Module 2: Cardiovascular And Hemodynamics Pathology Flashcards

Question

Two Pathways That Lead To The Activation Of Fibrinogen To Fibrin? Bot intrinsic and extrinsic pathways lead to activation of what?

Answer 1

• Intrinsic Pathway Both Intrinsic and Extrinsic —Factors required for activation found in the blood Pathways lead to activation of • Extrinsic Pathway Factor X — Activated by Tissue Factor • Found in the endothelial cells LEAD TO activation of FACTOR X (10)

Answer 2

Thrombin ** Fibrin is a soluble thread that creates a mesh around the platelet plug- stabilizing the clot

Answer 3

If the body is leaning Prothrombotic > Antithrombotic • DVT, stroke, MI and other vessel complications will occur • If the body is leaning Antithrombotic > Prothrombotic • Bleeding disorders, hemorrhage, and other blood loss complications will occur **** Diagram on slide 60

Answer 4

Endothelin Von Willebrand Factor (vWF) Vitamin K Plasminogen Activator Inhibitor-1 ADP & Thromboxane A₂ Serotonin

Answer 5

Nitric oxide Heparin/warfarin Thrombomodulin t-PA Antithrombin III Asprin

Answer 6

Enzymatic breakdown of the fibrin threads/mesh within a blood clot • Plasmin cuts up the fibrin fibers allowing the clot to dissolve • Plasminogen is plasmin’s precursor • t-PA is the enzyme that completes this process t-PA • Plasminogen Plasmin • t-PA is released by endothelial cells and increase production when activated clotting factors are near • BUT…..to balance out this process, endothelial cells also secrete out: • Plasminogen Activator Inhibitor 1 • Antiplasminogen

Answer 7

Breaks down fibrin (without breaking down fibrin the clot will not form)

Answer 8

Plasminogen is the precursor to plasmin Tissue plasminogen activator (t-PA) breaks down plasminogen to plasmin

Answer 9

This will covert plasminogen to plasmin and then the body can break down the clot. And fluid can move from the region

Answer 10

Medications • Commonly referred to as blood thinners or anti-clotting medication • Preventing clots from forming or getting larger Anticoagulants • Heparin • Inactivates Thrombin and Factor Xa • Intravenous injections- has immediate effects • Warfarin (Coumadin) • Blocks the effects of vitamin K • Clotting factors II, VII, IX, and X are not produced • Tablet; full effect in 2-3 days Antiplatelets • Blocks the formation of thromboxane a2 in platelets • Class of drugs that inhibit platelet aggregation • Aspirin is classified as an antiplatelet

Answer 11

• 1. Prothrombin time (PT) • Screens for the activity of the proteins in the extrinsic pathway • Factors VII, X, II, V, and fibrinogen • 2. Partial Thromboplastin Time (PTT) • Screens for the activity of the proteins in the intrinsic pathway • Factors XII, XI, IX, VIII, X, V, II, and fibrinogen

Answer 12

• 1. Hemorrhagic Disorders • Basically- inability to stop blooding from occurring • Body loses ability to clot blood • Leads to loss of blood from circulatory system- • 2. Thrombotic and Embolic Disorders • Basically- blood clots too easily or at inappropriate time/location • Blood will form abnormal clots due to some sort of vessel damage or chemical mediator response • Leads to blockage of vessels (ischemia) and even formation of an embolus

Answer 13

• Hemorrhage is the extravasation of blood from vessels • Thrombotic is the association of the formation of thrombus

Answer 14

• Amount of blood loss can vary drastically • Can be acute or chronic • Occur from a variety of causes —Trauma, atherosclerosis, inflammatory or neoplastic erosion of a vessel wall, medications, defects in the primary and secondary hemostasis • Can be external loss, internal loss, and even accumulate within a tissue — A Hematoma is pooling of blood in soft tissue —Commonly named according to location of pooling- Hemothorax

Answer 15

• Petechiae —1-2mm hemorrhages; red in color • Purpura — 3-5mm hemorrhages; purple in color • Ecchymosis — 1-2cm hematomas; (bruise or contusion) — Blood leaking from broken blood vessels just beneath the skin's surface • Hematoma — Localized bleeding outside of the blood vessels; generally pooling of clotted blood • Amount of blood loss, acute or chronic, and location are vital for outcomes • Blood Thinner Medication — Can lead to excessive hemorrhage time

