Chapter 26 Flashcards
1
Q
Impact of structural disorders on arteries and arterioles
A
Decreased blood flow to tissues, impaired delivery of oxygen and nutrients, accumulation of waste
2
Q
Impact of structural disorders on veins
A
Interference with blood outflow from capillary beds, trapping fluid, cellular waste products from tissues
3
Q
Function of the endothelium in vasculature
A
Homeostatic functions: transfer across vascular wall, platelet adhesion, blood clotting, modulation of blood flow and vascular resistance, metabolism of hormones, regulation of immune and inflammatory reactions, elaboration of factors that influence cell growth (eg: for SMCs)
4
Q
Endothelial dysfunction
A
Cell responses to various stimuli by structural and functional alterations
Cause: inflammation, hemodynamic stress, lipids, hypoxia
5
Q
What do SMCs in the tunica media d in response to hormone and neural stimulation?
A
Constrict and dilate blood vessels often due to ANS stimulation
Eg: NE diffuses into tunica media —> AP propagated along gap junctions —> contraction of muscle layer —> decreased radius —> increases resistance to flow through the vessels
6
Q
What biological molecules do vascular SMCs synthesize?
A
Collagen, elastin, growth factors, cytokines
7
Q
What does BP do during systole?
A
Rises as a result of left ventricular contraction
Rapid upstroke in pulse, then slower rise to peak blood pressure
End of systole: downward deflection and diacritic notch —> small rise in intra-aortic pressure due to continued contraction of the aorta and large vessels against the close aortic valve
8
Q
What does BP do during diastole?
A
BP falls as the heart relaxes
Blood flows into peripheral vessels —> arterial pressure falls rapaidaly, then decline more slowly
9
Q
Diacritic Notch
A
The point at which ventricular pressure fall below aortic pressure
Sudden closure of the aortic valve is triggered
10
Q
Pulse pressure
A
Difference between systole and diastole
Impact factors: volume of blood ejected form left ventricle during a beat and degree of distensibility within the arterial tree (ability of arterial vasculature to accept ejected blood)
11
Q
Arterial Distensibility determinants
A
Elastic properties of aorta and large arteries, degree of resistance to flow into smaller vessels
12
Q
Mean arterial pressure (MAP)
A
90-100 mmHg in adults
Average pressure in arterial system during ventricular contraction and relaxation
Indicator of tissue perfusion (60 percent diastolic pressure and 40 percent systolic pressure)
MAP= CO x PVR
13
Q
Peripheral vascular resistance
A
Reflects changes in arterioles radius and viscosity of the blood
14
Q
General mechanism of blood pressure regulation in the body
A
Adjusts CO to compensate for changes in PVR OR
Adjusts PVR to compensate for CO changes
15
Q
Why is it essential for arterial pressure to remain relatively constant?
A
To ensure adequate tissue perfusion
16
Q
Acute regulation of blood flow
A
Second to minutes to correct temporary imbalance during life-threatening situation
Neural and humoral mechanisms
17
Q
Neural mechanisms of acute regulation of BP
A
Regulated by the reticular formation of medulla and lower third of pons
Transmits parasympathetic impulses to the heart through vagus nerve and sympathetic impulses to heart and BVs through spinal cord and peripheral sympathetic nerves
18
Q
Impact on cardiac system when vagus nerve is stimulate
A
HR slows
Sympathetic stimulation increase HR and cardiac contractility, constricts small arteries and arterioles, increasing PVR
19
Q
Intrinsic reflexes
A
Baroreceptors and chemoreceptors reflexes
Rapid and short-term blood pressure regulation
Neural: hypothalamus which controls SNS responses
20
Q
Baroreceptors/ pressoreceptors
A
Pressure sensitive receptors in the walls of blood vessels and the heart
Eg: carotid and aortic baroreceptors sit in areas between the heart and brain, responding to changes in vessel wall stretch from impulses to cardio centers in the brain stem —> alteration of HR, strength of contractility, vascular smooth muscle tone
21
Q
Arterial chemoreceptors
A
Chemosensitive cells, sit in carotid and aortic bodies
Monitor blood levels of oxygen, carbon dioxide, hydrogen ions
Close contact with arterial blood, communicate with brain stem cardio centers for widespread vasoconstriction
Main function is to regulate ventilation
22
Q
Humoral mechanisms of BP regulation
A
RAAS system—> renin released in response to increased SNS activity or decreased BP —> vasoconstriction —> increase PVR —> increase sodium reabsorption —> increasing salt and water retention
Vasopressin/ ADH: responds to decreased blood volume or BP or increased osmolality of body fluid —> vasoconstriction of abdominal viscera
Epinephrine/ norepinephrine: increasing HR and cardiac contractility
Regulate BP by altering vascular tone
23
Q
Long-term BP regulation
A
Largely regulated by kidneys and their role in regulation of extra cellular fluid volume near an equilibrium point
24
Q
How does increased water and salt intake impact arterial pressure?
