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Pathophysiology Atherosclerosis and Atrial Fibrillation.pdf Flashcards
Study
What is atherosclerosis characterized by?
Atherosclerosis is characterized by patchy intimal plaques (atheromas) that encroach on the lumen of medium-sized and large arteries. The plaques contain lipids, inflammatory cells, smooth muscle cells, and connective tissue.
What are the risk factors for atherosclerosis?
Risk factors for atherosclerosis include dyslipidemia, diabetes, cigarette smoking, family history, sedentary lifestyle, obesity, and hypertension.
How is the diagnosis of atherosclerosis made?
The diagnosis of atherosclerosis is clinical and confirmed by angiography, ultrasonography, or other imaging tests.
What are the treatments for atherosclerosis?
Treatment for atherosclerosis includes risk factor modification, lifestyle and dietary changes, physical activity, antiplatelet drugs, and antiatherogenic drugs.
What is arteriosclerosis?
Arteriosclerosis is a general term for several disorders that cause thickening and loss of elasticity in the arterial wall.
Why is atherosclerosis considered the most serious form of arteriosclerosis?
Atherosclerosis is considered the most serious and clinically relevant form of arteriosclerosis because it causes coronary artery disease and cerebrovascular disease.
Which arteries can be affected by atherosclerosis?
Atherosclerosis can affect all large and medium-sized arteries, including the coronary, carotid, cerebral arteries, the aorta and its branches, and major arteries of the extremities.
What is the leading cause of morbidity and mortality in developed countries like the US?
Atherosclerosis is the leading cause of morbidity and mortality in the US and most developed countries.
How many deaths worldwide were attributed to cardiovascular disease, primarily coronary and cerebrovascular atherosclerosis, in 2019?
In 2019, cardiovascular disease, primarily coronary and cerebrovascular atherosclerosis, caused about 18 million deaths worldwide accounting for 30% of all deaths.
How many people died of cardiovascular disease in the US in 2019?
In 2019, about 558,000 people died of cardiovascular disease in the US.
What is the clinically relevant form of arteriosclerosis that causes coronary artery disease and cerebrovascular disease?
Atherosclerosis
Which arteries can be affected by atherosclerosis?
Coronary, carotid, cerebral, aorta, branches of the aorta, and major arteries of the extremities
What is the leading cause of morbidity and mortality in the US and most developed countries?
Atherosclerosis
How many deaths worldwide were caused by cardiovascular disease primarily coronary and cerebrovascular atherosclerosis in 2019?
About 18 million deaths worldwide
How many people died of cardiovascular disease in the US in 2019?
About 558,000
Where is atherosclerosis rapidly increasing in prevalence?
Low and middle-income countries
What is the earliest visible lesion of atherosclerosis?
Fatty streak
What are the three major components of an atherosclerotic plaque?
Lipids, inflammatory cells, smooth muscle cells
What is the connective tissue matrix that may contain thrombi and calcium deposits in an atherosclerotic plaque?
A connective tissue matrix
What is considered to be an inflammatory response to injury in atherosclerosis?
All stages of atherosclerosis, from initiation and growth to complication of the plaque (e.g., myocardial infarction, stroke)
What role is thought to have a primary initiating role in atherosclerosis?
Endothelial injury
What kind of blood flow is associated with the initiation of atherosclerosis?
Non-laminar or turbulent blood flow (e.g., at branch points)
What are the three major components of the atherosclerotic plaque?
Lipids, inflammatory and smooth muscle cells, connective tissue matrix
What is the primary initiating role in endothelial injury leading to atherosclerosis?
Nonlaminar or turbulent blood flow
What is inhibited by nonlaminar or turbulent blood flow in the arterial tree?
Endothelial production of nitric oxide
What stimulates endothelial cells to produce adhesion molecules that recruit inflammatory cells?
Nonlaminar or turbulent blood flow
What are some risk factors for atherosclerosis mentioned in the text?
Dyslipidemia, diabetes, cigarette smoking, hypertension, oxidative stressors, systemic infection, and inflammation
What is the net effect of risk factors on endothelial cells in atherosclerosis?
Endothelial binding of monocytes and T cells, migration of these cells, and initiation of vascular inflammatory response
What do monocytes in the subendothelium transform into?
Macrophages
What happens to lipids in the blood, particularly LDL and VLDL cholesterol, in atherosclerosis?
They bind to endothelial cells and are oxidized in the subendothelium
What is the result of oxidized lipids and macrophage transformation in atherosclerosis?
Lipid-laden macrophages
What inhibits nitric oxide production and stimulates the production of adhesion molecules, proinflammatory cytokines, chemotactic proteins, and vasoconstrictors?
Superoxide radicals, angiotensin II, and systemic infection and inflammation
What is the net effect of the inhibition of nitric oxide production and stimulation of proinflammatory molecules on endothelial cells?
Endothelial binding of monocytes and T cells, migration of these cells to the subendothelial space, and initiation and perpetuation of a local vascular inflammatory response
What do monocytes in the subendothelium transform into?
Macrophages
What binds to endothelial cells and oxidizes in the subendothelium, leading to the formation of fatty streaks in atherosclerotic lesions?
Lipids in the blood, particularly low-density lipoprotein (LDL) cholesterol and very-low-density lipoprotein (VLDL) cholesterol
What result from the uptake of oxidized lipids and transformation of macrophages into lipid-laden foam cells in the subendothelium?
Early atherosclerotic lesions called fatty streaks
What may serve as an additional source of lipids within atherosclerotic plaques, resulting from degradation of erythrocyte membranes due to intraplaque hemorrhage?
Degraded erythrocyte membranes from the rupture of vasa vasorum
What do macrophages elaborate in the subendothelium that recruit smooth muscle cell migration and stimulate growth of macrophages?
Proinflammatory cytokines
What components make up a subendothelial fibrous plaque in atherosclerosis?
Fibrous cap made of intimal smooth muscle cells, connective tissue, and intracellular and extracellular lipids
What process causes calcification within atherosclerotic plaques, similar to bone formation?
A process similar to bone formation
What has been observed as a potential link to atherosclerosis, particularly an association with coronary artery disease?
Serologic evidence of certain infections, like Chlamydia pneumoniae and cytomegalovirus
What are the putative mechanisms linking infection and atherosclerosis?
Indirect effects of chronic inflammation in the bloodstream, crossreactive antibodies, and inflammatory responses
What factors promote smooth muscle cell replication and increase production of dense extracellular matrix?
Various factors promote smooth muscle cell replication and increase production of dense extracellular matrix.
What is the result of the stimulation of macrophage growth and smooth muscle cell replication?
The result is a subendothelial fibrous plaque with a fibrous cap made of intimal smooth muscle cells surrounded by connective tissue and intracellular and extracellular lipids.
