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Pathology 1 > Week 4 > Flashcards

Week 4 Flashcards

1
Q

What are the (2) lipid pathways?

A
  • Exogenous lipid pathway
  • Endogenous lipid pathway
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2
Q

Absorption of fats from the digestive tract into the circulation describes which lipid pathway?

A

Exogenous lipid pathway

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3
Q

Transporting of fats synthesized in the liver between the liver and the
peripheral tissues describes which lipid pathway?

A

Endogenous lipid pathway

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4
Q

Cholesterol/triglycerides levels that are too high can increase your chance of getting __________, _________, etc.

A
  • heart disease
  • stroke
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5
Q

(2) The medical term for high blood cholesterol are?

A

lipid disorder or hyperlipidemia.

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6
Q

How many types of lipoproteins are there?

A

5

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7
Q

Excess LDL binds to ____________________?

A

endothelial cells

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8
Q

Too much fats = ________________ = too much in blood

A

Saturation of liver

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9
Q

What oxidizes LDL?

A

Macrophages

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10
Q

Phagocytic macrophages have ____________ that bind to LDL

A

receptors

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11
Q

Oxidized LDL by Macrophages are key component of ________________?

A

atherosclerosis

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12
Q

______________________ is a condition with a high amount of LDL, or the bad cholesterol

A

Hypercholesterolemia

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13
Q

Increase _________________ = increase HDLs

A

unsaturated fats

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14
Q

_________________ is formation of
fibro-fatty lesions in the intimal lining of
large and medium- sized arteries

A

Atherosclerosis

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15
Q

What is the leading cause of CAD,
stroke, peripheral arterial disease?

A

Atherosclerosis

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16
Q

Accumulation of _______________________ forming a lesion called a plaque

A

lipid- loaded macrophages

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17
Q

Pathogenesis of Atherosclerotic Lesions (4) in order?

A
  1. Endothelial injury
  2. Migration of inflammatory
    cells
  3. Lipid accumulation and
    smooth muscle proliferation
  4. Gradual development of the
    atheromatous plaque
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18
Q

Endothelial cells express ________________________molecules that bind monocytes and other inflammatory cells.

Which stage of atherosclerosis lesions is this?

A
  1. selective adhesion
  2. Inflammatory cells migrate
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19
Q

_______________ adhere to endothelium, transform into macrophages and engulf LDLs

Which stage of atherosclerosis lesions is this?

A
  1. Monocytes
  2. Inflammatory cells migrate
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20
Q

In which stage of atherosclerosis lesions do macrophages engulf LDLs then releases toxic oxygen species that oxidize LDL?

A

Lipid accumulation

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21
Q

When macrophages engulf LDLs, they release toxic oxygen and also this leads to ________________________?

A

platelet aggregation

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22
Q

Oxidized LDL (ingested by macrophage) becomes?

A

foam cells

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23
Q

Foam cells leads to ___________________ streaks covered by fibrous cap of tissue

A

lesions/fatty

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24
Q

Rupture or erosion of an unstable
fibrous cap may lead to _______________
into the plaque or ____________________ of the vessel lumen

A
  1. hemorrhage
  2. thrombotic occlusion
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25
Q

Core contains ________ filled macrophages and __________ smooth muscle debris

A
  1. lipid
  2. necrotic
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25
Q

unstable plaques are characterized by (4):

A
  • 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
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26
Q

Stable plaques are characterized by (3):

A
  • Thick fibrous caps
  • Partially block vessels
  • Do not tend to form clots or emboli
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26
Q

______________________ is the force that that moves blood through arterial
system

A

Arterial Blood Pressure

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27
Q

What is the most common of all health problems?

A

Hypertension

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28
Q

Arterial Blood Pressure is the contraction & relaxation of the _____________________?

A

left ventricle

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29
Q

HTN = Caused by (3)?

A
  • Increase cardiac output
  • Increase total peripheral resistance (PR)
  • or both
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30
Q

CO is increased by any condition that increases (2)?

A
  • Heart rate
  • stroke volume
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31
Q

PR is increased by any factor that (2)?

