exam 2 (ch. 11, 12, 14) Flashcards
chapters 11, 12, 14
hemostasis
- hemo = blood
- stasis = remain
- the stopping of bleeding
- the process is rapid and localized
the primary layers in hemostasis include
- blood vessels
- platelets
- plasma proteins (coagulent proteins)
What are plasma proteins made by
liver
Vascular system
Intact endothelial cells inhibit platelet adherence and blood coagulation
Injury to endothelial cells promotes…
localized clot formation
Injury to endothelial cells: Phases
Phase 1: vasoconstriction
Phase 2: Platelets
Phase 3: Coagulation
First phase: Vasoconstriction
- Narrows the lumen of the vessel to minimize the loss of blood
- Brings the hemostatic components of the blood (platelets and plasma proteins) into closer proximity to the vessel wall
- Collagen = enhances contact activation of platelets
- Von Willebrand factor = made by endothelial cells
What does collagen initiate
vasoconstriction
Second phase: Platelets
- Circulate in resting state approximately 10 days
2. At rest = minimal interaction with other blood components or the vessel wall
When stimulated by endothelial damage, platelets function to…
- Plug the defect = round and sticky platelets, aggregate to site and build a hemostatic plug
- Release vasoconstrictors
- Cause more platelets to aggregate
- Secretion of active substances to initiate coagulation
Platelets are cells fragments of what?
megakarocyte
When platelets aggregate to site, the release what?
- ADP (recruit more platelets)
- Vasoconstrictive amines
- epinephrine (vasoconstrictor) - Thromboxane A2
- amplifies the initial aggregation of platelets into a large platelet mass
Von Willebrand Factor
Secreted by endothelial cells
- important for adhesion and aggregation of platelets
Third phases: Coagulation
To go from liquid to semisolid mass.
- need calcium and vitamin K
what are the two pathways of coagulation
- Extrinsic
- Intrinsic
- they both come together to form a common pathway; you need both for normal coagulation
Describe the coagulation cascade
Phase 1: intrinsic and extrinsic pathways come together and form common pathway
Phase 2: Prothrombin to thrombin
Phase 3: Fibrinogen to fibrin
Platelets and coagulation factors
Distinct but complimentary and mutually dependent
- platelets interact with coagulation factors by providing binding sites
- thrombin activates platelets
Coagulation Inhibitors
Counterbalance coagulation factors; restrict clot by keeping it at one location. Substances: - Antithrombin - Protein C - Plasminogen
Fibrinolysis
Plasminogen activated to plasmin
- by Tissue plasminogen Activator (TPA), released by endothelial cells
- plasmin dissolves fibrin
Fibrinolysis is activated at the same time as what?
Coagulation
Disturbances of Blood Coagulation: 4 types
- Abnormalities of small blood vessels
- Abnormality of platelet formation
- Deficiency of one or more plasma coagulation factors
- Liberation of thromboplastic material into circulation
Abnormalities of small blood vessels
Abnormal bleeding resulting from failure of small blood vessels to contract after tissue injury
- rare genetic disease
Reduced platelet numbers or function
- Thrombocytopenia (reduced platelet number in blood)
- Causes: genetic, acquired (radiation)
- Disease: leukemia
- Autoimmune
- Hypersplenism
- Leads to petechiae
Petechiae
small pinpoint hemorrhages
Hypersplenism
Spleen normally removes platelets after about 10 days, but sometimes the spleen gets too big/active and will remove platelets before 10 days.