What causes calcification within the atherosclerotic plaque?
A process similar to bone formation causes calcification within the plaque.
What is the observed link between infection and atherosclerosis according to the text?
An association between serologic evidence of certain infections (e.g., Chlamydia pneumoniae, cytomegalovirus) and coronary artery disease (CAD) has been observed.
What are the characteristics of unstable atherosclerotic plaques?
Unstable plaques are vulnerable to spontaneous erosion, fissure, or rupture causing acute thrombosis, occlusion, and infarction.
What enzymes are involved in plaque rupture according to the text?
Plaque rupture involves secretion of metalloproteinases, cathepsins, and collagenases by activated macrophages in the plaque.
What can unstable plaques cause?
Unstable plaques are vulnerable to spontaneous erosion, fissure, or rupture, causing acute thrombosis, occlusion, and infarction.
What may result from unstable plaques that are often not hemodynamically significant on angiography?
Most clinical events, including acute thrombosis, occlusion, and infarction.
What may be a way to reduce morbidity and mortality related to unstable plaques?
Plaque stabilization.
What factors contribute to the strength and resistance to rupture of the fibrous cap in a plaque?
The relative balance of collagen deposition and degradation.
What enzymes are secreted by activated macrophages in the plaque to digest the fibrous cap and cause rupture?
Metalloproteinases, cathepsins, and collagenases.
What role do T cells play in the plaque leading to rupture?
T cells secrete cytokines that inhibit smooth muscle cells from synthesizing and depositing collagen, which reinforces the plaque.
What triggers thrombosis when a plaque ruptures?
The exposure of plaque contents to circulating blood.
What factor present in macrophages stimulates thrombosis by promoting thrombin generation in vivo?
Tissue factor.
What are the five possible outcomes when a plaque ruptures and triggers thrombosis?
1. The thrombus may organize and be incorporated into the plaque, changing its shape and causing rapid growth. 2. The thrombus may rapidly occlude the vascular lumen, precipitating an acute ischemic event. 3. The thrombus may embolize. 4. The plaque may fill with blood, balloon out, and immediately occlude the artery. 5. Plaque contents may embolize, occluding vessels downstream.
What is one of the key factors influencing plaque stability?
Plaque composition, including the relative proportion of lipids, inflammatory cells, smooth muscle cells, and connective tissue.
What is tissue factor's role in thrombosis?
Tissue factor promotes thrombin generation in vivo.
What are the 5 potential outcomes of a thrombus formation?
1. The thrombus may organize and be incorporated into the plaque. 2. The thrombus may rapidly occlude the vascular lumen and cause an acute ischemic event. 3. The thrombus may embolize. 4. The plaque may fill with blood, balloon out, and occlude the artery immediately. 5. Plaque contents may embolize, occluding vessels downstream.
What factors contribute to plaque stability?
Plaque stability depends on factors such as plaque composition, proportion of lipids, inflammatory cells, smooth muscle cells, connective tissue, wall stress, cap fatigue, core size, location, and plaque configuration in relation to blood flow.
What role does intraplaque hemorrhage play in plaque transformation?
Intraplaque hemorrhage contributes to rapid growth and lipid deposition, playing an important role in transforming stable plaques into unstable plaques.
What are the characteristics of unstable coronary artery plaques?
Unstable coronary artery plaques have high macrophage content, a thick lipid core, a thin fibrous cap, narrow the vessel lumen by 50%, and tend to rupture unpredictably.
How do unstable carotid artery plaques differ from unstable coronary artery plaques?
Unstable carotid artery plaques have a similar composition but typically cause problems through severe stenosis, occlusion, or deposition of platelet thrombi which embolize rather than rupture.
What are the characteristics of low-risk plaques?
Low-risk plaques have a thicker cap, contain fewer lipids, narrow the vessel lumen by 50%, and may produce predictable exercise-induced stable angina.
What factors determine the clinical consequences of plaque rupture in coronary arteries?
The clinical consequences depend not only on the anatomical location of the plaque but also on relative factors.
What are the characteristics of unstable carotid artery plaques?
High macrophage content, thick lipid core, thin fibrous cap, tend to narrow the vessel lumen by 50, and tend to rupture unpredictably.
What are the clinical consequences of plaque rupture in coronary arteries dependent on?
Dependent on the anatomical location of the plaque, relative balance of procoagulant and anticoagulant activity in the blood, and vulnerability of the myocardium to arrhythmias.
What risk factors tend to cluster as the metabolic syndrome?
Abdominal obesity, atherogenic dyslipidemia, hypertension, insulin resistance, a prothrombotic state, and a proinflammatory state in sedentary patients.
How do insulin resistance, dyslipidemia, hypertension, and diabetes promote atherosclerosis?
By amplifying or augmenting endothelial dysfunction and inflammatory pathways in the vascular endothelium.
What are the effects of dyslipidemia in promoting atherosclerosis?
Subendothelial uptake and oxidation of LDL, production of adhesion molecules and inflammatory cytokines, incitement of a T cell-mediated immune response, and inflammation in the arterial wall.
What may be key in the etiology of the metabolic syndrome in sedentary patients?
Insulin resistance
What promotes atherosclerosis by amplifying or augmenting endothelial dysfunction and inflammatory pathways in vascular endothelium?
Dyslipidemia, high total LDL or low HDL cholesterol, hypertension, and diabetes
What increases oxidized lipids leading to the production of adhesion molecules and inflammatory cytokines in dyslipidemia?
Subendothelial uptake and oxidation of LDL
What may lead to a T cell-mediated immune response and inflammation in the arterial wall?
Oxidized lipids from LDL in dyslipidemia
What is the main determinant for the risk of atherogenic cardiovascular disease?
Concentration of atherogenic lipoproteins, best reflected by apo B concentration or nonHDLC concentration if apo B is unavailable
How does hypertension lead to vascular inflammation?
Through angiotensin II-mediated mechanisms, stimulating production of proatherogenic mediators
What does diabetes lead to the formation of, increasing the production of proinflammatory cytokines from endothelial cells?
Advanced glycation end products
What increases in diabetes, leading to the generation of oxidative stress and reactive oxygen radicals?
Production of advanced glycation end products
What is the best indicator of atherogenic lipoproteins concentration in the body?
Apolipoprotein B (apo B) concentration or nonHDL-C concentration if apo B is unavailable
How does hypertension contribute to vascular inflammation?
Hypertension may lead to vascular inflammation via angiotensin II-mediated mechanisms
What are some proatherogenic mediators produced by angiotensin II?
Proinflammatory cytokines, superoxide anions, prothrombotic factors, growth factors, and lectin-like oxidized LDL receptors
How does diabetes contribute to atherogenesis?