A
  • Increases blood viscosity
  • Decreases in vessel diameter
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32
Q

_________________________ is force opposing the movement of blood within the blood vessels

A

Systemic vascular resistance (SVR)

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33
Q

Primary hypertension is AKA?

A

essential hypertension

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34
Q

Chronic elevation of BP occurs without
evidence of other disease conditions is what kind of hypertension?

A

Primary hypertension

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35
Q

Elevation of BP results from some other
disorder is what kind of hypertension?

A

Secondary hypertension

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36
Q

__________________________ is markedly high BP is accompanied by progressive target-organ damage

A

Hypertensive crisis

Systolic >180mmHg
Diastolic >120 mmHg

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37
Q

_______________ is abnormal drop in BP when assuming the standing position

A

Orthostatic hypotension

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38
Q

_______________ is a heart disease caused by impaired coronary blood flow

A

Coronary artery disease (CAD)

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39
Q

_______________ is the most common cause of CAD

A

Atherosclerosis

40
Q

CAD does not produce
symptoms until it is advanced
because of ________________?

A

collateral flow

41
Q

______________________ is your body’s way of working around blood flow blockages.

A

Collateral circulation

42
Q

CAD is divided into (2) types of disorders:

A
  • Acute coronary syndromes (ACS)
  • Chronic ischemic heart disease
43
Q

What type of CAD is the following symptoms:

  • Caused by acute plaque disruption
  • Range from unstable angina to MI
A

Acute coronary syndrome (ACS)

44
Q

What type of CAD is the following symptoms:

  • Caused by atherosclerotic or vasospastic obstruction of coronary arteries (i.e. stable angina)
A

Chronic ischemic heart disease

45
Q

Pathogenesis of CAD with Stable plaque will lead to _________________?

A

Stable angina

46
Q

Pathogenesis of CAD with unstable plaque will lead to what (4) events in order?

A
  1. Plaque disruption
  2. Platelet aggregation
  3. Thrombus formation
  4. Unstable angina and MI
47
Q

Pathophysiology of CAD - 1st step

A

Occlusion of arteries

48
Q

Pathophysiology of CAD - 2nd step

A

After a few minutes, contractility stops depriving the heart’s cells of glucose for aerobic metabolism.

49
Q

Pathophysiology of CAD - 3rd step

A

Lactic acid accumulates: myocardial fibers are irritated by the lactic acid

50
Q

Pathophysiology of CAD - 4th step

A

Pain ensues- angina

51
Q

Pathophysiology of CAD - 5th step

A

Lead to MI

52
Q

What are the (3) Types of Angina?

A
  • Stable angina
  • Variant angina (Printzmetal’s)
  • Silent myocardial ischemia
53
Q

What type of angina is the following:

Pain when heart’s oxygen demand increases

A

Stable angina

54
Q

What type of angina is the following:

Pain when coronary arteries spasm

A

Variant angina (Printzmetal’s)

55
Q

What type of angina is the following:

Myocardial ischemia without pain

A

Silent myocardial ischemia

56
Q

_____________ is a sudden attack of chest pain or pressure due to transient myocardial ischemia

A

Angina pectoris

57
Q

Chronic Stable Angina is often associated with ______________?

A

atherosclerosis

58
Q

Chronic Stable Angina is felt in what area?

A

substernal area

59
Q

ACS classified based on presence or
absence of ______________ elevation on
ECG

A

ST-segment

60
Q

Classic changes that occur with ACS include (3):

A
  • T wave inversion
  • ST elevation
  • development of an abnormal Q wave
61
Q

Diagnosis of ACS uses ____________________?

A

serum biomarkers

62
Q

___________ assays are the primary biomarker tests for the diagnosis of MI.

63
Q

Serum biomarkers for ACS include (2):

A

troponin I and troponin T

64
Q

Troponin levels begin to rise ___ hours after onset of MI. They may stay elevated for _______ days (useful for late diagnosis

A
  1. 3 hours
  2. 7-10 days
65
Q

__________________ is an isoenzyme highly specific for injury to myocardial tissue

A

CK-MB or creatine-kinase

66
Q

Creatine-kinase becomes elevated within _____ hrs after injury

67
Q

NSTEMI means?

