Contributing factors: Vomiting, coughing, lifting, bending Can lead to Barrett's esophagus due to chronic irritation |
|
|
Paraesophageal Hiatal hernia
|
Stomach bulges through a new opening in diaphragm near the esophagus that is not supposed to be there
Major risk of "strangling" the esophagus by having the stomach wrap around it |
|
|
Sliding Hiatal Hernia
|
Part of the stomach moves through the diaphragm where the esophagus is supposed to be
Stomach bulges up above the diaphragm Causes: congential variation, trauma, weak diaphragmatic muscles |
|
|
Pyloric obstruction
|
Blocking of the pylorus
D.T. Peptic ulcer disease as the ulcerations cause inflammation, edema, spasms, fibrosis, scarring or Cancer |
|
|
Intestinal obstruction
|
Blockage that stops or impairs passage of intestinal contents in the intestines
Simple: Mechanical blockage Fxnal: Failure of motility (paralytic ileus) D.T. Hernia, torsion, intussusception, diverticulosis, tumor, paralytic ileus S/S's dependant on area of obstruction: Pyloric- profuse, clear, gastric emesis Proximal small intestine- mild distension, bile colored emesis Lower intestinal- More pronounced distension, late vomiting with fecal type emesis |
|
|
Gastritis
|
Inflammatory disorder of the gastric mucosa
Acute: Erosion of surface epithelium Usually D.T. drugs/ chemicals Chronic: Thinning & degeneration of stomach wall |
|
|
Peptic Ulcer Disease
|
Erosion of the GI mucosa D.T. the digestive action of HCl + pepsin
Can be acute, chronic, superficial, or deep Superficial ulcers not "true" |
|
|
Duodenal peptic ulcers
|
Most common
Primary cause: hypersecretion of HCl + Pepsin Contributing factors: H. Pylori infection(damages mucosal cells + stims gastrin + acid secretion) NSAID use(decrease mucous) Smoking (Increases acid production) |
|
|
Gatric peptic ulcer
|
Less common
Chronic gastritis associated with gastric ulcers Major causes: H. Pylori NSAIDS Drugs Duodenal reflux of bile |
|
|
Stress peptic ulcers
|
An acute form of peptic ulcer
Develops after severe illness, systemic trauma, neural injury Emotion stress may be a cause Ischemic: Develops within hours of major physiological event (hemorrhage, burn) Cushing: Associated with severe head trauma as result of decreased mucosal blood flow + hypersecretion of acid |
|
|
Pancreatic Insufficiency
|
Deficient production of panc. enzymes
Result= fat maldigestion Causes: Chronic pancreatitis Pancreatic carcinoma Pancreatic resection Cystic fibrosis Most common sign = steatorrhea |
|
|
Ulcerative collitis
|
Chronic inflammation that causes ulceration of colonic mucosa
Lesions appear btwn 20-40 yrs Lesions form erosions which develop into ulcers, abscess formation, necrosis follows Increased risk of colon CA D.T. chronic irritation S/S's= mucosal bleeding, cramping, urge to defecate, frequent diarrhea ( up to 20x/day) with blood + purulent mucous dehydration, weight loss, anemia, fever (secondaryto bleeding, fluid loss, inflammation) |
|
|
Crohn's disease
|
Inflammatory disorder affecting all of GI tract
Affects all layers of the colon Cobblestone pattern ulcers Increased risk for colon CA S/S's= May have no "specific" systems other than "irritable bowel" Diarrhea, RLQ tenderness, weight loss may be anal involvement including fissure, abscess, fistula |
|
|
Diverticular disease
|
POuching of mucosa through muscle layers of colon wall
S/S's are vague or absent: cramping of lower ABD, constipation, diarrhea, distension, gas |
|
|
Appendicitis
|
Age 20-30 yrs
S/S's= vague epigastric or periumbilical pain that worsens over 3-4 hrs, pain then moves to RLQ N+V, anorexia, fever, Increased WBC, rebound tenderness |
|
|
Portal hypertension
|