Diabetes leads to the formation of advanced glycation end products, which increase the production of proinflammatory cytokines and cause oxidative stress that directly injures the endothelium
How does chronic kidney disease promote the development of atherosclerosis?
Chronic kidney disease promotes atherosclerosis via worsening hypertension, insulin resistance, decreased apolipoprotein A I levels, and increased levels of lipoproteina, homocysteine, fibrinogen, and C-reactive protein
What effects does tobacco smoke have on the cardiovascular system?
Tobacco smoke contains toxins that are toxic to the vascular endothelium, increases platelet reactivity, promotes plasma fibrinogen levels and hematocrit, increases blood viscosity, LDL levels, and decreases HDL levels, and promotes vasoconstriction
What is the impact of smoking cessation on HDL levels?
HDL levels increase rapidly within 1 month of smoking cessation
What is Lipoprotein a (Lp(a)) and its association with cardiovascular disease?
Lp(a) is proatherogenic and is an independent risk factor for cardiovascular disease, including myocardial infarction, stroke, and aortic valve stenosis. It has a structure similar to LDL but also has a hydrophilic apolipoprotein(a) component
What chemicals in smoking are toxic to the vascular endothelium?
Nicotine and other chemicals
How does smoking affect platelet reactivity?
Increases platelet reactivity possibly promoting platelet thrombosis
What effect does smoking have on plasma fibrinogen levels and hematocrit?
Increases plasma fibrinogen levels and hematocrit, increasing blood viscosity
What effect does smoking have on LDL and HDL levels?
Increases LDL and decreases HDL levels
What is Lipoprotein a (Lpa) and its association with cardiovascular disease risk?
Lpa is proatherogenic and is an independent risk factor for cardiovascular disease including myocardial infarction, stroke, and aortic valve stenosis
How long does it take for HDL levels to increase after smoking cessation?
HDL levels increase rapidly within 1 month of smoking cessation
What are the levels of Lpa considered pathogenic?
Lpa levels above 50 mg/dL are considered pathogenic
What is Apolipoprotein B (apoB) responsible for in cholesterol transport?
ApoB is responsible for cholesterol transport and for the transport of oxidized phospholipids with proinflammatory properties
What is the initiating event for the development of atherosclerotic lesions according to the text?
The presence of the apoB particle within the arterial wall
What is highly atherogenic and characteristic of diabetes?
High level of small dense LDL
Does a high C-reactive protein (CRP) level reliably predict the extent of atherosclerosis?
No, a high CRP level does not reliably predict the extent of atherosclerosis but can predict increased likelihood of ischemic events
What is responsible for cholesterol transport and can bind the LDL receptor?
ApoB particle
What properties does the ApoB particle have besides transporting cholesterol?
Transport of oxidized phospholipids and proinflammatory properties
What is thought to be the initiating event for the development of atherosclerotic lesions in the arterial wall?
Presence of the ApoB particle
What characteristic of diabetes is highly atherogenic and may include increased susceptibility to oxidation and nonspecific endothelial binding?
High level of small dense LDL
Does a high C-reactive protein (CRP) level reliably predict the extent of atherosclerosis?
No, but it can predict increased likelihood of ischemic events
What may elevated levels of CRP indicate in the absence of other inflammatory disorders?
Increased risk of atherosclerotic plaque rupture, ongoing ulceration or thrombosis, or increased activity of lymphocytes and macrophages
Does CRP itself have a direct role in atherogenesis?
No
What is accelerated coronary atherosclerosis often followed by in heart transplantation?
Immunemediated endothelial injury
What is the likely cause of accelerated coronary atherosclerosis after thoracic radiation therapy?
Radiation-induced endothelial injury
How can infections like C. pneumoniae or H. pylori cause endothelial dysfunction?
Direct infection exposure, endotoxin stimulation, or systemic inflammation
What has been robustly associated with atherosclerosis and cardiovascular events, and when summed, strongly associates with advanced atherosclerosis and cardiovascular events?
Common and rare genetic variants
What has been shown to strongly associate with more advanced atherosclerosis and primary and recurrent cardiovascular events when the total number of risk variants is summed up?
Genetic risk scores
What is a potential cause of accelerated coronary atherosclerosis after thoracic radiation therapy?
Radiation-induced endothelial injury
How can C. pneumoniae infection or other infections cause endothelial dysfunction?
Through direct infection exposure to endotoxin or stimulation of systemic or subendothelial inflammation
What has been associated with atherosclerosis and cardiovascular events, with genetic risk scores showing a strong association with advanced atherosclerosis and cardiovascular events?
Several common and rare genetic variants
What condition increases the risk of atherosclerosis, but no longer thought to directly cause it due to lack of evidence from trials?
Hyperhomocysteinemia
What is the reason behind the association between elevated homocysteine levels and atherosclerosis?
Unclear
According to the information, what happens when atherosclerotic disease is documented in one vascular territory?
Increases the likelihood of disease in other vascular territories
How are patients with non-coronary atherosclerotic vascular disease classified in terms of cardiovascular risk?
Considered to have a CAD risk equivalent and should be treated aggressively
What is the association between elevated homocysteine levels and atherosclerosis?
The reason for the association is unclear.
How does the presence of atherosclerotic disease in one vascular territory affect the likelihood of disease in other vascular territories?
It increases the likelihood of disease in other vascular territories.
How do the cardiac event rates of patients with noncoronary atherosclerotic vascular disease compare to those with known CAD?
They are comparable, and patients with noncoronary atherosclerotic vascular disease are considered to have a CAD risk equivalent.
When was the association of an irregular pulse and mitral stenosis first described, and who described it?
It was first described by Robert Adams in 1827.
What technology was instrumental in recording atrial fibrillation (AF) on an electrocardiogram for the first time?
Electrocardiography, invented by William Einthoven.
Which community-based study provided critical epidemiological data on associated risk factors and clinical outcomes related to atrial fibrillation (AF)?
The Framingham Heart Study (FHS).
What does AF stand for in the context of the document?
Atrial Fibrillation.
How is AF characterized?
AF is characterized by high-frequency excitation of the heart.
When was atrial fibrillation AF first recorded on the electrocardiogram?
AF was first recorded on the electrocardiogram in the 1990s.
What critical epidemiological data on associated risk factors related to AF was provided by the Framingham Heart Study FHS?
The Framingham Heart Study provided critical epidemiological data on associated risk factors and clinical outcomes of AF.
What is the prevailing hypothesis of AF genesis?
The prevailing hypothesis of AF genesis is that rapid triggering initiates propagating reentrant waves in a vulnerable atrial substrate.
What role do myocyte sleeves within the pulmonary veins PV play in the initiation of AF?