A
Causes it to rise due to increased extracellular fluid —> increases rate or pressure diuresis and pressure natriuresis
25
Pressure diuresis
Kidney water excretion
26
Pressure natriuresis
Salt excretion
27
Impact of increased fluid volume on cardiac function
Leads to elevated BP
Directly on preload of CO: with increased extracellular fluid volume —> increased CO —> generalized constriction of arterioles —> increased PVR and BP
Indirectly on PVR through autoregulation
28
Function of large, elastic arteries
Transport of blood
29
Function of medium-sized arteries
Distribution of blood flow is controlled by contraction and relaxation of the vessel smooth muscle
30
Function fo small arteries and arterioles
Regulate capillary blood flow
31
Ischemia
Reduction in arterial flow to a level that is insufficient to meet the oxygen demands of the tissues
32
Infarction
An area of ischemic necrosis in an organ produced by occlusion of its arterial blood supply or venous drainage
33
Atherosclerosis
Progressive disease
Formation of fibroblasts plaques in the intima of large and medium vessels
Risk factors: hypercholesterolemia, elevations in LDL, and inflammation, increasing age, family history of heart disease, male sex, cigarette smoking, obesity, visceral fat, hypertension, diabetes mellitus, physical inactivity, stressful life patterns, blood levels of CRP, serum homocysteine levels
34
Vasculitis/ angitis/ arteritis
Inflammation of the blood vessel wall —> tissue injury and necrosis
Impacts: arteries, capillaries, and veins
Inflammatory process initiated by direct injury, infections agents, or immune processes
35
Aneurysms
Abnormal localized dilation of an artery due to weakness in the vessel wall
As it increases in size, tension in vessel wall increase, putting it at risk for rupture
Increased size may also exert pressure on adjacent structures
36
Dyslipidemia
Condition of imbalance of lipid components (triglycerides, phospholipids, cholesterol) of the blood
Diagnostics: elevated serum cholesterol levels, increased triglycerides, increased LDL, decreased HDL
Types: primary (independent) and secondary (caused by something)
Impact factors: nutrition, genetics, medications, comorbid conditions, metabolic diseases
37
Triglycerides
Used in energy metabolism
38
Phospholipids
Important structure of lipoproteins, blood-clotting components, myelin sheath, cell membranes
39
Lipoproteins
Transport cholesterol and triglycerides to various tissues for energy utilization, lipid deposition, steroid hormone reduction, and bile acid formation
40
Apoprotein B
Involved in lipid metabolism, primary protein of VLDL and LDL
Contributes to plaque formation and atherosclerosis
41
VLDL
Body’’s main source of energy during prolonged fasting
Carry triglycerides to fat and muscle cells, where triglycerides are removed
42
What does uptake of LDL by macrophages in arterial wall lead to ?
Atherosclerosis
43
What can increase HDL levels?
Exercise, moderate alcohol consumption, lipid medication
44
What can decrease HDL levels?