Answer 16

• A blood clot that forms, commonly from abnormal causation, and stays in the blood vessel • Condition is referred to as thrombosis • Can occur in veins or arteries • Can partially or completely block vessel flow

Answer 17

1. Endothelial injury 2. Stasis or turbulent blood flow 3.Hypercoagulability of the blood • Having all three is referred to as the Virchow triad (NBCE loves this)

Answer 18

• Pathological formation of a blood clot (thrombus) within intact vessels • Basically- a blood clot that forms abnormally in a blood vessel • Referred to as thrombosis or thrombus • Can occur in veins or arteries • Can partially or completely block vessel flow

Answer 19

• Dissolution —Activation of fibrinolytic factors may lead to its rapid shrinkage and complete dissolution • Propagation — Thrombus enlarges • Embolization (Embolus) — Part or all of the thrombus is dislodged and transported elsewhere in the vasculature • Organization and Recanalization — Older thrombi become fibrotic and absorbed into the vessel wall

Answer 20

• Clinical Manifestations • Pain in leg or arm or location of thrombus • Swelling in one leg or arm or location of thrombus • Ischemia • Numbness or weakness on one side of the body • Diagnosis • Ultrasound and venography • Treatment • Medications called tissue Plasminogen Activator (tPA) • Clot dissolving medication

Answer 21

• 1. Occlusion of the vessel, especially an artery • 2. Emboli formation

Answer 22

Within the heart • Myocardial infarction Within the brain • Thrombotic stroke Within the lower extremity • Deep Vein Thrombosis

Answer 23

1. Pulmonary Thromboembolism • Embolus is lodged within the pulmonary arteries • DVT is most common causation 2. Systemic Thromboembolism • Emboli that travel through the systemic arterial circulation • Arise within the heart • Secondary to atrial fibrillation or some other heart complication 3. Fat Embolism • Initiated by severe trauma, especially bone break • What type of bone? Long bone (diaphysis) • Releases microscopic fat globules into the circulation 4. Amniotic Fluid Embolism • Underlying cause is entry of amniotic fluid (and its contents) into the maternal circulation via tears in the placental membranes and/or uterine vein rupture • It accounts for 10% of maternal deaths in the United States 5. Air Embolism • Gas bubbles within the circulation can form together to create a large gas bubble and obstruct vascular flow and cause distal ischemic injury • During surgeries and even with syringes/needle injections with air in it

Answer 24

An abnormal clot formation in a deep vein of the lower extremity • Leads to partial or complete occlusion of venous flow • Could be life threatening situation • If it causes swelling of the leg Clinical Manifestations: • Leads to swelling, pain , warmth, and redness • Obstruction of venous return

Answer 25

• Thrombophlebitis —Presence of a thrombus in a vein with associated inflammation • Phlebothrombosis —Presence of a thrombus in a vein without associated inflammation

Answer 26

The sudden or insidious onset of widespread thrombosis within the blood • Basically clots in the blood form all over the place (NBCE loves this) • Leads to circulatory insufficiency, particularly in the brain, lungs, heart, and kidneys • Widespread microvascular thrombosis consumes platelets and coagulation proteins and fibrinolytic mechanisms are activated • A thrombotic disorder can evolve into a bleeding catastrophe • DIC is not a primary disease but rather a potential complication of numerous conditions associated with widespread activation of thrombin

Answer 27

is a localized abnormal dilation of a blood vessel due to a weakening in the vessel wall that may be congenital or acquired

Answer 28

• Inadequate or abnormal connective tissue synthesis • Marfan’s disease and Ehlers-Danlos syndrome • Excessive connective tissue degradation • Loss of smooth muscle cells • **Atherosclerosis • **Hypertension

