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Pathophysiology > Exam 1 > Flashcards

Exam 1 Flashcards

1
Q

what is the leading cause of death i the US and the world

A

CV disease

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2
Q

what are causes of cardiovascular disease

A

genetic
neurohumoral
inflammatory mechanisms

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3
Q

what are the underlying cellular processes of cardiovascular diseases

A

endothelial injury
remodeling
stunning
reperfusion injury
autoimmune disease

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4
Q

what is a varicose vein

A

a vein in which blood has pooled
distended, tortous, palpable veins

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5
Q

what is the usual vein for varicose vein

A

spahenous

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6
Q

what causes varicose veins

A

-Trauma or gradual venous distention, rendering valves incompetent (standing on hard floor for long periods of time)
-altered connective tissue proteins
-increased proteolytic enzyme activity
-decreased transforming growth factor B in vein walls

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7
Q

what is normal arterial pressure

A

120/80 mmHg

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8
Q

what is normal venous pressure

A

0-8

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9
Q

what is normal pressure going into RA

A

5

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10
Q

veins have a _______ muscle layer

A

thin
have great distendability

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11
Q

arteries have a _________ muscle layer

A

thick

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12
Q

anytime you have inflammation what are three sings

A

heat
redness
swelling

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13
Q

what does inflammation trigger

A

inflammatory mediators, cytokines then neutrophils, macrophages then elastase protease
these dissolve damaged tissue and replace it with fibrin

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14
Q

what can inflammatory mediators lead to

A

further damage (dissolving of damaged tissue to replace it with fibrin)

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15
Q

what does fibrin from damaged tissue lead to? what property is lost in this process

A

scar tissue (fibrin)
elasticity/stretch (no collagen)

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16
Q

what can chronic venous insufficiency lead to

A

venous stasis ulcers

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17
Q

what is chronic venous insufficiency

A

inadequate venous return over a long period of time as a result of varicose veins, valvular incompetence

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18
Q

how does the heart compensate for venous insufficiency

A

increased HR

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19
Q

what causes varicose veins in saphenous to be painful

A

runs with the saphenous nerve

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20
Q

what is treatment for varicose veins and chronic venous insufficiency

A

-leg elevation, compression stockings, physical exercise
-endovenous ablation (radiofrequency and laser)
-ultrasound-guided foam sclerotherapy
-surgical ligation and vein stripping

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21
Q

what can DVT lead to

A

thromboemboli then PE

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22
Q

what is a blood clot that is attached

A

thrombus

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23
Q

what is a blood clot loose in venous system

A

emoboli

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24
Q

what is Virchows triad

A

For DVT
1. Venous stasis
2. Hypercoagulability
3. Venous endothelial damage

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25
Q

how many miles of vessels are in body

A

64,000 miles

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26
Q

what does the venous system rely on for return from legs

A

muscular contraction

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27
Q

how do you prevent DVTS

A

1 mobilization after sx, illness, bed rest, injury

2 prophylactic LMWH, antithrombin agents, warfarin, pneumatic devices

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28
Q

how do you prevent DVT from causing PE

A

IVC filter

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29
Q

what are tests for DVT

A

d dimer
CT
MRI

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30
Q

where do saddle thrombus form

A

pulmonary artery biforcation

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31
Q

what is treatment for DVT/PE

A

LMWH, unfractionated heparin, antithrombin agents, sub q heparin
thrombolytic therapy
ASA

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32
Q

what are risk factors for DVT

A

smoking
overweight
truck driver

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33
Q

T/F Heparin dissolves clots?

A

false
prevents more clots,
prevents current clot from growing

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34
Q

what is a D-dimer

A

fibrin degradation product elevated when clot is present

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35
Q

what does ASA prevent

A

platelet function

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36
Q

what are values for HTN

A

> 140 sys or >90 diastolic

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37
Q

what is pre htn

A

120-139/80-89

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38
Q

what is isolated systolic HTN

A

elevated SBP with normal DBP

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39
Q

what is primary/essential HTN

A

unknown cause
95% of all HTN cases

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40
Q

what does HTN increase with age

A

decreased flexibility of arteries/hardening of plaque formation

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41
Q

what is secondary HTN

A

HTN due to underlying primary disease or drugs

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42
Q

what is the most significant factor in causing target organ damage

A

systolic HTN

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43
Q

systolic HTN puts at an increased risk for

A

stroke (more pressure change between diastolic and systolic)

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44
Q

a higher diastolic pressure puts more pressure on the

A

heart

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45
Q

Why is BP important?

