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Patho Test #2 > Cardiovascular > Flashcards

Cardiovascular Flashcards

1
Q

What are varicose veins?

What are they caused by?

Treatment options?

A

Veins in which blood has pooled

Caused by:

  • trauma or gradual venous distention
  • Defective valves from birth - (congenitally defective valves)
  • Pregnancy
  • Thrombophlebitis

Treatment:

  • External compression stockings
  • Surgery
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2
Q

What are the typical sites of varicose veins?

A

legs, anus, and lower esophagus

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3
Q

What is Thrombophlebitis?

A

swelling of a vein caused by a blood clot

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4
Q

What is venous insufficiency?

Why does it occur?

A

condition in which the veins have problem getting blood from the legs back to the heart
Long-term condition (goes from varicose veins to venous insufficiency).

Occurs b/c a vein a partly blocked or if blood is leaking around the valves of the veins.

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5
Q

If venous insufficiency is not treated, what can it lead to?

A

Stasis Ulcers.

Where:
Below the knee-primary found on the inner part of the leg just above the ankle.

Ulcers may affect one or both legs.

Base-red in color and may be covered with yellow fibrous tissue.

There may be a green or yellow discharge if the ulcer is infected. Fluid drainage can be significant.

Boarders-usually irregularly shaped.

The surrounding skin is often discolored and swollen. It may even feel warm or hot.

The skin may appear shiny and tight, depending on the amount of edema.

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6
Q

What is a DVT?

Where is it commonly found?

A

Deep Vein Thrombosis - Obstruction of venous flow leading to increased venous pressure

Blood clot that forms in a vein deep inside a part of the body. Mainly affects large veins in the lower leg or thigh.

DVTs are most common in adults over age of 60. Clot breaks off and moves through the blood stream=embolism. Embolism can get stuck in brain, lungs, heart, or other area….leading to damage.

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7
Q

Triad of Virchow

A

Venous stasis
Venous endothelial damage
Hypercoagulable states

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8
Q

What causes a clot in a DVT?

A

Accumulation of clotting factors causing a clot to form and an inflammatory response.

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9
Q

Symptoms of a DVT

A

may not have symptoms or may cause pain, redness, warmth, and edema

Problem is that it may totally occlude the vein and lead to ulceration or break off and move the lungs (pulmonary embolus)

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10
Q

What is Essential Arterial Hypertension?

A

BP of 140/90 or greater

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11
Q

What are the primary and secondary causes of Essential Arterial Hypertension?

A

Primary: The disease
Secondary: Medications or other disorders

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12
Q

Hypertension

A

Elevations of systolic pressure are caused by increases in cardiac output, total peripheral vascular resistance, or both

Isolated systolic hypertension—becoming prevalent in all age groups

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13
Q

Primary hypertension

A

Also known as essential (familial) or idiopathic (unknown) hypertension

Genetic and environmental factors
Affects 92% to 95% of individuals with hypertension

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14
Q

What are some risk factors for Hypertension?

A 
Risk factors: 
High sodium intake
Natriuretic peptide abnormalities
Obesity
Insulin resistance
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15
Q

Secondary Hypertension

A

Caused by a systemic disease (underlying) process that raises peripheral vascular resistance or cardiac output

less than 10% of people have this

Renal artery stenosis, renal parenchymal disease, pheochromocytosis, drugs

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16
Q

What are the symptoms of Hypertension?

A

Early stages may not have symptoms other than increased blood pressure

Silent disease

Most the clinical presentation is due to organ damage

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17
Q

How is hypertension diagnosed?

A

at least (2) readings, (2) minutes apart
Person at rest for 5 minutes
Arm supported at level of the heart
No cigarettes or caffeine in previous 30 minutes

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18
Q

Test(s) and treatment(s) for hypertension

A

Test: 24 hour serial BP monitoring, CBC, urinalysis, BMP for creatinine, cholesterol, and triglycerides and electrolytes, glucose

Tx: exercise, weight loss/control, diet

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19
Q

A-type natriuretic peptides

A

also called atrial natriuretic peptides.

They’re made/stored/released largely by the atria,

High BP = body makes more A-type NP

*seen in congestive heart failure, where increased blood volume and higher levels of extracellular fluid (fluid overload) stretch the heart’s walls.

In patients with heart failure, A-type natriuretic peptides are also made by the ventricles

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20
Q

Where are A & B Natriuretic Peptides made?