Smoking, metabolic syndrome, excess alcohol consumption
45
Familial Hypercholesterolemia
Deficient or defective LDL receptor as a result of an autosomal dominant disorder
The gene is mutated that codes for this receptor
Leads to elevated cholesterol levels
Heterozygous: blood LDL mean value of 350 mgdl, but don’t develop symptoms until adult life (xanthomas and atherosclerosis)
Homozygous: experience LDL levels up to 1000 mgdl and develop symptoms during childhood; significantly higher risk of death from myocardial ischemic disease during young adulthood
46
Secondary Dyslipidemia
Causes: diet, obesity, metabolic changes associated with type 2 diabetes mellitus
Treatment: adopt diet high in fruits, veggies, whole grains, dairy, chicken, fish, legumes, and nuts; limi intake of sweets and red meet (DASH diet)
Diagnostics: elevated triglycerides, elevated LDL, decreased HDL, related to chemical activity of adipose tissue
47
Why do some people with obesity develop chronic low-grade states of systemic inflammation?
Due to the combination of adipokine secretion and macrophage activity
Elevated fatty acids and systemic inflammation may disrupt glucose homestasis —> can lead to insulin resistance development
48
Insulin resistance
Results in use of no glucose energy sources, leading to further increased blood lipid levels
49
Type 2 diabetes
Development of insulin in resistance and a collection of metabolic alterations (dyslipidemia AKA metabolic syndrome)
50
Metabolic Syndrome
Defined the presence of three or more of the following:
1- Elevated fasting blood glucose or current treatment for diabetes
2- Elevated BP or current treatment fo hypertension
3- Elevated waist circumference and increased abdominal fat deposits I
4- Dyslipidemia reflected by increased blood triglycerides and/ or decreased HDL cholesterol in the blood or received current treatment for dyslipidemia
51
What are some other syndromes that can elevate lipids apart from type 2 diabetes?
Hypothyroidism
Nephrotic syndrome
Obstructive liver disease
Meds: beta-blockers, estrogens, protease inhibitors (used to treat HIV)
52
Atherosclerotic lesions
Fatty streak
Fibrous atheromatous plaque
Complication lesion
53
What is the most important complication of atherosclerosis?
Thrombosis that could cause occlusion of small vessels in the heart and brain
Aneurysms ma develop in arteries weakened by extensive plaque formation
54
Clinical manifestations of atherosclerotic plaques
Narrowing of the vessel —> produce ischemia —> sudden vessel obstruction due to plaque hemorrhage or rupture, thrombosis and formation of emboli —> damage to the vessel endothelium or aneurysm formation due to weakened vessel wall
55
Clinical manifestations of vasculitis
Fever
Mayalgia
Arthritis
Malaise
56
Giant Cell Temporal Arteriti
Focal inflammatory condition of medium-sized ad large arteries; predominantly those that originate from the aortic arch
Clinical manifestations: sudden onset of headache, tenderness over the artery, swelling and redness of the overlying skin, blurred vision or diplopia, facial pain
57
Peripheral Vascular Disorders
Disorders of circulation in the extremities
Symptoms: ischemia, pain, impaired function, infarction, tissue necrosis
58
Acute Arterial Occlusion
Sudden event that interrupts arterial flow to the affected tissues or organ
Cause: often are result of an embolus or a thrombus; less common: trauma or arterial spasm from arterial cannulation'
Symptoms: 7 P’s —> pistol shot (acute onset), pallor, polar (cold), pulselessness, pain, paraesthesia, paralysis
Clinical Manifestations: absent pulse below level of occlusion, cyanosis, mottling, loss of sensory, reflex, motor function, tissue death if blood flow is not restored
Diagnosis: visual assessment, palpation of pulses, methods to assess blood flow
Tx: aimed to restore blood flow; embolectomy; thrombocytes therapy; anticoagulant therapy (heparin)
59
Embolus
Freely moving particle (eg: blood clot) that breaks loose and travels in the larger vessels of circulation until lodging in a smaller vessel and occluding blood flow
Cause: typically a complication of heart disease, atrial fibrillation, rheumatic heart disease, fat emboli from bone marrow, amniotic fluid, prosthetic heart valves
