Week 4 Flashcards
1
Q
What are the (2) lipid pathways?
A
- Exogenous lipid pathway
- Endogenous lipid pathway
2
Q
Absorption of fats from the digestive tract into the circulation describes which lipid pathway?
A
Exogenous lipid pathway
3
Q
Transporting of fats synthesized in the liver between the liver and the
peripheral tissues describes which lipid pathway?
A
Endogenous lipid pathway
4
Q
Cholesterol/triglycerides levels that are too high can increase your chance of getting __________, _________, etc.
A
- heart disease
- stroke
5
Q
(2) The medical term for high blood cholesterol are?
A
lipid disorder or hyperlipidemia.
6
Q
How many types of lipoproteins are there?
A
5
7
Q
Excess LDL binds to ____________________?
A
endothelial cells
8
Q
Too much fats = ________________ = too much in blood
A
Saturation of liver
9
Q
What oxidizes LDL?
A
Macrophages
10
Q
Phagocytic macrophages have ____________ that bind to LDL
A
receptors
11
Q
Oxidized LDL by Macrophages are key component of ________________?
A
atherosclerosis
12
Q
______________________ is a condition with a high amount of LDL, or the bad cholesterol
A
Hypercholesterolemia
13
Q
Increase _________________ = increase HDLs
A
unsaturated fats
14
Q
_________________ is formation of
fibro-fatty lesions in the intimal lining of
large and medium- sized arteries
A
Atherosclerosis
15
Q
What is the leading cause of CAD,
stroke, peripheral arterial disease?
A
Atherosclerosis
16
Q
Accumulation of _______________________ forming a lesion called a plaque
A
lipid- loaded macrophages
17
Q
Pathogenesis of Atherosclerotic Lesions (4) in order?
A
- Endothelial injury
- Migration of inflammatory
cells - Lipid accumulation and
smooth muscle proliferation - Gradual development of the
atheromatous plaque
18
Q
Endothelial cells express ________________________molecules that bind monocytes and other inflammatory cells.
Which stage of atherosclerosis lesions is this?
A
- selective adhesion
- Inflammatory cells migrate
19
Q
_______________ adhere to endothelium, transform into macrophages and engulf LDLs
Which stage of atherosclerosis lesions is this?
A
- Monocytes
- Inflammatory cells migrate
20
Q
In which stage of atherosclerosis lesions do macrophages engulf LDLs then releases toxic oxygen species that oxidize LDL?
A
Lipid accumulation
21
Q
When macrophages engulf LDLs, they release toxic oxygen and also this leads to ________________________?
A
platelet aggregation
22
Q
Oxidized LDL (ingested by macrophage) becomes?
A
foam cells
23
Q
Foam cells leads to ___________________ streaks covered by fibrous cap of tissue
A
lesions/fatty
24
Q
Rupture or erosion of an unstable
fibrous cap may lead to _______________
into the plaque or ____________________ of the vessel lumen
A
- hemorrhage
- thrombotic occlusion
25
Core contains ________ filled macrophages and __________ smooth muscle debris
1. lipid
2. necrotic
25
unstable plaques are characterized by (4):
- Thin fibrous caps
- May completely block artery
- Plaque can rupture and cause a thrombus to form
- The clot may break free and become an embolus
26
Stable plaques are characterized by (3):
- Thick fibrous caps
- Partially block vessels
- Do not tend to form clots or emboli
26
______________________ is the force that that moves blood through arterial
system
Arterial Blood Pressure
27
What is the most common of all health problems?
Hypertension
28
Arterial Blood Pressure is the contraction & relaxation of the _____________________?
left ventricle
29
HTN = Caused by (3)?
- Increase cardiac output
- Increase total peripheral resistance (PR)
- or both
30
CO is increased by any condition that increases (2)?
- Heart rate
- stroke volume
31
PR is increased by any factor that (2)?
- Increases blood viscosity
- Decreases in vessel diameter
32
_________________________ is force opposing the movement of blood within the blood vessels
Systemic vascular resistance (SVR)
33
Primary hypertension is AKA?
essential hypertension
34
Chronic elevation of BP occurs without
evidence of other disease conditions is what kind of hypertension?
Primary hypertension
35
Elevation of BP results from some other
disorder is what kind of hypertension?
Secondary hypertension
36
__________________________ is markedly high BP is accompanied by progressive target-organ damage
Hypertensive crisis
Systolic >180mmHg
Diastolic >120 mmHg
37
_______________ is abnormal drop in BP when assuming the standing position
Orthostatic hypotension
38
_______________ is a heart disease caused by impaired coronary blood flow
Coronary artery disease (CAD)
39
_______________ is the most common cause of CAD
Atherosclerosis
40
CAD does not produce
symptoms until it is advanced
because of ________________?
collateral flow
41
______________________ is your body's way of working around blood flow blockages.
Collateral circulation
42
CAD is divided into (2) types of disorders:
- Acute coronary syndromes (ACS)
- Chronic ischemic heart disease
43
What type of CAD is the following symptoms:
- Caused by acute plaque disruption
- Range from unstable angina to MI
Acute coronary syndrome (ACS)
44
What type of CAD is the following symptoms:
- Caused by atherosclerotic or vasospastic obstruction of coronary arteries (i.e. stable angina)
Chronic ischemic heart disease
45
Pathogenesis of CAD with Stable plaque will lead to _________________?
Stable angina
46
Pathogenesis of CAD with unstable plaque will lead to what (4) events in order?
1. Plaque disruption
2. Platelet aggregation
3. Thrombus formation
4. Unstable angina and MI
47
Pathophysiology of CAD - 1st step
Occlusion of arteries
48
Pathophysiology of CAD - 2nd step
After a few minutes, contractility stops depriving the heart's cells of glucose for aerobic metabolism.