A

pressure of oxygen delivery

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46
Q

what does HTN increase the risk of

A

MI
kidney disease
stroke

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47
Q

how does HTN lead to kidney disease

A

damages glomerulus

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48
Q

how does HTN lead to stroke

A

HTN causes generalized dilation of vessels in vein in head, ruptures and causes hemmg stroke

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49
Q

why does HTN lead to MI

A

heart has to pump faster/harder to overcome pressure
heart receives blood in diastole
inadequate time to oxygenate heart

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50
Q

when does heart receive blood flow

A

diastole

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51
Q

what are risk factors for HTN

A

family hx
age
female >70, male <55
black
sodium intake
DM
alcohol use
obesity
smoking
low K, Mg, Ca

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52
Q

what are the two causes of HTN

A

increased CO or SVR (or both)

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53
Q

what causes HTN from increased CO

A

increased HR or stroke volume

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54
Q

what causes HTN from increased SVR

A

any factor that increases blood viscosity or causes vasoconstriction

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55
Q

how is HTN treated lifestyle

A

-reducing risk factors
-sodium restriction 2.4g/day
-increased K intake
-decreased saturated fat
-weight control
-DASH diet
-stop smoking
-exercise program

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56
Q

what are pharm treats for lifestyle

A

thiazide diuretics,
beta blockers
ACEI
ARBs
CCBs

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57
Q

why thiazide diuretic in HTN

A

k sparing, longer lasting

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58
Q

why do we use ACEI first for HTN

A

stopping a normal physiologic process, doesnt impact heart at all, decreases fluid retention and prevents vessel constriction

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59
Q

what do pharmacologic therapies reduce risk of

A

end-organ damage
prevent MI stroke

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60
Q

what are thiazide diuretics and beta blockers associated with

A

lipid disorders
glucose intolerance

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61
Q

what are ACEI and ARBs effective for

A

HF, CKD, after MI, recurrent stroke

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62
Q

what is an aneurysm

A

local dilation of vessel wall

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63
Q

what is a true aneurysm

A

all three layers of the arterial wall
fusiform aneurysm
circumferential aneurisms

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64
Q

what are the three layers of the artery

A

intima
media
adventitia

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65
Q

what is a false aneurism

A

tear in intima and media that pouches in adventitia
saccular aneurism

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66
Q

most cerebral aneurisms are

A

saccular (false)

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67
Q

what is present in 50% of people with aneurisms

A

arteriosclerosis and HTN

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68
Q

where do aneurisms usually occur

A

increased pressure or branching

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69
Q

how do aneurisms in heart present

A

dysrhythmias, HF, embolism of clots to the brain

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70
Q

how do aortic aneurisms present

A

asymptomatic till it ruptures, then it is painful

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71
Q

what are clinical signs of thoracic aneurism

A

dysphagia, dyspnea

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72
Q

what are signs of abdomen aneurism

A

flow to an extremity is impaired, causing ischemia

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73
Q

where does an Abdomen Aneurism occur

A

where the iliacs branch off

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74
Q

most of the time saccular refers to an aneurism that ___________ involve all three layers

A

does not

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75
Q

a false aneurism is really a

A

hematoma (clot formation)

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76
Q

what is a dissecting aneurism

A

form of false
rips through intima and media, blood collets in adventitia

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77
Q

what is the most serious/fatal of all aneurism

A

dissecting, saccular

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78
Q

what are treatments for aneurism

A

maintain low blood volume
low BP
smoking cessation
B blockers
Surgery

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79
Q

which aneurism is a surgical emergency

A

aortic dissecting aneurism

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80
Q

why are aneurisms formed in aorta

A

high BP in aorta hits the curved wall of aorta with high pressure causing damage of lining

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81
Q

what causes arterial thrombus formation

A

athersosclerosis roughening the intima activates the clotting cascade
high BP causes high flows that damage intima lining (
trauma like car crash

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82
Q

what areas do arterial thrombi from htn occur

A

anywhere with a branch, carotid artery,

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83
Q

what is arteriosclerosis

A

hardening of the arteries, media looses elasticity, not as expanded

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84
Q

what is atheroscleosis

A

disruption of intima with plaque formation, a form of arteriosclerosis

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85
Q

what is treatment for arterial thrombus

A

heparin, warfarin, thrombin inhibitors, thrombolytic agents
balloon tipped catheter used to remove or compress an arterial thrombi

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86
Q

what do arterial thombi damage

A

heart
kidney
brain

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87
Q

what is an embolism

A

bolus of matter circulates in the bloodstream then lodges and obstructs blood flow

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88
Q

what are examples of emboli

A

thrombus from DVT
air
amniotic fluid
aggregate of fat
bacteria
cancer cell
foreign substance

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89
Q

what causes arterial emboli from heart

A

MI, valve disease, endocardidits, dysrhythmias, HF

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90
Q

what can an embolism cause

A

occlusion of coronary artery
occlusion of cerebral artery (stroke)
ischemia or infarction or necrosis distal to obstruction

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91
Q

does heparain dissolve clots

A

no, it prevents new clots from forming or clot from getting larger

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92
Q

when can you use a thrombolytic agent

A

within 4 hours, must have a good history

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93
Q

how does an extremity appear distal to a arterial occlusion

A

waxy whiteness of skin do to lack or erythrocytes
numbness and pain from neuronal ischemia

