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Module 2: Cardiovascular And Hemodynamics Pathology Flashcards

(89 cards)

1
Q

Two Classifications of Hypertension

A

• Secondary Hypertension
• Under 10% of cases
• Due to an underlying condition
• Renal or adrenal disease • Essential (Idiopathic)

Hypertension
• 90-95% of all hypertension cases
• No known direct cause
• Influenced by genetics and environmental factors

Mechanisms of Essential Hypertension
• Reduced renal sodium excretion —> Na in blood so water follows Na (increase blood volume and blood pressure)
• Increased vascular resistance
—Chronic vasoconstriction may result in permanent thickening of the walls of affected vessels
• Genetic factors
—Possible susceptible genes influencing the renin-angiotensin system
• Environmental factors
— Stress, obesity, smoking, physical inactivity, and high levels of salt consumption
• All can influence epigenetics which influence genes being expressed

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2
Q

HTN treatment

A

Lifestyle Changes
• DASH diet or diets less in salt • Exercise / Weight loss • Smoking cessation

Medications
• Thiazide Diuretics (water pills)
• Eliminate water and sodium • Angiotensin-converting enzyme (ACE) inhibitors • Angiotensin II receptor blockers (ARBs) • Beta blockers
• Decrease the workload on your heart
• Vasodilation
• Slows the heart rate

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3
Q

All of the options are true regarding hypertension, except?
• A. Secondary hypertension can be due to a renal disorder
• B. Reduced renal sodium excretion is associated with essential hypertension
• C. A complication of hypertension is cardiac hypertrophy
• D. Actually, all of the options are true

A

D

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4
Q

All of the statements are true, except?
• A. Increased risk of stroke is a complication of hypertension.
• B. Stage 1 hypertension needs both high readings of systolic and diastolic
• C. Decreased renal sodium excretion is a mechanism of hypertension
development • D. Medications that block the effect of RAAS is a treatment of hypertension

A

B

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5
Q

Tunic Intima and Tunic Media thicken
with damage

A

Referred to as: Intimal Thickening and
Intima-Media Thickness

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6
Q

Intimal Hyperplasia

A

• Process that the intimal layer of the blood
vessel becomes thickened • Due to presence and increase of smooth
muscle and extracellular matrix
components • Between the endothelium and internal
elastic membrane

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7
Q

Arteri/o

A

Refers to an artery or arteries

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8
Q

Sclerosis

A

Abnormal and pathological hardening of body tissue
• Mostly from scar tissue

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9
Q

Arteriosclerosis

A

Literally means hardening of an artery or arteries
• “Chronic disease characterized by abnormal thickening and hardening of the
arterial walls with resulting loss of elasticity”

Mainly associated with hypertension, diabetes mellitus, and smoking

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10
Q

Three Types Arteriosclerosis

A
  1. Arteriolosclerosis
    —Arteriol/o = arterioles
  2. Atherosclerosis
    —Most common type of arteriosclerosis
  3. Mönckeberg Medial Sclerosis
    • Calcium deposits in muscular arteries
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11
Q

Arteriolosclerosis vs atherosclerosis • Arteriolosclerosis

A

• Arteriolosclerosis
— Hardening and thickening of arterioles

• Atherosclerosis
— Hardening of an artery specifically due to an atheromatous plaque

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12
Q

Atherosclerosis: Overview

A

Build of fat, cholesterol, and other substances
underneath the endothelium
• Build-up is called an Atherosclerotic Plaque
• Plaques also weaken the underlying media tunics
• Can lead to aneurysm
• Atherosclerosis basically hardens the vessel and narrows
the lumen space

** Coronary Artery Disease (CAD) & Peripheral Artery Disease (PAD)**
• Dangerous manifestation of atherosclerosis
• Deaths caused by ischemic heart disease (IHD)
• Myocardial infarction
• Lower extremity complications

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13
Q

Pathogenesis

Steps to Atherosclerosis Development

A
  1. Endothelial Damage

• Damage to the endothelium
• High blood pressure, smoking, high cholesterol
• Initiates the inflammatory process

