Patho Exam 2
Chapter 12 Study Questions
1. What are the 3 factors involved in the pathogenesis of intravascular clotting (Virchow’s Triad)?
· Slowing or stasis of blood flow
· Blood vessel wall damage
· Increased coagulability of blood
2. What is the relationship between the following: a thrombus, an embolus, and an infarct?
· Thrombus- Intravascular clot can occur in any vessel or within the heart
· Embolus- Detached clot (or other material) carried into pulmonary or systemic circulation. Plugs vessel of smaller caliber than diameter of clot blocking blood flow and causing necrosis
· Infarct- Tissue necrosis caused by interruption in blood flow
3. What are the predisposing factors for venous thromboses? Where do the majority form? What are possible outcomes?
· Majority form in the deep veins of the legs
o Prolonged bed rest
o Cramped position for extended period of time
o Impaired milking action of leg , musculature that normally promotes venous return resulting in stasis of blood in veins
o Varicose veins or any condition preventing normal emptying of veins
o Increased blood coagulability
· Outcomes
o Leg swelling from partial blockage of venous return in leg
o Pulmonary embolism- clot detaches and lodges in pulmonary artery or on of its branches
4. Differentiate between the lung damage seen in small and large pulmonary emboli? What are the signs and symptoms or each? How are pulmonary emboli diagnosed and treated?
· Large
o Severe dyspnea
o Cyanosis
o Shock
o Sudden death
· Small
o Dyspnea
o Pleuritic chest pain
o Cough
o Hemoptysis due to leakage of blood from infarcted lung tissue into bronchi
5. What is the main cause of an arterial thrombus? What is gangrene?
· Main cause- Injury to vessel wall from arteriosclerosis, causing ulceration, roughening of arterial lining with thrombi formation
· Gangrene- when thrombosis blocks major leg artery
6. What are causes of intracardiac thrombi? What may result from the formation of intracardiac thrombi?
· Clot forms
o Within atrial appendages: heart failure or arrythmia
o Surfaces of heart valves: valve injury
o Wall of left ventricle: myocardial infarction
· May dislodge into systemic circulation and cause infarction: spleen, kidneys, brain
7. What are the factors that lead to thrombosis by increased coagulability?
· Rise in coagulation factors following surgery or injury
o Due to release of thromboplastin
· Estrogen in contraceptive pills stimulates synthesis of clotting factors
o Also occurs during pregnancy
· Hereditary gene mutations
o Mutation of gene that codes for factor V Leiden
- More resistant to inactivation, prolonged activity, increased coagulability
o Mutation of gene regulating prothrombin synthesis
- Risk for venous thrombosis increases as prothrombin level rises
· Thrombosis in pts with cancer from increased platelets and coagulation factors
o Predisposes to both arterial and venous thromboses
o Hyper coagulability due to the release of thromboplastic materials into circulation from tumor deposits
- Tumors release thromboplastic material slowly but continuously
- Production of coagulation factors exceeds destruction leading to hypercoagulability
8. What is edema and what causes it? What are the factors regulating fluid flow between capillaries and interstitial tissue? What are pitting edema, pleural effusions, and ascites?
· Accumulation of fluid in tissues
o Often first noted in ankles and legs
· Results from disturbance of extracellular fluid circulation between capillaries and interstitial fluid
9. What are the four causes of edema? What are some examples of each?
· Capillary hydrostatic pressure
o Force pushing fluid from capillaries into extracellular space
· Capillary permeability
o Determines ease of fluid flow through capillary endothelium
· Osmotic pressure
o Water-attracting property of a solution exerted by proteins in the blood that attract fluid from interstitial space back into the capillaries
· Open lymphatic channels
o Collect fluid forced out of capillaries by the hydrostatic pressure and return fluid into circulation
10. What is shock? What are the various categories and some causes of each? What are the signs and symptoms? What is the treatment and prognosis?