Deficiencies in blood coagulation: Phase 1
- remember that phase 1 is when intrinsic and extrinsic pathways come together and form common pathway*
- usually hereditary; relatively rare
- hemophilia A or B, or Von Willebrand’s disease
Hemophilia
X-linked hereditary disease affecting males
- most common and best known
Hemophilia A
Classic hemophilia = factor 8; (antihemophilic factor); more common that Hemophilia B
Hemophilia B
Christmas disease (after affected patient) = factor 9
Signs / Symptoms of Hemophilia A
- Spontaneous or traumatic subcutaneous bleed
- Blood in urine
- Bleeding in the mouth, lips, tongue
- Bleeding in the joints, CNS, GI tract
Hemophilia A treatment
a. Transfusions (blood)
b. treated with missing factor
Deficiencies in blood coagulation (Phase 1): Von Willebrands disease
Decrease in von Willebrand factor
- autosomal dominant (only one copy needed)
- more common and less severe then hemophilia
Signs / Symptoms of Von Willebrands disease
bruise easily
do not bleed in joints
Deficiencies in blood coagulation: Phase 2
Deficiency of prothrombin or factors required for the conversion of prothrombin to thrombin
Deficiencies in blood coagulation: Phase 2 examples
a. liver disease (not making bile)
- bile makes some coagulant proteins
b. lack of vitamin K
- vitamin K synthesized by intestinal bacteria
- bile required for its absorption
Deficiencies in blood coagulation: Liberation of Thromboplastin Material into Circulation
Liberation of Thromboplastin Material into Circulation can start to form clot.
- this abnormal release of thromboplastin material can jumpstart the coagulation cascade
Liberation of Thromboplastin Material into Circulation is a result of several pathological processes such as…
- snakebites
- gram negative bacteria
- surgery
- disease associated with shock and tissue necrosis
- overwhelming bacterial infections
- other causes of tissue necrosis (burn)
Laboratory Tests to Evaluate Hemostasis
- Platelet count
- Bleeding time –> make small cut to see how long it takes to clog
- Clotting time –> test tube, sample of venous blood
Laboratory Tests to Evaluate Hemostasis: Partial Thromboplastin time (PTT)
Clotting time
- measures time it takes for blood plasma to clot after adding lipid and calcium
- measures overall efficiency
Laboratory Tests to Evaluate Hemostasis: Prothrombin time (PT)
Measures coagulation in extrinsic pathway
Laboratory Tests to Evaluate Hemostasis: Thrombin time = Fibrinogen Assay
Measures the level of fibrinogen
Anti-Coagulants
- Asprin
- inhibits Thromboxane A2 formation; acts on platelets - Warfarin (aka coumadin)
- reduced amount of Vitamin K availability; acts on coagulant proteins
- decreased risk of clot formation
- used chronically - Heparin
- used acutely
- inactivates thrombin (which inhibits fibrinogen to fibrin)
Anatomy of Heart
a. 4 Chambers (2 atria that receive blood, 2 ventricles that pump blood)
b. 2 sets of valves = function to maintain unidirectional BF
- AV valves (between atria and ventricles)
- semilunar valves
Right side of heart
Receive oxygenated blood from body; pulmonary circuit
Left side of heart
Receive oxygenated blood thats been oxygenated by lungs from pulmonary veins; systemic circuit
What are the AV valves?
Tricuspid valve
Mitral valve
What are the semilunar valves called?
pulmonary valve
aortic valve
Review of coronary circulation
- main blood supply to the heart
- myocardium is too thick for the diffusion of nutrients
- branches off of aorta
- venous blood collected by cardiac veins
- empties blood into the RA
Review conduction system of heart
The heart has a normal sinus rhythm so the heart can beat as one unit
The main components of the cardiac conduction system
SA node, AV node, bundle of His, bundle branches, and Purkinje fibes
Electrocardiogram (ECG, EKG)
A tool used to examine Cv function.
- electrodes are placed on external surface around heart and they measure electrical activity of the heart
What is an Electrocardiogram (ECG, EKG) used for?
- normal sinus rhythm
- block in conduction system
- rate too fast / slow
- irregular heart beat
What are the waves that you see from an Electrocardiogram (ECG, EKG)
P wave: atria depolarization
QRS complex: ventricular depolarization
T wave: ventricular repolarization
you do not see atria repolarization because it’s hidden by QRS complex
Echocardiography (echo, sonogram)
A tool used to examine Cv function.