  1. Accumulation of Lipoproteins and Monocytes

LDL (“bad” cholesterol) particles enter the damaged area and get stuck in
the vessel wall • Monocytes move to the area to “clean up” the excess LDL particles

  1. Immune Response and Fatty Streak Formation

Monocytes differentiate into macrophages that phagocytize the LDL
particles and become foam cells • Foam cells pile up and form a fatty streak, the earliest visible lesion • Fatty Streak is visible and thrombogenic

  1. Smooth Muscle Proliferation and Plaque Formation

Smooth muscle cells migrate from the tunica media into the intima
• Produce ECM components to form a fibrous cap over the lipid core

  1. Plaque Rupture or Calcification of Plaque

If the fibrous cap ruptures, the lipid core is exposed to the bloodstream
• Will cause a thrombosis (an abnormal blood clot) which can block the artery
• Leads to a heart attack or stroke or blood vessel blockage

6.*Calcification of plaque

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14
Q

Clinical complications of atherosclerosis

A

Atherosclerosis Leads To:
• Coronary Artery Disease (CAD)
• Peripheral Artery Disease (PAD)
• Transient Ischemic Attack
• Cerebral Vascular Accident

  • infarction (partially block vessel lumen, clot forms and completely blocks vessel lumen)
  • Aneurysm and rupture (plaque build up weakens vessel wall
  • Embolism formation
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15
Q

All of the options are TRUE, except?
• A. Arteriosclerosis is hardening of the arterioles
• B. Foam cells are macrophages that phagocytize LDL particles
• C. The fatty streak is formed due to the foam cells
• D. Fibrous cap formation is due to smooth muscle cells
• E. Actually, all of the options are true

A

A

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16
Q

All of the options are TRUE, except?
• A. Tremendous and serious complications are associated with atherosclerosis
• B. Endothelial damage associated with atherosclerosis can be caused from
hypertension
• C. Coronary artery disease is primarily associated with atherosclerosis
• D. Intimal hypertrophy naturally occurs as an individual ages
• E. The process of atherosclerosis occurs quickly, typically within months

A

E

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17
Q

Hemostasis

A

Process of stopping the flow of blood (bleeding) • Formation of blood clots at a site of injury

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18
Q

Homeostasis Process

A

• Hemostasis is a cascade of reactions involving clotting factors,
platelets, and the endothelium (at site of injury)

Vital process for survival • Delicate balance of having clotting blood when needed and not clotting
blood when not needed

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19
Q

Hemostasis Disorders Breakdown Into 2 Broad Categories

A

• 1. Hemorrhagic disorders

• 2. Thrombotic disorders

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20
Q

General Sequence Of Hemostasis

A

• 1. Vascular spasm

HEALTHY endothelial cells normally release nitric oxide (NO) and
prostaglandins
• Cause vasodilation AND no platelet aggregation
• Endothelial Injury Immediately Causes Vasoconstriction
• Causes the release of Endothelin
• Potent vasoconstrictor chemical mediator released by damaged endothelial cells
• After a few moments– inflammation kicks in

• 2. Primary hemostasis (platelet plug formation)

• AKA: Platelet Plug Formation
• Ultimately want to activate platelets
circulating in the blood to form a PLATELET
PLUG
• Activated platelets stick to each other and the damaged area of the blood vessel
• Forms a PLATELET PLUG (that’s the goal)

• 3. Secondary hemostasis (coagulation)

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21
Q

How Do Platelets Become Activated?

A

• Collagen Fibers
— Exposed when the endothelial lining is damaged
• Von Willebrand Factor (vWF)
— Binds to collagen and helps platelets attach to vessel wall and activates them
• Thrombin
— Potent platelet activator from the coagulation cascade • ADP and Thromboxane A₂ (TxA₂)
—Released by activated platelets
to the area and activate more platelets.
— Recruit and activate more platelets (positive feedback loop)
• Serotonin and Calcium
—Also released by activated platelets to enhance activation and aggregation

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22
Q

Hemostasis Step 2: Primary Hemostasis

Once platelets become activated…>

A

• 1. Change their shape- form arm like extensions (tentacles)
— Grab on to other platelets

