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M3 Path Block 2 > 7 - Hemodynamics (2nd Half) > Flashcards

7 - Hemodynamics (2nd Half) Flashcards

1
Q

Abnormal Blood Flow (Virchow): Turbulence contributes

A

To arterial and cardiac thrombosis by causing endothelial or dysfunction

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2
Q

Abnormal Blood Flow (Virchow): Turbulence and stasis contribute to thrombosis in several clinical settings (6)

A

Ulcerated atherosclerotic plaques

Aneurysms

Acute MI

Acute myocardial infarctions

Rheumatic mitral valve stenosis

Hyperviscosity

Sickle cell anemia

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3
Q

Hypercoagulability (Virchow)

A

AKA Thrombophilia

Is any alteration of the coagulation pathways that predisposes to thrombosis

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4
Q

Hypercoagulability (Virchow) is divided into

A

Primary (genetic)

Secondary (acquired) disorders

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5
Q

Hypercoagulability: Primary (Genetic) - Common (3)

A

*Mutation in Factor V (Leiden)

Mutation in prothrombin gene

Mutation in methyltetrahydrofolate gene

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6
Q

Hypercoagulability: Primary (Genetic) - Rare (3)

A

Anti-thrombin III Deficiency

Protein C Deficiency

Protein S Deficiency

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7
Q

Hypercoagulability: Primary (Genetic) - Very Rare

A

Fibrinolytic defects

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8
Q

Hypercoagulability: Secondary (Acquired) - High Risk for Thrombosis

A
  • Prolonged bed rest or immobilization
  • MI
  • AFib (a SA node)
  • Tissue damage (surgery, fracture, burns)
  • Cancer (Pancreas)
  • Prosthetic cardiac valves
  • DIC
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9
Q

Hypercoagulability: Secondary (Acquired) - Low Risk for Thombosis

A
  • Hyper estrogenic states (pregnancy)

- OCPs

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10
Q

Mnemonic to remember thrombophilia

A

THROMBI

T - Tissue Damage 
H - Hereditary (V leiden) 
R - Rest (prolonged) 
O - Obstetrics (eclampsia, abruptio) 
M - Malignancy 
B - Blood flow disturbances (MI, aneurysms, varicose veins) 
I - Immune mechanisms
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11
Q

Factor V (Leiden) Mutation is called the

A

G1691A mutation

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12
Q

Factor V (Leiden)/G1691A Mutation

A

Results in glutamine to arginine substitution at position 506 that renders factor V resistant to cleavage by Protein C

Important anti-thrombotic counter-regulatory pathway is lost

Recurrent DVT

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13
Q

Prothrombin gene mutation

A

Single nucleotide change (G20210A)

Elevated prothrombin levels

Threefold increased risk of venous thrombosis

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14
Q

Protein C

A

Anti-thrombotic factor made by liver

Vit. K Dependent

Binds to activated Facts 5 and 8

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15
Q

If patient has a clot in leg before age 50, suspect?

A

Genetic abnormality rather than environmental

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16
Q

Heparin-Induced thrombocytopenia (HIT) Syndrome

A

IOccurs following administration of unfractionated heparin

Antibodies to heparin +Platelet factor (pf)-4 complex and Pf-44 like proteins on the endothelial cells

Binding of antibodies results in activation, aggregation, and consumption (thrombocytopenia)

Low molecular weight heparin has less frequency

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17
Q

If you give unfractionated heparin, some part of heparin protein will also resemble proteins in the bod, so what ocurrs?

A

Cross reaction

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18
Q

Antiphospholipid Antibody Syndrome (APLA)

A

Previously called lupus anticoaglant syndrome

Name derived from binding of antibodies to epitopes on plasma proteins (e.g. prothrombin) that are induced or ‘unveiled’ by phospholipids

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19
Q

Antiphospholipid Antibody Syndrome (APLA):

The autoantibodies INDUCE a hypercoagulable state by? 3

A

Causing endothelial injury

Activating platelets and complement directly

Interactions with the catalytic domains of certain coagulation factors

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20
Q

Antibodies to beta-2 glycoprotein are expressed on?