Focal ectopic firing arising from myocyte sleeves within the pulmonary veins can initiate AF.
What progress has research yielded in the clinical treatment of AF over the last 3 decades?
Research has yielded progress in the clinical treatment of AF, especially as AF is reaching epidemic proportions.
What is the prevailing hypothesis of AF genesis?
Rapid triggering initiates propagating reentrant waves in a vulnerable atrial substrate.
Who first identified focal ectopic firing from myocyte sleeves within the pulmonary veins in patients with paroxysmal AF?
Haissaguerre and colleagues.
What reduces AF burden in patients with paroxysmal AF by targeting ectopic foci within the pulmonary veins?
Ablation of the ectopic foci.
What are some of the unique properties of the pulmonary veins that promote reentry and ectopic activity for AF initiation?
Unique electrical properties and a complex fiber architecture.
What cells have been identified within the pulmonary veins in autopsy studies that play a role in triggering AF?
Pacemaker cells, transitional cells, and Purkinje cells.
What is the primary molecular basis for pulmonary vein triggers in AF?
Abnormal calcium (Ca2) handling, specifically diastolic leak of Ca2 from the sarcoplasmic reticulum.
What proteins/enzymes contribute to SR Ca2 overload and diastolic membrane instability, leading to AF triggers in the pulmonary veins?
Protein kinase A, calmodulin kinase II, phospholamban, and the ryanodine receptor type 2.
What mechanism describes PV triggers where localized reentry is enabled by decremental conduction and repolarization heterogeneity?
A reentrant mechanism.
What kind of firing arises from muscle sleeves of the pulmonary veins and propagates into the atria, contributing to AF initiation?
Focal trigger firing.
What are some important contributors to SR Ca2 overload and diastolic membrane instability in the heart?
Hyperphosphorylation of key regulatory proteins and enzymes including protein kinase A, calmodulin kinase II, phospholamban, and the ryanodine receptor type 2
What mechanism has been described for PV triggers in atrial fibrillation?
A reentrant mechanism
What enables localized reentry and may foster a focal driver for atrial fibrillation within the pulmonary veins?
Decremental conduction and repolarization heterogeneity
What is a focal trigger arising from the muscle sleeve of the pulmonary vein that propagates into the left atrium and initiates atrial fibrillation?
Focal trigger from PV muscle sleeve
What acts as a driver for atrial fibrillation and can be a fixed or moving spiral rotor resulting from functional reentry?
Fixed or moving spiral rotor
What is a circus movement around anatomic structures or scar that generates micro and macro reentrant circuits in the heart?
Circus movement
What perpetuates atrial fibrillation through the propagation of multiple simultaneous wavelets mediated by both functional and structural reentry?
Perpetual propagation of multiple wavelets
What type of conduction acts as a driver for the persistence of atrial fibrillation and results in fibrillatory conduction from a point source?
Point source with fibrillatory conduction
In the context of atrial fibrillation, what enables reentry in a three-dimensional construct by causing electrical dissociation between myocardial layers?
Electrical dissociation in myocardial layers
What is the mechanism that promotes the perpetuation of atrial fibrillation (AF) by stabilizing reentry?
Structural architectural and electrophysiological atrial abnormalities
What are the two dominant hypotheses for the mechanism of reentry in AF?
Reentrant rotors or multiple independent wavelets
What is the third hypothesis, supported by recent data, regarding the mechanism of reentry in AF?
The double layer hypothesis, suggesting electrical dissociation of epicardial and endocardial layers
What are atrial substrates that promote reentry characterized by?
Atrial cardiomyocyte abnormalities, fibrotic changes, alterations in the interstitial matrix
What do molecular and histologic changes in atrial substrates that promote reentry impair?
Normal anisotropic conduction, fibrosis, reduced cell coupling, and may shorten atrial ERP
What type of abnormalities in atrial substrates can lead to a gain in K channel function and shorten ERP of atrial cardiomyocytes in familial AF?
Congenital abnormalities
What combination of factors in heart failure (HF) can result in both a slowing of conduction velocity and atrial fibrosis?
Atrial fibrosis and alterations in cardiomyocyte function
What are the characteristics of atrial substrates that promote reentry?
Abnormalities of the atrial cardiomyocyte, fibrotic changes, alterations in the interstitial matrix with primarily non-collagen deposits
What molecular and histologic changes impair normal anisotropic conduction in atrial substrates?
Fibrosis and/or reduced cell coupling, shorten atrial effective refractory period (ERP)
How do congenital abnormalities in familial AF and heart failure HF affect atrial cardiomyocytes?
Congenital abnormalities in familial AF lead to a gain in K channel function and shorten ERP, while in HF, atrial fibrosis and alterations in cardiomyocyte function result in a slowing of conduction velocity and shortening of ERP
What was the prevailing notion about the progression of AF in the past?
The prevailing notion was that AF began with paroxysmal episodes that increased in frequency and duration, leading to progression to more persistent AF subtypes
What is the 'AF begets AF' postulate based on?
It is based on early experimental data showing that tachycardia induces electrophysiologic atrial remodeling, resulting in the persistence of AF
What does the AF postulate suggest regarding the persistence of atrial fibrillation (AF)?
The AF postulate suggests that tachycardia induces electrophysiologic atrial remodeling, leading to the persistence of AF.
What was the progression rate of paroxysmal AF to more persistent chronic AF subtype in the Canadian Registry of Atrial Fibrillation (CARAF) after 1 year and 5 years?
86% at 1 year and 24% by 5 years.
In the Euro Heart Survey, what percentage of patients with paroxysmal AF remained paroxysmal after one year?
80% of patients with paroxysmal AF remained paroxysmal after one year.
What percentage of patients with persistent AF progressed to permanent AF in the Euro Heart Survey after one year?
30% of patients with persistent AF progressed to permanent AF after one year.
What was the percentage of patients with paroxysmal AF who remained paroxysmal in studies involving patients with pacemakers?
54-76% of patients with paroxysmal AF remained paroxysmal.
In one study involving patients with paroxysmal AF, what percentage progressed to persistent AF in one year?
Only 24% of patients with paroxysmal AF progressed to persistent AF in one year.
What pattern of arrhythmia burden was observed in patients with paroxysmal AF before developing persistent AF?
There was a progressive pattern of increasing arrhythmia burden in patients with paroxysmal AF, except in the days prior to the development of persistent AF.
What is a remarkable observation about persistent AF mentioned in the text?
Persistent AF may spontaneously switch to paroxysmal subtype, highlighting the complex natural history of AF.
What are some limitations and uncertainties regarding the mechanisms and factors governing the clinical course of AF?
There are limitations in experimental data, uncertainties in mechanisms, and factors contributing to the clinical course of AF.