60
Thrombus
Blood clot on the wall of a vessel that continues to grow until obstructing blood flow
Cause: due to erosion or rupture of the fibrous cap of an arteriosclerosis plaque
61
Peripheral artery disease
Common in lower extremities (superficial femoral and popliteal arteries)
Risk factors: cigarette smoking progresses atherosclerosis of lower extremities and development of symptoms of ischemia, diabetes mellitus
Clinical manifestations: 50% narrowing before ischemia arises, intermittent claudication, calf pain, vague aching feeling, numbness, thinning of skin/ subcutaneous tissues, cool foot, weak or absent popliteal pulses, limb color blanches with elevation and deep red when dependent
Diagnosis: inspection of limbs for ischemia (atrophy, brittle toenails, hair loss, pallor, coolness, dependent rubor), palpation or Doppler ultrasound, BP taken on leg to determine obstruction, MRI, CT
Tx: decrease cardio risk and decrease symptoms —> removing cardiovascular risk factors, medications (anti platelet agents to minimize thrombosis), walking slowly, surgical vascular intervention
62
Thromboangiitis Obliterans
AKA Buerger disease
Inflammatory arterial disorder that causes thrombus formation (medium-sized arteries in plantar and digital vessels in the foot and lower leg)
Symptoms: thrombosis and acute inflammation; can spread
Risk factors: less than 35 years old, heavy cigarette smokes
Clinical manifestations: pain related to distal arterial ischemia, intermittent claudication (arch and digits of foot), impaired circulation, increased sensitivity to cold, peripheral pulses diminished or absent, changes in extremity color, cyanosis when dependent, digits reddish blue, skin is think and shiny, little hair growth, thick, malformed nails, gangrene, ulceration
Tx: extreme —> amputation, nicotine and tobacco use eliminated
Diagnosis: same as those for atherosclerosis
63
Raynaud Disease
Functional disorder caused by intense vast spasm of the arteries and arterioles in the fingers and less often, toes
Etiology: common in females over males; vasospasm leading to vasoconstriction; limited to fingers
Clinical manifestations: ischemia due to vasospasm —> changes in skin color —> pallor —> cyanosis, sensation of col, changes in sensory perception (numbness and tingling) —> hyperemia —> intense redness, throbbing, parenthesis —> Trenton to normal color
Severe cases: nails become brittle, skin over tips may thicken, ulceration, gangrene
Diagnosis: history of vasospasm is attacks
Tx: eliminate factors that cause vasospasm and protect digits from trauma during an ischemic episode, smoking abstinence, cold protection, emotional stress control
Impact factors: cold and strong emotions; severe tissue necrosis; associate with previous vessel injury, neurological disorder, occupational trauma alternating hot and cold temperatures, chronic arterial occlusive disorders, collagen disease (scleroderma, lupus)
64
Aneurysm
Abnormal localized dilation of the blood vessel (arteries and veins, but most common in the aorta)
Classified according to their cause, location, and anatomical features
65
True aneurysm
Bounded by a complete vessel wall
Blood remains within the vascular compartment
66
False aneurysm
Localized dissection or tear in the inner wall of the artery with formation of an extra vascular hematoma that causes vessel enlargement
Only outer layers of the vessel wall or supporting tissues bound false aneurysms
67
Berry aneurysm
True aneursym that consists of a small, spherical dilation of the vessel at the bifurcation
Typically at circle of Willis
68
Fusiform aneursym
True aneurysm that involves the entire circumference of the vessel with gradual and progressive vessel dilation
Vary in diameter and length
may involve ascending and transverse portion of the thoracic aorta
May extend over large segment of the abdominal aorta
69
Saccular aneurysm
True aneurysm that extends over part of the circumference of the vessel (appears saclike)
70
Dissecting aneurysm
False aneurysm resulting from a tear in the intimacy layer of the vessel that allows blood to enter the vessel wall, dissecting its layers to create a blood-filled cavity