Shock
- A condition in which the circulatory system is not providing enough blood to all parts of the body causing organs to fail to function properly
· Blood flow/pressure too low to adequately supply body
o Circulating blood volume < capacity of vascular system
· Causes inadequate perfusion of the organs and tissues
o They begin to fail
· Always life-threatening
Categories
· Hypovolemic shock: low blood volume leading to low blood pressure
- Causes
o Hemorrhage
o Dehydration
o Severe burns
o Vomiting/Diarrhea
o Diuretic use
· Cardiogenic shock: inadequate cardiac output of blood by the heart when it fails to pump effectively
- Causes
o Myocardial infarction: Damage to the heart muscle reduces pumping function
o Pericardial effusion: Prevents heart from filling
o Valvular disease: Interferes with forward blood flow
· Septic shock: excessive vasodilatation secondary to release of microbial toxins and inflammatory mediators
· Anaphylactic shock: excessive vasodilatation from release of inflammatory mediators due to severe allergic reaction
Signs and Symptoms
· Skin is cool, clammy, and pale
· Weakness, dizziness, thirst, or nausea
· Breathing may be shallow and rapid
· Pulse is weak and rapid
· BP is low
· Lips and fingernail beds may be cyanotic
· Pt may be confused or suddenly become
unconscious
Chapter 14 Study Questions
11. What are the factors concerned with hemostasis?
· Integrity of small vessels
· Adequate number of platelets
· Normal coagulation factors
· Normal coagulation inhibitors
· adequate number of calcium ions
12. What roles do small vessels play in hemostasis?
· First line of defense, constrict on injury to facilitate closure by clotting, Exposure of underlying connective tissue of endothelium causes platelet adhesion and activates coagulation
13. What three functions do platelets play in hemostasis?
· Platelet functions, plug defect in vessel wall, liberate vasoconstrictors and compounds causing platelets to aggregate, release substances that initiate coagulation.
14. What are the three phases of blood coagulation? What happens in each phase?
· Phase 1- prothrombin activator generated. Phase 2- Conversion of prothrombin into thrombin. Phase 3- Conversion of fibrinogen into fibrin by thrombin à Blood clot
15. What roles do coagulation inhibitors, antithrombin, and plasmin in regulating blood coagulation?
· Coagulation factors are counterbalanced by inhibitors, restrict clotting process to certain areas
· Antithrombin inhibits thrombin and other activated coagulation factors in the clotting process
· Plasmin dissolves fibrin, Plasminogen activated to form plasmin (fibrinolysin), Fibrinolytic system activated at same time
16. What are the four classes of disturbances of blood coagulation? What causes each class?
· Abnormalities of small blood vessels:
o Abnormal bleeding resulting from failure of small blood vessels to contract after tissue injury
o Abnormality of blood vessel formation
· Abnormality of platelet formation
· Deficiency of one or more plasma coagulation factors
· Liberation of thromboplastic material into circulation
17. What is thrombocytopenia and what are some causes?
· Thrombocytopenia is a platelet deficiency that could be caused by:
o Injury or disease of bone marrow damaging the megakaryocytes (precursors of platelets
o Infiltration of bone marrow by leukemic cells or cancer cells, crowding out the megakaryocytes
o Antiplatelet antibodies destroy platelets in peripheral blood (autoimmune disease)
o Abnormal function of platelets despite normal count
18. What are petechiae and what causes them?
· Small red or red-blue spots about 1-5mm
· Pinpoint sized hemorrhages or small capillaries in skin or mucous membranes
· Indicative of defective or inadequate platelets or capillary defect
19. What are some causes of disturbances of phase 1 and phase 2 of the blood coagulation cascade? What are some signs and symptoms that were discussed?
- Phase 1
· Usually hereditary, relatively rare except: Hemophilia- X-linked hereditary disease affecting males
o Most common/best known
o Episodes or hemorrhage in joints and internal organs after minor injury
o Hemophilia A- Classic hemophilia = Factor Vlll (Antihemophilic factor)
o Hemophilia B- Christmas disease (after affected pt) = Factor lX (Christmas Factor)
- Phase 2
· Deficiency of prothrombin or factors required for the conversion of prothrombin into thrombin
o Factors produced in liver
o Vitamin K required for synthesis of most factors (Vitamin K synthesized by intestinal bacteria or obtained by food)
o Bile required for its absorption
20. What are some causes of thromboplastin being released into the circulation?
· Diseases associated with shock and tissue necrosis
· Overwhelming bacterial Infections
· Other causes of tissue necrosis
21. What is disseminated intravascular coagulation syndrome? What are some signs and symptoms?
· Thromboplastic substances in circulation
· Activation of coagulation
· Clotting platelets and plasma coagulation factors are utilized causing levels to drop rapidly in the blood
· Activate fibrinolytic system to defend body from widespread intravascular clotting
