Septic Shock and Vascular Biology Quiz

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Questions and Answers

What is the primary cause of the initial endothelial activation in septic shock?

Activation of the coagulation cascade leading to microthrombi formation

Release of cytokines by immune cells in response to infection (correct)

Direct damage to the endothelium by toxins released by bacteria

Direct bacterial invasion of the endothelium

What is the main consequence of smooth muscle relaxation in septic shock?

Reduced vascular resistance and a drop in blood pressure (correct)

Increased blood flow to the affected tissues

Increased permeability of the blood vessels leading to fluid leakage

Increased blood clotting and formation of microthrombi

How does septic shock contribute to hypercoagulation?

Inhibition of the clotting cascade by cytokines

Increased blood viscosity due to the presence of bacteria

Activation of the fibrinolytic pathway leading to excessive breakdown of clots

Increased production of tissue factor and decreased production of clotting inhibitors (correct)

What is the primary reason for the development of hyperglycemia in septic shock?

Increased production of stress hormones like cortisol and glucagon (D) Signup and view all the answers

What is the effect of lactic acidosis on the blood pH?

Decreases blood pH (C) Signup and view all the answers

Which of the following is NOT a major consequence of reduced tissue perfusion in septic shock?

Increased blood pressure due to vasoconstriction (B) Signup and view all the answers

What is the primary characteristic that differentiates compensated shock from irreversible organ failure?

The presence of irreversible organ damage (C) Signup and view all the answers

The clinical manifestations of shock are primarily determined by which of the following?

The initial underlying cause (C) Signup and view all the answers

Which of the following is a primary threat to life in a patient with shock?

Underlying initiating event (B) Signup and view all the answers

What is the main difference between arteries and veins?

Both A and B (C) Signup and view all the answers

Which of the following is NOT a layer of a blood vessel?

Endocardium (A) Signup and view all the answers

What is the function of the internal elastic lamina?

Separates the intima from the media (A) Signup and view all the answers

Which of the following is NOT a form of vascular disease?

Osteoporosis (A) Signup and view all the answers

What is the difference between arteriosclerosis and atherosclerosis?

Arteriosclerosis is a general term for hardening of the arteries, while atherosclerosis is a specific type of arteriosclerosis caused by plaque buildup. (D) Signup and view all the answers

Which of the following is a potential complication of a weakened blood vessel?

Aneurysm (B) Signup and view all the answers

Which of the following is NOT a potential cause of vascular disease?

Diabetes (B) Signup and view all the answers

Which of these conditions is associated with hypercoagulability and is often related to smoking?

Oral contraceptives (D) Signup and view all the answers

What are thrombi called when they are found in the aortic lumen and heart chambers?

Mural thrombi (C) Signup and view all the answers

In what direction do arterial thrombi typically grow?

Away from the heart (D) Signup and view all the answers

Which of these factors can lead to the dissolution of a thrombus?

Fibrinolytic factors (C) Signup and view all the answers

What is the process by which an old thrombus is replaced by new tissue called?

Organization (A) Signup and view all the answers

Which type of infarct is associated with venous occlusion?

Red infarct (A) Signup and view all the answers

What is the primary factor that determines whether an infarct will be white or red?

Type of tissue affected (C) Signup and view all the answers

Which of the following is NOT a factor that affects the outcome of an infarct?

Size of the thrombus (B) Signup and view all the answers

What is the most common type of vasculitis?

Giant Cell (temporal) arteritis (B) Signup and view all the answers

Which of the following is NOT a contributing factor to essential hypertension?

Renal disease (A) Signup and view all the answers

What is a major sequelae of untreated hypertension?

Cardiac hypertrophy (C) Signup and view all the answers

What is the primary mechanism of peripheral resistance control?

Arterioles (D) Signup and view all the answers

What is the primary factor that affects stroke volume?

Filling pressure (B) Signup and view all the answers

What is the main characteristic of giant cell (temporal) arteritis?

All of the above (D) Signup and view all the answers

What is the key characteristic of malignant hypertension?

Rapid progression to severe hypertension above 200/120 mmHg (A) Signup and view all the answers

What is a key feature of Kawasaki disease?

Fever lasting for 5 days (B) Signup and view all the answers

Which of these are affected by both alpha and beta adrenergic inputs?

Cardiac contractility (D) Signup and view all the answers

Which of the following is NOT a factor that can affect arterial tone and perfusion?