- ultrasound examination
What is Echocardiography (echo, sonogram) used for?
- valve structure
- chamber size
- abnormal clot formation
- looks at anatomy/structure
Heart Disease classifications
congenital
genetic
infection
environmental
Congenital heart disease
Atrial and Ventricular Septal Defects (most common)
Manifestations:
- murmur (not unidirectional, stethoscope)
- easily fatigued because oxygenated and deoxygenated blood mix
- heart failure if not discovered
usually detective at birth
Atrial Septal Defect
Left to right shunt
- oxygenated blood flowing to deoxygenated side which overloads right side of the heart (RV)
Atrial Septal Defect: complications
pulmonary hypertension
right ventricular hypertrophy
Atrial Septal Defect: treatment
surgery to close hole
Ventricular Septal Defect
Left to right shunt
- overloading blood on right side of the heart which can lead to pulmonary hypertension
- makes left side of heart pump harder because some blood is leaving by aorta but some is mixing with deoxygenated side
Ventricular Septal Defect: complications
pulmonary hypertension
right ventricular hypertrophy
Ventricular Septal Defect: treatment
surgery to close hole
Congenital heart disease: Tetralogy of Fallot
Four heart defects:
- VSD (ventral septum defect)
- pulmonary stenosis
- right ventricular hypertrophy
- overriding aorta
Rare: 5 in 10,000 infants
Overriding Aorta
aorta is between left and right ventricles, over VSD
Tetralogy of Fallot: manifestations
- cyanosis (blood is well oxygenated –> purple lips etc.)
- slow growth
- heart failure
- variable life expectancy
Tetralogy of Fallot: treatment
surgery soon after birth
Valvular Heart Disease
There are 3 types of valvular dysfunctions
- Valvular Stenosis
- Valvular Regurgitation
- Mitral valve prolapse syndrome (MVPS)
Valvular Heart Disease: Aortic Stenosis
Leaflets undergo degenerative changes –> fibrotic, calcified, rigid –> restricts valve mobility, stenosis
Clinical outcomes of Aortic Stenosis
increase strain of heart –> left ventricular hypertrophy –> heart failure
*more common with aging
Valvular Heart Disease: Rheumatic fever (Scarlet Fever)
a. Commonly encountered in children
- streptococcal bacterial
b. NOT due to bacterial infection per se, but a hypersensitivity reaction
c. Antigen-antibody reaction injures CT and causes fever
Prevention of Rheumatic fever (Scarlet Fever)
antibiotics as soon as streptococcal bacterial is found
Clinical outcomes of Rheumatic fever (Scarlet Fever)
a. healing with scarring of tissues (heart valves)
b. death from severe inflammation and acute heart failure
c. can recur if another streptococcal infection reactivates hypersensitivity and tissue damage
Valvular Heart Disease: Rheumatic Heart Disease
a. scarring of heart valves following rheumatic inflammation
b. primarily affects mitral and aortic valves
Clinical outcome of Rheumatic Heart Disease
valve regurgitation or stenosis –> impairs cardiac function, increases strain on heart –> eventually leads to heart failure
Valvular Heart Disease: Mitral valve prolapse
a. Common but only few develop problems
b. Leaflets enlarge, stretch, prolapse into LA –> blood leaks back into LA; mitral regurgitation
c. On auscultation: “faint systolic murmur” from reflux of blood in between closed valve leaflets
Causes of Mitral valve prolapse
genetic
CT disease
Cardiac Arrhythmias
Disturbance of the heart rhythm (irregular heart beat)
Cardiac arrhythmias range from…
They range from occasional “missed” or rapid beats to severe disturbances that affect the pumping ability of the heart
Cause of cardiac arrhythmias
an abnormal rate of impulse generation or abnormal impulse conduction
Cardiac Arrhythmia: rate
a decrease or increase in heart rate
Cardiac Arrhythmia: Premature
Premature = extra beats
- flutter
- premature atrial contraction
- premature ventricular contraction (PVCs); common
Cardiac Arrhythmia: Atrial fibrillation
- Disorganized electrical impulses
- Atria quiver instead of contract (incomplete emptying)
- Common with age
Cardiac Arrhythmia: Ventricular fibrillation
life threatening; paddles, quivering, blood not being distributed
Cardiac Arrhythmia: heart block (complete or incomplete)
common due to athersclerosis
What do we mean by “heart attack”? Myocardial Infarction
Acute Coronary Syndrome
- blood supply is compromised to heart
- spectrum of clinical presentations
Categories of Acute Coronary Syndrome
- stable angina
- unstable angina
- acute coronary syndrome
Pathogenesis of Myocardial Infarction
athersclerosis
Atherosclerosis: pathogenesis
Endothelial injury
- increased permeability
- monocyte margination, become macrophages sub-endothelial
- induction of smooth muscle cells
Where does Atherosclerosis occur?