o Clots are dissolved to prevent lethal obstruction of circulatory system
· End result is an abnormal bleeding state
Chapter 11 Study Questions
22. What does each layer of the heart consist of? Understand the structure of the pericardium.
· Epicardium- Outer layer of connective tissue
o Coronary arteries
o Covered by visceral pericardium
· Myocardium- Middle layer, muscular, thickest layer, workhorse of the heart
· Endocardium- Innermost layer
o Double-walled sac that surrounds the
heart
23. Differentiate between the right and left sides (pulmonary and systemic circulations) of the heart.
· Right half (right atrium, RA and right
ventricle, RV)
o Pulmonary pump, circulates blood into
pulmonary artery, lungs
· Left half (left atrium, LA and left
ventricle, LV)
o Systemic pump, circulates blood into aorta,
organs and tissues
24. What are the locations and functions of the heart valves?
· AV valves: flap-like
valves between atria and ventricles
o Prevent back flow of blood into atria when ventricles
contract
· Tricuspid valve: three flexible flaps; directs
blood flow from RA to RV
o prevents backflow to RA when RV contracts
· Bicuspid valve or mitral valve: directs blood flow from LA to LV
o prevents backflow to LA when LV contracts
· Semilunar valves
o Cup-shaped
o Surround orifices of aorta and pulmonary artery
o Free margins of valves face upward
o Prevent backflow of blood into ventricles
during diastole
· Pulmonary valve: directs blood flow
from RV to pulmonary trunk
· Aortic valve: directs blood flow from LV to aorta
25. Describe the blood flow through the heart including valves that are encountered.
· Pulmonary circulation
o Oxygen-poor blood enters RA → RV
through tricuspid valve → pulmonary
artery → lungs
· Systemic circulation
o Freshly oxygenated blood leave lungs
through pulmonary veins → LA → LV
through mitral valve → aorta → rest of the body
26. What is the purpose of the coronary circulation?
· Main blood supply of the heart
o Myocardium is too thick for the diffusion of
nutrients
· Aorta branches to right and left coronary arteries that carry arterial blood to the heart when relaxed
· Blood passes through capillary beds of myocardium
· Venous blood collected by cardiac veins
· Cardiac veins join together and form the coronary sinus that empties blood into the RA
27. How does the cardiac conduction system work? In what order does current flow through this system?
· Sinoatrial node (SA node)
· Atrioventricular node (AV node)
· Bundle of His (AV bundle)
· Right and left bundle branches
· Purkinje fibers
28. What happens at each phase of the cardiac cycle?
· Diastole: Chambers relaxed
o Venous blood returning to atria flows into ventricles through open atrioventricular (AV) valves
o Semilunar (SL) valves closed
o Additional blood pumped into ventricles during atrial systole
· Ventricular systole: ventricles contract
o AV valves close as pressure rises in ventricles
o SL valves open when intraventricular pressures exceed pressure in aorta and pulmonary artery
· Diastole: chambers relax and a new
cycle begins
o SL valves close as ventricular pressures fall
o AV valves open as chambers relax, and venous blood flows into chambers
29. What are the different types of blood vessels?
· Large elastic arteries – conduct the blood to various locations throughout the body.
· Arterioles – smaller vessels with muscular walls that regulate flow from the large arteries into the capillaries.
· Capillaries – thin endothelium-lined channels that deliver nutrients to cells and
remove waste products.
· Veins – return blood to the heart under low pressure and usually travel with the arteries.