A

Endothelial cells

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21
Q

Antibodies against anion phosphoplipids

A

Cardiolipin

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22
Q

What type of reaction is there for VDRL?

A

False positive

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23
Q

What happens in vitro? (I think it’s referring to VDRL)

A

Inhibits coagulation

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24
Q

What happens in vivo? (I think it’s referring to VDRL)

A

Hypercoagulable state

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25
Q

Clinical Features of APLA (10)

A
  1. Pulmonary embolism (following lower extremity venous thrombosis)
  2. Pulmonary hypertension (from recurrent subclinical pulmonary emboli)
  3. Stroke
  4. Bowel infarction
  5. Renovascular hypertension
  6. Renal microangiopathy
  7. Recurrent thrombosis
  8. Repeated miscarriages (due to ab-mediated inhibition of t-PA activity necessary for trophoblastic invasion of the uterus)
  9. Cardiac valve vegetations
  10. Thrombocytopenia
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26
Q

Morphology of Thrombus 3

A
  1. Develop anywhere in the cardiovascular system

2. Size and shape of thrombi depend on the site of origin and the cause

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27
Q

Sizes and shapes of thrombi depending on the site of origin and the cause

A

Venous thombi: at sites of stasis; extend IN DIRECTION of blood flow

Arterial thrombi: grow retrograde from the point of attachment

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28
Q

Lines of Zahn

A

Represent pale platelet and fibrin deposits alternating with darker red cell-rich layers

Are laminations seen in thrombi

*Signigy that a thrombus has formed in flowing blood

Distinguish ante mortem thrombosis from the bland non-laminated clots that occur postmortem

Thrombi occurring in heart are known as mural thrombi

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29
Q

Ante mortem Clot Characteristics (4)

A
  1. Adhere to vessel
  2. Have lines of Zahn
  3. Can’t be washed away
  4. Buffed in color
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30
Q

Postmortem Clot Characteristics (4)

A
  1. Do not adhere to vessel
  2. Absent Lines of Zahn
  3. Easily washed away
  4. Chicken fat appearance
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31
Q

Mural thombus

A

Occur in heart chambers or in the aortic lumen

  • abnormal myocardial contraction
  • Endomyocardial injury
  • **Precursors of aortic thrombi
    • ulcerated atherosclerotic plaque
    • aneurysmal dilation
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32
Q

Cardiac Vegetations

A
  • Thrombi on heart valves
  • Infective endocarditis
  • Nonbacterial thrombotic endocarditis
  • *Libman-Sack’s endocarditis
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33
Q

Fate of Thrombus: 1st - Propagation

A

Thrombi accumulate additional platelets and fibrin

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34
Q

Fate of Thrombus: 2nd - Embolization

A

Thrombi dislodge and travel to other sites in the vasculature

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35
Q

Fate of Thrombus: 3rd - Dissolution

A

Result of fibrinolysis, which can lead to the rapid shrinkage and total disappearance of recent thrombi

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36
Q

Fate of Thrombus: 4th - Organization and recanalization

A

Older thrombi become organized by the ingrowth of endothelial cells, smooth muscle cells, and fibroblasts

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37
Q

Venous Thrombosis (Phlebothrombosis): Superficial Venous Thrombi

A

Saphenous veins affected in the setting of varicosities

Local congestion, pain, and if edema superadded, impaired blood supply –> ulcer

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38
Q

Venous Thrombosis (Phlebothrombosis): Deep Vein Thrombosis (DVT)

A

Larger leg veins: at or above the knee (e.g. popliteal, femoral, and iliac veins) - is more serious

More often embolize to the lungs and give rise to pulmonary infarction

C/F - local pain and edema

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39
Q

Causes of for Venous Thrombosis (5)

A

Migratory thrombophlebitis or Trousseau syndrome (seen in pancreatic carcinoma)