Sodium levels (C) Signup and view all the answers

What does the term "edema" refer to?

An accumulation of fluid in tissues caused by net movement of water into the extravascular spaces (D) Signup and view all the answers

Which of the following is NOT a cause of edema?

Hemostasis (C) Signup and view all the answers

Which of these is NOT a cause contributing to venous return related edema?

Protein-losing glomerulopathies (D) Signup and view all the answers

What is the primary cause of ascites?

Liver cirrhosis (B) Signup and view all the answers

Which of the following is a condition that can lead to reduced oncotic pressure and edema?

Nephrotic syndrome (B) Signup and view all the answers

Besides protein-losing glomerulopathies, what other condition is a major contributor to decreased oncotic pressure?

Liver cirrhosis (D) Signup and view all the answers

What is the role of lymphatics in maintaining fluid balance?

To help remove excess fluid from tissues (B) Signup and view all the answers

What is the primary mechanism by which sodium retention leads to edema?

It increases the hydrostatic pressure (D) Signup and view all the answers

Which of these is NOT a consequence of inflammation that contributes to edema?

Increased lymphatic drainage (C) Signup and view all the answers

What is the effect of angiotensin II on blood pressure?

Increases blood pressure (A) Signup and view all the answers

Which of these is NOT a direct effect of angiotensin II on blood pressure regulation?

Increased heart rate (A) Signup and view all the answers

What is the role of aldosterone in regulating blood pressure?

Increases sodium reabsorption (A) Signup and view all the answers

Under what condition does the renin-angiotensin-aldosterone system become activated?

Decreased blood pressure (B) Signup and view all the answers

What is the primary function of the natriuretic peptides released by the myocardium?

Decrease sodium reabsorption (D) Signup and view all the answers

What is the main consequence of a combined failure of both heart and kidney function?

Increased fluid retention (A) Signup and view all the answers

What is the primary role of the kidneys in regulating blood pressure?

Regulating salt excretion (C) Signup and view all the answers

What is the most common form of arteriosclerosis?

Atherosclerosis (C) Signup and view all the answers

What is the main characteristic of Mönckeberg medial calcific sclerosis?

Calcium deposits in the muscle walls (C) Signup and view all the answers

What is the clinical significance of Fibromuscular Intimal Hyperplasia?

It can lead to luminal stenosis (C) Signup and view all the answers

What is the main characteristic of atheromas in atherosclerosis?

They are composed of friable lipid cores (A) Signup and view all the answers

What is the most common cause of stroke?

Atherosclerosis in cerebral arteries (A) Signup and view all the answers

What is the most common cause of a heart attack?

Atherosclerosis in the coronary arteries (C) Signup and view all the answers

What can happen when an atheroma ruptures?

The artery can become completely blocked by a thrombus (D) Signup and view all the answers

Which of the following vascular diseases is NOT considered a congenital anomaly?

Atherosclerosis (B) Signup and view all the answers

Which of the following is a characteristic of Berry aneurysms?

They frequently occur in the circle of Willis (C) Signup and view all the answers

Which of the following is true about Arteriovenous fistulas?

They can be created intentionally for medical purposes (C) Signup and view all the answers

Which of the following is considered a "clog the pipe" form of vascular disease?

Atherosclerosis (D) Signup and view all the answers

Which of the following is considered a "weaken the pipe" form of vascular disease?

Arteriosclerosis (C) Signup and view all the answers

What is the difference between Atherosclerosis and Arteriosclerosis?

Atherosclerosis is a specific type of arteriosclerosis (F) Signup and view all the answers

Which of the following conditions can result from atheroma rupture?

All of the above (D) Signup and view all the answers

Study Notes

Pathogen 4.1 Vessels - Study Notes

Objectives include illustrating fluid distribution between intravascular and extravascular spaces in normal circulation.
Objectives also cover distinguishing oncotic and hydrostatic causes of edema, analyzing the role of renal pathology in fluid balance and hemorrhage, and illustrating normal hemostasis.
Objectives further include analyzing hypercoagulability, illustrating infarction and shock, differentiating major types of vascular disease, and analyzing hypertension causes and types, and discussing vasculitis and vascular tumors.

Fluid Balance

Fluid balance involves two opposing forces: hydrostatic pressure and oncotic pressure.
Hydrostatic pressure typically "wins," but only slightly.
Lymphatics remove excess fluid.