Caused by any disorder that obstructs/hinders blood flo thru any part of portal venous system or vena cava
Common causes: Thromboses, inflammation, fibrosis May result in: Varices Splenomegaly Ascites Hepatic Encephalopathy |
|
|
Varices
|
Distended tortuous veins found in lower esophagus, stomach, rectum
Caused by prolonged elevation of pressure within the portal venous system Vomiting of blood from bleeding esophageal varices is most common sign of portal HTN |
|
|
Hepatic Encephalopathy
|
Deterioration of brain cell fxn
D.T. blood bypassing liver b/c of portal HTN = toxic blood being circulated to brain or Toxins in blood not being removed adequately because liver fxn impaired Primary culprit: NH4 |
|
|
Ascites
|
Fluid buildup in peritoneal cavity "3rd spacing"
Late stage S/S's or cirrhosis + portal HTN 3 causes: Portal HTN Hepatocyte failure Increased Hepatic Lymph production S/S's Weight gain, ABD distension, shiny tight skin of ABD, dyspnea, tachypnea, orthopnea, peripheral edema |
|
|
Obstructive Jaundice
|
Extrahepatic:
common bile duct occluded or compressed Bilirubin conjugated by hepatocytes but cant flow into duodenum Bilirubin then accumulates in liver + enters blood = hyperbilirubinemia Light color stool Intrahepatic: 1)Hepatocellular damage or 2)Obstruction of bile canaliculi 1) Damaged hepatocytes leak conjugated bilirubin and are unable to conjugate bilirubin = high plasma lvls of conjugated + unconjugated bilirubin 2) Flow of conjugated bilirubin through liver into common bile duct diminished = increased plasma concentration of conjugated bilirubin |
|
|
Hemolytic jaundice
|
Excess lysis of RBCs or absorption of hematoma
Excess of unconjugated bilirubin > hepatocytes ability to conjugate = unconjugated hyperbilirubinemia Unconjugated is NOT H2O soluble so it is not excreted in urine |
|
|
Hepatitis
|
Injury to the liver by presence of inflammatory cells in tissue
Causes: Viruses Toxins Drugs Autoimmune disease Alcohol Heredity |
|
|
Viral Hep
|
BCD are chronic, rest are acute
All types cause: Hepatic cell necrosis Kuppfer(recycled RBC) cell hyperplasia Phagocytes in liver |
|
|
Fulminant Hep
|
Can result as severe complication of Hep B or C
Causes wisespread hepatic necrosis + liver failure Treatment usually palliative |
|
|
Cirrhosis
|
Irreversible, slowly progressive inflammatory disease of liver that disrupts structure + fxn
Liver tissue undergoes fibrosis |
|
|
Cholelithiasis
|
Presence of gallstones in bladder
Develops when balance of cholesterol, bile salts, + Ca+ is disrupted Bile secreted by liver is supersaturated with cholesterol S/S's= Epigastric discomfort, fatty food intolerance, heartburn, gas, pruritis, jaundice, pain |
|
|
Cholecystitis
|
Inflammation of gallbladder or cystic duct
Usually b/c gallstone in duct Impairs blood flow causing ischemia, necrosis, perforations S/S's= pyrexia, increased WBC's, rebound tenderness, ABD muscle rigidity |
|
|
Cough
|
Protective reflex
Cleanses lower airways Acute= resolves in 2-3 weeks Chronic= persists >3weeks |
|
|
Green thick foul smelling sputum
|
Infection
|
|
|
Blood stained sputum
|
TB, PE, Lung cancer
|
|
|
White thick mucoid sputum in the absence of infection
|
COPD, asthma
|
|
|
Pink frothy sputum
|
HF, pulm. edema
|
|
|
Brown or brick color sputum
|
TB, infection
|
|
|
Kussmauls Respirations
|
Increased RR with no expiratory pause (DKA)
|
|
|
Cheyne-Stokes resps
|
Alternating deep + shallow resps with periods of apnea (decreased blood flow to brain stem)
|
|
|
Hypercapnia
|
Increased PaCO2