any artery, NOT veins
Atherosclerosis leads to…
Fatty streak
- lipid accumulation
and fatty streak leads to atheroma
Atherosclerosis: lifetime development
Begins early in life, asymptomatic for many years
- clinical in 6th decade
Myocardial Infarction leads to what?
Necrosis of the heart muscle from severe ischemia
ischemia
insufficient blood flow
Basic mechanisms that trigger heart attack
a. sudden blockage of a coronary artery from a thrombus
b. blockage of atherosclerotic plaque
c. sudden greatly increased myocardial oxygen requirements (vigorous PA)
Symptoms of Acute Myocardial Infarction
a. Angina
b. Sympathetic Nervous system response
c. Hypotension and shock
d. May be symptomatic
Symptoms of Acute Myocardial Infarction: Angina
Chest pain
- severe, crushing, constrictive OR like heartburn
Symptoms of Acute Myocardial Infarction: Sympathetic Nervous system response
a. GI distress, nausea, vomiting
b. Tachycardia and vasoconstriction
c. Anxiety, restlessness, feeling of impending doom
Symptoms of Acute Myocardial Infarction: Hypotension and shock
weakness in arms and legs
Symptoms of Acute Myocardial Infarction: men vs women
Men: angina
Women: Sympathetic Nervous system response
more likely
Angina pectoris
chest pain due to ischemia
Stable angina
Pain when heart’s O2 demand increases
- predictable
Unstable angina
Medical emergency, heart attack may follow
- no pattern
Features if Myocardial Infarction
a. 50% MI occur without warning
b. 50% preceded by episodes of angina
c. 80-90% MI patients arrive alive
- 10-20% die before cardiac arrhythmia
- minority recover without complications
- most develop clinical complications
Myocardial Infarction - Diagnosis
- Physical examination:
- usually not abnormal unless patient exhibits evidence of shock, heart failure, murmur - Laboratory Data:
- Electrocardiogram, ECG or EKG
- Enzyme tests; enzymes leak out from necrotic cells after an infarct –> the larger the infarct, the longer for elevated levels to return to normal of enzymes
Cardiac Enzymes
- Creatine Kinase
- Lactate Dehydrogenase
- Troponin
Coronary angiogram
Locate and determine degree of obstruction by injecting radioactive dye and using and Xray
Long term Complications of MI
- arrhythmia
- heart failure
- cardiogenic shock
- pericarditis
- thromboemboli
- cardiac rupture
- ventricular aneurysm
Coronary heart disease risk factors
- elevated blood lipids (high cholesterol/LDL/triglycerides)
- high BP
- Cig smoking
- diabetes
- obesity
- gender
- homocysteine
Likelihood of coronary heart disease and heart attack
a. 1 risk factor = 2x risk
b. 2 risk factors = 4x risk
c. 3 risk factors = 7x risk
Treatment for CAD: goal
restore blood flow
Treatment for CAD
a. destroy clot
- angioplasty
b. cardiac bypass
c. stent (brace lumen open)
what is cad
coronary artery disease
myocardial infarction treatment: Thrombolytic therapy
a. Thrombolytic therapy = tissue plasminogen activator
- reduces blood coagulability, dissolves clots
- effective but clot may not completely dissolve
- better outcome sooner the clot is dissolved (1 hr of MI symptoms)
- may cause bleeding issues
Explain the action of aspirin and how it reduces CVD risks
Action: Reduces platelet aggregation
- rapidly absorbed from stomach and SI
- inhibits platelet function within 1 hr of ingestion
- reduces risk of CVD and stroke
- increases risk of bleeding
myocardial infarction treatment: medical treatment
a. Medical treatment: control or eliminate risk factors
- stop smoking
- control hypertension
