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Patho 2 (Path 311) > Mod 5 Valvular/Vessels Disorders > Flashcards

Mod 5 Valvular/Vessels Disorders Flashcards

1
Q

What are murmurs associated with?

A

Aortic regurgitation (or mitral)

  • honestly, any regurg from a heart valv (4)
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2
Q

What are 2 types of mechanical disruptions for valvular disorders

A
  1. Stenosis (narrowing of valves = don’t open properly)
  2. Incompetence (distortion = don’t close aka regurg)
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3
Q

What effects do valvular disorders generally have?

A

Obstruct flow of blood or allow backward flow of blood

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4
Q

What is Systemic lupus erythematosus (SLE)?

A

A autoimmune condition where the body attacks its own tissue

  • causes widespread inflammation
  • affects joints, skin, brain, lungs, and blood vessels
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5
Q

What is Rheumatoid Arthritis (RA)

A

Immune system attacks healthy cells causing inflammation

  • Joints are most commonly affected, but the heart can be as well
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6
Q

What is Marfans Syndrome?

A

Genetic condition that affects connective tissue

  • causes damaged blood vessels, heart, eyes, skin, lungs and bones
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7
Q

Origin of valvular disorders

A
  • Congenital defects
  • Trauma
  • Ischemic damage
  • Degenerative changes
  • Inflammation/infection
  • Neoplasm
  • Long term cocaine use
  • Connective tissue diseases
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8
Q

What are degenerative changes associated with?

A

Diabetes mellitus and hypercholesteremia

  • risk factors of valv disorders
  • damage vessel walls over time (chronic)
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9
Q

Why are Stenotic valves a problem? (2)

A

Fighting against the valve to pump (obstructive shocks?)

  1. Distension of the chamber that pumps blood thru the diseased valves (Increased pressure)
  2. Impaired filling of chamber that receives the blood (decreased pressure)
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10
Q

Why are regurgitant/incompetent valves a problem? (3)

A
  1. Backflow thru valve
  2. Causes distension of the chamber prior to the diseased valve (Increased Pressure)
  3. This place increases work demands on this chamber
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11
Q

Would mild valvular disorders cause or produce any symptoms?

A

Other than a heart murmur, no.

  • only minimally impact the pressures seen
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12
Q

Clinical manifestations of valvular disorders?

A

Exertional dyspnea

  • syncope
  • Effort induced fatigue
  • Angina secondary to ischemia
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13
Q

Diagnostic Tests for Valvular disorders?

A
  1. Auscultation of heart sounds
  2. Echocardiogram -> Transesophageal echo (TEE) is particularly effective in identifying valve disorders
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14
Q

Why are Transesophageal echo’s effective for diagnosing/identifying valv disorders?

A

Allows for viewing of the internal structures of of the herat and blood flow patterns

  • helps visualize blood flow, and assesses visually if there is a clot
  • Used to confirm lack of blood clot in the atria in patients w/prolonged afib before performing cardioversion
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15
Q

What is the most common vessel for an aneurysm to occur?

A

Aorta

  • but can occur in arteries or veins throughout the body
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16
Q

What is a aneurysm?

A

A abnormal localized dilation of a blood vessel by > 50%

  • Classified by area of occurrence i.e triple A, cerebral aneursym etc. etc.
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17
Q

What are 4 variations of Aneurysms?

A
  • Abdominal aortic aneurysms (AAA)
  • Thoracic aortic aneurysms (TAA)
  • Cerebral aneurysm
  • peripheral aneurysm
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18
Q

What are 3 variations of Aneurysms (that haven’t bursted yet)?

A
  1. Saccular (berry)
  2. Fusiform
  3. Dissecting (false)
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19
Q

What is the etiology of aneurysms?

  • why are they able to form?
A

Aneurysms form where the vessel wall has been weakened

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20
Q

What are etiological risk factors of Aneurysms?

A
  • Atherosclerosis
  • Hypertension
  • Inherited condition? -> relative with 1 degree at increased risk
  • Marfans syndrome (connective tissue disease)
  • Collagen vascular disorders
  • Trauma
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21
Q

Pathophysiology: What are 4 outcomes that could emerge from a Aneurysm development?

A

All the following could develop and lead to a aneurysm rupture

  1. Rupture or leaking
  2. Impairment of blood flow distally
  3. Pressure on adjacent structures
  4. Thrombi at site form emboli
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22
Q

What are clinical manifestations of Aortic aneurysms?

A

Most are asymptomatic, those that are seen are late stage findings, such as:

  • Sensitivity to touch at area of aneurysm
  • Strong palpable pulse in the abdominal area
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23
Q

If a cerebral aneurysm ruptures, what signs and symptoms are seen?