30. Differentiate systolic and diastolic blood pressure.
· Pressure is highest when ventricles contract systolic pressure
· Pressure is lowest when ventricles relax diastolic pressure
31. What is an electrocardiogram used for? What does each wave of the tracing represent?
· Measures electrical activity of heart; diagnostic tool
o Detects disturbances in rate, rhythm,
conduction, muscle injury, extent of
muscle damage
32. What are the signs/symptoms and etiology of arrhythmias?
· Symptoms
o Palpitations
o Tachycardia
o Bradycardia
o Skipped heartbeats
o Syncope
o Fatigue
· Etiology
o Results when there is interference within the conduction system of the heart
o Ischemia and drugs cause many arrhythmias
33. What is the difference between a normal sinus rhythm, sinus bradycardia, and sinus tachycardia?
· Normal sinus rhythm
o ECG that is within normal limits with a heart rate between 60-100 bpm
· Sinus bradycardia
o A regular rhythm with a heart rate of <60 bpm
o This may be normal in an athlete
· Sinus tachycardia
o A regular rhythm with a heart rate of >100 bpm
34. What is atrial fibrillation? What does it look like on an ECG? Who is prone to it? How is it treated?
· Seen in older persons; those with CVD,
COPD, hyperthyroidism; occasionally in
normal individuals
· Multiple areas of atrial depolarization
o Characterized by extremely rapid, incomplete atrial contractions of 400-500 bpm
o Atria quiver versus contracting normally
· Only some of these impulses reach the ventricles
o Causes ventricles to beat irregularly at 140-160 bpm
o Leads to shortened filling time
35. What are premature ventricular contractions? What causes them? What do they look like on an ECG? Are they harmful?
· One of the most common and least
harmful arrhythmias
· The PVC is followed by a pause before the
occurrence of the next normal cycle
· Caused by
o Lack of Sleep
o Caffeine
o Nicotine
o Alcohol
o Anxiety/Stress
36. What is ventricular tachycardia? What type of patients is it often seen in? What does it look like on an ECG? Is it harmful?
· Seen in patients with cardiac disease
· Characterized by 3 or more PVCs that occur at a rate of 150-250 bpm
o There are no P waves and the QRS complexes
are distorted
· V-tach is life threatening and can rapidly deteriorate into ventricular fibrillation and cardiac arrest
37. What is ventricular fibrillation? What does it look like on an ECG? Is it harmful?
· One of the more serious arrhythmias
· Rapid and uncoordinated ventricular beat
o Heart cells are contracting spontaneously and the heart just quivers
· It is totally ineffective for pumping blood and will quickly lead to death if not
corrected
38. What is cardiac arrest? What are the signs/symptoms? What is the etiology? What is the treatment?
· The sudden, unexpected cessation of
cardiac activity
· Symptoms
o The patient is unresponsive, with no
respiratory effort and no palpable pulse
· Etiology
o Results from anoxia or interruption of the
electrical stimuli to the heart
· Treatment
o CPR must be initiated within 4-6 minutes
o Defibrillation
o Epinephrine or dobutamine to stimulate the heart
o Antiarrhythmic drugs (lidocaine, amiodarone)
39. What are the various treatments for arrhythmias? How do they work?
· Depends on the cause
· Antiarrhythmic drugs
· Drug induced arrhythmias usually resolve with the stoppage of the drug
· Anticoagulants are given to prevent thromboembolism
· Ischemia should respond to oxygen and increased blood flow to the myocardium
· Cardioversion (defibrillation) for serious
arrhythmias
o Electrical device that applies countershocks
to heart through electrodes or pads placed
on chest wall
o Purpose is to convert cardiac arrhythmia
into normal sinus rhythm
40. What are the 2 types of valvular malfunction? What are some causes?
Stenosis
· Hardening of cusps of valves that prevents
complete opening of valves
· Impedes blood flow into next chamber
o Causes the heart to have to work harder to
pump blood forward
· Common causes:
o Rheumatic heart disease
o Infective endocarditis
o Congenital malformations
o Calcification of the valve cusps
Insufficiency (incompetence, regurgitation)
· Failure of valves to close completely
o Allows blood to be forced back into the previous chamber as the heart contracts
· This exerts added pressure on that chamber and overloads the heart
o Ultimately the ventricle will dilate and fail
41. What is rheumatic fever? What causes it? What are the signs/symptoms? What are possible clinical outcomes? How is it treated?
- Immunologic reaction that develops weeks after initial streptococcal infection
Signs/Symptoms
· Fever
· Inflammation of connective tissue throughout the body, especially heart and joints
· Acute arthritis (multiple joints)
