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Cardiovascular PPT 1 Flashcards

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1
Q

cardiovascular disease

A

leading cause of death

disorders of veins, arteries, and heart wall

patho focused on genetic, neurohumoral, inflammatory, metabolic mechanisms that underlie tissue and cellular alterations

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2
Q

circulatory system: VEINS

A

> blood from tissues back to heart
surface of skin
veins contain valves
would collapse if blood flow stops

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3
Q

circulatory system: ARTERIES

A

> blood from heart to tissues
positioned deeper
more muscular
generally remain open if blood flow stopped

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4
Q

DISEASES of the VEINS

A

varicose veins
chronic venous insufficiency
DVT
superior vena cava syndrome

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5
Q

Varicose veins

A

caused by weak vein walls or valves

female:male predominance 3:1

blood back-up and pooling = distortion of veins, leakage, INC intravascular hydrostatic pressure, inflammation

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6
Q

Varicose veins CAUSES

A

incompetent valves
venous obstruction
muscle pump dysfunction
or a combo

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7
Q

Varicose veins progress to…

A

Chronic venous insufficency

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8
Q

Chronic Venous Insufficiency

A

persistent ambulatory lower extremity venous HTN

venous HTN, circulatory stasis, tissue hypoxia = inflammatory reaction in vessels and tissue

can cause: edema, pain, chronic skin change (hyperpigmentation), necrosis (venous statis ulcers)

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9
Q

Chronic Venous Insufficiency MANIFESTATION

A

along continuum

asymptomatic spider veins - varicose veins - chronic vascular insufficiency

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10
Q

Chronic Venous Insufficiency TREATMENT

A

conservative measures

weight loss
DEC time spent standing/sitting
leg elevation
compression stockings
physical exercise

endovenous ablation or foam sclerotherapy

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11
Q

Define Chronic venous insufficiency

A

persistent ambulatory lower extremity venous HTN

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12
Q

DVT

A

thrombosis: CLOT

detached thrombus: thromboembolism; can lead to PE

clot in large vein - cause obstruction of venous flow leading to INC venous pressure

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13
Q

DVT: Virchow Triad

A

1) venous statis (immobility, obesity, age, prolonged leg dependency)

2) venous intimal damage (PICC line, trauma, IV meds)

3) hypercoagulable states (CA, pregnancy, contraceptive use, HRT)

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14
Q

Post-thrombotic syndrome

A

1/3 of patients

ongoing pain, edema from outflow obstruction

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15
Q

PATHO of a CLOT (review)

A

Intrinsic: factor XII

Extrinsic: factor VII

common pathway: factor X

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16
Q

DVT Tests/Treatment

A

PREVENTION IS CRUCIAL
mobilization and prophylactic LMWH

Tests: D-dimer, doppler

Treatment:
LMWH
Direct thrombin inhibitors
ASA tx
Catheter directed thrombolytic tx

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17
Q

Superior Vena Cava Syndrome

A

progressive occlusion of SVC = venous distention in upper extremities and head

LEADING CAUSE: non-small cell lung CA, lymphoma

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18
Q

Superior Vena Cava Syndrome MANIFESTATIONS

A

edema
**venous distention (face, neck, trunk, upper extremities)
cyanosis
dyspnea
dysphagia
hoarseness, stridor
cough
chest pain
CNS changes
Resp distress

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19
Q

Superior Vena Cava Syndrome TREATMENT

A

radiation and chemo

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20
Q

DISEASES of the ARTERIES

A

HTN
Orthostatic hypotension
Aneurysm
Thrombus formation
Embolism
PAD
Atherosclerosis
CAD
MI
Acute coronary syndromes

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21
Q

HTN

A

consistent elevation of systolic arterial BP

sustained BP of 140/90 or higher

affects entire CV system:
systolic HTN most significant factor in causing target organ damage

INC risk of MI, kidney disease, stroke

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22
Q

Primary vs Secondary HTN

A

Primary HTN (essential, 95% of cases) : genetic and environmental factors

Secondary HTN: caused by altered hemodynamics from underlying primary disease or drugs