A

Same sign and symptoms of a stroke

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24
Q

What are the clinical manifestations of a ruptured aneurysm?

  • what are they outcomes?
A

Hypotension (bp diff in each arm, sometimes seen atherosclerosis)

  • Pale in color
  • Decreased LOC
  • Extreme pain in ab or back region
  • Dizziness/syncope
  • Palpating abdominal mass (30-50% of the time)
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25
Q

What is atherosclerosis?

A

Thickening or hardening of arteries caused by a buildup of plaque

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26
Q

What does infrarenal mean?

A

Issue below the kidneys

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27
Q

How are aneurysms diagnosed?

A
  • CxR
  • ultrasound can see flow of blood but can’t detect rupture/leak
  • CT scan is the gold standard
  • MRI
  • Angiography
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28
Q

What are treatments for a stable aneurysm?

A
  • Treat hypertension (b-blockers)
  • Follow up w/repeated imaging
  • Surgical repair
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29
Q

What are treatments for a ruptured aneurysm?

A
  • Treat shock
  • supportive care
  • Surgical repair
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30
Q

In the context of a ruptured aneurysm, how is the subsequent shock managed?

A
  • IV’s or fluid resuscitation
  • Blood
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31
Q

Left off @slide 85 (cardiomyopathies)

A
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32
Q

What is the definition of a Cardiomyopathy?

A

A group of of disorders that affect the heart muscle and diminishes cardiac performance.

  • Can develop as a primary or secondary disorder
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33
Q

What are the main variations of cardiomyopathy?(4)

A
  • Dilated
  • Restrictive
  • Hypertrophic
  • Congestive (can lead back to dilated)
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34
Q

What are the primary causes of Cardiomyopathies?

A
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35
Q

What are the secondary causes of origin for Cardiomyopathies?

A
  • Other CV disorders: Ischemia hypertension, valv disorers
  • Metabolic disorders (diabetes, hyperthyroidism)
  • Collagen Vascular disease (SLE,RA)
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36
Q

What are the primary characteristics of dilated cardiomyopathy?

A

Heart can fill, but cannot pump it. Its floppy.

  • Heart becomes enlarged and myocardium weak
  • Results in a systolic dysfunction
37
Q

What are the outcomes of Dilated Cardiomyopathy?

A

Depends on affected ventricle (its unable to pump blood it receives)

  • If LV is affected –> Left heart failure and its manifestations
  • If the RV is affected –> Right heart failure and its manifestations
38
Q

What are the characteristics of Hypertrophic Cardiomyopathy?

A

Hallmark is inappropriate, disorganized proliferation of myocardial cells.

  • Caused by genetic disorder
  • Affects the LV, frequently in the interventricular septal area
  • Results in systolic and diastolic dysfunction
39
Q

What are the outcomes of Dilated Cardiomyopathy?

A

Results in both systolic and diastolic dysfunction

  • Leading cause of sudden cardiac death in pre-adolescent and adolescent children
40
Q

What are the characteristics of Restrictive Cardiomyopathy?

A

Heart unable to move properly

  • Walls of the ventricle are stiff but not necessarily thickened
  • Impairs the filling of blood as ventricle doesn’t relax normally
  • Results in diastolic dysfunction
  • Most commonly associated w/foreign materials aka drugs
41
Q

What are the outcomes of Restrictive Cardiomyopathy?

A

Results in diastolic dysfunction.

  • If LV is affected –> Left heart failure and its manifestations
  • If the RV is affected –> Right heart failure and its manifestations
42
Q

What is Pericarditis?

A

Inflammation of the pericardium aka swelling around the heart

  • Can be acute or chronic
  • Inflammation can lead to accumulation of fluid in the pericardial sac
43
Q

What is Pericarditis characterized by?

  • how does it manifest?
A
  • Chest pain
  • Pericardial rub
  • Serial ECG changes
44
Q

Etiology of Pericarditis?

A

Its idiopathic

  • Infections, kidney failure, chest trauma, and prior MIs are the most common. More list in the pic.
45
Q

What is the pathophysiology of Pericarditis?

A

Etiological agent bypasses WBC affecting pericardial vascularization leading to several outcomes.

46
Q

What are the 3 main outcomes of Pericarditis?

A
  1. Pericardial effusion
  2. Fibrinous reaction and adhesion formation
  3. Formation of Granulomas
47
Q

What is the formation of Granulomas associated with?