• 2. Secrete:
— More Von Willebrand’s Factors
— Calcium (Ca2+)
— Serotonin- attracts more platelets
— ADP & Thromboxane A2
— Together, activate more platelets that haven’t bound to vWF

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23
Q

Hemostasis Step 2:Primary hemostasis

Balance Between
Platelet Activators and Platelet Inhibitors

A

• Activators: ADP and Thromboxane A2

• Inhibitors: Nitric Oxide and Prostaglandins

** Aspirin
• Prevents platelet aggregation
• Blocks the production of Thromboxane A2 (plays a role eon the plates ability to clot, this is limited)

Von Willebrand Disease (VWD)
• Genetically inherit low levels of von Willebrand factor (vWF)
(VWF helps stick and form clot factors)

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24
Q

Hemostasis Step 3: Secondary Hemostasis

A

AKA: Coagulation

• Need to REINFORCE the platelet plug formation

• Clotting factors get proteolytically activated to ultimately convert
fibrinogen to fibrin to form a fibrin mesh

• Fibrin mesh reinforces platelet plug

• Basically- fibrinogen is activated (converted) to fibrin which is a
net/mesh to hold the platelet plug together and secure it

• Platelet plug = bricks

• Fibrin mesh = mortar holding the bricks together
Fibrinogen—>Fibrin

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25
Two Pathways That Lead To The Activation Of Fibrinogen To Fibrin? Bot intrinsic and extrinsic pathways lead to activation of what?
• 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)
26
_______ converted fibrinogen to fibrin?
Thrombin ** Fibrin is a soluble thread that creates a mesh around the platelet plug- stabilizing the clot
27
Prothrombotic vs Anti-thrombotic
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
28
Name prothrombotic substances
Endothelin Von Willebrand Factor (vWF) Vitamin K Plasminogen Activator Inhibitor-1 ADP & Thromboxane A₂ Serotonin
29
Name antithrombotic substances
Nitric oxide Heparin/warfarin Thrombomodulin t-PA Antithrombin III Asprin
30
Fibrinolysis involves what?
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
31
What does plasmin do?
Breaks down fibrin (without breaking down fibrin the clot will not form)
32
Precursor to plasmin is ______. What coverts plasminogen to plasmin?
Plasminogen is the precursor to plasmin Tissue plasminogen activator (t-PA) breaks down plasminogen to plasmin
33
Why would giving a patient with DVT a t-PA be beneficial?
This will covert plasminogen to plasmin and then the body can break down the clot. And fluid can move from the region
34
Hemostasis: Influencing Variables Medications.. Anticoagulants.. Antiplatelets..
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
35
Clinical Tests of the Coagulation Process
• 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
36
All of the options have an antithrombotic / anticoagulation effect, except? • A. Warfarin • B. Tissue type plasminogen activator (t-PA) • C. von Willebrand’s factor • D. Nitric oxide
C
37
What substance has a prothrombotic effect? • A. ADP • B. Plasminogen activator inhibitor • C. Thromboxane A2 • D. All of the options have a prothrombotic effect
D
38
All of the options are true, except? • A. Thrombin converts fibrinogen to fibrin • B. Activation of t-PA leads to the breakdown of the fibrin mesh • C. Platelets are already activated as they circulate through the blood • D. Decreased levels of vitamin K leads to anti-thrombotic effects
C
39
The main goal of secondary hemostasis is to form a platelet plug. • A. True • B. False
B
40
Hemostasis Disorders: Overview Hemostasis Disorders Grouped Into 2 Broad Categories
• 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
41
What is a hemorrhage and thrombotic disorders?
• Hemorrhage is the extravasation of blood from vessels • Thrombotic is the association of the formation of thrombus
42
Hemorrhagic Characteristics
• 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
43
Hemorrhagic Disorders: Classifications Classified by Size
• 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
44
Thrombus
• 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
45
The Primary Abnormalities That Lead To Thrombosis
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)
46
Thrombotic Disorders: Overview
• 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
47
Fate/Outcomes Of A Thrombus
• 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
48
Thrombotic Disorders: Characteristics Clinical manifestations Diagnosis Treatment
• 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
49
Major Complications of Thrombosis
• 1. Occlusion of the vessel, especially an artery • 2. Emboli formation
50
Occlusion Of A Vessel Thrombotic disorders
Within the heart • Myocardial infarction Within the brain • Thrombotic stroke Within the lower extremity • Deep Vein Thrombosis
51
Embolic Disorders: Classifications
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
52
Deep Vein Thrombosis (DVT)
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
53
Thrombophlebitis vs Phlebothrombosis
• Thrombophlebitis —Presence of a thrombus in a vein with associated inflammation • Phlebothrombosis —Presence of a thrombus in a vein without associated inflammation