D.T. hypoventilation of alveoli RR + pattern may appear normal Must obtain ABG's Leads to hypoxemia Causes: Depression of resp center (drugs) Disruption of medulla (CNS infection or trauma) Disease of resp muslces Thoracic cage abnormalities Large airway obstruction (tumors, sleep apnea) Increased work breathing or dead space (emphysema) |
|
|
Hypoxemia
|
Decreased PaO2
Decreased oxygenation of cells D.T. Decreased O2 content of air Hypoventilation Diffusion abnormalities Abnormal ventilation-perfusion rations |
|
|
Hypoxia D.T. decreased O2 content of inspired gas
|
PaO2 depends on getting enough inspired O2 (PiO2)
Low PiO2 = less O2 to diffuse the blood Can be corrected by increased O2 in environment Can be caused by fires, high altitudes |
|
|
Hypoventilation hypoxemia
|
Causes hypercapnia
If O2 not delivered to alveoli then O2 content decreases + PaCO2 increases = less O2 diffusing in blood Can be corrected by increased rate + depth of breathing Can be caused by unconsciousness, COPD |
|
|
Diffusion abnormality Hypoxemia
|
Diffusion impaired D.T. thickened membrane (edema) or decreased surface area for diffusion
Edema increases time needed for diffusion Destroyed alveoli result in less surface area for diffusion |
|
|
Abnormal ventilation hypoxemia
|
Most common cause of hypoxemia
Abnormal distribution of ventilation + perfusion |
|
|
Acute respiratory failure
|
Inadequate gas exchange
Hypoxemia + hypercapnia present Caused either directly ( injury to lungs, airways, chest wall) or indirectly ( Injury to other body system, CNS) |
|
|
Pulmonary edema
|
Excess H2O in lungs D.T. Lt ventricular HF, cap injury, lympatic system obstruction
|
|
|
Pulm edema D.T. Lt. vent. HF
|
Increased vascular V in lungs= increased pulm. cap. hydrostatic psi whch causes fluid to shift into alveolar interstitial spaces in high enough amounts that lymphatic system cant drain it
|
|
|
Pulm. edema D.T. Cap injury
|
increased cap. permeability causes H2O + plasma proteins to leak into interstitial spaces + alveoli. This increases interstitial oncotic psi= H20 moves out of cap. + into lung
|
|
|
Lymphatic system obstruction pulm. edema
|
Lymphatic system is unable to remove excess fluid from interstitial spaces
|
|
|
Aspiration
|
Passage of particles into lung
Cough reflex/swallow impaired Food can obstruct the bronchus = bronchial inflammation + collapse of distal airways Gastric fluid can cause severe pneumonitits + damage to alveolocapillary membrane Can lead to bacterial aspiration pneumonia R. LUNG MORE SUSCEPTIBLE |
|
|
Absorption Atelectasis
|
Decreased air from obstructed or hypoventilated alveolior from inhalation of concentrated O2 or anesthetic agents
Tends to occur after surgery b/c of: Inhaled anesthetics Pain Secretions pooling |
|
|
Compression Atelectasis
|
Pressure on part of lung, alveolar collapse
Result: Lung cant inflate properly |
|
|
Pnemothorax
|
Air in pleural space
D.T. Rupture in visceral or parietal pleura and/or chest wall 2 kinds: Tension pneumothorax: Air goes into pleural space through rupture but is not able to escape through the same rupture: LIFE THREATENING Open Pneumothorax: Air enters rupture and is able to pushed back out when the diaphragm lifts S/S's: Severe hypoxemia, dyspnea, hypotension, tracheal shift |
|
|
Pleural effusion
|
Fluid in pleural space
Sources: Blood, lymphatic vessels, abscesses, lesions Can result in compression atelectasis Pleural friction rub on effected side |
|
|
Emphysema
|
Infected pleural effusion
Presence of pus in pleural space Usually result of bacterial pneumonia S/S's: Fever, cyanosis, tachycardia, cough, pleural pain |
|
|
Pleuritis
|
Inflammation of pleura
Often preceeded by URI May lead to pleural effusion S/S's: Chills, fever, pain on expiration, pleural frictin rub |
|
|
Pulmonary fibrosis
|
increased fibrous or C.T. in lungs D.T.