· Inflammation of heart
42. What is rheumatic heart disease? What causes it? How is it prevented?
- Complication of rheumatic fever
· Primarily affects mitral and aortic valves
- Etiology
· In acute disease, valves become red, thickened, and swollen
· Inflammatory damage produces scarring causing stenosis or incompetence
o Impairs cardiac function, increases strain on heart,
eventually leads to heart failure
43. What is mitral stenosis, what causes it, and how is it treated?
- Most common of all valve diseases
· Impairs the passage of blood from the left atrium to the left ventricle
- Etiology
· rheumatic heart disease is the cause of most cases
- Treatment
· Diuretics help reduce the workload on the heart
· Anticoagulants prevent the formation of thrombi
· Surgical intervention includes commissurotomy, balloon valvuloplasty, valve replacement
44. What are the types of non-rheumatic aortic stenosis? Clinical outcomes? Prevention? Treatment?
· Aortic stenosis secondary to bicuspid
aortic valve
o Aortic valve has 2 cusps rather than usual 3
cusps
o Functions satisfactorily for a time, then
becomes thickened, calcified, and rigid from
increased strain on valve, leads to heart failure
· Calcific aortic stenosis
o Common valvular heart disease
o Normal 3 cusps
o Leaflets undergo connective tissue degenerative changes → fibrotic, calcified, rigid → restricts valve mobility, stenosis
o Recent studies: also occurs with deposits of lipids and macrophages as in coronary atherosclerosis
· Clinical outcomes:
o ↑ strain → left ventricular hypertrophy →heart failure
· Prevention:
o Control risk factors (high cholesterol, diabetes, hypertension, smoking)
· Treatment
o Digitalis can be used as an inotropic agent
o Anticoagulants prevent the formation of thrombi
o Balloon valvuloplasty and valve replacement
45. What is mitral valve prolapsed? What causes it? Is it dangerous?
· Fairly common
· One or more of the cusps of the mitral valve protrudes back into the left atrium during ventricular contraction
· Prolapsing leaflets may not fit together tightly →blood leaks back into LA; mitral regurgitation
- Etiology
o Abnormally long or short chordae tendineae may not allow the valve to close properly
o Malfunctioning papillary muscles
o Usually a benign, asymptomatic condition and does not require treatment
46. What is infective endocarditis? What can it cause?
· Bacterial endocarditis is the most common
· Vegetations – build up of large, easily fragmented infective masses
· Can cause:
o Erosion of valve leaflets
o Seeding of the blood with infective agent
o Embolization
47. What is subacute infective endocarditis? What are the symptoms?
· Caused by organisms of low virulence
o Affects abnormal or damaged (mitral, aortic valves)
· Platelets and fibrin may deposit on abnormal or damaged valves; then serve as sites for bacteria to implant or for thrombi to form followed by emboli and tissue infarction
· Mild symptoms of infection
· Prophylactic antibiotics given prior to dental or
surgical procedures to prevent transient
bacteremia and resulting endocarditis
48. What is acute infective endocarditis? What are the symptoms? Who is at risk?
· Caused by highly pathogenic organisms, commonly staphylococci
o Affects normal heart valves
· Severe symptoms of infection and valve destruction
· At-risk groups:
o Intravenous drug users; affect tricuspid valve instead of mitral or aortic valves
o Unsterile materials or contaminants enter right side of heart, form large bacteria-laden vegetations on valve, lodge into lungs cause pulmonary infarct
49. How is infective endocarditis treated and prevented?
· Treatment
o IV anti-infective therapy
o Antipyretics
o Anticoagulants
o Damaged cardiac valves may need surgical repair or replacement
· Prevention
o Prophylactic antibiotics given prior to
dental or surgical procedures
50. What is hypertension and how does it develop? What are the current recommendations defining hypertension, pre-hypertension, and an ideal blood pressure? What are the signs/symptoms and risk factors?
· Excessive vasoconstriction of small arterioles resulting in:
· Increased peripheral resistance increased diastolic blood pressure
· Results in an increased force of ventricular contraction Compensatory
increase in systolic pressure
· Normal- Systolic <120 mmHg AND Diastolic <80 mm Hg
Elevated- Systolic 120-129mm Hg AND Diastolic <80 mmHg
Hypertension: Stage 1- Systolic 130-139mm Hg OR Diastolic 80-89 mmHg
Hypertension: Stage 2 - Systolic ≥140 mm OR Diastolic ≥90 mm
51. What is the difference between primary and secondary hypertension? What are some causes of secondary hypertension?
- Primary
· Also called essential hypertension (HTN)
· No specific cause can be identified
o Occurs in 90-95% of cases
· Thought to be due to some defect in the blood pressure control mechanism
· Has an insidious onset, with few if any symptoms until permanent damage has occurred