How can the natural history of AF change over time according to the text?
The natural history of AF may change as risk factors contributing to AF onset shift in prevalence and severity.
What is the most prominent risk factor for atrial fibrillation (AF)?
Advancing age
How does the incidence of AF change with advancing age?
The incidence of AF increases with advancing age
What are some examples of unmodifiable risk factors for AF?
Genetics and age
What are some examples of modifiable risk factors for AF?
Male sex, body mass index (BMI), diabetes, smoking, alcohol consumption, systolic blood pressure, hypertension treatment, left ventricular hypertrophy, heart murmur, heart failure, and myocardial infarction
What are some challenges in predicting the natural history of AF subtypes?
Inconsistent means for quantifying and assessing AF burden over time, leading to ascertainment bias
What is the complex natural history of persistent AF highlighted by?
The spontaneous switch to paroxysmal subtype
What factors contribute to the uncertainty in the mechanisms and factors governing the clinical course of AF?
Limitations of experimental data
How has age been observed to be the greatest risk factor for AF compared to other risk factors?
During the last 5 decades, age was observed to be the greatest risk factor for AF compared to other risk factors including male sex, BMI, diabetes, smoking, alcohol consumption, systolic blood pressure, hypertension treatment, left ventricular hypertrophy, heart murmur, heart failure, and myocardial infarction
Why is understanding the influence of age on AF risk important?
For assessing how changes in life expectancy will affect the prevalence of AF
What is the incidence rate of AF per 1000 persons for age 45-54 years in the Scottish study?
0.5
What is the incidence rate of AF per 1000 persons for age 55-64 years in the Scottish study?
1.1
What is the incidence rate of AF per 1000 persons for age 65-74 years in the Scottish study?
3.2
What is the incidence rate of AF per 1000 persons for age 75-84 years in the Scottish study?
6.2
What is the incidence rate of AF per 1000 persons for age 85+ years in the Scottish study?
7.7
What has been observed as the greatest risk factor for AF compared to other risk factors in the last 5 decades?
Age
In the most recent time period studied (1998-2007), what were the risk ratios for AF in individuals aged 60-69, 70-79, and 80-89 years compared to those aged 50-59 years?
5.98, 7.35, 9.33
What has been incorporated in AF risk prediction scores due to its stepwise increment in risk with age?
Age
How do AF patients with age <65 years compare to those with age ≥65 years in terms of health, risk factors, and in-hospital deaths?
Healthier, different risk profile, less in-hospital deaths
In North American and European populations, is the age-adjusted incidence of AF higher in men or women?
Men
What was the AF incidence per 1000 person-years in men and women in the FHS study?
Men: 3.8, Women: 1.6
What were the AF incidence per 1000 person-years in men in the Olmsted County Minnesota Study and Rotterdam Study compared to women?
Olmsted County Minnesota Study: Men 4.7, Women 2.7; Rotterdam Study: Men 11.5, Women 8.9
What is the age-adjusted incidence of AF in men and women in North American and European populations?
Higher in men compared to women
What was the AF incidence per 1000 person-years in men and women in the FHS study?
38 in men and 16 in women
Which studies reported different AF incidence rates in men and women (per 1000 person-years)?
The Olmsted County Minnesota Study and the Rotterdam Study
What is the lifetime risk for AF between men and women in North American and European populations?
Similar despite higher AF incidence in men due to shorter life expectancy
Pathophysiology Atherosclerosis and Atrial Fibrillation.pdf Flashcards
Study
What were the lifetime risks to develop AF at age 40 years for men and women in the Framingham Heart Study?
Men: 26, Women: 23
What were the lifetime risks to develop AF at age 55 years for men and women in the Rotterdam study?
Men: 23.8, Women: 22.2
What factor largely explains the higher incidence of AF in men compared to women, according to the text?
Underlying risk factors of AF and taller stature in men
After adjusting for AF-related risk factors, what did the CHARGE-AF Consortium report about male sex as an independent risk factor for AF?
Male sex was no longer an independent risk factor for AF
Which population had a consistently lower lifetime risk for AF in men compared to women across all age groups?
Chinese adults
Which racial group is reported to have a lower prevalence of AF compared to individuals of European ancestry?
Individuals of African ancestry
What did the Multi-Ethnic Study of Atherosclerosis (MESA) report about the prevalence of AF in Hispanic and Asian individuals in the United States compared to white and African American individuals?
Hispanics: 61, Asians: 39, White: 112, African American: 58
What racial and ethnic differences in AF prevalence have been observed in studies?
AF is less prevalent in individuals of African descent compared to European ancestry. Hispanics and Asians in the United States have lower incidence rates of AF compared to whites and African Americans.
What did the MultiEthnic Study of Atherosclerosis (MESA) report about the prevalence of AF in Hispanics and Asians in the United States?
MESA reported a lower prevalence of AF in Hispanics and Asians, with age and sex-adjusted incidence rates of 61 in Hispanics and 39 in Asians compared to 112 in whites and 58 in African Americans.
Which racial and ethnic groups have been found to have a lower risk of AF compared to whites, according to The Healthcare Cost and Utilization Project?
Hispanics and Asians have been found to have a lower multivariable-adjusted risk of AF compared to whites, with a hazard ratio of 0.78 and 95% CI of 0.77-0.79.
What are some modifiable risk factors for AF related to physical activity and lifestyle?
Physical inactivity and sedentary lifestyle, hypertension, obesity, and diabetes are known risk factors for AF. Obstructive sleep apnea (OSA) is common in obese individuals and has been associated with a sedentary lifestyle.
How does a sedentary lifestyle contribute to the risk of AF?
A sedentary lifestyle is known to increase the risk of AF by inducing structural and electrical remodeling of the atrium. Conditions such as hypertension, obesity, diabetes, and obstructive sleep apnea (OSA) are associated with sedentary behavior and can lead to AF.
What are the primary mechanisms contributing to the pathogenesis of AF in endurance athletes?
The pathogenesis of AF in endurance athletes is attributed to increased vagal tone, which may shorten and increase the dispersion of atrial effective refractory period (ERP), promoting pulmonary vein firing and localized reentry.
What is a modifiable risk factor for atrial fibrillation specifically in comparison to whites?
Hypertension
How does a sedentary lifestyle increase the risk of atrial fibrillation?
By inducing structural and electrical remodeling of the atrium
What is obstructive sleep apnea (OSA) associated with in obese individuals?
Sedentary lifestyle
What are the two primary mechanisms attributed to the pathogenesis of atrial fibrillation in endurance athletes?
Increased vagal tone and progressive cardiac remodeling
What are some of the factors contributing to the excess risk of atrial fibrillation in obesity?