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23
Q

HTN CAUSES

A

INC in cardiac output or total peripheral resistance, or both

cardiac output INC: condition that INC HR or stroke volume

peripheral resistance INC: INC blood viscosity, vasoconstriction

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24
Q

primary HTN (polygenetic) CAUSES

A

mediated by neurohumoral effects

overactivity of sympathetic nervous system and RAAS, and alterations in natriuretic peptides

age range to develop usually 25-55 (before 20 usually not primary HTN)

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25
secondary HTN CAUSES
identifiable cause Caused by systemic disease that INC peripheral vascular resistance and/or cardiac output CAUSES: polycystic kidney, RAS, pheochromocytomas, Cushing syndrome, OSA
26
Hypertensive crisis (malignant HTN)
rapidly progressive (dramatic rise) HTN diastolic pressure usually >120-140 Can LEAD to encephalopathy, severe HA, CVA (CNS involvement), AKI, CHF, aortic dissection
27
HTN RISK FACTORS
positive family hx advancing age gender: female race: AA INC sodium intake glucose intolerance (DM) insulin resistance heavy ETOH obesity cigarettes LOW K+, Mg+, Ca+
28
HTN MANIFESTATIONS
early stages: elevated BP, asymptomatic "silent disease"
29
HTN DIAGNOSIS
BP at least 140/90 on 2 or more occasions
30
HTN TREATMENT
DEC or eliminating risk factors dietary changes (DASH) Smoking cessation exercise program Pharmacologic tx: ACE-I, ARBs, aldosterone antagonists CCB, combo thiazide diuretic and other antihypertensives
31
Orthostatic Hypotension
DEC in systolic (20mmHg) and diastolic (10mmHg) pressures on STANDING Primary (SNS) vs secondary (disease, meds) orthostatic hypotension manifestation: fainting upon standing TX: DEC salt intake, raise HOB, wear compression stockings, expand volume w/ mineralcorticoids, administer vasoconstrictors (midodrine)
32
Aneurysm
local dilation or outpouching of a vessel wall occur in either vein or artery most occur in arteries
33
True Aneurysm
ALL LAYERS BULGE involve all three layers of arterial wall most occur in aorta
34
False Aneurysm
hole in wall = HEMATOMA leak usually from sx and occurs between vascular graft and natural artery
35
Aneurysm MANIFESTATIONS (based on location/size)
1)ascending aorta - dysrhythmias, AI, HF, LV dysfunction, embolism of clots to brain and other vital organs 2)descending aorta - asymptomatic until RUPTURE, painful, chest/back pain, hypotension, pulsating mass in abdomen 3)thoracic - dysphagia, dyspnea caused by pressure 4)abdomen - flow to LEs impaired = ischemia, cold foot
36
Aneurysm CAUSES
anything that disrupts vasa vasorum blunt trauma **atherosclerosis Marfan syndrome pregnancy **HTN infectious syphilis coarctation of aorta
37
Aneurysm TREATMENT
BP maintenance = LOW blood volume and LOW BP = DEC mechanical forces smoking cessation B-adrenergic blockage Surgery
38
Aneurysm COMPLICATIONS
Aortic dissection (type A & B) can disrupt the flow through the arterial branches Type A = surgical emergency
39
Embolism
bolus of matter circulates in the bloodstream and then lodges, obstructing blood flow can occur in veins or arteries occlusion of a coronary artery (MI) or cerebral artery (stroke) Can lead to ischemia or infarction or necrosis DISTAL to the obstruction
40
Embolism TYPES
1) thromboembolism (blood clot) 2) air embolism 3) amniotic fluid embolism 4) bacterial embolism 5) fat embolism 6) foreign matter
41
PVD Thromboangiitis Obliterans (Buerger disease)
occurs mainly in SMOKERS inflammatory disease of peripheral arteries obliterates small and medium sized arteries pain and tenderness develop in affected part sluggish blood flow, rubor, and cyanosis TX: smoking cessation; vasodilators; exercise; bone marrow transplantation
