Hemodynamic disorders Flashcards by Annabella Moody

______ delivers oxygen and nutrients to tissues & removes wastes

blood circulation

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Three functions of circulation:

delivers oxygen to tissues
delivers nutrients to tissues
wastes are removed

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Blood clotting that prevents excess bleeding after blood vessel damage:

hemostasis

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inappropriate clotting:

thrombosis

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migration of clots:

embolism

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active process, arteriolar dilation and increased blood inflow:

hyperemia

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Describe the color of the blood associated with hyperemia:

red color- due to oxygenated hemoglobin

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In hyperemia we see ______ colored blood due to ______ hemoglobin

red; oxygenated

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passive process, impaired outflow of venous blood from a tissue:

congestion

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Describe the color of blood associated with congestion:

blue/red color (cyanosis)- deoxygenated hemoglobin

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In congestion we see _____ colored blood due to _____ hemoglobin

blue/red (cyanosis); deoxygenated

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Hyperemia is a ____ process

Congestion is a ____ process

active; passive

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What is seen in this image? Is the specimen from a living or dead individual?

Liver with chronic passive congestion & hemorrhagic necrosis; dead specimem

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_____ % of the body weight is water, ______ intracellular

60%; 2/3

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Two thirds of the 60% water comprising our body weight is:

Intracellular

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The remaining fluid in the body (not including water) is comprised by mostly:

Interstitial fluid

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Around _____ % blood plasma is found in the body

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accumulation of interstitial fluid in tissues:

edema

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Edema is the accumulation of ____ in tissues

interstitial fluid

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Extravascular fluid that collects in body cavities:

Effusions

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Effusions are _____ that collects in body cavities

extravascular fluid

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Effusion in the pleural cavity:

hydrothorax

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Effusion in the pericardial cavity:

hydropericardium

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Effusion in the peritoneal cavity:

hydroperitoneum or ascites

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Severe generalized edema due to fluid retention in tissues and cavities:

anasarca

Causes of edema include: (5)

1. increased hydrostatic pressure 2. reduced plasma osmotic pressure (hypoproteinemia) 3. lymphatic obstruction 4. sodium retention 5. inflammation

What may cause increased hydrostatic pressure that leads to edema? (2)

1. impaired venous return 2. arterial dilation

-CHF -Constrictive pericarditis -Ascites (liver cirrhosis) -Venous obstruction or compression -Thrombosis -External pressure (e.g. mass) -Lower extremity inactivity with prolonged dependency These are all examples of:

impaired venous return (leading to increased hydrostatic pressure which is a cause of edema)

-Heat -Neurohumoral dysregulation These are all examples of:

Ateriolar dilation (leading to increased hydrostatic pressure which is a cause of edema)

-Protein-losing glomerulopathies (nephrotic syndrome) -Liver cirrhosis (ascites) -Malnutrition -Protein-losing gastroenteropathy These are all examples of:

Reduced plasma osmotic pressure (hypoproteinemia) (which is a cause of edema)

-Inflammatory -Neoplastic -Postsurgical -Postirradiation These are all examples of conditions leading to:

Lymphatic obstruction (which is a cause of edema)

-Excessive salt intake with renal insufficiency -Increased tubular reabsorption of sodium -Renal hypoperfusion -Increased renin-angtiotensin-aldosterone secretion These are all causes of:

Sodium retention (which is a cause of edema)

-Acute inflammation -Chronic inflammation -Angiogenesis Theses are all causes of:

Inflammation (which is a cause of edema)

What is responsible for dictating fluid movement between vascular & interstitial spaces?

-vascular hydrostatic pressure -colloid osmotic pressure (plasma proteins)

What causes colloid osmotic pressure?

Plasma proteins

Vascular hydrostatic pressure and colloid osmotic pressure (plasma proteins) dictate fluid movement between:

vascular & interstitial spaces

Arterial outflow is normally balanced by:

inflow at the venous end

_____ is normally balanced by inflow at the venous end

arterial outflow

Arterial outflow is normall balanced by inflow at the venous end: Results in small net ______----> drained by ______

outflow of fluid in interstitial space; lymphatics

Capillary hydrostatic and osmotic forces are normally balanced so there is little net movement of fluid into the:

Interstitium

Capillary hydrostatic and osmotic forces are normally balanced so there is little net movement of fluid into the interstitium. However, ________ hydrostatic pressure or _______ plasma osmotic pressure leads to extravascular fluid accumulation (edema)

increased hydrostatic pressure diminished plasma osmotic pressure

When extravascular fluid accumulates, tissue lymphatics drain much of the excess fluid back to the circulation by the way of ____. However, if the capacity for lymphatic drainage is exceeded, _____ results.