54
Disseminated Intravascular Coagulation (DIC
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
55
An embolus can only be caused by a thrombus. • A. True • B. False
B
56
Endothelial damage, such as atherosclerosis, can lead to a thrombus. • A. True • B. False
A
57
Thrombi always lead to an embolus. • A. True • B. False
B
58
A DVT would cause unilateral redness and swelling. • A. True • B. False
A
59
Aneurysm
is a localized abnormal dilation of a blood vessel due to a weakening in the vessel wall that may be congenital or acquired
60
Pathogenesis of aneurysms
• Inadequate or abnormal connective tissue synthesis • Marfan’s disease and Ehlers-Danlos syndrome • Excessive connective tissue degradation • Loss of smooth muscle cells • **Atherosclerosis • **Hypertension
61
Classification of Aneurysms
**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)
62
Where do most aneurysms most commonly occur in the Circle of Willis?
Anterior communicating artery
63
Vasculitis: Overview
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
64
Vasculitis Etiology
• 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
65
Veins: Varicose Veins
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
66
Varicose Veins Clinical Manifestations
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
67
Veins: Other Varicosities
• 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
68
1. All of the options are TRUE, except? • A. Brain aneurysms symptoms are a gradual onset • B. Aortic abdominal aneurysm can be detected on an X-ray • C. Vasculitis can occur from a type III hypersensitivity reaction • D. Varicose veins is associated with valve dysfunction
A
69
What option is TRUE? • A. Esophageal varices can be caused from stomach complications • B. Hemorrhoids are a result of stagnant arterial blood flow in the anorectal junction • C. A saccular aneurysm, the most common type of aneurysm, is when there is outpouchings on both sides of the artery • D. Hypertension is a possible causation to an aneurysm • E. Two of the options are correct
D
70
If a patient states their headache is the worst headache they ever have had and nothing helps the pain- there is nothing to worry about, right? • A. True • B. False
B
71
Inflammation Related Edema and Effusions
• EXUDATES: Protein-rich fluid • Accumulate due to increases in vascular permeability caused by inflammatory mediators
72
Non-Inflammatory Related Edema and Effusions
• TRANSUDATES: Low protein fluid • Noninflammatory edema and effusions are common in many disorders, including heart failure, liver failure, renal disease, and malnutrition
73
Edema Has Four Main Causations:
• 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
74
Hyperemia
• 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
75
Congestion
• 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
76
Shock: Categories of Shock
• 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
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Sepsis and Septic Shock
• 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
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Shock: Overview
• 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
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Septic Shock Concerns
• 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
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Hypovolemic and Cardiogenic Shock
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
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Infarction
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
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Classification of Infarcts Based On
• 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
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All of the following options are true regarding increased hydrostatic pressure, except? • A. Can be caused from a deep vein thrombosis • B. Can cause an exudate or transudate edema fluid • C. Can be localized or systemic • D. It will lead to edema
B
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Ascites occurs when there is fluid build up in the pericardium? • A. True • B. False
B
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Hyperemia will lead to cyanosis due to the increased blood flow? • A. True • B. False
B
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Edema from inflammatory processes will have transudates rather than exudates. • A. True • B. False
B
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This type of shock is caused by a significant loss of blood over a short period of time? • A. Cardiogenic shock • B. Septic shock • C. Anaphylactic shock • D. Hypovolemic shock
D
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This type of morphology occurs when there is an infarct associated with ischemia? • A. Liquefactive necrosis • B. Red necrosis • C. White necrosis • D. Ischemic coagulative necrosis
C
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Shock occurs when there is hypoperfusion to tissues? • A. True • B. False
A