Causes of Edema

Edema results from issues with venous return, oncotic pressure, lymphatic obstruction, or sodium retention.
Causes include issues with venous return, congestive heart failure, constrictive pericarditis, ascites, venous obstruction, thrombosis, and external pressure.
Oncotic pressure causes include protein-losing glomerulopathies, liver cirrhosis, malnutrition, protein-losing gastroenteropathy, lymphatic obstruction, inflammatory diseases, and neoplasms.
Sodium retention causes include too much salt and/or kidney function issues, increased Na+ uptake, renal hypoperfusion, and increased renin-angiotensin-aldosterone secretion.

Terms

Edema is fluid accumulation in tissues.
Hyperemia is excessive arterial blood flow.
Congestion is excess venous blood in tissues.
Hemostasis is blood clotting.
Thrombosis is a blood clot.
Embolism is a dislodged clot.
Infarction is tissue death due to ischemia (lack of blood supply).
Effusion is extravascular fluid collected in body tissues.

Renin, Angiotensin, Aldosterone

Renin, released by hypoperfused kidneys, activates angiotensinogen to angiotensin I.
Angiotensin I is converted to angiotensin II in the lungs.
Angiotensin II increases blood pressure by constricting blood vessels and releasing aldosterone.
Aldosterone promotes sodium retention, which in turn increases water retention, and further elevates blood pressure, which, in turn, relieves the renin trigger.

BP regulation

Blood pressure regulation involves the kidneys, adrenals, and heart.
Kidneys regulate salt, renin-angiotensin-aldosterone (RAAS).
Myocardium releases natriuretic peptides to inhibit sodium reabsorption when volume expansion is sensed.
The system works to control blood volume, blood pressure, and maintains a balance.

One Thing Leads to Another (Heart/Kidney Failure)

Heart failure can lead to decreased kidney blood flow resulting in renal failure.
This can lead to increased fluid in the heart.
Albumin issues can further impact oncotic force.

Hemorrhage Terms

Hemorrhage is blood leakage.
Hematoma is a blood mass.
Petechiae/Purpura are small hemorrhages into the skin, mucous membranes.
Ecchymoses are bruises under the skin.
RBC degradation creates hemosiderin.

Clinical Tie-ins for Hemorrhage

Massive hemorrhage causes exsanguination and potentially death.
Hematoma can compress tissues.
Intracerebral hemorrhage leads to stroke and potentially death.
Chronic hemorrhage causes iron deficiency anemia.

Hemostasis Review

Hemostasis is the process of stopping bleeding.
Steps include arteriolar vasoconstriction, platelet plug formation, and fibrin clot formation.
Then, clot stabilization and resorption follow.

Clinical Point (Clotting Testing)

D-dimer is a measurable fibrin breakdown product.
Elevated D-dimer indicates ongoing clotting activity.

Clotting Pathway

PT/INR assesses the extrinsic pathway.
PTT assesses the intrinsic pathway.
Feedback loops amplify the clotting cascade.

Clotting Inhibition - Heparin-Like Molecules

Heparin-like molecules activate antithrombin, disrupting thrombin activity during coagulation.
Endothelial cells release anticoagulants in their passive state.
After injury, endothelial cells become procoagulant for a time to balance coagulation.

Clotting Inhibition - Thrombomodulin and endothelial protein C receptor

Thrombomodulin and endothelial protein C receptor disrupt the clotting pathway by binding factors.
This prevents thrombin activation from causing clots.

Clotting Inhibition - t-PA and Other endothelial products

t-PA and other products like prostacyclin, nitric oxide, and adenosine diphosphatase inhibit clotting.

Medicinal Clotting Inhibition

Warfarin inhibits vitamin K-dependent clotting factors.
Heparin activates antithrombin.
Xa inhibitors and low molecular weight heparins act directly on clotting factors.

Clinical Point (Bridge to Warfarin)

Initial heparin use helps resolve clotting issues before warfarin reduces synthesis of Protein C and S.

Clinical Points (Factor V Leiden/Other Pathology)

Genetic mutations (Factor V Leiden, Protein C/S deficiency, Antithrombin III deficiency, Von Willebrand disease) can affect hemostasis.
Use anticoagulants (heparin, NOAC, DOAC) to manage blood clots.
Use antiplatelets (ASA, P2Y12 inhibitors) to manage platelets.
Use thrombolytic therapy (tPA) to dissolve clots

Virchow's Triad

Endothelial injury, abnormal blood flow, and hypercoagulability are the major factors that trigger clotting.