A

In the Ventricles

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21
Q

What is the function of the A-Natriuretic Peptides?

A

causes a reduction in blood volume and therefore a reduction in heart output and blood pressure

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22
Q

What is the funciton of B-Natriuretic Peptides?

A

acts as a natural diuretic, eliminating fluid, relaxing blood vessels and funneling sodium into the urine.

When the heart is damaged, the body secretes very high levels of B-type natriuretic peptide into the bloodstream in an effort to ease the strain on the heart

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23
Q

What is the function of C-Natriuretic Peptides?

A

They cause relaxation of blood vessels, helping to lower blood pressure.

produced by cellsthat line the blood vessels.

Unlike A-type and B-type natriuretic peptides, they don’t have direct natriuretic activity.

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24
Q

Complicated Hypertension

A

Chronic hypertensive damage to the walls of systemic blood vessels

Smooth muscle cells undergo hypertrophy and hyperplasia with fibrosis of the tunica intima and media

Affects heart, kidneys, retina most especially
Can result in transient ischemic attack/stroke, cerebral thrombosis, aneurysm, dementia

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25
Q

Malignant Hypertension

A

Rapidly progressive hypertension

Diastolic pressure is usually >140 mm Hg

Life-threatening organ damage

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26
Q

Postural Hypotension

A

Decrease of BP 20/10 within 3 minutes of moving

Can be acute or chronicto a standing position

S/Sx: dizziness, blurring or loss of vision, syncopy or fainting

*Can be controlled with drugs or by increasing fluid and salt intake, wearing thigh-high compression stocking

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27
Q

atherosclerosis

A

chronic inflammatory process in blood vessels. Endothelial injury plays a critical role in initiating the process. (plaque builds up)

Circulating lipids in the blood are instrumental in the evolution of a lesion.

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28
Q

Aneurysms

A

Weakening and rupture of vessels

The majority occur in the abdomen.

are typically without s/sx until they rupture…severe pain and hypotension

Marfan syndrome individuals are at high risk

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29
Q

Blood Clot

How is it diagnosed?

Tx?

A

Pooling blood

Diagnosed via doppler ultrasound or angiography

Tx blood thinners, thrombolytics

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30
Q

What is one of the most important observations to make in a post-operative patient?

A

observe for presence of thrombus formation, prevention

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31
Q

Thrombus formation

A

Blood clot that remains attached to the vessel wall

Risk factors include intimal injury/inflammation, obstruction of flow, pooling (stasis)

Thromboembolus
Thrombophlebitis
Arterial thrombi
Venous thrombi

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32
Q

Embolism

A

can be any bolus of matter that is circulating in the bloodstream

Dislodged thrombus
Air bubble
Amniotic fluid
Aggregate of fat
Bacteria
Cancer cells
Foreign substance
33
Q

Thromboangiitis obliterans (Buerger disease)

A

Occurs mainly in young men who smoke

Inflammatory disease of peripheral arteries resulting in the formation of nonatherosclerotic lesions (Hands and feet)

Obliterates the small and medium-sized arteries

S/Sx: pain and tenderness of the extremity, b/c blood flow slows down in the vessels and it causes the skin to have a red color (rubor)

Tissue does not get enough oxygen, it becomes thin and shiny, nails become malformed and thickened…can progress to gangrene

Dx is based on age < 45, history of smoking, and S/Sx

Tx: Stop smoking, drugs to relax vasospasms, exercise to increase blood flow to the extremity

34
Q

Raynaud phenomenon and Raynaud disease

A

small vessels of the hands and feed constrict excessively in an exaggerated response to cold.

The fingers and toes become cold and blue.

Stress has also been implicated in triggering this response.

Raynaud disease is a primary vasospastic disorder of unknown origin

Manifestations include pallor, cyanosis, cold, pain

Tx: prevention (avoid cold environments, dress warmly, decrease stress)
Some medications can be use to dilate the blood vessels if symptoms become hard for the patient to control.

35
Q

Raynaud phenomenon

A 
secondary to other systemic diseases or conditions:
Collagen vascular disease
Smoking
Pulmonary hypertension
Myxedema
Cold environment
36
Q

Arteriosclerosis

A

Chronic disease of the arterial system

Abnormal thickening and hardening of the vessel walls

Smooth muscle cells and collagen fibers migrate to the tunica intima

37
Q

Atherosclerosis

A

Form of arteriosclerosis

Thickening and hardening caused by accumulation of lipid-laden macrophages in the arterial wall

Plaque development

38
Q

Intermittent Claudication

A

muscle cramp like pain which comes on with exercise. most often occurs as a pain in the calf, thigh or buttock after walking a certain distance and is relieved by rest.

caused by narrowing or blockage in the arteries taking blood to the leg.