Left atrial enlargement, increased left ventricular mass, and diastolic dysfunction
According to the Framingham Heart Study, how much increased risk of atrial fibrillation was observed in men and women with diabetes respectively?
40% in men and 60% in women
What may be more predictive of atrial fibrillation risk than the actual diagnosis of diabetes in older adults?
Level of blood glucose
How do glucose intolerance and insulin resistance contribute to the development of the atrial fibrillation substrate in diabetes mellitus?
They mediate the development by altering cardiac structure through impaired mitochondrial function and oxidative stress
What is a well-established independent predictor of atrial fibrillation related to high blood pressure?
Increased left atrial size
What is the increased risk of atrial fibrillation (AF) in men with diabetes?
40% increased risk of AF in men with diabetes
What is the increased risk of AF in women with diabetes?
60% increased risk of AF in women with diabetes
What may be more predictive than the actual diagnosis of diabetes in older adults in relation to AF?
Level of blood glucose
What pathophysiological factors mediate the development of the AF substrate in individuals with glucose intolerance and insulin resistance?
Glucose intolerance and insulin resistance
What molecular mechanism is involved in the alteration of cardiac structure due to insulin resistance in individuals with AF?
Impaired mitochondrial function and oxidative stress
What is a well-established independent predictor of AF related to chronic hypertension?
Increased left atrial size
Apart from left atrial size, what other pathologic features of chronic hypertension are associated with AF?
Left ventricular hypertrophy and impaired diastolic dysfunction
What common factor among individuals with chronic hypertension increases left atrial pressure and volume, leading to AF?
Elevated left ventricular end-diastolic pressure
What is atrial remodeling associated with in individuals with chronic hypertension and AF?
Slower and more heterogeneous atrial conduction and increased PV firing
What supports multiple reentry circuits in individuals with chronic hypertension and AF?
Increased left atrial mass
What is the increased risk of stroke and transient ischemic attack associated with AF?
Increased risk of stroke and transient ischemic attack
What is the attributable risk of AF for stroke in individuals aged 50-59 years old?
15% in individuals aged 50-59 years old
What is the attributable risk of AF for stroke in individuals aged 80-89 years old?
23.5% in individuals aged 80-89 years old
How can the burden of AF, including subclinical AF, be accurately assessed in patients with implanted cardiac devices?
Through atrial tachyarrhythmia with an atrial rate of 190 beats per
What does increased left atrial mass support in relation to AF?
Multiple reentry circuits
What is the attributable risk of AF for stroke among 50-59 years olds in the FHS study?
15
What has been associated with an increased risk of clinical AF and ischemic stroke?
Atrial tachyarrhythmia with an atrial rate of 190 beats per minute for longer than 6 minutes
What are some risk factors that modulate the risk of stroke with AF?
Age 65, hypertension, diabetes, prior stroke/transient ischemic attack/thromboembolism history, vascular disease, heart failure, and female sex
In the Copenhagen Stroke Study, what outcomes were observed in patients with AF compared to those without?
Higher rates of in-hospital death, longer hospital stay, lower rates of discharge home, larger infarcts involving the cerebral cortex
What are AF patients at increased risk of according to the Copenhagen Stroke Study?
In-hospital death, longer hospital stay, lower rates of discharge home, larger infarcts, and involvement of the cerebral cortex
What did the Copenhagen Stroke Study show about the odds of silent infarcts in patients with AF compared to non-AF patients?
Similar odds for silent infarcts were observed in patients with AF and non-AF
What did the Framingham Heart Study show about 30-day mortality in AF-associated strokes compared to non-AF strokes?
Increased 30-day mortality was observed in AF-associated strokes compared to non-AF strokes in the Framingham Heart Study
What did individuals with AF have worse outcomes in following stroke according to the Framingham Heart Study?
Individuals with AF had worse 1-year survival following stroke and increased risk of stroke recurrences compared to those with non-AF strokes
What factors have been implicated in thrombogenesis in AF?
Blood stasis, endothelial dysfunction, and prothrombotic state are factors implicated in thrombogenesis in AF
What has attention focused on regarding thrombogenesis in AF?
Attention has focused on the left atrial appendage (LAA) in thrombogenesis in AF
What is associated with the presence of spontaneous echo contrast, increased LAA thrombus, and stroke in AF patients according to the text?
Clinically reduced LAA emptying velocity on transesophageal echocardiography
What factor supports the role of LAA in AF-related stroke according to the text?
The efficacy of LAA closure devices for reducing strokes in patients with AF supports the role of LAA in AF-related stroke
What abnormalities in coagulation have been observed in patients with AF-related strokes according to observational studies?
Increases in prothrombin fragment and thrombin-antithrombin complexes
What other hemostatic factors have been implicated in contributing to the hypercoagulable state in AF patients?
Other hemostatic factors such as fibrinogen, D-dimer, and factor VIII have been implicated in contributing to the hypercoagulable state in AF patients
What is the significance of reduced LAA emptying velocity on transesophageal echocardiography?
Associated with presence of spontaneous echo contrast, increased LAA thrombus, and stroke
What observational studies support the role of LAA in AF-related stroke?
Efficacy of LAA closure devices for reducing strokes in patients with AF
What abnormalities in coagulation have been observed in patients with AF-related strokes?
Increases in prothrombin fragment and thrombinantithrombin complexes
Which hemostatic factors contribute to the hypercoagulable state in AF-related strokes?
Fibrinogen, D-dimer, factor VIII, and von Willebrand factor
According to the Framingham Heart Study (FHS), what is the reason for abnormalities in coagulation in AF-related strokes?
Attributed to AF risk factors and presence of cardiovascular disease rather than AF alone
How may inflammation mediate in AF-related strokes?
By mediating endothelial dysfunction and hypercoagulability
What are the shared risk factors between dementia and AF?
Advancing age, obesity, diabetes, and hypertension
What is the adjusted increased risk associated with AF in regards to cognitive impairment and dementia?
Increased risk of cognitive impairment, Alzheimers dementia, and vascular dementia in patients with and without a history of stroke
What does meta-analysis show regarding incident dementia in patients with AF and no history of stroke?
Significantly increased risk of incident dementia
How is AF associated with cognitive impairment and dementia in patients with a history of stroke?
AF is associated with 25-fold adjusted risk of cognitive impairment and dementia in patients with a history of stroke
What are some risk factors associated with an increased risk of cognitive impairment, dementia, and Alzheimer's disease in patients with AF?
Advancing age, obesity, diabetes, and hypertension
In patients with normal baseline cognitive function and no history of stroke, what did a meta-analysis of eight studies find regarding the risk of incident dementia in those with AF?
A significantly increased risk of incident dementia
In patients with a history of stroke, what is the adjusted risk of cognitive impairment and dementia associated with AF?