Bed rest and immobilization

CHF

Trauma, surgery, burns

Advanced age

40
Q

Mnemonic to remember risk factors for DVT/Pulmonary embolism: 5H

A

Hypercoagulability (sickle cell, polycythemia)

Hypomobility (Prolonged bed rest)

Hereditary (Factor V)

Hormones (OCP)

Hyperhomocysteinemia

41
Q

Causes of Arterial and Cardiac Thrombosis and Consequences (4)

A

Atherosclerosis

MI

Rheumatic heart disease

Consequences:

  • local obstruction
  • embolize peripherally - brain, kidneys, and spleen are particularly likely targets because of their rich blood supply
42
Q

Disseminated Intravascular Coagulation (DIC): Defined

A

Sudden or insidious onset of widespread fibrin thrombi in the microcirculation

43
Q

DIC: Causes (23)

A

Obstetrics complications

Advanced malignancy

44
Q

DIC: Pathogenesis

A

Release of tissue factor and widespread endothelial injury

45
Q

DIC: Complications

A

Platelet and coagulation protein consumption

Diffuse circulatory insufficiency, particularly in the brain, lungs, heart and kidneys

46
Q

Embolism: Definied

A

Detached intravascular solid, liquid, or gaseous mass that’s carried by blood to a site distant from its point of origin

47
Q

Pulmonary Embolism: Stats (4)

A

95% originate from leg (DVTS)

60-80% are clinically silent

Risk for more after having 1

Usually multiple

48
Q

Course of an Embolus

A
  1. DVT
  2. Reaches the right side of the heart and into the pulmonary arterial tree (deoxygenated blood)

Can have 3 pathways

a. Main pulmonary arteries
b. Straddle the pulmonary arterial bifurcation (saddle embolism)
c. Pass out into smaller, branching arteries

49
Q

In what conditions can an emboli go from right side to left and into systemic circulation (paradoxical embolism)?

A

ASD, VSD

50
Q

Embolism: Clinical Features (5)

A

Sudden death

Right heart failure (cor pulmonale)

Cardiovascular collapse

Pulmonary infarction - embolus in the setting of left-sided cardiac failure (and compromised bronchial artery flow)

Pulmonary hypertension

51
Q

Systemic Thromboembolism: Defined

A

Emboli in the arterial circulation

52
Q

Systemic Thromboembolism: Source (3)

A

Intracardiac mural thrombi

Unknown origin

Can travel to a variety of sites

53
Q

Systemic Thromboembolism: Major Sites (2)

A

Lower extremities (75%)

Brain (10%)

54
Q

Systemic Thromboembolism: Causes

A

Infarction of the affected tissues due to atherosclerosis

Majority occur in the heart

55
Q

Fat and Marrow Embolism (Rare)

A

Microscopic fat globules: with or without associated hematopoietic marrow elements in the circulation impacted in the pulmonary vasculature

56
Q

Fat and Marrow Embolism (Rare): Causes (3)

A

Fracture of long bones (which have fatty marrow)

Soft tissue trauma (MVA)

Burns

Slide 70

57
Q

Fat and Marrow Embolism (Rare): Pathogenesis (2)

A

Mechanical obstruction: Fat, micro emboli and associated red cell and platelet aggregates occlude the pulmonary and cerebral microvasculature

Biochemical injury: Release of free FAs from the fat globules exacerbates the situation by causing local toxic injury to endothelium and platelet activation and granulocyte recruitment

58
Q

Fat and Marrow Embolism (Rare): Clinical Features (8)

A
  1. Pulmonary Insufficiency
  2. Neurologic Symptoms
  3. Anemia: red cell aggregation and/or hemolysis
  4. Thrombocytopenia - splenic sequestration
  5. Fatal in about 5 - 15%
  6. Sudden onset of tachypnea, dyspnea, and tachycardia
  7. Irritability and restlessness can progress to delirium or coma
  8. A diffuse petechial rash from thrombocytopenia
59
Q