A

Non-ST Segment Elevation MI

68
Q

Is NSETMI or unstable angina related to sufficient myocardial damage to release detectable quantities of troponin?

69
Q

Are there serum biomarker changes in unstable angina?

70
Q

What meds are a good treatment for Unstable Angina/NSTEMI?

A

Meds that decrease platelet aggregation and workload of the heart

71
Q

Ischemic death of myocardial tissue is a _______?

72
Q

Pathologic Changes of STEMI - 1st step

A

Metabolism changes from aerobic to
anaerobic with inadequate energy production to sustain normal myocardial function

73
Q

Pathologic Changes of STEMI - 2nd step

A

Striking loss of contractile function within 60 seconds of onset

74
Q

Pathologic Changes of STEMI - 3rd step

A

Cell structure changes within minutes

75
Q

Pathologic Changes of STEMI - 4th step

A

Ischemic area ceases to function within
minutes

76
Q

Pathologic Changes of STEMI - 5th step

A

Irreversible myocardial cell death (necrosis) occurs after 20 to 40 minutes of severe ischemia

77
Q

For clinical manifestations of MI, elderly people complain of _______________?

A

shortness of breath

78
Q

for STEMI, Reestablish blood flow using ______________ therapy or ______________ procedures

A
  • fibrinolytic
  • revascularization
79
Q

Recovering area of the heart is called?

A

stunned myocardium

80
Q

What are the (3) zones of cardiac tissue
damage?

A

1) Zone of infarction
2) Zone of Injury
3) Zone of Ischemia

81
Q

Fibrinolytic Drug example?

A

Tenectaplase (TNKase)

82
Q

Tenectaplase (TNKase) interacts with plasminogen to form plasmin which
________ fibrin clots and digests ______________?

A
  1. lysis
  2. clotting factors
82
Q

Percutaneous Coronary Intervention
(PCI) includes (2):

A

coronary angioplasty and stent implantation

83
Q

___________________ is an emergency treatment for STEMI within 4-6 hours of symptom onset

A

Coronary artery bypass graft (CABG)

83
Q

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.

A
  1. revascularization
  2. saphenous
84
Q

_______________ is a complex syndrome that results from any functional or structural disorder of the heart

A

Heart failure (HF)

85
Q

Heart failure results in or increases the risk of developing manifestations of low ________________ and/or pulmonary or systemic ___________?

A
  1. cardiac output (CO)
  2. congestion
86
Q

____________________ is a type of heart muscle disease that causes the heart chambers (ventricles) to thin and stretch, growing larger

A

Dilated cardiomyopathy

87
Q

________________ is when the valves of the heart do not open or close properly

A

Valvular heart disease

88
Q

Persons with heart failure use their _____________________ at rest

A

cardiac reserve

89
Q

____________________ is the ability of the heart to increase its output during increased activity

A

Cardiac reserve

90
Q

Types of Heart Failure (6):

A
  • High-output failure
  • Low- output failure
  • Systolic failure
  • Diastolic failure
  • Right-sided failure
  • Left-sided failure
91
Q

Is decreased myocardial contractility systolic or diastolic heart failure?

A

Systolic heart failure

92
Q

Is inability for left ventricle to fill sufficiently systolic or diastolic heart failure?

A

Diastolic heart failure

93
Q

___________________________________ 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)

A

The Frank-Starling mechanism

94
Q

_______________ are peptides that constrict blood vessels and raise blood pressure

A

Endothelins

95
Q

(3) general concepts that indicate heart failure:

A
  1. Effects of impaired pumping
  2. Effects of decreased renal blood flow
  3. Effects of the sympathetic nervous system
96
Q

Severe ___________________ is due to elevated left ventricular filling
pressures with or without low cardiac output

A

pulmonary edema

97
Q

Frothy blood tinged sputum is a sign of __________________?

A

pulmonary edema

98
Q

Acute pulmonary edema is when capillary fluid moves into the ________?

Pathology 1 (14 decks)

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