A
  • Pericarditis
  • TB
  • rheumatoid arthritis (RA)
  • Fungal infections
48
Q

What is Constrictive Pericarditis characterized by?

A

Fibrinous reaction and adhesion formation caused by scarring of the pericardium after one or more episodes of pericarditis

  • Pericardium becomes thickened and stiff
  • Results in impaired filling of the heart –> Diastolic dysfunction
  • Blood backup
49
Q

What are 2 outcomes of pericardial effusions (blood around the heart)?

A
  1. Formation of cardiac tamponade
  2. Exudative effusion aka serous fibrinous hemorrhagic, purulent, or chylous infections
50
Q

Clinical Manifestations of Pericarditis?

A
  • Chest pain
  • Pericardial rub
  • Signs of tamponade if large effusion present (becks triad and Kussmauls sign)
51
Q

What is the Becks triad?

A

Sign of large effusion or tamponande via 3 signs:

  • JVD
  • Distant heart sounds
  • hypotension
52
Q

What is Kussmauls sign?

A

Increased right atrial pressure on inspiration –> Increased JVD on inspiration

  • Its pardoxical because JVP normally decreases on inspiration due to increased thoracic pressure and has resulting decreased venous return to R.atrium
  • TLDR: Swelling JVD during insp
53
Q

What is the difference between Kussmauls sign and Kussmauls breathing?

A
  1. K.Sign Refers to parodical pressure chances in jugular venous pressure on inspiration (it increases when it normally decreases)
  2. K.Breathing refers to deep, rapid, labored breathing pattern that is associated with metabolic acidosis and diabetic ketoacidosis (DKA)
54
Q

What does untreated constrictive pericarditis result in?

A

Impaired filling of the heart, aka diastolic dysfunction

55
Q

Clinical manifestations of Constrictive Pericarditis?

A

Bc it results in blood backing up into extremities and lungs. S & S are similar to heart failure

56
Q

What would be the expected diagnostics for Pericarditis?

A
  • Lab studies would display infectious origin (increased WBC + blood cultures) and increase in cardiac enzymes (if MI)
  • CxR could show pericardial effusion
  • Analysis of pericardial fluid should be done
57
Q

What are the 4 classic ECG stages for Pericarditis?

A
58
Q

What is the first classic ECG stage for Pericarditis?

A

Stage 1:

  • ST elevation in all leads
  • PR depression
59
Q

What is the second classic ECG stage for Pericarditis?

A

Stage 2: Pseudonormalization (transition)

  • generalized T wave flattening
  • 1-3 wks
60
Q

What is the third classic ECG stages for Pericarditis?

A

Stage 3: Inverted T-Waves

  • 3 to several wks
61
Q

What is the fourth classic ECG stages for Pericarditis?

A

Stage 4: Normalization

  • Several weeks onwards
62
Q

General treatment for Pericarditis?

A

Depends on etiology (i.e antibiotics for bacterial pericarditis etc.). General tx involve:

  • Analgesics for pain
  • Steroids for inflammation
63
Q

Treatment for Pericarditis if effusions are present? (4)

A
  • Pericardiocentesis
  • Pericardial window
  • Pericardiodesis
  • Pericardiectomy
64
Q

What is pericardiocentesis?

A

Procedure to remove fluid that has built up in the sac around the heart (pericardium)

  • done via needle/catheter to drain excess fluid
65
Q

What is the Pericardial Window?

A

Procedure done on the sac around the heart.

  • surgically cuts open apart of the sac to allow drainage of excess fluids
  • Prevents recurrence of pericardial effusion
  • Apparently allowed to drain into the chest
66
Q

What is Pericardesis?

A

Sac is fused to the heart (no longer outside, its apart of it)

  • Prevents further recurrences of effusions
  • Fuse layers of the pericardium by injecting sclerosant. Sclerosant causes local inflammation, which leads to decreased blood flow to the area.
  • TLDR: Agent is used to prevent sac from sticking together
67
Q

What is Pericardiectomy?

A

Excision of part of the pericardium (similar to pericardial window)

  • Done in severe cases
  • Done for constrictive pericarditis or for chronic recurring pericarditis
68
Q

What is Cardiac Tamponade?

A

Condition where elevated intra-pericardial pressures impair the filling of the heart during diastole..

  • Increased pressure results from a build up of fluid in the pericardial sack
  • Results in decreased SV and decreased CO
69
Q

Etiology of Cardiac Tamponade

A
  • Trauma, cardiac surgery
  • Cardiac rupture secondary to MI
  • Pericarditis (all etiologies)
  • Neoplasm
70
Q

What does the Pathophysiology of Cardiac Tamponade generally involve?