thoracic duct; tissue edema

Usually caused by disorders that impair venous return:

increased hydrostatic pressure

Increased hydrostatic pressure is usually caused by disorders that:

impair venous return

Disorders that can cause impaired venous return: (2)

1. deep venous thrombosis 2. congestive heart failure

Reduced plasma albumin concentration will lead to:

Reduced plasma osmotic pressure

Reduced plasma albumin concentration may be result from:

loss in circulation or reduced synthesis

Nephrotic syndrome and severe liver disease are both causes for:

Reduced plasma albumin concentration (wich reduces plasma osmotic pressure)

Fill in the highlighted portions:

A) Heart failure B) Malnutrition C) Decreased hepatic synthesis D) Nephrotic syndrome E) Renal failure F) Edema

Fill in the highlighted portions:

Green: DECREASED plasma albumin Blue: DECREASED plasma osmotic pressure

Fill in the highlighted portions:

Green: INCREASED capillary hydrostatic pressure Blue: DECREASED renal blood flow Orange: Activation of the RENIN-ANGIOTENSIN-ALDOSTERONE SYSTEM Pink: Retention of Na+ & H2O Purple: INCREASED blood volume

Pathways leading to ______ can result from heart failure, renal failure, or reduced plasma osmotic pressure

systemic edema

Compromises resorption of fluid from interstitial spaces leading to edema:

Lymphatic obstruction

What conditions can lead to lymphatic obstruction? (3)

1. inflammatory conditions 2. neoplastic conditions 3. congenital lymphedema

What does lymphatic obstruction compromise?

Resorption of fluid from interstitial space (ultimately leading to edema)

Stage of lymphedema in which the lymphatic system experiences abnormal flow but no fluid-build up:

Stage 1 (asymptomatic)

Stage of lymphedema which is due to an accumulation of lymph fluid that may subside when elevated:

Stage 2 (swelling)

Stage of lymphedema categorized by permanent swelling that cannot be relieved through elevation, accompanied by changes in the skin (fibrosis):

Stage 3

Stage of lymphedema characterized by elephantiasis or the deformation of a limb due to extensive swelling, skin thickening and scarring:

Stage 4

Extravasation of blood from vessels:

Hemorrhage

Defective clot formation, trauma, atherosclerosis, inflammatory, neoplastic conditions, inherited/acquired defects are all causes:

hemorrhage

Hemorrhage manifestations include: (4)

1. hematoma 2. ecchymoses 3. purpura 4. petechiae

Large collection of hemorrhage in a tissue:

hematoma

1-2 cm subcutaneous hemorrhage (bruises):

ecchymoses

3-5 mm hemorrhages:

purpura

1-2 mm minute hemorrhage:

petechiae

Often a consequence of thrombocytopenia or Vitamin C deficiency:

Petechiae

What can be seen in this image?

Petechiae

Clot formation steps include: (4)

1. vasoconstriction 2. platelet plug forms 3. fibrin clot deposition 4. clot stabilization and resorption

_______ are the primary regulators of hemostasis through changes in expression of procoagulant or anticoagulant factors

Endothelial cells

Endothelial cells are the primary regulators of hemostasis through changes in expression of ____ or ____ factors

procoagulant; anticoagulant

Disk-shaped, enucleate fragments of megakaryocytes:

Platelets

Platelet adhesion is mediated by:

Von Willenbrand factor

Congenital deficiency of receptors or molecules may lead to:

Bleeding disorders

Functions as an adhesion bridge between subendothelial collagen and the glycoprotein 1b (Gp1b) platelet receptor:

Von Willebrand factor

Platelet aggregation is accomplished by ____ binding to platelet Gp1b-3b receptors on different platelets

fibrinogen

Deficiency due to Gp2b-3a complex:

Ganzmann thrombasthenia

Deficiency due to Gp1b:

Bernard-Soulier syndrome

Deficiency due to Von Willebran factor:

Von Willebrand disease

A series of amplifying enzymatic reactions that lead to the deposition of an insoluble fibrin clot:

Coagulation cascade

The coagulation cascade is also known as:

Secondary hemostasis

Coagulation cascade pathway that is spontaneous and occurs in response to internal injury to the vascular endothelium:

Intrinsic pathway

Coagulation cascade pathway that is activated by external trauma:

Extrinsic pathways

Contact activation due to damaged surface occurs with what coagulation cascade pathway?

Intrinsic

Label the following pathways of the coagulation cascade:

1. Intrinsic pathway 2. Common pathway 3. Extrinsic pathway

The intrinsic pathway of the coagulation cascade is activated by _____ (____)

Contact activation (damaged surface)

The extrinsic pathway of the coagulation cascade is activated by ______

Injury

Factors form the intrinsic pathway & factors from the extrinsic pathway merge to the common pathway at: What do they act on?

