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Pathophysiology > Chapter 26 > Flashcards

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

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2
Q

Impact of structural disorders on veins

A

Interference with blood outflow from capillary beds, trapping fluid, cellular waste products from tissues

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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)

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4
Q

Endothelial dysfunction

A

Cell responses to various stimuli by structural and functional alterations

Cause: inflammation, hemodynamic stress, lipids, hypoxia

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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

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6
Q

What biological molecules do vascular SMCs synthesize?

A

Collagen, elastin, growth factors, cytokines

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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

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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

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9
Q

Diacritic Notch

A

The point at which ventricular pressure fall below aortic pressure

Sudden closure of the aortic valve is triggered

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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)

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11
Q

Arterial Distensibility determinants

A

Elastic properties of aorta and large arteries, degree of resistance to flow into smaller vessels

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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

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13
Q

Peripheral vascular resistance

A

Reflects changes in arterioles radius and viscosity of the blood

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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

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15
Q

Why is it essential for arterial pressure to remain relatively constant?

A

To ensure adequate tissue perfusion

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16
Q

Acute regulation of blood flow

A

Second to minutes to correct temporary imbalance during life-threatening situation

Neural and humoral mechanisms

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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

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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

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19
Q

Intrinsic reflexes

A

Baroreceptors and chemoreceptors reflexes

Rapid and short-term blood pressure regulation

Neural: hypothalamus which controls SNS responses

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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

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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

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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

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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

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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

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25
Q

Pressure diuresis

A

Kidney water excretion

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26
Q

Pressure natriuresis

A

Salt excretion

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27
Q

Impact of increased fluid volume on cardiac function

A

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

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28
Q

Function of large, elastic arteries

A

Transport of blood

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29
Q

Function of medium-sized arteries

A

Distribution of blood flow is controlled by contraction and relaxation of the vessel smooth muscle

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30
Q

Function fo small arteries and arterioles

A

Regulate capillary blood flow

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31
Q

Ischemia

A

Reduction in arterial flow to a level that is insufficient to meet the oxygen demands of the tissues

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32
Q

Infarction

A

An area of ischemic necrosis in an organ produced by occlusion of its arterial blood supply or venous drainage

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33
Q

Atherosclerosis

A

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

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34
Q

Vasculitis/ angitis/ arteritis

A

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

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35
Q

Aneurysms

A

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

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36
Q

Dyslipidemia

A

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

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37
Q

Triglycerides

A

Used in energy metabolism

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38
Q

Phospholipids

A

Important structure of lipoproteins, blood-clotting components, myelin sheath, cell membranes

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39
Q

Lipoproteins

A

Transport cholesterol and triglycerides to various tissues for energy utilization, lipid deposition, steroid hormone reduction, and bile acid formation

40
Q

Apoprotein B

A

Involved in lipid metabolism, primary protein of VLDL and LDL

Contributes to plaque formation and atherosclerosis

41
Q

VLDL

A

Body’’s main source of energy during prolonged fasting

Carry triglycerides to fat and muscle cells, where triglycerides are removed

42
Q

What does uptake of LDL by macrophages in arterial wall lead to ?

A

Atherosclerosis

43
Q

What can increase HDL levels?

A

Exercise, moderate alcohol consumption, lipid medication

44
Q

What can decrease HDL levels?

A

Smoking, metabolic syndrome, excess alcohol consumption

45
Q

Familial Hypercholesterolemia

A

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
Q

Secondary Dyslipidemia

A

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
Q

Why do some people with obesity develop chronic low-grade states of systemic inflammation?

A

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
Q

Insulin resistance

A

Results in use of no glucose energy sources, leading to further increased blood lipid levels

49
Q

Type 2 diabetes

A

Development of insulin in resistance and a collection of metabolic alterations (dyslipidemia AKA metabolic syndrome)

50
Q

Metabolic Syndrome

A

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
Q

What are some other syndromes that can elevate lipids apart from type 2 diabetes?