Scar tissue from lung disease After effects of a disease (TB) Inhalation of harmful substances Leads to stiffness in lungs and decreased alveolocapillary diffusion |
|
|
Flail Chest
|
Results from breaking several consecutive ribs
Multiple fractures cause chest wall instability= paradoxic movement with breathing S/S's: Unequal chest expansion, pain, dyspnea, hypoventilation, hypoxemia |
|
|
Exposure to toxic gases
|
Leads to severe inflammation
Alveolar + cap damage Pulm. edema High concentrations of O2 can lead to O2 toxicity Other sources: Smoke, ammonia, Hydrogen chloride, sulfer dioxide, chlorine |
|
|
Pneumoconiosis
|
Any change in lung D.T. inhalation of inorganic dust particles
Usually occupational Occurs after yrs of exposure= progressive fibrosis Tx usuall palliative |
|
|
Allergic allveolitis
|
Inhaling organic dusts= allergic inflammatory response
Prolonged, repeated exposure can lead to pulmonary fibrosis |
|
|
ARDS
|
Acute respiratory distress syndrome
Fulminant form of resp failure Characterized by: Acute lung inflammation Diffuse alveolocapillary (AC) injury Injured AC membranes result in massive inflammatory response = severe pulm. edema Elderly + patient with severe infections have high mortality rate Usually caused by: Sepsis Trauma Others: Pneumonia, burns, aspiration, bypass surgery, drug OD, DIC etc |
|
|
Asthma
|
Chronic inflammatory airway disorder
Airway inflammation, hyperresponsiveness, bronchoconstriction, air hunger First affects bronchial airways, causes mucosal edema, secretion of mucous, + airway inflammation Triggers release of leukotrienes + histamine = inflammation + bronchospasm S/S's: Prolonged expiration, tachycardia, tachypnea, dyspnea, increased resp. effort, chest constriction, decreased breath sounds with wheezes, dry non productive cough STATUS ASTHMATICUS: Develops it bronchospasm not reversed Results in: Hypoxemia= acidosis Life threatening! Silent chest + PCO2>70mmHg = bad sign |
|
|
Chronic Bronchitis
|
Form of COPD
Chronic inflammation leading to scarring + damage to mucociliary lining... results= hyper secretion of mucous, swelling + thickening of bronchioles 1) Inspired irritants = inflammed airways with neutrophils, macrophages, lymphocytes 2) Chronic inflammation = bronchial edema + increase in size + # of mucous glands + goblet cells 3) Thick tenacious mucous production, not able to clear 4) Increased susceptibility to chest infection 5) Frequent infections complicated by bronchospasm |
|
|
Emphysema
|
Form of COPD
permanent enlargement of sac exchange airways (acini) + destruction of alveolar walls Air flow further limited b/c of decreased elastic recoil of bronchial walls Obstruction results from change in lung tissue Destruction of alveoli + loss of elastic recoil = increased amount of air in Acinus Experation becomes difficult Hyperinflation of alveoli produces large air spaces Each inspiration becomes trapped in Acinus Air trapping causes hyper expansion of chest |
|
|
Pneumonia
|
Acute inflammation of LRT, results in inflammation
Caused by pathogens being inhaled or aspirated 4 types: Lobular (one lobe) Lobar (entire lung) Bronchopneumonia (lobes adjacent to bronchi) Interstitial (in 3rd spaces) Mortality + incidence higher in elderly Risk factors: Immunosuppression immobility dysphagia intubation |
|
|
Tuberculosis
|
Infection by mycobaterium tuberculosis
Airborne droplets enter lungs, multiply in alveoli, enters lympatic + blood stream, neutrophils go to lungs to attack bacilli, engulfs + isolates bacilli forming a tubercle When bacilli are isolated + immunity is developed TB may remain dormant for rest of life Can be reactivated if immunosuppressed S/Ss: Fatigue, weight loss, lethargy, anorexia, cough with sputum, night sweats, anxiety, fever, dyspnea, chest pain, hemoptysis |
|
|
Embolus
|
A bolus of matter travelling in bloodstream
|
|
|
Embolism
|
Obstruction of vessel by an embolus (stationary)
|
|
|
Pulmonary embolism
|
Occlusion of pulmonary vessel by an embolus
Embolus can be: Thrombus (blood clot), tissue fragment; lipid, tumor piece, air Medical emergency!!!! Risk factors: Conditions that promote clotting secondary to venous stasis Hypercoagulability Injuries to endothelial cells that line vessels S/S's: Tachycardia, tachypnea, dyspnea, anxiety, syncope, pleural pain |