- anti-coronary diet: low cholesterol and fat (sat./trans)
- weight reduction
- exercise program
Cocaine-Induced Arrhythmia’s and Infarcts
Prolongs and intensifies effects of sympathetic nervous system:
a. increases heart rate: increased O2 demand
b. increased muscle irritability: predisposes to arrhythmia
c. increased peripheral vasoconstriction and coronary artery spasm: high BP
d. fatal arrhythmia’s and MI can occur even among those with normal coronary arteries
cardiomyopathy: causes
genetic mutations
environment
types of cardiomyopathy
- Dilated cardiomyopathy (congestive cardiomyopathy)
- weakened, enlarged (all chambers), poor pumping, problem in systole - Hypertrophic cardiomyopathy
- can lead to sudden cardiac arrest
- leading cause of death in young athletes
- diminished outflow
- less room for heart to fill (problem in diastole) - Restrictive cardiomyopathy
- heart is rigid, restricted from stretching
- decrease in diastole
- decreased outflow
complications of cardiomyopathy
- heart failure
- blood clots - pulmonary embolism
- valves problems
- cardiac arrest
- sudden death
Heart failure
General term used to describe several types of cardiac dysfunction that result in inadequate perfusion of tissues with blood-borne nutrients
Heart failure: types
Left Heart failure
Right Heart failure
usually you have both
Is damage to heart muscle reversible?
No. It is either turned into scar tissue or fibrosis
Sudden cardiac death
Natural death from cardiac causes within one hour of acute symptoms (not a heart attack per se)
Sudden cardiac death may be due to
- arrhythmia
- MI
- aortic aneurysm
- electrocution
- drugs (coke)
Fluid compartments in the body
ICF, Interstitial fluid, plasma
interstitial fluid and plasma are ECF
Factors that regulate fluid flow
- hydrostatic pressure
- capillary permeability
- osmotic (colloid) pressure
- open lymphatic channels
osmotic (colloid) pressure
pressure exerted by proteins
What are some things that influence circulatory disturbances?
- Blockage
- Thrombus
- Atherosclerosis - Dilation
- varicose veins - Damage to wall
- Alterations in permeability
- edema - Pressure changes
- increase (hypertension)
- decrease (shock)
Thrombus vs blood clots
Normally, blood does not clot within the vascular system without injury.
Thrombus = pathological
Blood clot = physiological; normal response when you have external injury
Thrombus
Hemostasis activated without external vessel injury; abnormal intravascular blood clot
- can occur in any vessel or within the heart
- stationary
Thrombosis
formation of thrombus
Pathogenesis of thrombus: Virchow’s Triangle
- Slowing or stasis of blood flow (abnormal blood flow)
- Blood vessel wall damage (intrinsic endothelial damage)
- Increased coagulability of blood
Embolus
A detached clot carried into pulmonary or systemic circulation; plugs vessel of smaller caliber than diameter of clot, blocking blood flow and causing necrosis
Infarct
Tissue necrosis from interruption in blood flow
Thrombus formation: common sites
bifurcation of artery or veins
Venous Thrombosis: Thrombophlebitis
Clot formed in vein which leads to inflammation; typically in leg
Predisposing factors leading to clot formation in leg veins
- prolonged bed rest
- cramped position for long period (impaired “milking action”)
- genetic factors
Venous Thrombosis outcome
- Leg swelling from partial blockage of venous return in leg
- pulmonary embolism
For a Pulmonary Embolism, clinical manifestations depend on what?