A

Hypothyroidism
Nephrotic syndrome
Obstructive liver disease

Meds: beta-blockers, estrogens, protease inhibitors (used to treat HIV)

52
Q

Atherosclerotic lesions

A

Fatty streak
Fibrous atheromatous plaque
Complication lesion

53
Q

What is the most important complication of atherosclerosis?

A

Thrombosis that could cause occlusion of small vessels in the heart and brain

Aneurysms ma develop in arteries weakened by extensive plaque formation

54
Q

Clinical manifestations of atherosclerotic plaques

A

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
Q

Clinical manifestations of vasculitis

A

Fever
Mayalgia
Arthritis
Malaise

56
Q

Giant Cell Temporal Arteriti

A

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
Q

Peripheral Vascular Disorders

A

Disorders of circulation in the extremities

Symptoms: ischemia, pain, impaired function, infarction, tissue necrosis

58
Q

Acute Arterial Occlusion

A

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
Q

Embolus

A

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
Q

Thrombus

A

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
Q

Peripheral artery disease

A

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
Q

Thromboangiitis Obliterans

A

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
Q

Raynaud Disease

A

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
Q

Aneurysm

A

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
Q

True aneurysm

A

Bounded by a complete vessel wall

Blood remains within the vascular compartment

66
Q

False aneurysm

A

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
Q

Berry aneurysm

A

True aneursym that consists of a small, spherical dilation of the vessel at the bifurcation

Typically at circle of Willis

68
Q

Fusiform aneursym

A

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
Q

Saccular aneurysm

A

True aneurysm that extends over part of the circumference of the vessel (appears saclike)

70
Q

Dissecting aneurysm

A

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
Q

Causes of aneurysms

A

Congenital defects, trauma, infections, and atherosclerosis

72
Q

Aortic aneurysm

A

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
Q

Aortic dissection

A

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

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

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
Q

Skeletal muscle pump

A

Leg muscles increase flow in the deep venous channels and return venous home blood to the heart when a person walks

75
Q

Varicose veins

A

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
Q

Chronic Venous Insufficiency

A

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
Q

Venous thrombosis (thrombophlebitis)

A

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
Q

Hyper-coagulability state

A

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
Q

Virchow’s triad

A

Illustrates three key factors that lead to thrombus formation
1- vessel wall injury
2- stasis
3- hypercoagulability state

80
Q

General risk factors for hypertension

A 
Age
Gender
Race
Family History and genetics 
Diet
Dyslipidemia
Tobacco
Alcohol consumption 
Fitness level
Obesity
Insulin resistance and metabolic abnormalities
Obstructive sleep apnea
81
Q

Secondary hypertension

A

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
Q

Renal Hypertension

A

Renal disease causing secondary hypertension

Decreased ruin formation —> retention of salt and water

83
Q

Disorders of Adrenocortical hormones

A

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
Q

Pheochromocytoma

A

Cause hypertensive crisis as a result of tumor in the adrenal medulla

Tumor of chroma fin tissue that release catecholamine

85
Q

Coarctation of the aorta

A

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
Q

Target organ systems

A

Kidneys
Heart
Eyes
Blood vessels

87
Q

Consequence of target-organ damage in hypertension

A

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
Q

Pathophysiology of hypertension

A

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
Q

Hypertensive emergency

A

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
Q

Preeclampsia-eclampsia

A

Multisystem disorder that includes hypertension during pregnancy

Thrombocytopenia
Impaired liver function
Renal insufficiency
Pulmonary edema
Vision disturbances
Cerebral disturbances
91
Q

Gestational Hypertension

A

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
Q

Orthostatic Hypertension

A

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
Q

What is orthostatic hypotension often an early sign of?

A

Reduced blood volume or fluid deficit

Common cause: hypovolemia, excessive diuretics and diaphoresis, loss of GI fluids, prolonged bed ret

94
Q

Why is bed rest and impaired mobility so damaging for cardiac health?

A

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
Q

Drug-induced hypotension

A

Anti hypertensive drugs and psychotropic drugs

Pathophysiology (9 decks)

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