Answer 29

**Wall Structure** —Which layers of the vessel are involved • 1. True Aneurysm —All three layers of the vessel wall are involved: intima, media, and adventitia —The wall bulges outward but remains intact —Common causes: Atherosclerosis, hypertension, congenital weaknesses • Examples: Abdominal aortic aneurysm (AAA) • 2. False Aneurysm (Pseudoaneurysm) —Breached vessel wall: blood leaks out and is contained by surrounding tissue —Looks like an aneurysm but isn’t a true dilation —Can present as a pulsatile hematoma • 3. Dissecting Aneurysm —Blood enters a tear in the intima and tracks between the layers of the vessel wall —Not a true aneurysm, but often grouped in discussions —Aortic dissection is the prime example—very high mortality if not managed emergently **Morphology** —What their shape looks like 1. Saccular Aneurysm (berry aneurysm) • Small, rounded, pouch-like bulge on one side of the vessel • Common in cerebral arteries (esp. Circle of Willis) • More prone to rupture due to the focused wall stress • Most Common! 2. Fusiform Aneurysm • Uniform, circumferential dilation along a segment of a vessel • Seen in aortic aneurysms, especially abdominal and thoracic types • More gradual development and progression **Location** —Where they are located in the body 1. Intracranial Aneurysms • Commonly occur at Circle of Willis • SUDDEN HEADACHE • WORSE HEADACHE OF LIFE • NOTHING IMPROVES PAIN • Saccular (Berry) Aneurysms of the Circle of Willis • Anterior Communicating Artery • 2. Abdominal Aortic Aneurysm (AAA) • X-ray • Atherosclerotic aneurysms occur most frequently in the abdominal aorta • Common iliac arteries, aortic arch, and descending thoracic aorta can also be involved • Occurs more frequently in men and in smokers and rarely develops before the age of 50 years • Concern is the obstruction it can cause to a vessel branching off it AND Rupture into the peritoneal cavity or retroperitoneal tissues 3. Thoracic Aortic Aneurysm • Most commonly associated with hypertension • Can be ascending or descending 4. Aortic Dissection • Occurs when blood separates the laminar planes of the tunics to form a blood-filled channel within the aortic wall • Basically blood flows between the layers of the aorta forcing them apart • Can be catastrophic if the dissecting blood ruptures through vessel wall and escapes into adjacent spaces **Etiology** — What caused them • Atherosclerotic —Often in abdominal aorta; due to chronic wall damage • Congenital — Connective tissue disorders like Marfan or Ehlers-Danlos • Infectious —From sepsis • Traumatic —Including iatrogenic causes- catheter-induced • Inflammation — Vasculitis-related aneurysms (Takayasu arteritis, Kawasaki disease)

Answer 30

Anterior communicating artery

Answer 31

General term for inflammation of the blood vessels • Generally Causes: • Vessel Damage • Can Affect… • Any vessel (artery, vein, or capillary) • Affect any organ system • Due to inflammation • Thickening of blood vessel layers leading to narrowing of blood vessel • Ischemia • Can even lead to an aneurysm formation

Answer 32

• Autoimmune: most common • Infectious: Hepatitis B/C, HIV, syphilis • Drug-induced • Paraneoplastic: Cancer • Idiopathic • Classified by blood vessel size • Specific blood vessels affected will have their own disease name • Giant cell arteritis (temporal vasculitis) • Treatment • Immunosuppressants and steriods

Answer 33

Varicose Veins • Abnormally dilated, tortuous veins produced by prolonged, increased intraluminal pressure with vessel dilation and incompetence of the venous valves • Superficial veins of the upper and lower leg are commonly involved • Venous pressures in these sites can be markedly elevated • Obesity, pregnancy, standing/sitting in prolonged postures

Answer 34

Leads to stasis, congestion, edema, pain, and thrombosis • Commonly occurs in deep veins • Secondary tissue ischemia results from chronic venous congestion and poor vessel drainage Treatment • Self-Care: losing weight, exercising, elevating legs, do not stand/sit for long periods of time • Compressions stockings • Different types of medical procedures including surgery

Answer 35

• Esophageal Varices (NBCE loves this) —Blood flow to liver is blocked and then blood flows into smaller veins that are not able to handle the blood flow • Hemorrhoids — Result from primary varicose dilation of the venous plexus at the anorectal junction —Prolonged pelvic vascular congestion due to pregnancy or straining to defecate • Spider Veins — Smaller version of varicose veins — Superficial, small veins

Answer 36

• EXUDATES: Protein-rich fluid • Accumulate due to increases in vascular permeability caused by inflammatory mediators

Answer 37

• TRANSUDATES: Low protein fluid • Noninflammatory edema and effusions are common in many disorders, including heart failure, liver failure, renal disease, and malnutrition