39
Q

Coronary Artery Disease

A

coronary arteries which deliver oxygen and nutrients to the heart’s own tissue become blocked by a buildup of cholesterol fats, often referred to as “plaque”.

Plaque deposits can make the arteries stiff and irregular (atherosclerosis).

Any narrowing, or blockage, of the coronary arteries reduces the blood supply to the heart tissue, therefore reducing the amount of oxygen and nutrients delivered. This inhibits the normal function of the heart muscle.

40
Q

Myocardial ischemia

A

Local, temporary deprivation of the coronary blood supply

When a thrombus forms over a ruptured plaque, unstable angina can be a “red flag”…when the plaque is becoming eroded, it can cause episodes of occlusion and vasoconstriction for about 10-20 minutes with return to normal perfusion.

41
Q

Stable angina

A

pain with exercise or stress; when oxygen demand outweighs oxygen supply; once blood flow is restored, the pain subsides (usually treated with rest and nitrates)

42
Q

Prinzmetal angina

A

(variant angina) as a result of vasospasms and can happen at rest (during sleep)

43
Q

Silent ischemia

A

can be asymptomatic; person may complain of fatigue, dyspnea or feeling of unease…this type of ischemia may be heralding an imminent MI.

44
Q

3 types of Angina

“C.U.P.”

A

(C) Chronic Stable Angina (fixed stenosis)
-Demand Ischemia
(U) Unstable Angina (thrombus)
-Supply Ischemia
(P) Printzmetal’s Variant Angina (vasospasm)
-Supply Ischemia

45
Q

Myocardial Infarction

A

when coronary blood flow is interrupted for an extended period of time.

46
Q

non-STEMI

A

When the occlusion in an MI resolves before necrosis of distal tissues occurs

47
Q

STEMI

A

When necrosis occurs in a MI

characterized by an elevated ST segment on ECG

48
Q

Hyperglycemia occurs about _______ after an MI and is associated with an increased risk of death.

A

72 hours

49
Q

What does Ang. II do during a MI?

A

causes an increase in water and salt in the circulation and vasoconstriction of blood vessels->increase work load on the heart.

Ang II also causes cardiac remodeling

50
Q

Remodeling

A

the heart’s attempt to compensate for damage that has resulted from ischemic tissues; over time the changes will not continue to function.

walls of the ventricles thicken

The left ventricle becomes non-compliant to blood volume changes…becomes ridged…can cause problems with pumping against increased peripheral resistance.

a process caused by angiotensin II, aldosterone, catecholamines, adenosine, and inflammatory cytokines that cause hypertrophy of cardiac cells but in the changes, they lose contractility.

51
Q

How long does it take for cardiac cells to die without access to oxygen?

A

20 minutes

52
Q

What are the manifestations of a MI?

A 
Manifestations:
Sudden severe chest pain; may radiate
Nausea, vomiting
Diaphoresis
Dyspnea
53
Q

What are (3) major disorders of the pericardium:

“Pericardial C.A.P.”

A

(C) Constrictive pericarditis
(A) Acute pericarditis
(P) Pericardial effusion (Tamponade)

54
Q

Acute pericarditis

A

is an inflammation of the sac surrounding the heart

the area becomes roughened and scarred. Exudates develop and pericardial effusions are possible.

55
Q

Pericardial effusions

A

refer to an accumulation of fluid in the pericardial cavity due to inflammation or infection

Accumulation of fluid in the pericardial cavity
May be exudate
Serosanguineous
Frank blood

56
Q

Pericardial Effusion: Cardiac Tamponade

What is the treatment?

A

fluid compresses the heart…this is life-threatening because it limits ventricular filling reducing stroke volume and cardiac output.
May develop right-sided heart failure

Treatment: pericardiocentesis (aspiration of excessive pericardial fluid)

57
Q

Constrictive Pericarditis

Treatment?

A

is due to fibrous scar tissue that develops gradually.

It puts too much pressure on the heart.

treatment: initially to restrict sodium intake and to give medications to improve cardiac output.

58
Q

Dilated Cardiomyopathy

A

The left ventricle becomes enlarged.

