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Patho > Cardiovascular PPT 1 > Flashcards

Cardiovascular PPT 1 Flashcards

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
Q

secondary HTN CAUSES

A

identifiable cause

Caused by systemic disease that INC peripheral vascular resistance and/or cardiac output

CAUSES: polycystic kidney, RAS, pheochromocytomas, Cushing syndrome, OSA

26
Q

Hypertensive crisis (malignant HTN)

A

rapidly progressive (dramatic rise) HTN

diastolic pressure usually >120-140

Can LEAD to encephalopathy, severe HA, CVA (CNS involvement), AKI, CHF, aortic dissection

27
Q

HTN RISK FACTORS

A

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
Q

HTN MANIFESTATIONS

A

early stages: elevated BP, asymptomatic

“silent disease”

29
Q

HTN DIAGNOSIS

A

BP at least 140/90 on 2 or more occasions

30
Q

HTN TREATMENT

A

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
Q

Orthostatic Hypotension

A

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
Q

Aneurysm

A

local dilation or outpouching of a vessel wall

occur in either vein or artery

most occur in arteries

33
Q

True Aneurysm

A

ALL LAYERS BULGE

involve all three layers of arterial wall

most occur in aorta

34
Q

False Aneurysm

A

hole in wall = HEMATOMA

leak usually from sx and occurs between vascular graft and natural artery

35
Q

Aneurysm MANIFESTATIONS (based on location/size)

A

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
Q

Aneurysm CAUSES

A

anything that disrupts vasa vasorum

blunt trauma
**atherosclerosis
Marfan syndrome
pregnancy
**HTN
infectious syphilis
coarctation of aorta

37
Q

Aneurysm TREATMENT

A

BP maintenance = LOW blood volume and LOW BP = DEC mechanical forces

smoking cessation

B-adrenergic blockage

Surgery

38
Q

Aneurysm COMPLICATIONS

A

Aortic dissection (type A & B)

can disrupt the flow through the arterial branches

Type A = surgical emergency

39
Q

Embolism

A

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
Q

Embolism TYPES

A

1) thromboembolism (blood clot)
2) air embolism
3) amniotic fluid embolism
4) bacterial embolism
5) fat embolism
6) foreign matter

41
Q

PVD Thromboangiitis Obliterans (Buerger disease)

A

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
Q

PVD Raynaud Phenomenon

A

secondary to other systemic diseases or conditions, such as scleroderma, CA, hypothyroidism, pHTN

TX: arm exercises, medications

43
Q

PVD Raynaud Disease

A

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
Q

Atherosclerosis

A

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
Q

Atherosclerosis PROGRESSION

A

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
Q

Atherosclerosis MANIFESTATIONS

A

depends on the organ affected

s/sx result of inadequate perfusion of tissues

47
Q

Atherosclerosis TREATMENT

A

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
Q

PAD

A

atherosclerotic disease of arteries that perfuse limbs&raquo_space; 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
Q

PAD TREATMENT

A

vasodilators
antiplatelet
antithrombotic meds
cholesterol lowering meds

exercise rehabilitation

50
Q

CAD

A

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
Q

CAD Modifiable RISK FACTORS

A

dyslipidemia
HTN
smoking
DM/insulin resistance
obesity and/or sedentary lifestyle
atherogenic diet (causes inflammation)

52
Q

CAD Dyslipidemia

A

strong link b/w lipoproteins and CAD

LDL - monitor in CAD

INC LDL = role in endothelial injury, inflammation, immune responses

53
Q

CAD Angina Pectoris

A

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&raquo_space; fatigue, nausea, SOB

54
Q

CAD Angina Pectoris TX

A

nitrates
B-adrenergic receptor blockers
CCB
Statins
anti-thrombotics

CABG

55
Q

Unstable Angina

A

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
Q

Unstable Angina TREATMENT

A

immediate hospitalization w/ administration of nitrates, antithrombotics, anticoagulants

ASA
BB and ACE-I
Emergent PCI

57
Q

MI

A

prolonged ischemia causes IRREVERSIBLE damage to heart muscle

structural and functional changes:
1)myocardial stunning
2) hibernating myocardium
3) myocardial remodeling

Repair

58
Q

MI Types (STEMI and NSTEMI)

A

NSTEMI: subendocardial infarction (partial thickness MI)

STEMI: transmural infarction (full thickness MI)
>ST elevation = immediate intervention (CATH LAB)

59
Q

MI MANIFESTATIONS

A

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
Q

MI TREATMENT

A

hospitalization
immediate administration of supplemental O2 and ASA
morphine sulfate
bed rest
cardiac meds
percutaneous coronary intervention (PCI)
surgery

61
Q

MI COMPLICATIONS

A

dysrhythmias
HF
cardiogenic shock
pericarditis
ventricular aneurysm

Patho (2 decks)

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