Clinical manifestations depend on size of embolus and where it lodges in the pulmonary artery
Explain potential risks of a large pulmonary embolism
Large pulmonary emboli may completely block main pulmonary artery or major branches obstructing blood flow to lungs
Symptoms of a large pulmonary emboli
a. cyanosis and shortness of breath due to inadequate oxygenation of blood
b. right ventricular dysfunction
c. decreased return of blood to left heart
- systemic BP falls and patient may go into shock
Explain a small pulmonary emboli
a. small emboli may pass through main pulmonary arteries, becoming stuck in peripheral arteries supplying lower lobes of the lungs
b. raises pulmonary pressure and inadequate collateral circulation
c. affected lung segment undergoes necrosis; pulmonary infarct
General symptoms of a pulmonary embolism
a. dyspnea - shortness in breath
b. chest pain
c. cough and expectoration of bloody sputum due to leakage of blood from infarcted lung tissue into bronchi
Diagnosis of pulmonary embolism
Pulmonary angiogram (gold standard): detects blocked pulmonary artery - inject dye and look with XRAY
Treatment of pulmonary embolism
- Anticoagulants: heparin initially followed by Warfarin
- Angioplasty
- Thrombectomy (clot extraction surgery)
- General supportive care
Varicose veins
Dilated tortuous (twisty) veins. - common, tend to run in families
Varicose veins Etiology
incompetent valves
Complications of Varicose veins
- pain
- thinning of skin fed by vein
- thrombophlebitis (not risk for PE)
Treatment for Varicose veins
small incision and pull vein out
Arterial thrombosis
Can happen in artery or vein
a. blood stasis is not a factor due to rapid blood flow and high BP
b. can grow to occlude vessel
Main cause of Arterial thrombosis
Injury to vessel wall from arteriosclerosis, smoking, hypertension
Explain how and where Arterial thrombosis may affect and individual
- Coronary artery: myocardial infarction
- Major leg artery: gangrene
- Cerebral artery: stroke
Arterial thrombosis: Intracardiac thrombosis
Within chambers of heart.
- Clot forms
a. within atrial –> heart failure
b. surfaces of heart valves –> valve injury (stenosis)
c. wall of left ventricle –> MI
d. chambers –> may dislodge into systemic circulation and cause infarction in spleen, kidneys, or brain
Thrombosis due to increased coagulability
A rise in coagulation factors following surgery or injury
What is a chemical that my stimulate the synthesis of clotting factors ?
Estrogen in contraceptive pills because it stimulates the liver to make coagulants
Thrombosis due to increased coagulability: hereditary gene mutations
There is a mutation in the gene regulating prothrombin synthesis
- risk for venous thrombosis increases as prothrombin level rises
Why might patients with cancer be likely to develop a thrombosis?
Due to rapid release of thromboplastic materials into circulation from tumor
What are some sources of an embolism?
- thrombus
- atherosclerotic debris
- bone marrow fat
- air
- amniotic fluid
Amniotic Fluid embolism
Complication of pregnancy
a. amniotic fluid enters maternal circulation through a tear in fetal membranes
b. fetal cells, hair, fat, and amniotic debris fluid blocks maternal pulmonary capillaries causing severe respiratory distress
c. Thromboplastic material in fluid activates coagulation mechanism leading to disseminated intravascular coagulation syndrome (DIC)
Air embolism
Large amount of suck sucked into circulation from lung injury due to chest wound
- may be accidentally injected into circulation
- air carried into right heart chambers and prevents filling of heart by returning venous blood
- heart is unable to pump blood and person dies rapidly of circulatory failure
Arteriosclerosis
Thickening and hardening of arteries
what is one cause of Arteriosclerosis
atherosclerosis
Risk factors for developing atherosclerosis
High levels of blood lipids
- hypertension
- smoking
- diabetes
- physical inactivity
- age
- overweight
- family history
- gender
dyslipidemia
high LDL, low HDL
Low-density Lipoprotein (LDL)
bad cholesterol
High-density Lipoprotein (HDL)
good cholesterol; protective; increases with regular exercise, smoking cessation, modest alcohol intake
Hypertension is due to
due to excessive vasoconstriction of small arterioles
Explain how hypertension results in cardiac effects
Increased peripheral resistance –> higher workload –> heart enlarges –> heart failure
Explain how hypertension results in vascular effects
Increased pressure –> premature wearing out of vessels; accelerates atherosclerosis; injury to vessels –> rupture and hemorrhage
Explain how hypertension results in renal effects
Narrowed renal arterioles –> decreased blood supply to kidneys –> injury and degenerative changes in glomeruli and tubules –> renal failure
Criteria for BP vs high BP
good: 120/80
high: 140/90
How do you treat hypertension?