5a The form the prothrombinase complex which act on prothrombin to convert it to thrombin

What is the ultimate result of the various pathways of the coagulation cascade?

Clot formation

A coagulation cascade assay is an:

evaluation of coagulation function

_____ evaluates intrinsic pathway factors

Partial prothrombin time (PTT)

PTT evaluates ____ factors including: (8)

Intrinsic factors: XII, XI, IX, VIII, X, V, prothrombin (II), fibrinogen (I)

_____ evaluates the extrinsic pathway factors:

Prothrombin time (PT)

PT evaluates ____ factors including: (5)

Extrinsic factors: VII, X, V, prothrombin (II), fibrinogen (I)

important for regulation of coagulation, plays a key role in synthesis of factors II, VII, IX & X:

Vitamin K

vitamin K plays a key role in the synthesis of factors:

II, VII, IX, X

Vitamin K helps synthesize ____ & _____. What are these proteins important for?

Protein C & S; important for negative feedback regulation of clotting cascade

Vitamin K deficiency results in:

increased bruising & bleeding

Anticoagulant mediation; antagonist for vitamin K:

Warfarin

Warfarin is a ____medication that is an antagonist for _____ and functions to inhibit _____

anticoagulant; antagonist; clotting

List some foods rich in Vitamin K: (10)

-Kale -green snap beans -brussel sprouts -kiwi -brocoli -collard greens -asparagus -turnip greens -cabbage -spinach

MOST important coagulation factor:

Thrombin

Thrombin is responsible for conversion of:

Fibrinogen into cross-linked fibrin

Responsible for conversion of fibrinogen into cross-linked fibrin:

Thrombin

What activates platelets?

Thrombin

The effects of thrombin can be described as:

Pro-inflammatory effects & anti-coagulation effects

Thrombin displays anti-coagulation effects after encountering:

normal endothelium

Factors limiting coagulation include:

1. dilution of blood past the site of injury 2. negatively charged phospholipids required- activated platelets 3. regulation by neighboring intact endothelium 4. fibrinolytic cascade limits size of clot

Fibrinolytic cascade limits the size of the clot but ____ activation is essential for this to occur

Plasmin

The _____ serves as a barrier to platelets resulting in lack of access to ____ & ____

Endothelium; VWF & collagen

Release of nitric oxide, prostacyclin, & adenosine diphosphate by the endothelium result in:

Barrier to the platelets- coagulation limitation

The endothelium expresses factors that inactivate _____ resulting in _____

thrombin; anticoagulant effects

Synthesis of tissue plasminogen activator (tPA) is considered a ____ effect

Fibrinolytic effect

Coronary artery disease, MI & chronic inflammation are a result of:

Endothelial injury leading to thrombosis

Endothelial injury can cause

thrombosis

Physical injury, infectious agent, abnormal flood flow, inflammatory mediators, toxins=

Chronic inflammation (may lead to thrombosis)

Abnormal blood flow promoting endothelial procoagulant activity may result in:

Thrombosis

Abnormal blood flow can lead to stasis which allows:

Platelets & leukocytes to associated with endothelial cells (leading to thrombosis)

Abnormal blood can lead to stasis which slows:

the removal of activated clotting factors, and impedes inflow of clotting factor inhibitors

Abnormally high tendency for blood to clot:

Hypercoagulability

What is an important risk factor for venous thrombosis?

Hypercoagulability

Hypercoagulabiity may be classified as:

Primary (genetic) or Secondary (acquired)

Hypercoagulability that is genetic in nature:

Primary disorder

Hypercoagulability that is acquired:

Secondary disorder

Virchow's train in thrombosis:

1. endothelial injury 2. abnormal blood flow 3. hypercoagulability

What is the most important factor in thrombosis?

Endothelial integrity

Abnormalities of procoagulants or anticoagulants can tip the balance in favor of:

Thrombosis

______ (______) can lead to hypercoagulability directly and also indirectly though endothelial dysfunction

Abnormal blood flow (stasis or turbulence)

Where can thrombi develop?

Anywhere in cardiovascular system

What type of thrombi often occur at sites of injury?

Arterial thrombi

What type of thrombi occur in the heart chambers or aorta?

cardiac mural thrombi

What type of thrombi occur often at sites of stasis?