Answer 38

• 1. Increased hydrostatic pressure —> Localized • Caused by impaired venous return ( deep venous thrombosis) • Generalized (systemic) • Most commonly caused by congestive heart failure (CHF) • 2. Reduced osmotic pressure —> • Conditions in which albumin is either lost from the circulation or synthesized in inadequate amounts • Nephrotic syndrome —Loss in urine • Severe liver disease —Reduced albumin production • Protein malnutrition • 3. Lymphatic obstruction —> Lymphedema • Primarily caused by lymphadenopathy or damage/removal of lymph nodes • About 20 liters lost with capillaries • About 17 liters recovered • About 3 liters of fluid to be recovered by lymphatic system — Damage or surgical removal associated with cancer — Lymphatic filariasis • Decreases ability to absorb and filter excessive fluid • 4. Increase vascular permeability (inflammation) —> • Important to identify what is causing edema • Is it inflammatory or non-inflammatory • If non-inflammatory, it could be: • Kidney • Heart • Liver • Lymphatic

Answer 39

• Increased vasodilation and inflow of arterial blood- active process • Inflammation and skeletal muscle when working out • Redder in color due to the increased blood flow of oxygenated blood

Answer 40

• Decreased and impaired outflow of venous blood- passive process • Can occur systemically or locally • Cyanotic in • Chronic passive congestion can lead to chronic hypoxia may result in ischemic tissue injury and scarring

Answer 41

• Cardiogenic Shock — Results from low cardiac output due to myocardial muscle inability to pump blood — Caused by myocardial damage (infarction), ventricular arrhythmias, extrinsic compression • Hypovolemic Shock — Results from low cardiac output due to loss of blood or plasma volume — Caused from hemorrhage or fluid loss from severe burns • Septic Shock — Results from arterial vasodilation and venous blood pooling — Stems from the systemic immune response to microbial infection • Random • Neurogenic (ANS) Shock • Anaphylactic Shock

Answer 42

• Sepsis — Systemic response to infection — Inflammatory response becomes dysregulated and can lead to widespread inflammation and organ dysfunction • Septic Shock — Advanced and life-threatening stage of sepsis — Occurs when sepsis progresses and the body's response to infection becomes severely impaired, leading to a profound drop in blood pressure

Answer 43

• Condition where the cells, tissues, and organs of the body are not getting enough blood flow • Characterized by systemic hypoperfusion of tissues —It can be caused by diminished cardiac output or by reduced effective circulating blood volume — Basically, a critical situation created by a sudden drop in blood flow within the body • Consequences are impaired tissue perfusion and cellular hypoxia • Although shock initially is reversible, prolonged shock eventually leads to irreversible tissue injury that often proves fatal

Answer 44

• Responsible for 2% of all hospital admissions in the United States • Of these, 50% require treatment in intensive care units • Mortality rate is around 50% • Infections (primarily gram + bacteria) lead to complex inflammatory reactions (NCBE loves this) • Bacterial infections (Staphylococcus aureus) • Also be caused by viral infections, such as COVID-19 or influenza **SLIDE 125

Answer 45

Exhibit hypotension, a weak rapid pulse, tachypnea, and cool, clammy, cyanotic skin Primary Threat to Life is The Initiating Event • Myocardial infarction • Cardiac, cerebral, and pulmonary changes rapidly aggravate the situation • Clinical manifestations of shock depend on the causation

Answer 46

An infarct is an area of ischemic necrosis caused by occlusion of the vascular supply to the affected • Infarction: process by which an infarct lesion forms • Roughly 40% of all deaths in the United States are a consequence of cardiovascular disease, with most of these deaths stemming from myocardial infarction or cerebral infarction Arterial thrombosis or arterial embolism underlies the vast majority of infarctions

Answer 47

• 1. Basis of their color (amount of hemorrhage) • 2. Presence or absence of microbial infection • Red (hemorrhagic) (NBCE loves this) • Loss of blood leads to red color (NBCE loves this) • White (anemic/ischemic) • Lack of blood supply leads to white color • Ischemic Coagulative Necrosis • Main histologic finding associated with infarcts • Liquefactive Necrosis • Commonly ischemic tissue injury in the central nervous system

Module 2: Cardiovascular And Hemodynamics Pathology Flashcards

(89 cards)