49
Pathophysiology of CAD - 3rd step
Lactic acid accumulates: myocardial fibers are irritated by the lactic acid
50
Pathophysiology of CAD - 4th step
Pain ensues- angina
51
Pathophysiology of CAD - 5th step
Lead to MI
52
What are the (3) Types of Angina?
- Stable angina
- Variant angina (Printzmetal’s)
- Silent myocardial ischemia
53
What type of angina is the following:
Pain when heart’s oxygen demand increases
Stable angina
54
What type of angina is the following:
Pain when coronary arteries spasm
Variant angina (Printzmetal’s)
55
What type of angina is the following:
Myocardial ischemia without pain
Silent myocardial ischemia
56
_____________ is a sudden attack of chest pain or pressure due to transient myocardial ischemia
Angina pectoris
57
Chronic Stable Angina is often associated with ______________?
atherosclerosis
58
Chronic Stable Angina is felt in what area?
substernal area
59
ACS classified based on presence or
absence of ______________ elevation on
ECG
ST-segment
60
Classic changes that occur with ACS include (3):
* T wave inversion
* ST elevation
* development of an abnormal Q wave
61
Diagnosis of ACS uses ____________________?
serum biomarkers
62
___________ assays are the primary biomarker tests for the diagnosis of MI.
Troponin
63
Serum biomarkers for ACS include (2):
troponin I and troponin T
64
Troponin levels begin to rise ___ hours after onset of MI. They may stay elevated for _______ days (useful for late diagnosis
1. 3 hours
2. 7-10 days
65
__________________ is an isoenzyme highly specific for injury to myocardial tissue
CK-MB or creatine-kinase
66
Creatine-kinase becomes elevated within _____ hrs after injury
4-8hrs
67
NSTEMI means?
Non-ST Segment Elevation MI
68
Is NSETMI or unstable angina related to sufficient myocardial damage to release detectable quantities of troponin?
NSETMI
69
Are there serum biomarker changes in unstable angina?
No
70
What meds are a good treatment for Unstable Angina/NSTEMI?
Meds that decrease platelet aggregation and workload of the heart
71
Ischemic death of myocardial tissue is a _______?
STEMI
72
Pathologic Changes of STEMI - 1st step
Metabolism changes from aerobic to
anaerobic with inadequate energy production to sustain normal myocardial function
73
Pathologic Changes of STEMI - 2nd step
Striking loss of contractile function within 60 seconds of onset
74
Pathologic Changes of STEMI - 3rd step
Cell structure changes within minutes
75
Pathologic Changes of STEMI - 4th step
Ischemic area ceases to function within
minutes
76
Pathologic Changes of STEMI - 5th step
Irreversible myocardial cell death (necrosis) occurs after 20 to 40 minutes of severe ischemia
77
For clinical manifestations of MI, elderly people complain of _______________?
shortness of breath
78
for STEMI, Reestablish blood flow using ______________ therapy or ______________ procedures
- fibrinolytic
- revascularization
79
Recovering area of the heart is called?
stunned myocardium
80
What are the (3) zones of cardiac tissue
damage?
1) Zone of infarction
2) Zone of Injury
3) Zone of Ischemia
81
Fibrinolytic Drug example?
Tenectaplase (TNKase)
82
Tenectaplase (TNKase) interacts with plasminogen to form plasmin which
________ fibrin clots and digests ______________?
1. lysis
2. clotting factors
82
Percutaneous Coronary Intervention
(PCI) includes (2):
coronary angioplasty and stent implantation
83
___________________ is an emergency treatment for STEMI within 4-6 hours of symptom onset
Coronary artery bypass graft (CABG)
83
Coronary artery bypass graft (CABG) works by _________________ of myocardium by placing a ___________ vein
graft between the aorta and the affected coronary artery distal to the site of occlusion.
1. revascularization
2. saphenous
84
_______________ is a complex syndrome that results from any functional or structural disorder of the heart
Heart failure (HF)
85
Heart failure results in or increases the risk of developing manifestations of low ________________ and/or pulmonary or systemic ___________?
1. cardiac output (CO)
2. congestion
86
____________________ is a type of heart muscle disease that causes the heart chambers (ventricles) to thin and stretch, growing larger
Dilated cardiomyopathy
87
________________ is when the valves of the heart do not open or close properly
Valvular heart disease
88
Persons with heart failure use their _____________________ at rest
cardiac reserve
89
____________________ is the ability of the heart to increase its output during increased activity
Cardiac reserve
90
Types of Heart Failure (6):
- High-output failure
- Low- output failure
- Systolic failure
- Diastolic failure
- Right-sided failure
- Left-sided failure
91
Is decreased myocardial contractility systolic or diastolic heart failure?
Systolic heart failure
92
Is inability for left ventricle to fill sufficiently systolic or diastolic heart failure?
Diastolic heart failure
93
___________________________________ is a principle in cardiac physiology that explains how the heart adjusts its contraction strength based on the volume of blood filling it (called preload)
The Frank-Starling mechanism
94
_______________ are peptides that constrict blood vessels and raise blood pressure
Endothelins
95
(3) general concepts that indicate heart failure:
1. Effects of impaired pumping
2. Effects of decreased renal blood flow
3. Effects of the sympathetic nervous system
96
Severe ___________________ is due to elevated left ventricular filling
pressures with or without low cardiac output
pulmonary edema
97
Frothy blood tinged sputum is a sign of __________________?
pulmonary edema
98
Acute pulmonary edema is when capillary fluid moves into the ________?
alveoli