Air Embolism: General (5)

A

Gas bubbles within the circulation can coalesce to form frothy masses that obstruct vascular flow

Decompression sickness: seen when there is sudden decrease in atmospheric pressure

Scuba and deep sea divers

Underwater construction workers

Indivduals in unpressureized aircraft in rapid ascent

60
Q

Air Embolism: Course (for skeletal muscles and joints)

A

If the diver ascends (depressurizes) too rapidly

The nitrogen comes out of solution in the tissues and the blood, causing

Rapid formation of gas bubbles within skeletal muscles and supporting tissues in and about joints, leading to

Painful conditions called the bends

61
Q

Air Embolism: Course (Lungs)

A

If the diver ascends (depressurizes) too rapidly

The nitrogen comes out of solution in the tissues and the blood in the LUNGS, forming

Gas bubbles in the vasculature, which can cause

Edema, hemorrhage, and focal atelectasis or emphysema, leading to

A form of respiratory distress called the chokes

62
Q

Air Embolism: Caisson Disease (3)

A

Chronic form of decompression sickness

Persistence of gas emboli in the skeletal system leads to multiple foci of ischemic necrosis;

Common sites: femoral heads, tibia, and humeri

63
Q

Amniotic Fluid Embolism (3)

A

Sudden sever dyspnea, cyanosis followed by shock

Neurological impairment

Pulmonary edema and septic shock

64
Q

Amniotic Fluid Embolism: Course

A

Tear in placental membranes or rupture of uterine veins, causing

Infusion of amniotic fluid or fetal tissue into the maternal circulation –> causing amniotic fluid embolism

65
Q

Amniotic Fluid Embolism: Histological Findings (4)

A

Squamous cells shed from fetal skin, lanugo hair, fat from vernix caseosa, in the maternal pulmonary microvasculature

Marked pulmonary edema

Diffuse alveolar damage

Presence of fibrin thrombi in many vascular beds due to DIC

66
Q

What is vernix caseosa?

A

White, cheesy surface coating to the skin of infants

67
Q

Infarction: Defined

A

Area of ischemic necrosis caused by occlusion of either the arterial supply or the venous drainage

68
Q

Infarction: Causes (8)

A
  1. Thrombotic or embolic arterial occlusions
  2. Local vasospasm
  3. Hemorrhage into an atheromatous plaque
  4. Extrinsic vessel compression (e.g. by tumor)
  5. Torsion of a vessel (e.g. in testicular torsion or bowel volvulus)
  6. Traumatic Rupture
  7. Vascular compromise by edema (e.g. anterior compartment syndrome)
69
Q

Morphology of an Infarct: According to Color

A

Red - hemorrhagic

White - anemic

70
Q

Morphology of an Infarct: Based on Presence or Absence of Infection

A

Septic

Bland

71
Q

Morphology of an Infarct: Wedge-Shaped

A

With the occluded vessel at the apex and the periphery of the organ forming the base

72
Q

Red Infarcts occur (5)

A
  1. With venous occlusions (e.g. ovary)
  2. In loose tissues (e.g. lung) where blood can collect in the infarcted zone
  3. In tissues with dual circulations (e.g. lung and small intestine)
  4. In tissues previously congested by sluggish venous outflow
  5. When flow is re-established to a site of previous arterial occlusion and necrosis
73
Q

Red Infarcts: Course

A

Extravasated red cells in hemorrhagic infarcts then

Phagocytosed by macrophages, then

Converts heme iron into hemosiderin, and then

Small amounts do not grossly impart any appreciable color, brown residuum

74
Q

White Infarcts Occur With (3)

A
  1. Arterial occlusions in solid organs with end-arterial circulation (e.g. heart, spleen, and kidney)
  2. Where tissue density limits the seepage of blood from adjoining capillary beds into the necrotic area
  3. Infarcts resulting from arterial occlusions in organs without a dual blood supply typically become progressively paler and more sharply defined with time
75
Q