25-fold increased risk
What did a twenty-year follow-up of the Rotterdam Study report about AF patients aged 67 years in terms of the risk of dementia?
They had the greatest risk of dementia
How does the dementia risk associated with AF change with AF duration exposure in patients 67 years of age?
Increases with AF duration exposure
What did the Framingham Heart Study show about the incidence of dementia, including dementia associated with AF, over the last three decades?
Decreased
What has led to the decreased incidence of dementia, including dementia associated with AF, according to the Framingham Heart Study?
Improved use of anticoagulation in individuals with AF
What does a retrospective study of patients receiving long-term warfarin show about the incidence of dementia in individuals with AF compared to those without AF?
Incident dementia was 2.4 times higher in individuals with AF
What are some possible mechanisms implicated in the development of dementia associated with atrial fibrillation (AF)?
Brain infarcts on brain magnetic resonance imaging and micro thromboembolisms with covert infarction, improved use of anticoagulation in individuals with AF
What did the Framingham Heart Study (FHS) show regarding the incidence of dementia, including dementia associated with AF, over the last three decades?
The incidence of dementia, including dementia associated with AF, has decreased over the last three decades
How does anticoagulation use in individuals with AF support the hypothesis that anticoagulation may reduce AF-associated dementia?
Improved use of anticoagulation in individuals with AF has shown to reduce incident dementia, with dementia risk significantly mitigated by increasing time in therapeutic range
What did a retrospective study of patients receiving long-term warfarin show regarding incident dementia in individuals with AF compared to those without AF?
Incident dementia was 2.4 times higher in individuals with AF versus those without AF, and the dementia risk in those with AF and non-AF was significantly mitigated by increasing time in therapeutic range
What is one possible mechanism that may involve cerebral hypoperfusion associated with AF and how does it affect different age groups?
Cerebral hypoperfusion associated with AF may influence the risk of dementia more in younger patients (50 years) than in older patients (65 years), consistent with the age-dependent dementia risk in AF patients
How did the Framingham Heart Study (FHS) uniquely report the joint incidence of atrial fibrillation (AF) and heart failure (HF) and their temporal relationship?
The FHS reported that among 931 participants with HF, 24 had prior or concurrent AF, and 17 subsequently developed AF. One fifth of participants had AF and HF detected on the same day, showing their closely interlinked pathophysiology
What is the incidence of first HF in FHS participants with AF?
The incidence of first HF in FHS participants with AF is 33 per 1000 person-years
What is the epidemiological data showing agedependent dementia risk in AF patients?
Agedependent dementia risk is observed in those 65 years of age in AF patients.
What was uniquely reported by the Framingham Heart Study (FHS) regarding AF and HF?
FHS reported the joint incidence of AF and HF and their temporal relationship.
What is the incidence of first HF in FHS participants with AF?
The incidence of first HF in FHS participants with AF is 33 per 1000 person-years.
What is the relationship between AF and HF based on the contemporary FHS cohort?
The incidence of HF was markedly higher in participants with AF than the incidence of AF in those with antecedent HF, suggesting AF begets HF more than HF begets AF.
What shared mechanisms are attributed to the strong association of HF and AF?
Neurohormonal and proinflammatory activation leading to myocardial inflammation and fibrosis are shared mechanisms between HF and AF.
What characterizes the atrial substrate with HF?
The atrial substrate with HF is characterized by atrial fibrosis and abnormalities in Ca2 handling.
What factors are associated with venous thromboembolism (VTE) and AF according to epidemiological data?
Increased BMI, obesity, and smoking are associated with VTE as well as AF.
What potential direct causal relationship has been proposed between AF and VTE?
A potential direct causal relationship between AF and VTE has been proposed but needs further study.
What is reported by few studies regarding the risk of VTE in AF and vice versa?
Few studies have reported an increased risk of VTE in AF and vice versa.
What are the shared mechanisms that lead to neurohormonal and proinflammatory activation in HF and AF?
Atrial substrate with HF is characterized by atrial fibrosis and abnormalities in Ca2 handling.
What epidemiological factors are associated with venous thromboembolism (VTE) and atrial fibrillation (AF)?
Increased BMI, obesity, and smoking
What is the proposed relationship between AF and VTE?
Potential direct causal relationship has been proposed but needs further study.
What are the mechanisms underlying the association between AF and VTE?
Studies show AF is associated with a hypercoagulable state attributed to elevated hemostatic factors.
What did the Framingham Heart Study (FHS) find regarding the levels of fibrinogen, von Willebrand factor, and tissue plasminogen activator in relation to AF?
Adjusted model showed no significant difference in levels, suggesting coexisting risk factors may explain elevated thrombotic risk.
What did the FHS report regarding AF and risk of death?
Multivariable adjusted association with increased risk of death, diminishing survival advantage generally enjoyed by women.
What was one of the first studies to report an association between AF and increased risk of death?
FHS (Framingham Heart Study)
What was the observed trend in mortality among men with AF compared to those without AF in the FHS study?
615 of men with AF between 55 to 74 years of age had died compared to 300 of men in the same age group without AF
What was the observed trend in mortality among women with AF compared to those without AF in the FHS study?
576 of women with AF had died by the 10-year follow-up compared to 209 in those without AF
What was the multivariable-adjusted odds ratio (OR) for death in men and women with AF in the FHS study?
15 for men and 19 for women
What was the increased risk associated with AF across all decades of age from 55-95 years, according to the FHS study?
Consistent increased risk of death
What is the risk of death associated with AF even in individuals without clinical evidence of cardiovascular or valvular disease at baseline?
2 fold increased risk of death
What does growing evidence suggest regarding AF and the risk of sudden cardiac death (SCD)?
AF is associated with an increased risk of sudden cardiac death (SCD)
What was the absolute risk reduction in all-cause mortality shown in a meta-analysis of antithrombotic studies with oral anticoagulation compared to control or placebo?
16
What have epidemiological studies like FHS provided insight into regarding AF risk factors (RFs) and their link to AF genesis?
Data associating various RFs with risk of AF and insight into their mechanistic link to AF genesis
What are some of the questions that remain unanswered regarding AF and risk assessment, therapeutic targets, and treatment strategies?
Will genetic studies improve AF risk assessment, identify novel therapeutic targets, and help guide treatment strategies for both primary and secondary prevention of AF
What are the target goals for RF modification in patients with AF?
To improve clinical outcomes
How will genetics alter the target goals for RF modification in patients with AF?
Genetics may alter these targets
What may ongoing and future epidemiological translational and clinical studies provide insight into?
Unanswered questions and improve clinical outcomes in patients with AF
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Unit 6 Nerve ID.pdf Flashcards
Study
What is the capital city of France?