Hypercoagulability

Various conditions can increase clotting risk, including Factor V Leiden mutation, Anti-thrombin III deficiency, Protein C/S deficiency, immobility, cancer, surgery, tissue injury, prosthetic valves, antiphospholipid antibody syndrome, smoking, atrial fibrillation, pregnancy, and oral contraceptives (especially in smokers).

Thrombi and Emboli

Thrombi (blood clots) can form in arteries or veins, growing towards the heart.
Emboli are dislodged thrombi that travel through the bloodstream to other parts of the body.

Embolism

Pulmonary emboli are common, arising from deep vein thrombosis in legs, potentially causing various fatal complications.
Systemic emboli can arise from the heart, targeting lower extremities, brain, and other areas causing tissue infarction.
Other embolism types include fat emboli (from bone fractures) and amniotic fluid emboli (from complications during pregnancy).

Fate of the Thrombus

Thrombi can grow (propagate), travel (embolize), or dissolve.
Other steps can result in dissolution, organization, and recanalization.

Infarct

An infarct is a region of ischemic necrosis (tissue death) due to blood vessel blockage.
Infarct risk factors include vascular supply anatomy, occlusion rate, and tissue vulnerability to hypoxia.
White infarcts result from arterial occlusion (aneomic).
Red infarcts result from venous occlusion (hemorrhagic).

Factor V Leiden

Factor V Leiden is an inherited condition that increases risk of blood clotting.
It has varying degrees of dominance.

Two Clinically Important Conditions

Heparin-induced thrombocytopenia (HIT) occurs when patients develop antibodies against heparin-platelet complexes, leading to severe thrombocytopenia (low platelet count) and potentially a prothrombotic state.
Disseminated intravascular coagulation (DIC) features widespread clotting in the microcirculation of the body, often as a complication of widespread infections, injuries, or malignancies. This results in thrombosis in various parts of the body, but also results in a deficiency of clotting factors, leading to profuse bleeding.

Shock

Shock is inadequate blood flow to tissues.
Types include cardiogenic, hypovolemic, and septic, each with particular underlying causes.
The initial stages in shock are often reversible with treatment.
Subsequent cellular injury in severe shock usually leads to an irreversible state.

Septic Shock and Hypotension

Endothelial activation, cytokine release, and vessel leakiness cause reduced blood flow to tissues.
These issues also result in hypercoagulation.
Metabolic derangements develop that include elevated blood sugars and lactic acidosis.
This can compromise organ function and lead to death.

Stages of Shock

Shock has different stages—a nonprogressive stage with compensatory mechanisms, a progressive one with hypoperfusion and metabolic imbalances, and an irreversible phase with damage leading to organ failure, sometimes fatal.

Clinical Manifestations of Shock

Specific manifestations depend on the underlying cause of the shock.
Manifestations may include hypotension, rapid weak pulse, tachypnea, cold and/or clammy skin, etc.

Normal Blood Vessels

Arteries have thicker walls with more smooth muscle cells compared to veins.
Veins have valves to prevent backflow, and are generally compressible.

Structural Aspects of Vessels

Blood vessels are organized in layers: intima, media, and adventitia.
Layers are separated by elastic laminae.

The Main Forms of Vascular Disease

Vascular diseases can involve clogging (e.g., atherosclerosis), weakening (e.g., aneurysms), or having anatomical issues (congenital, genetic).

Congenital Anomalies of Vasculature

Congenital issues affecting vascular structures include berry aneurysms, arteriovenous fistulas, and fibromuscular dysplasia.

Arteriosclerosis

This generic term ("hardening of the arteries") refers to arterial wall thickening and loss of elasticity.
This can occur in various ways - including hyaline, or hyperplastic; calcium buildup in media (Monckeberg medial sclerosis.
An additional process is Fibromuscular intimal hyperplasia.

Atherosclerosis

Characterized by atheromas, composed of friable lipid cores (cholesterol with necrosis) covered by a fibrous cap.
Can impact many major vascular areas (generalized or located).
This disease can impact arteries and arterioles.

Atherosclerosis → Aneurysm

Atherosclerosis can lead to aneurysms due to progressive weakening of the arterial wall.