- increase PA
- diet
- reduce salt
- increase fruits and veggies - medication
- diuretics (decrease blood vol)
- angiotensin-converting enzyme (ACE) inhibitors
Aneurysm
Dilation or out-pouching of portion of arterial wall
causes of Aneurysm
- Arteriosclerosis
a. causes narrowing, thrombosis, and weakening of vessel wall - Congenital
Explain and Aneurysm in the aorta
most common in distal part of aorta; may rupture, leading to massive and fatal hemorrhage
Dissecting Aneurysm of aorta
Spitting of elastic and muscle tissues
What are some symptoms of Aneurysm in aorta?
severe chest and back pain
What are risk factors for developing an Aneurysm
hypertension, atherosclerosis
Ischemia is due to
- Obstruction
- Vascular occlusion
a. torsion (twisting of BV)
b. drowning
c. CO
long periods of ischemia lead to
infarct
Factors influencing the development of an infarct
- Single or dual vascular supply (more the better)
- Rate at which obstruction develops (atherosclerosis or embolus)
- Sensitivity of downstream tissue to oxygen deprivation
- oxygen content in blood
Edema
Shift of water from vascular space into another compartment (usually interstitial)
- result of underlying condition
Two types of edema
Exudate: fluid w protein
Transudate: fluid w low protein
How can edema be fatal?
Cerebral edema
Pulmonary edema
Pathogenesis of Edema
- Increased capillary permeability
a. causes swelling of tissues with acute inflammation
b. increase in capillary permeability from some systemic diseases - Low plasma proteins
a. excess protein loss (kidney disease)
b. inadequate synthesis (malnutrition) - Increased hydrostatic pressure
a. heart failure
b. localized venous obstruction - Lymphatic obstruction
Lymphedema
Edema of Lymphatic Obstruction
- build up of fluid when lymphatics damaged or blocked
- high protein edema
- most common cause is due to removal of lymph nodes (secondary lymphedema)
Why would you need to remove lymphnodes
cancer
Shock
Inability to meet the O2 demands of the body
Shock could be the final stage of what?
- severe hemorrhage
- bacterial sepsis
- burns
- MI
- severe soft tissue damage
What is the end result of shock?
often times the end result is multi-organ failure and death
Cardiogenic shock
Pump failure
Cannot maintain perfusion pressure
Hypovolemic Shock
decreased blood volume
Anaphylactic shock
A severe, potentially life-threatening allergic reaction.
Septic (sepsis) shock
Systemic bacterial infection
- gram negatives
Septic (sepsis) shock leads to
- vasodilation
- decreased myocardial contractility
- endothelial cell damage which may start DIC
Effects of irreversible shock
- circulatory collapse
- marked hypo-perfusion of vital organs
- loss of vital functions
- multi-organ failure
- death
Prognosis of shock
Prognosis of shock depends on early recognition and rapid appropriate treatment
How could you treat shock?
- Drugs that promote vasoconstriction
- Use of intravenous fluids or blood to restore blood volume secondary to fluid loss or hemorrhage
- Treat underlying cause