Paris
What is the largest planet in our solar system?
Jupiter
Who wrote the play 'Romeo and Juliet'?
William Shakespeare
What is the chemical symbol for gold?
Au
What is the powerhouse of the cell?
Mitochondria
What is the tallest mountain in the world?
Mount Everest
What is the capital city of Japan?
Tokyo
Who painted the Mona Lisa?
Leonardo da Vinci
What is the largest ocean on Earth?
Pacific Ocean
What year did the Titanic sink?
1912
What is the currency of Germany?
Euro
Who discovered penicillin?
Alexander Fleming
What is the largest desert in the world?
Sahara Desert
What is the chemical symbol for iron?
Fe
Who is known as the 'Father of Modern Physics'?
Albert Einstein
What are the components and functions of the Glossopharyngeal nerve?
1. Special Sensory (Taste from the Posterior 1/3 of the tongue) 2. Visceral sensory from the carotid sinus and carotid body 3. Visceral Motor (Parasympathetic Preganglionic motor fibers to the otic ganglia and then to the parotid gland secretomotor - Lesser petrosal nerve) 4. Somatic branchial Motor to stylopharyngeus muscle (nucleus ambiguous) 5. Somatic general Sensory from the posterior 1/3 of the tongue and oropharynx (Inner surface of tympanic membrane - Afferent limb of the gag reflex) 6. Superior and inferior ganglia at the level of the jugular foramen that contain sensory cell bodies
What are the components of the Lingual branch of the Glossopharyngeal nerve when tagged in the tonsillar bed?
1. Special sensation from the posterior third of the tongue 2. Somatic sensation from the posterior third of the tongue
What are the components and functions of the Superior Laryngeal nerve?
1. Somatic motor (External laryngeal nerve to cricothyroid) 2. Somatic general Sensation above the true vocal folds (Cough reflex) 3. Special sensation (Taste fibers from the epiglottis and root or very posterior of the tongue)
What are the components of the Internal Laryngeal nerve?
1. Somatic general Sensation above the true vocal folds (Cough reflex) 2. Special sensation (Taste fibers from the epiglottis and root or very posterior of the tongue) 3. Preganglionic parasympathetic secretomotor fibers to the mucosal glands
What are the functions of the Vagus nerve?
1. Special Sensation (Taste fibers from the epiglottis and the very root posterior of the tongue) 2. Visceral Sensory a. Monitors the Viscera (e.g., Heart and Baroreceptors at arch of aorta, Chemoreceptors of aortic bodies, Thoracic and Abdominal viscera) b. Sensory from the mucosa above and below the vocal folds (Afferent of the cough reflex) 3. Visceral Motor (Parasympathetic Preganglionic Motor Fibers to the Viscera - Heart, Lungs, Esophagus, Abdominal Organs, Microscopic ganglia in the walls of the organs, Secretomotor to the glands in mucosa - Dorsal motor nucleus) 4. Somatic Motor (Branchial motor - Motor fibers to the Muscles of the Palate, Larynx, and Pharynx - nucleus ambiguous, Efferent of the cough reflex) 5. Somatic Sensory (General sensation from some of the external meatus and part of the tympanic membrane - auricular branch, Dura of posterior cranial fossa) 6. Superior ganglia of the Vagus has cell bodies of the somatic sensory fibers 7. Inferior or Nodose ganglia has cell bodies of the visceral sensory fibers
What are the cell bodies of the somatic sensory fibers in the auricular branch of the posterior cranial fossa?
Superior ganglia of the Vagus
What are the cell bodies of the visceral sensory fibers in the auricular branch of the posterior cranial fossa?
Inferior or Nodose ganglia
Which muscle of the soft palate is innervated by V3 instead of the vagus nerve?
Tensor palatini
Which muscle of the pharynx is innervated by the glossopharyngeal nerve instead of the vagus nerve?
Stylopharyngeus
Which muscle of the tongue is innervated by the vagus nerve instead of the hypoglossal nerve?
Palatoglossus
Which nerve innervates all of the laryngeal muscles except the cricothyroid muscle?
Inferior Recurrent laryngeal nerve
Which nerve innervates the cricothyroid muscle instead of the inferior recurrent laryngeal nerve?
External laryngeal nerve
Which pharyngeal arch is associated with the Glossopharyngeal nerve and its functions?
Arch 3
Which pharyngeal arch is associated with the Vagus nerve, swallowing, superior laryngeal nerve, and pharyngeal branches?
Arch 4
Which pharyngeal arch is associated with the Vagus nerve, recurrent laryngeal nerves, and speaking functions?
Arch 6
Unit 6 Nerve ID.pdf Flashcards
Study
Controls voluntary movements and sensory information
Motor nerves
Regulates involuntary functions like heart rate and digestion
Autonomic nerves
Transmits information from the body to the brain and vice versa
Sensory nerves
Coordinates muscle movements and maintains balance
Cerebellum nerves
Regulates hormone production and the body's internal environment
Endocrine nerves
Controls conscious thoughts, reasoning, and decision-making
Cerebral cortex nerves
Regulates sleep, mood, and emotions
Limbic system nerves
Facilitates communication between the brain and spinal cord
Brainstem nerves
Controls reflex actions such as pulling hand away from a hot surface
Spinal cord nerves
Sensory fibers: Inferior or Nodose ganglia has cell bodies of the visceral sensory fibers
Innervation of muscle groups
Muscles of the soft palate innervation
Vagus except tensor palatini (V3)
Muscles of the pharynx innervation
Vagus except stylopharyngeus which is glossopharyngeal
Muscles of the tongue innervation
Hypoglossal except palatoglossus which is vagus
Innervation of laryngeal muscles
Inferior Recurrent laryngeal nerves except for the cricothyroid from external laryngeal nerve
Auricular branch Dura of posterior cranial fossa
Innervation of the Dura of posterior cranial fossa
Superior ganglia of the Vagus
Contains cell bodies of the somatic sensory fibers
Inferior or Nodose ganglia
Contains cell bodies of the visceral sensory fibers
Innervation of muscle groups
1. All muscles of the soft palate are vagus except tensor palatini which is V3 2. All muscles of the pharynx are vagus except stylopharyngeus which is glossopharyngeal 3. All muscles of the tongue are hypoglossal except palatoglossus which is vagus 4. All laryngeal muscles are innervated by the inferior recurrent laryngeal nerves except cricothyroid which is from the external laryngeal nerve
Branchial Pharyngeal Arches Arch 3
Glossopharyngeal nerve components and functions listed above
Branchial Pharyngeal Arches Arch 4
Vagus: Swallowing - Superior laryngeal nerve and Pharyngeal Branches Vagus: Recurrent Laryngeal nerves - Speaking
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