- Secondary
· Some other specific disorder can be identified as the cause of the elevated BP
· Kidneys
o Chronic kidney disease
· Excessive levels of various hormones
o Pituitary or adrenal tumor
o Hyperthyroidism
52. What are the consequences of hypertension and why do they develop? How is hypertension treated?
· Cardiac effects: increased peripheral resistance →higher workload → heart enlarges →heart failure
· Vascular effects: increased pressure →premature wearing out of vessels; accelerates atherosclerosis; injury to arterioles → weakened areas may rupture and hemorrhage
o Linked to strokes and heart attacks
· Renal effects: narrowed renal arterioles →decreased blood supply to kidneys → injury and degenerative changes in glomeruli and tubules →renal failure
- Treatment
· Reduction of unfavorable factors
o Weight loss
o Increased exercise
o Smoking cessation
o Salt restriction
o Stress reduction
53. What is myocarditis, what usually causes it, and what is the typical course of the disease?
· Active inflammation of heart muscle associated with injury and necrosis of individual muscle fibers
o Usually viral cause
o Abrupt onset may lead to acute heart failure
o Usually complete recovery
54. What is cardiomyopathy? What is dilated cardiomyopathy? What is hypertrophic cardiomyopathy?
· Diverse group of diseases of the myocardium associated with mechanical and/or electrical dysfunction
o Frequently causes ventricular hypertrophy
or dilation
o Due to a variety of causes
o Genetics often plays a role
- Hypertrophic cardiomyopathy
· Disorganized muscle fibers
· The left ventricular wall and interventricular septum hypertrophies
o So pronounced reduces ventricular volume and obstructs outflow
from the heart
· Hypertrophy reduces size of ventricles and do not
readily dilate in diastole – diastolic dysfunction
· Septal muscles more hypertrophied than rest of myocardium → impedes flow into aorta
· Thick septum impinges on anterior mitral valve
leaflet → intermittently blocks outflow from left
ventricle
- Dilated cardiomyopathy
· Diffuse degeneration of myocardial fibers leading to decreased contractile effort
· Heart becomes enlarged and dilated, impairing ventricular action and leading to chronic heart failure
55. What causes dilated cardiomyopathy, what are the signs/symptoms, how is it treated?
- Causes
· Can be the result of chronic alcoholism, infections, chemotherapy, drugs, toxins
· Familial transmission in 30% – 50% of cases,
usually autosomal dominant
- Symptoms
· As with CHF
- Treatment
· Similar to heart failure
o Diuretics, beta blockers, ACE inhibitors
· Anticoagulants
· ICD reduces risk of death by 50%
56. What causes hypertrophic cardiomyopathy, what are the signs/symptoms, how is it treated?
- Causes
· Autosomal dominant transmission
- Symptoms
· Most remain asymptomatic throughout life
· Angina pectoris
· Fatigue
· Dyspnea
· Syncope
· Arrhythmias
· Heart failure
57. Have a general understanding of the fetal circulation. Particularly how blood flow through the foramen ovale and ductus arteriosus.
58. Why do congenital heart diseases usually occur, what are some causes, and how are they prevented?
· Usually due to persistence of normal fetal blood channels or faulty embryologic development
· Causes: German measles, Down syndrome, drugs, genetic factors
o Over 90% are idiopathic
· Prevention: protect developing fetus
from intrauterine injury
59. What is the difference between right-to-left and left-to-right shunting? What results from each?
- Left-to-right shunt:
· Blood is diverted from systemic circulation to the lungs
o Causes pulmonary hypertension and damage lungs
o Eventually, right-sided heart failure
- Right-to-left shunt:
· Blood is diverted from pulmonary circulation to systemic circulation
· Blood is poorly oxygenated
o Cyanosis
o Polycythemia
o Clubbing
60. What are the 4 main causes of congenital heart disease? What are some examples of each?
· 1. Fetal bypass channels fail to close
normally
o Patent ductus ateriosus
o Patent foramen ovale (PFO)
· 2. Atrial, ventricular, or combined septal
defects
· 3. Abnormalities obstructing flow
o Pulmonary stenosis
o Aortic stenosis
o Coarctation of the aorta
· 4. Abnormal formation of aorta and
pulmonary artery or abnormal connection
of vessels
o Tetralogy of Fallot
o Transposition of great vessels
61. What is a patent ductus arteriosus? What type of shunting does this cause? What are the signs/symptoms? How is it treated? If left unrepaired, what will be the result?