A

Rapid accumulation of fluids in pericardium that reduce CO and SV

  • Effusions can be serous (clear), serosanguineous (clear w/blood tinge) or chylous (milky)
  • Path can change depending on acute/chronic status of pericardial effusion
71
Q

What is the pathophysiology cardiac tamponade if the initial pericardial effusion is acute?

A

Results in decreased SV and CO that have the same S and S of shock and heart failure

72
Q

What is the pathophysiology cardiac tamponade if the initial pericardial effusion is chronic?

A

S and S of pericardial effusion, due to stretching of the pericardium (normalizes?)

73
Q

What are the primary clinical manifestations used to diagnose Cardiac Tamponade? (3)

A

Becks triad (hypotension, increased JVP, Diminished heart sounds)

  • Tachycardias
  • Decreased pulse pressure or pulsus paradoxus
  • May present w/PEA
74
Q

What is the relationship between Pulse pressure and Pulsus paradoxus?

A
  • Pulse pressure = normal (diastolic 40 is normal)
  • Pulsus paradoxus = fall in systolic BP > 10 on insp
75
Q

What are immediate treatments of Cardiac Tamponade?

A
  1. Pericardiocentesis
  • Acute = subxiphoid percutaneous drainage w/18 gauge needle
  • less acute = fluroscopy/echo to aid
  1. Treat underlying cause
76
Q

For recurring tamponade secondary to effusions, what are the treatment options? (3)

A
  • Pericardial Window
  • Pericardiodesis: Agents introduced into pericardial sac to sclerose the tissue. (prevents the sac from sticking together)
  • Pericardiectomy
77
Q

What is Disseminating Intravascular Coagulation (DIC)

A

A stimulus causes hyperstimulation of the clotting pathways…resulting in formation of diffuse clots in the microvasculature and depletion of the clotting factors…leading to generalized bleeding

  • Widespread coagulation and bleeding
  • TLDR: Clotting everywhere bc hyperstimulated -> used up all your clotting factors = no more clot factors left.
  • not a primary disease; complication of something else
78
Q

What is the Etiology of DIC?

A

Its a complication of other pathos and conditions, such as:

  • Infections and Shocks
  • Surgery and traumas
  • Obstetric conditions (childbirth related)
  • Hematologic conditions (transfusion related)
79
Q

What is the pathophysiology of Disseminating Intravascular Coagulation (DIC)?

A

Generally, a stimulus disrupts the clotting pathway leading to a cascade of bleeding and depletion of clotting factors. End result is organ failure.

80
Q

How does diffuse clotting and micro emboli lead to organ failure?

A

They lead to organ and tissue ischemia and widespread fibrinolysis (excessive bleeding)

  • fibrinolysis results from excessive bleeding with depleted clotting factors
81
Q

What are specific clinical manifestations of Disseminating Intravascular Coagulation (DIC)? (4)

A
  1. Petechiae (purplish hemorrhagic spots on skin)
  2. Ecchymosis (Bruise)
  3. Bleeding (via Epistaxis, bleeding gums, or from surgical sites)
  4. S & S of thrombosis and resulting ischemia
82
Q

what is Epistaxis?

A

Nose bleeding

83
Q

What is the end result of thrombosis and resulting ischemia?

A

DVT and/or Renal failure

84
Q

Why is it bad when a DVT (deep vein thrombosis) breaks away?

A

Can lead to pulmonary embolism and stroke

85
Q

What lab findings can be used to diagnose Disseminating Intravascular Coagulation (DIC)? (5)

A
  1. Decreased platelet count
  2. D dimer (highly specific test)
  3. Abnormal clotting times (prolonged aPTT time)
  4. Anemia
  5. Decreased coagulation factors
86
Q

What are treatments for Disseminating Intravascular Coagulation (DIC)? (3)

A
  1. Address primary disease
  2. Replacement clotting components (transfusion of Fresh frozen plasma (FFP), Platelets, cryoprecipitate)
  3. Prevention of further activation of clotting factors (heparin therapy)
87
Q

What site is most affected by or is the most senstive to multi organ system failure (MOSF)

A

Kidneys

88
Q

What are complications of Disseminating Intravascular Coagulation (DIC)? (3)

A
  1. Death
  2. organ infarction (obstruction of blood vessels = tissue hypoxia)
  3. Limb/digit ischemia
89
Q

How do infarctions occur in organs because of Disseminating Intravascular Coagulation (DIC)?

A

Micro emboli may obstruct blood vessels and cause tissue hypoxia leading to potential necrotic damage to organs

Patho 2 (Path 311) (15 decks)

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