|
|
S/Ss of lung cancer
|
Non specific until later in disease
Cough Hemoptysis Chronic sputum Pain Dyspnea Malaise |
|
|
Pathway of blood
|
1) Blood drains into R. atrium from SVC + IVC
2) R. atrium -> R. Ventricle 3) R. Ventricle -> Lungs via pulm. A. 4) Lungs oxygenate blood 5) Oxygenated blood flows to L. Atrium 6) L. Atrium -> L. Ventricle 7) L. ventricle to rest of body via aorta + aortic arch |
|
|
Arteriosclerosis
|
Thickening + hardening of arterial walls= narrow arterial lumen
|
|
|
Atherosclerosis
|
Form of arteriosclerosis= thickening + hardening of vessel secondary to cholesterol plaque build up
Inflammatory disease Narrowed vessel = decreased blood supply to tissue = ischemia Typical in coronary vessels Leads to CAD, CVA, TIA |
|
|
Stroke Volume (SV)
|
Amount of blood pumped by L. Ventricle per beat
|
|
|
Cardiac Output (CO)
|
Total blood flow through systemic or pulmonary circulation per min
|
|
|
Systemic Vascular Resistance (SVR)
|
Force opposing movement of blood within blood vessels
|
|
|
Hypertension
|
Sustained elevated arterial BP
Results from: Increase CO (Increase HR + SV) Increased Pulmonary vascular resistance (PVR) Heart works harder |
|
|
BP's for:
Normal Prehypertensive Stage 1 hypertensive Stage 2 hypertensive |
Systolic Diastolic
<120 <80 120-139 80-89 140-159 90-99 >160 >100 |
|
|
Primary hypertension
|
Increased systolic + diastolic
Contributing factors: Heredity, stress, hyperactive SNS, hyperactive RAA, endothelial cell dysfxn, insulin resistance, increased Na+ intake |
|
|
Secondary HTN
|
Caused by systemic disease processes such as:
Renal disease ( Na+ + H2O retention= release of renin) Endocrine disorders(adrenal adenoma= increased aldosterone) Vascular disorders (artherosclerosis) Stress (SNS activity) |
|
|
Isolated systolic HTN
|
Increased vascular resistance secondary to increased rigidity of proximal large arteries (arteriosclerosis)
|
|
|
Complicated HTN
|
From chronic HTN
Damages walls of systemic blood vessels Lumen narrows significantly= decreased blood flow to organs |
|
|
Malignant HTN
|
Rapidly increasing BP
Excessive arterial psi HTN emergency |
|
|
Orthostatic hypotension
|
Decrease in systolic + diastolic when first standing up
Systolic BP drop >20mmHg or Diastolic BP drop > 10 mmHg Acute: Delay in normal regulatory mechanisms D.T. anatomic variation, drugs, prolonged immobility, starvation, physical exhaustion, volume depletion Chronic: Secondary to some diseases |
|
|
Aneurysm
|
Dilation of vessel wall or heart chamber
Most common cause artherosclerosis Aorta most affected 2 types: True: affects all 3 layers of arterial wall False: extravascular hematoma (a "leak" from trauma, surgery etc.) |
|
|
Thrombus
|
Blood clot attached to vessel wall
Develops where coagulation cascade activation has occured (inflammation, rough area, injury, infection) Artherosclerosis is primary cause Can be venous or arterial |
|
|
Peripheral artery disease
|
Artherosclerotic disease of the arteries that perfuse the limbs
Usually lower limbs Leading cause of leg amputation |
|
|
Raynauds's phenomenon
|
Vasospasm in small arteries + arterioles of fingers or toes
Secondary to systemic disease, long term exposure to cold Raynauds disease: Idiopathic vasospastic disorder S/S's: D.T. ischemia + vasospasm Skin color change Change in sensation Bilateral presentation |
|
|
DVT
|
Deep vein thrombosis
Formation of blood clot in a deep vein Usually in leg Contributing factors: Venous stasis Venous endothelial damage Hypercoaguable states S/Ss: Discoloration, calf or leg pain/tenderness, swelling of leg, warmth Pulmonary embolism: SERIOUS complication of DVT Clot dislodges from initial site in the bloodtream to the lungs MEDICAL EMERGENCY |
|
|
Myocardial Ischemia
|
Supply of coronary blood does not meet demands of myocardium for O2 + nutrients
Most common cause atherosclerotic plaques Myocardial cells become ischemic after 10 SECS of occlusion Cells can remain usable for 20 mins under ischemic conditions |
|
|
Stable Angina
|
Caused by myocardial ischemia
Occurs when myocardial demand increases Often mistaked for indigestion |
|
|
Variant (Prinzmetal) angina
|
Unpredictable chest pain