71
Causes of aneurysms
Congenital defects, trauma, infections, and atherosclerosis
72
Aortic aneurysm
Involves any part of the aorta
Etiology: atherosclerosis and degeneration of the vessel media, hypertension (50% of cases), males after the age of 50 years who smoke cigarettes
Clinical manifestations: asymptomatic, compression of superior vena cava, DVT, edema
Thoracic aneurysm: substernal, back, and neck pain, dyspnea, strider, brassy cough (pressure on trachea), hoarseness
Diagnosis: ultrasonography, echocardiography, CT, MRI, surgery
73
Aortic dissection
Hemorrhage into the vessel wall with longitudinal tearing to form a blood-filled channel
Etiology: conditions that weaken or degenerate the elastic and smooth muscle layers of the aorta cause this
Risk factors: 40-60 year olds, males, hypertension, degeneration of the medial layer of the vessel wall, connective tissue disease (Marfan syndrome), pregnancy, congenital defects of aortic vale, aortic coarctation, cardiac surgery, catheterization
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Classifications: type a (lesions involving the ascending aorta or both the descending and ascending aorta)
Type b (not involving the ascending aorta and beginning distal to the subclavian artery)
Time after onset: acute or chronic
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Symptoms: abrupt excruciating pain (tearing or ripping), chest, bp elevated and later unobtainable, syncope, hemiplegia, paralysis of lower extremities, heart failure
Diagnosis: history, physical, imaging, CT, mir
Treatment: control of hypertension and drugs that lessen force of systolic blood ejection form the heart, surgery
74
Skeletal muscle pump
Leg muscles increase flow in the deep venous channels and return venous home blood to the heart when a person walks
75
Varicose veins
Can lead to venous insufficiency;
Primary: originate in superficial saphenous veins
Secondary: develop when flow in deep channels is impaired or blocked; commonly caused by DVT, congenital or acquired arteriovenous fistula, congenital venous malformation, pressure on abdominal veins due to pregnancy or tumor
Risk factors: obesity, people who stand a lot due to increase of venous pressure and vasodilation/ stretching of vessel wall, prolonged heavy lifting
Signs and symptoms: primary (aching in lower extremities, edema)
Diagnosis: history and physical, inspection of extremities, Doppler, angiography
Tx: weight loss and avoid continuous standing, elastic support stockings, sclerotherapy, surgery (if deep venous channels are patent)
76
Chronic Venous Insufficiency
Persistent venous hypertension on the structure and function of the venous system of the lower extremities
Unidirectional flow and empty of deep veins is not possible
etiology prolonged standing, incompetent valves in the veins, DVT, decreased skeletal muscle pump function, inflammatory processes, endothelial dysfunction
Clinical manifestations: tissue congestion, edema, necrosis, skin atrophy, brown pigmentation, sclerosis of lymph handles, stiffening of ankle joint, loss of muscle mass
Sever: stasis dermatitis, venous ulcers, difficult to heal ulcers/ lesions
Treatment: compression therapy
77
Venous thrombosis (thrombophlebitis)
Presence of thrombus and the accompanying inflammatory response in the vein wall (superficial or deep veins —> SVT or DVT)
Etiology: stasis of blood, increased blood coagulability, vessel wall injury
Risks: bed rest and immobilization, acut MI, CHF, older adults, long airplane travel, hyper-coagulability
Symptoms: pain, swelling, deep muscle tenderness, fever, general malaise, elevate wbc count, ERS, tenderness along vein, calf pain, swelling
Diagnosis: vena graphs, ultrasonography, plasma d-dimmer assessment
Treatment: anti embolism stockings, prevention, leg elevation, heat, anticoagulation drug therapy (heparin and warfarin), intravascular filters
78
Hyper-coagulability state
Increased clot formation that increase the likelihood of DVT
Cause: issues with plasma proteins that typically inhibit thrombus formation, oral contraceptive, hormone replacement therapy, smoking cigarettes, cancers, antiphospholipid syndrome, myeloproliferative disorders
79