This type can be caused by:
Alcoholism
Pregnancy
Genetic
Diffuse ischemic injury
59
Q

Hypertrophic Cardiomyopathy

A

The walls of the left ventricle become so enlarged that they encroach on the space inside the ventricle.

60
Q

Restrictive Cardiomyopathy

A

The heart muscle becomes stiff and cannot accommodate the usual volume of blood during diastole.

61
Q

Aortic Valve Stenosis

A

narrowing of the valve that causes resistance to the outflow (flow of blood moving forward) of blood through that valve.

62
Q

Valve Regurgitation

A

Regurgitation of the valve is when the valve does not close properly allowing blackflow (reverse flow of blood) of blood.

63
Q

Rheumatic Fever

A

Systemic, inflammatory disease caused by a delayed immune response to pharyngeal infection by the group A beta-hemolytic streptococci

Febrile illness (Inflammation of the joints, skin, nervous system, and heart)

untreated = rheumatic fever causes rheumatic heart disease

64
Q

Rheumatic Heart Disease

Treatment?

A

Vegetation accumulates on the valves causing lesions; these eventually cause scarring and cause the valves to lose their eleacity and may cause the leaflets to adhere to each other.

Tx: 10 days of oral penicillin or erythromycin and NSAIDS

65
Q

Infective Endocarditis

Treatment?

A

Infections and inflammation of the endocardium; can be bacterial or viral.

Tx: anti-infectives, may need surgery to excise infected tissues, valve replacement

66
Q

Heart Failure

A

When the heart is not able to pump blood to perfuse tissues or when there is an increase diastolic filling pressure of the left ventricle or both of these situations heart failure can occur

67
Q

Systolic heart failure

A

Inability of the heart to generate adequate cardiac output to perfuse tissues
Ventricular remodeling
Causes include myocardial infarction, myocarditis, cardiomyopathy

68
Q

Diastolic heart failure

A

Pulmonary congestion despite normal stroke volume and cardiac output
Causes include myocardial hypertrophy and ischemia, diabetes, valvular and pericardial disease

69
Q

Manifestations of left heart failure:

A

Result of pulmonary vascular congestion and inadequate perfusion of the systemic circulation–

Include dyspnea, orthopnea, cough of frothy sputum, fatigue, decreased urine output, and edema

Physical examination often reveals pulmonary edema (cyanosis, inspiratory crackles, pleural effusions), hypotension or hypertension, an S3 gallop, and evidence of underlying CAD or hypertension

70
Q

Right heart failure

Signs and symptoms?

A

Most commonly caused by a diffuse hypoxic pulmonary disease

Can result from an increase in left ventricular filling pressure that is reflected back into the pulmonary circulation

S/Sx:
Shortness of breath
Swelling of feet and ankles
Voiding frequently
Fatigue
Weakness
Fainting
71
Q

What is Shock?

A

Cardiovascular system fails to perfuse the tissues adequately

Leads to impaired cellular metabolism
Impaired oxygen use
Impaired glucose use

Manifestations:
hypotension, tachycardia, increased respiratory rate

72
Q

What are the (4) types of shock?

“CHampS rN” or “CHaNS -pron. like chance”

A

Cardiogenic
Hemorrhagic
Septic
Neurogenic

73
Q

Cardiogenic shock

A

is caused by heart failure. Essentially, the heart cannot maintain cardiac output for adequate perfusion.

74
Q

Hemorrhagic Shock

A

when there is such a low volume of blood that the heart cannot pump it adequately

75
Q

Septic shock

A

when there is a systemic dilation of small vessels due to the toxins released by bacteria…causes pooling of blood in the periphery.

76
Q

Neurogenic shock

A

when there is a systemic dilation of the small vessels due to problems with neuronal innervation…causes an inadequate return of blood to the heart, causing it to pool in the periphery.

77
Q

Multiple Organ Dysfunction Syndrome (MODS)

A

Progressive dysfunction of two or more organ systems resulting from an uncontrolled inflammatory response to severe illness or injury.
Triggered by: chronic inflammation, necrotic tissue, severe trauma, burns

Most common: sepsis, septic shock (low grade fever, tachycardia, dyspnea, altered mental state)

78
Q

MODS manifestations

A

Manifestations:
Respiratory-lungs are the first to fail (Adult respiratory distress syndrome-ARDS)

Hepatic-7-10 days then the liver fails

Renal-14-21 days, the kidneys and the GI fails

Myocardial failure-eventually the heart fails

Patho Test #2 (2 decks)

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