- The ductus arteriosus does not close after birth
· Blood is shunted from aorta to pulmonary artery
· Often asymptomatic
o Pressure overload can lead to pulmonary hypertension and eventually causes right-sided CHF
- Treatment
· Indomethacin (NSAID) inhibits prostaglandin synthesis and can induce closure
· PDAs may be surgically repaired by tying the vessel closed or by using a catheter device.
·
62. What is an atrial septal defect? What type of shunting does this cause? What are the signs/symptoms? How is it treated? If left unrepaired, what will be the result?
· Abnormal opening between the right and
left atria
· Blood is shunted from the left to the right
side
· Often go undetected in childhood
· Often asymptomatic in children
· Catheter closures with amplatzer device is
most common
· If unrepaired, will cause right-sided CHF
63. What is a ventricular septal defect? What type of shunting does this cause? What are the signs/symptoms? How is it treated? If left unrepaired, what will be the result?
· Abnormal opening between the right and left ventricles
· Small defect usually remain asymptomatic and don’t progress
· In larger defects, there is more left to the right shunting
o Pulmonary congestion
o Dyspnea
o Fatigue
o Susceptibility to pulmonary infections
64. What is a coarctation of the aorta? What are the signs/symptoms? How is it treated? If left unrepaired, what will be the result?
· Narrowing of the aortic lumen causes a partial obstruction of the flow of blood
· Occurs primarily in males
· Large pressure gradient across narrowing
o Hypertension in the head and upper limbs
o Hypotension in the abdomen and lower limbs
o Left ventricular hypertrophy
· Repaired by surgically removing the defective area and reconstructing the aorta
· Untreated, will cause left-sided CHF if not repaired
65. What is tetralogy of fallot? What type of shunting does this cause? What are the signs/symptoms? How is it treated? If left unrepaired, what will be the result?
- Is a combination of 4 defects
· Ventricular septal defect
· Pulmonary stenosis a tightening of the pulmonary valve or vessel
· Displacement of the aorta receives blood from both ventricles
· Right ventricular hypertrophy an adaptation of the right ventricle to the high afterload caused by the pulmonary stenosis
66. What is transposition of the great vessels? What are the signs/symptoms? How is it treated? If left unrepaired, what will be the result?
· The aorta and pulmonary arteries are
reversed
· Results in 2 closed-loop circulatory
systems
· Prostaglandins are administered to keep
the ductus arteriosus and the foramen
ovale from closing
· Blood flow is redirected by surgical
correction
67. What is an aneurysm? What causes them? What are possible consequences? What are the signs/symptoms?
- A weakening and resulting local dilation or
outpouching of portion of arterial wall
- Etiology
· The most common cause is the build up of
atherosclerotic plaque that weakens the vessel wall
· Congenital
- Risk factors for aortic aneurysms
· Elevated blood lipids/atherosclerosis
· Hypertension
· Smoking history (75% of AAA have a smoking history)
68. What are abdominal aortic aneurysms? What are the signs/symptoms? How are they detected?
- Abdominal aortic aneurysms are the most common
· As the aneurysm enlarges, the patient may experience abdominal or back pain and a pulsating mass in the abdomen
· May rupture leading to massive and fatal hemorrhage
· Hard to detect clinically
· Current guidelines recommend routine ultrasound screening for adults over age 65 with risk factors for arteriosclerosis, or history of aneurysm in a family member
69. What is a dissecting aneurysm of aorta? What are the signs/symptoms?
· Degenerative changes causes middle layer to loose cohesiveness and separate
· Pressure forces blood through a tear and causes separation of the layers
70. How are aneurysms treated?
· Depends on size, location, and likelihood of rupture
· Most should be treated with surgical repair before they leak or rupture
· May be done by replacing the damaged area with a synthetic graft, by endovascular stenting, or coiling
· If the aneurysm is small or the patient is not a good surgical candidate, watchful waiting is employed
71. What is thrombophlebitis? What are some causes? What are the signs/symptoms? How is it treated?
· Inflammation of a vein caused by or
associated with the formation of a blood clot
· Often occurs in the leg veins
- Etiology
· Disruptions in blood flow
· Hypercoagulable state
· Injury or infection to the venous wall
72. What are varicose veins? What are some causes? What are the signs/symptoms? How are they treated?
· Dilated, tortuous, and knotted veins
· Usually occur in superficial veins of the legs
- Etiology
· Thought to arise as a result of elevated venous pressure
· Dilation leads to failing of the valves and worsening of the problem