Virchow’s triad
Illustrates three key factors that lead to thrombus formation
1- vessel wall injury
2- stasis
3- hypercoagulability state
80
General risk factors for hypertension
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Age
Gender
Race
Family History and genetics
Diet
Dyslipidemia
Tobacco
Alcohol consumption
Fitness level
Obesity
Insulin resistance and metabolic abnormalities
Obstructive sleep apnea
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81
Secondary hypertension
Elevation in BP because of another disease conditions (eg: Cochin, amphetamines, erythropoietin, licorice, kidney disease, disorder of adrenal cortical hormones, pheochromocytoma, coarctation of aorta, oral contraceptives)
82
Renal Hypertension
Renal disease causing secondary hypertension
Decreased ruin formation —> retention of salt and water
83
Disorders of Adrenocortical hormones
Hypertension as a result of increased levels of adrenocortical hormones due to hormonal lay induced renal retention of salt and water
Eg: primary hyperaldosteronism (excess production of aldosterone) and excess levels of glucocorticoid (Cushing disease)
84
Pheochromocytoma
Cause hypertensive crisis as a result of tumor in the adrenal medulla
Tumor of chroma fin tissue that release catecholamine
85
Coarctation of the aorta
Narrowing in area of arch of the aorta —> increases resistance to blood flow —> LV to increase pressure to overcome resistance —> low BP in lower extremities/ high BP in upper extremities
Treatment: surgery
86
Target organ systems
Kidneys
Heart
Eyes
Blood vessels
87
Consequence of target-organ damage in hypertension
Heart
- Angina (due to myocardial ischemia)
- MI
- Heart Failure
Brain
- Stroke or transient ischemic attack
Chronic kidney disease or kidney failure
PAD
Retinopathy
Sexual dysfunction
88
Pathophysiology of hypertension
Increases workload of LV by increase in pressure against which heart must pump as it ejects blood —> LV wall remodels —> hypertrophy
Risk for: coronary heart disease, cardiac dysarthria, sudden death, CHF since heart cannot pump effectively
89
Hypertensive emergency
Rare, sudden elevations in BP (>180/120) complicated by acute or worsening target-organ damage
Impacts: ischemic stroke, hypertensive encephalopathy, cardiac ischemia, retinal hemorrhage
Diagnosis: sequential BP measurements
Treatments: reducing effects through lifestyle, behavior changes, medication therapy
90
Preeclampsia-eclampsia
Multisystem disorder that includes hypertension during pregnancy
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Thrombocytopenia
Impaired liver function
Renal insufficiency
Pulmonary edema
Vision disturbances
Cerebral disturbances
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91
Gestational Hypertension
Elevation of BP occurring after 20 weeks gestation without evidence of proteinuira or other clinical manifestations diagnostic of preeclampsia
Might be a risk factor for later development of chronic hypertension
92
Orthostatic Hypertension
AKA postural hypotension
Abnormal drop in BP on assumption of the standing position of at least 20 mmHg or a diastolic BP of 10 mmHg
Other symptoms: associated dizziness and syncope, weakness, nausea, blurred vision, palpitations, lightheadedness
Etiology: when standing, blood pools in lower part of body —> CO falls —> BP drops —> blood flow in the brain is inadequate
More frequent in older adults
Diagnosis: auscultatory method, history, physical exam
Treatment: gradual ambulatory, avoidance of situation that encourage excessive vasodilation, avoidance of excess diuresis, diaphoresis, or loss of body fluids, compression hose around abdomen may help
93
What is orthostatic hypotension often an early sign of?
Reduced blood volume or fluid deficit
Common cause: hypovolemia, excessive diuretics and diaphoresis, loss of GI fluids, prolonged bed ret
94
Why is bed rest and impaired mobility so damaging for cardiac health?
Promotes a reduction in plasma volume, a decrease in venous tongue, failure of peripheral vasoconstriction, and weakness of skeletal muscles that support the veins and assist in returning blood to the heart
95
Drug-induced hypotension
Anti hypertensive drugs and psychotropic drugs