Venous thrombi

Observed grossly & microscopically; differentiates antemortem clots from postmortem clots:

Lines of Zahn

Thrombi occur in heart chambers or aortic lumen:

Cardiac mural thrombi

Thrombi that are typically rich platelets, often formed by endothelial injury:

Arterial thrombi

Thrombi that contain a high volume of red blood cells:

Venous thrombi

Venous thrombi may also be termed:

Phlebothrombosis

____% of venous thrombi occur in the _____

90% legs

Fate of thrombi includes: (4)

1. propogation 2. embolization 3. dissolution 4. organization and recanalization

What fate of thrombi is described below? Clot enlarges:

Propogation

What fate of thrombi is described below? Clot disparaged and moved by circulatory system

Embolization

What fate of thrombi is described below? Activation of fibrinolytic factors

Dissolution

What fate of thrombi is described below? Older thrombi are reorganized to facilitate some function

Organization & recanalization

Clot in the leg that is described as "local congestion & swelling from impaired venous flow":

Superficial vein clot

Give an example of a superficial vein that a clot may occur in:

Varicose veins

Deep venous thrombosis occur in larger veins called:

Deep veins

What are two risks with deep vein thrombosis?

1. may be asymptomatic in 50% of patients 2. may embolize to lungs

Atherosclerosis is a major cause of:

Arterial & cardiac thrombosis

What is a major cause of arterial & cardiac thrombosis?

Atherosclerosis

Atherosclerosis results in ____ which leads to:

Results in loss of endothelial integrity & abnormal blood flow; leads to MI, ischemia to organs (especially brain, kidneys, spleen)

DIC:

Disseminate intravascular coagulation

DIC- Disseminated intravascular coagulation can be described as:

Widespread thrombosis within microcirculation

Disseminated intravascular coagulation (DIC) involves the consumption of:

Platelets & clotting factors

DIC may occur form:

Complications in obstetrics, injuries, cancer & more

What is the net result of DIC?

Excessive clotting & bleeding

May be a solid, liquid or gaseous mass, carried by the blood from its point of origin to a distant site:

Embolism

Most common embolism:

Pulmonary embolism

Most common embolism; mostly from upper deep leg veins proximal to popliteal fossa. They pass through the larger high heart vessels and lodge in the pulmonary artery or arterioles:

Pulmonary embolisms

Most pulmonary embolisms are small & then progressively become organized, but large ones can cause _______, and multiple emboli over time can cause ____ & _____

sudden death; pulmonary hypertension; right ventricular failure

May arise from intracardiac mural thrombi (80%). Can embolize to lower extremities most frequently, CNS. intestines, kidney and spleen:

Systemic thromboembolism

Injury to bone marrow can cause release of fat globules into circulation but rarely show clinical manifestations. Less than 10% show pulmonary problems, neurologic problems, anemia, thrombocytopenia, and petechial rash:

Fat embolism

Severe post-birth complication with 80% mortality rate due to biochemical activation of coagulation system and immune system from entry of amniotic fluid into circulation system of mother:

Amniotic fluid embolism

Gas in circulation can come together to obstruct vascular flow- example decompression sickness in scuba divers:

Air embolism

How does a pulmonary embolism form?

1. embolus breaks off 2. embolus travels through vein to lung 3. embolus travels through heart and gets lodged in blood vessel of lungs

Area of ischemic necrosis caused by occlusion of the vascular supply to the affected tissue:

Infarction

Most infarctions are caused by:

arterial thrombosis or embolism

What are the most common complication of infarctions?

Involvement of the heart & brain

Infarctions are classified according to:

color

Infarct that contains hemorrhage:

Red infarct

A red infarct can be caused by:

Venous occlusion, loose tissue, tissue with dual circulation, previously congested tide, reperfusion injury

Infarct that is an arterial occlusion in solid organs:

White infarct

A white infarct can occur in the:

Heart, liver, spleen

A state in which diminished cardiac output to reduced effective circulating blood volume impairs tissue perfusion & leads to cellular hypoxia:

shock

Prolonged shock leads to:

Irreversible tissue injury

Three types of shock include:

1. cardiac shock 2. hypovolemic shock 3. septic shock

Failure of myocardial pump resulting from intrinsic myocardial damage, extrinsic pressure, or obstruction to outflow resulting in shock:

Cardiogenic shock

Inadequate blood flow or plasma volume resulting in shock:

Hypovolemic shock

Peripheral vasodilation and pooling of blood; endothelial activation/injury; leukocyte-induced damage; disseminated intravascular coagulation; activation of cytokine cascades resulting in shock:

Septic shock

-myocardial infarction -ventricular rupture -arrythmia -cardiac tamponade -pulmonary embolism These are all potential causes of:

Cardiogenic shock

-hemorrhage -fluid loss (vomiting, diarrhea, burns, trauma) These are all potential causes of:

Hypovolemic shock