Types of Aneurysms

True aneurysms (saccular or fusiform) involve wall bulging.
False aneurysms (pseudoaneurysms) involve a tear in the vessel wall resulting in blood accumulation outside the vessel.
Dissection involves blood penetrating into aortic layers.

AAA (Abdominal Aortic Aneurysm) – Clinical Consequences

Obstructed blood supply is a major factor.
The loss of supply can lead to tissue damage.
Compression and rupture are common and fatal complications.

Aortic Dissection

Blood tears the layers of the aortic media, resulting in a blood-filled channel.
Rupture into body cavities can cause fatal hemorrhaging and tamponade, especially impacting the pericardium.

Marfan Syndrome

A genetic disorder characterized by connective tissue abnormalities, primarily affecting the skeletal, cardiovascular, and ocular systems.
Fibrillin 1 gene mutations are the cause.

Cardiovascular Effects of Marfan Syndrome

Connective tissue weakness around the aortic root leads to potential problems like aortic aneurysmal dilation and subsequent rupture.

Hypertension

Primary hypertension has unclear etiology.
Secondary hypertension commonly has underlying issues with renal or adrenal disease.
Hypertension, if untreated, can lead to multiple cardiac, vascular, and cerebrovascular sequelae.

Vasculitis and Vascular Tumor

These diseases encompass a range of inflammation affecting blood vessels (Vasculitis) and benign/malignant tumors derived from the vascular system (vascular tumors).

Vasculitis

Giant cell (temporal) arteritis, Polyarteritis Nodosa, Kawasaki disease, and Thrombangitis Obliterans (Buerger disease) are all types of vasculitis.

Giant Cell Arteritis

This type of vasculitis impacts the temporal artery commonly affecting people over 50 years old.

Polyarteritis Nodosa

This involves necrotizing inflammation of medium-sized arteries, commonly found in young adults and often associated with hepatitis B.

Kawasaki Disease

Characterized by fever and inflammation, often related to upper respiratory issues, impacting primarily infants and young children. Also the most common cause of acquired heart disease in children under 4 years old.

Thrombangitis Obliterans (Buerger Disease)

Almost entirely linked to heavy smoking and affects younger individuals, causing inflammation and thromboses in vessels of the extremities.

Raynaud Phenomenon

Characterized by exaggerated digital artery vasoconstriction, often benign, leading to pallor or even cyanosis in the extremities, primary affects women.

Vascular Tumors

Types of vascular tumors include benign (hemangioma, lymphangioma, glomus tumors) and malignant (Angiosarcoma, Hemangiopericytoma).

Hemangioma

Benign vascular tumors characterized by varying amounts of normal or abnormal vessels.
Commonly encountered in young children (up to 7% of all benign tumors).

Kaposi Sarcoma

Associated with immunosuppression conditions such as HIV/AIDS.

Angiosarcoma

A malignant tumor derived from endothelial cells typically affecting the skin, tissues, and organs.

Familial Hypercholesterolemia

Inherited disorder from low-density lipoprotein receptor (LDLR) disruptions.
Results in significantly elevated LDL cholesterol.
Leads to various problems including xanthomas and early onset cardiovascular issues.

Familial Hypercholesterolemia: Disease Etiology and Incidence

FH is a disorder of cholesterol and lipid metabolism.
FH affects all races but presents differently.

Familial Hypercholesterolemia: Pathogenesis

LDL receptor function is disrupted (due to mutations), resulting in LDL accumulation.

Familial Hypercholesterolemia: Phenotype and Natural History

Heterozygotes exhibit elevated cholesterol from birth.
Arcus corneae and tendon xanthomas may appear in heterozygotes' second decade.
Homozygotes may have high cholesterol from birth, and early onset cardiovascular disease (usually by age 30), with a risk of death.

Familial Hypercholesterolemia: Management

Treatment includes diet (low-fat, high-carbs), bile acid sequestrants, statins to inhibit cholesterol synthesis, and LDL apheresis (filtering LDL from blood).

Familial Hypercholesterolemia: Inheritance Risk

Autosomal dominant disorder, so each child of an affected heterozygous parent has a 50% risk of inheriting the mutation.

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Description

Test your knowledge on the physiological aspects of septic shock and vascular biology. This quiz covers key concepts such as endothelial activation, smooth muscle relaxation, and the consequences of shock on the body. Explore the differences between arteries and veins while understanding vascular diseases.