Exception to white infarcts

A

Brain – liquefactive necrosis

76
Q

Shock: Is a systemic hypoperfusion due to reduction in? 2

A

Cardiac Output

Effective circulating blood volume

77
Q

Shock: Result

A

Hypotension

Impaired tissue perfusion and cellular hypoxia

78
Q

Shock: Main Categories

A
  1. Cardiogenic
  2. Hypovolemic
  3. Septic
79
Q

Shock: Others

A
  1. Neurogenic Shock

2. Anaphylactic Shock

80
Q

Shock: Cardiogenic Shock (4)

A

Failure of myocardial pump

Intrinsic Myocardial Damage
- Infarction, Ventricular rupture, arrhythmia

Extrinsic compression
- Cardiac tamponade

Outflow obstruction
- Pulmonary embolism

81
Q

Shock: Hypovolemic

A

Due to loss of blood of plasma volume

Hemorrhage
Fluid loss
- From severe burns, trauma, vomiting, diarrahea

82
Q

Shock: Septic

A

Most common cause of death in ICU’s in USA

Dissemination of infection into vasculature

Causes: G(+), G(-) infection (endotoxic shock), fungal infections, superantigens

Endothelial cell activation and injury –> hypercoagulable state –> DIC

83
Q

Shock: Septic - Components

A

Inflammatory Mediators: TNF, IL-1, IFN-γ, IL-12, and IL-18. high mobility group box 1 protein (HMGB1).

Reactive oxygen species and lipid mediators such as prostaglandins and platelet activating factor (PAF)

Endothelial cell activation and injury: (1) thrombosis; (2) increased vascular permeability; and (3) vasodilation –> DIC

84
Q

Shock: Septic - *Metabolic Abnormalities

A

Insulin resistance and hyperglycemia. TNF and IL-1, stress-induced hormones
(Such as glucagon, growth hormone, and glucocorticoids), and catecholamine’s –> gluconeogenesis

  • Frank adrenal necrosis due to DIC (*Waterhouse-Friderichsen syndrome)

Immune Suppression

Organ dysfunction

85
Q

Shock: Septic - Symptoms (7)

A
  1. Systemic Vasodilation (Hypotension)
  2. Diminished cardiac contractility
  3. Endothelial injury and activation (Adult Resp. Distress Sydrome, ARDS)
  4. Activatation of coagulation system (DIC)
  5. Multi-organ system failure
  6. Liver, Kidney, CNS
  7. Death
86
Q

Morphology of Shock: General and Brain

A

Failure of multiple organ systems

Brain: ischemic encephalopathy

87
Q

Morphology of Shock: Heart (2)

A

Focal or widespread coagulation necrosis

Sub-endocardial hemorrhage

88
Q

Morphology of Shock: Kidney

A

*Acute Tubular Necrosis

Extensive tubular ischemic injury

C/F - Oliguria, anuria, electrolyte disturbances

89
Q

Morphology of Shock: Lungs

A

Pure Hypovolemic Shock
- Rarely affected as they are resistant to hypoxic injury

Shock caused by bacterial sepsis or trauma
- Diffuse alveolar damage (shock lung)

90
Q

Morphology of Shock: GIT

A

Hemorrhagic enteropathy

Patchy mucosal hemorrhages and necroses

91
Q

Morphology of Shock: Liver

A

Fatty Change

Central hemorrhagic necrosis with severe perfusion deficits

92
Q

Stages of Shock: Non-Progressive (Early)

A

Compensatory Mechanisms: Increase HR and peripheral resistance and maintain perfusion of vital organs

93
Q

Stages of Shock: Progressive

A

Tissue hypoperfusion

Renal insufficiency and electrolyte imbalance –> metabolic acidosis from lactic acidosis

94
Q

Stages of Shock: Irreversible

A

Survival is not possible

95
Q

Hypovolemic, Cardiogenic, Septic Shock Chart (Slide 103)

A

Check Slide 103

M3 Path Block 2 (10 decks)

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