42
PVD Raynaud Phenomenon
secondary to other systemic diseases or conditions, such as scleroderma, CA, hypothyroidism, pHTN TX: arm exercises, medications
43
PVD Raynaud Disease
primary vasospastic disorder of UNKNOWN origin can be triggered by cold, emotional stress TX: avoidance of emotional stress and cold and cessation of cigarette smoking
44
Atherosclerosis
plaque builds up in arterial wall pathologic process thickening and hardening or arterial wall caused by the accumulation of lipid-laden macrophages -- plaque develops LEADING CAUSE: CAD and cerebrovascular disease
45
Atherosclerosis PROGRESSION
chronic inflammatory condition BEGINS w/ injury to endothelial cells that line artery walls 1)endothelium injury 2)inflammation of endothelium 3)cytokines released 4)cellular proliferation 5)macrophage migration 6)LDL oxidation w/ oxidative stress 7)fatty streak 8)fibrous plaque 9)complicated plaque
46
Atherosclerosis MANIFESTATIONS
depends on the organ affected s/sx result of inadequate perfusion of tissues
47
Atherosclerosis TREATMENT
focuses on DEC risk factors, removing initial causes of vessel damage, preventing lesion progression exercising, smoking cessation, controlling HTN/DM, DEC LDL levels by diet or meds or both
48
PAD
atherosclerotic disease of arteries that perfuse limbs >> especially limbs prevalent: DM or smokers Intermittent claudication: obstruction of arterial blood flow in the iliofemoral vessels, resulting in pain w/ ambulation advanced PAD can lead to "rest" pain
49
PAD TREATMENT
vasodilators antiplatelet antithrombotic meds cholesterol lowering meds exercise rehabilitation
50
CAD
any vascular disorder that narrows or occludes the coronary arteries reversible MI or irreversible infarction may result COMMON CAUSE: atherosclerosis Non-modifiable risk factors: advanced age, family hx, males, females after menopause
51
CAD Modifiable RISK FACTORS
dyslipidemia HTN smoking DM/insulin resistance obesity and/or sedentary lifestyle atherogenic diet (causes inflammation)
52
CAD Dyslipidemia
strong link b/w lipoproteins and CAD LDL - monitor in CAD INC LDL = role in endothelial injury, inflammation, immune responses
53
CAD Angina Pectoris
supply of coronary blood NOT EQUAL to demand of myocardium oxygen/nutrients 1) stable 2) unstable 3) prinzmetal (variant) 4) silent ischemia: does NOT cause angina >> fatigue, nausea, SOB
54
CAD Angina Pectoris TX
nitrates B-adrenergic receptor blockers CCB Statins anti-thrombotics CABG
55
Unstable Angina
chest pain at rest reversible MI transient episodes of thrombotic vessel occlusion and vasoconstriction occur at the site of plaque damage w/ return of perfusion before significant myocardial necrosis occurs
56
Unstable Angina TREATMENT
immediate hospitalization w/ administration of nitrates, antithrombotics, anticoagulants ASA BB and ACE-I Emergent PCI
57
MI
prolonged ischemia causes IRREVERSIBLE damage to heart muscle structural and functional changes: 1)myocardial stunning 2) hibernating myocardium 3) myocardial remodeling Repair
58
MI Types (STEMI and NSTEMI)
NSTEMI: subendocardial infarction (partial thickness MI) STEMI: transmural infarction (full thickness MI) >ST elevation = immediate intervention (CATH LAB)
59
MI MANIFESTATIONS
sudden severe chest pain (+SOB, N/V, radiating pain to neck, jaw, arm) EKG changes or not, if NSTEMI Troponin I: most specific hyperglycemia
60
MI TREATMENT
hospitalization immediate administration of supplemental O2 and ASA morphine sulfate bed rest cardiac meds percutaneous coronary intervention (PCI) surgery
61
MI COMPLICATIONS
dysrhythmias HF cardiogenic shock pericarditis ventricular aneurysm

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