Caused by transient ischemia secondary to coronary artery vasospasm Occurs at rest, sleep, or while smoking |
|
|
Silent Ischemia
|
Asymptomatic myocardial ischemia
Present in patients with acute + chronic coronary symptoms |
|
|
Unstable angina
|
Labile blood clot forms on complicated plaque, increases blockage in coronary artery
Can be reversible Warning sign for MI |
|
|
Acute myocardial infarcation
|
Plaques rupture in coronary artery
Blood clot occludes vessel for increased amounts of time Myocardial ischemia= death/necrosis Complications: Dysrhythmias, pericarditis, organic brain syndrome, rupture of heart structures, thromboembolism Cardiac enzymes elevated |
|
|
Acute pericarditis
|
Acute inflammation of pericardium
Caused by: MI, surgery, infection, flu, Epstein Barr, hepatitis, mumps, HIV, C.T. diseases, radiation Associated with: Increased cap permeability S/Ss: Sharp chest pains that worsen with breathing, cardiac friction rub, fever, tachycardia |
|
|
Constrictive pericarditis
|
Fibrous scarring between visceral + parietal layers of pericardium
Starts with pericarditis Interferes with diastolic filling of heart S/Ss: Ascites, pedal edema, dyspnea, fatigue, JVD |
|
|
Pericardial effusion
|
Accumulation of fluid in pericardial cavity
Fluid can be: Serous (HF, overhydration) Serosanguineous (TB, neoplasm) Sanguineous (aneurysm, trauma) Purulent (infection) Psi can lead to a tamponade |
|
|
Dilated cardiomyopathy
|
Severe dilation
Ventricular contractility reduced= decreased cardiac output= HF |
|
|
Hypertrophic cardiomyopathy
|
1) Asymmetrical
Inherited Abnormal interventricular septum thickening L. ventricle chamber size decerases 2. Hypertensive Increased resistance |
|
|
Restrictive cardiomyopathy
|
Heart chambers unable to fill with blood properly b/c of rigidness + stiffness of ventricular walls
Amount of blood ejected is poor = decreased CO |
|
|
Valvular stenosis
|
Narrowing of valve so blood cant move through as freely as needed
Heart chamber above the narrowed valve needs to work harder = myocardial hypertrophy |
|
|
Valvular insufficency
|
AKA regurgitation
Incompetent valves do not close completely= failure of one way valve Blood re-enters atrium during systole Causes: Inflammation, Infection, Calcificationm Ischemia, Trauma Usually affects mitral or aortic valve |
|
|
Rheumatoid fever
|
Diffuse inflammatory disease
Caused by abnormal delayed immune response to infection by group A beta hemolytic streptococci Toxins produced stimulate immune system + Abs produced by body also attack C.T. of heart If valves become inflamed, lesions develop on cusps and scar tissue is formed |
|
|
Infective endocarditis
|
Infection + inflammation of endocardium
Increases D.T. IV drug use 3 Processes: 1) Bacteremia: Delivers organisms to valve 2) Organisms adhere to damaged surface 3) Organisms invade valvular leaflets |
|
|
Heart Failure
|
Heart fails to pump enough oxygenated blood to meet metabolic needs of body
Causes include: Atheroclerosis, HTN, MI, valvular disease, cardiomyopathy, arrhythmias |
|
|
Lt Ventricular Failure (CHF)
|
L. ventricle is weak, cant adequately pump blood = decreased CO
Weakened L. Ventricle unable to empty all blood from chamber = increased L. ventricular preload Residual volume of blood in L. Ventricle= L atrium cant empty all its contents into L. Ventricle during diastole L. Atrium overfills= pulmonary vein cant return all blood from pulmonary arteries into L. atrium= backs up Buildup of blood in pulmonary arteries = congestion= high psi= forcing fluid from arteries into alveoli= pulmonary edema |
|
|
R. Ventricular failure
|
Veins in body are unable to pump blood into R atrium b/c R. ventricle is backed up b/c too much psi + congestion in pulmonary artery = venous congestion
Systemic signs= JVD, peripheral edema, hepatomegaly |
|
|
Diastolic HF
|
Heart is thick + stiff
HTN most common cause |
|
|
Systolic HF
|
Weak heart muscle
Prior heart attack most common cause Heart too damaged to pump well |
|
|
P wave
|
Depolarization of atria
|
|
|
PR interval
|
start of P wave to start of QRS complex (time needed for atrial depolariztion + time for impulse to travel through AV node to ventricles)
|
|
|
QRS complex
|
Depolariztion of ventricles
|
|
|
T wave
|
Repolarization of ventricles
|