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94
Q

any time you get an arterial occlusion you get what

A

avascular necrosis

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95
Q

what is raynaud disease

A

episodic vasospasms (ischemia) in the arteries and arterioles of the fingers

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96
Q

how does reynauds manifest

A

changes in skin color and sensation caused by ischemia

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97
Q

what is reynaud phenomenon

A

same thing but secondary to other systemic diseases or conditions

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98
Q

how do you treat Reynaud’s phenomenon

A

arm exercises
medications

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99
Q

why are decubitus ulcers difficult to heal

A

need blood flow and epithelization, doesnt occur in dead tissue

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100
Q

what does debridement do for ulcer

A

cuts away dead tissue so that there is live tissue that can grow

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101
Q

what causes raynauds disease

A

primary vasospastic disorder of unkown origin

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102
Q

how do you treat raynauds disease

A

avoidance of emotional stress and cold and cessation of smoking

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103
Q

what causes atherosclerosis

A

thickening and hardening caused by the accumulation of lipid-laden macrophages in the arterial wall
-plaque development

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104
Q

what is a trigger for reynauds

A

stress

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105
Q

what is the leading cause of coronary artery and cerebrovascular disease

A

atherosclerosis

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106
Q

T/F atherosclerosis only occurs in one area

A

F, process occurs throughout the body

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107
Q

what are steps of atherosclerosis

A

1-endothelium injury
2-inflammation of endothelium
3-cytokines released
4-cellular proliferation
5-macrophage migration (gobble up ldl)
6-LDL oxidation (foam cells)
7-fatty streak (formed by LDL)
8=fibrous plaque
9-complicated plaque

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108
Q

where does atherosclerosis most commonly occur

A

branches
carotid
coronary vessels
abd aorta splits
aortic arc

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109
Q

why kind of blood flow does a branch create

A

turbulent

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110
Q

what are the layers of the artery

A

intima, media, adventitia

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111
Q

where do fatty streaks develop in atherosclerosis

A

between intima and media (pushes it away)

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112
Q

what is fatty streak made from

A

LDLs

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113
Q

what makes an unstable plaque

A

fatty core (foam cells) and thin fibrous outer shell
can rupture easier

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114
Q

what makes a stable plaque

A

thick fibrous shell around plaque
less likely to break off

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115
Q

what happens when part of plaque ruptures

A

thrombosis (blood clot) begins at the site of the plaque rupture

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116
Q

what happen when blood clot on plaque enlarges

A

occlusion, blocks artery and all tissues supplied by that artery begin to die
heart attack, stroke etc

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117
Q

where does atherosclerosis occur (what layer)

A

media, this is where muscle and elasticity is from

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118
Q

what happens when artery is made smaller by plaque formation

A

increased pressure, increased turbulent flow, increased damage, so increased plaque formation
decreased flow to organs distal to narrowing

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119
Q

how does atherosclerosis manifest

A

depends on organ affected, will inadequately perfuse tissue the artery supplies

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120
Q

what is treatment on atherosclerosis

A

focuses on reducing risk factors
removing initial causes of vessel damage
prevent lesion progression

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121
Q

what are lifestyle changes for atherosclerosis

A

exercising
smoking cessation
controlling HTN
controlling DM
reducing LDL cholesterol by diet and medications

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122
Q

what is coronary artery disease

A

Any vascular disorder that narrows or occludes the coronary arteries

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123
Q

what does a CAD lead to

A

imbalance between coronary supply of blood and myocardial demand for oxygen and nutrients

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124
Q

what is the most common cause of CAD

A

atherosclerosis

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125
Q

what are non-modifiable risk factors for CAD

A

advanced age, family history
male gender, women after menopause

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126
Q

carotid artery occlusoin causes

A

stroke

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127
Q

coronary artery occlusion causes

A

MI

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128
Q

what is prolonged ischemia causes irreversible damage to the heart muscle

A

MI

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129
Q

50% of all aneurisms have

A

arteriosclerosis and aneurism

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130
Q

arthersclerosis is a form of

A

arteriosclerosis

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131
Q

what is myocardial stunning

A

temporary loss of contractile function that persists for hours to days after perfusion has been restored

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132
Q

What is hibernating myocardium?

A

Tissue that is persistently ischemic undergoes metabolic adaptation to prolong myocyte survival
(adapts to less O2)

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133
Q

What is remodeling?

A

process that occurs in the myocardium after an MI

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134
Q

we have __________% more mitochondria in heart than in any othermuscle

A

20%

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135
Q

a heart muscle cell can live for _________ without fresh O2

A

20 min

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136
Q

when do electrical signals send with myocardial ischemia

A

6-8 seconds after blockage

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137
Q

what are ECG changes with MI

A

ST depression
T wave inversion
ST elevation

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138
Q

what are the two major types of MI

A

subendocardial and transmural

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139
Q

what is a subendocardial MI

A

under the surface, heart can still pump because deeper muscle layers can still function

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140
Q

what is a transmural MI

A

MI through all layers of heart, worse kind

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141
Q

what ECG signs of MI require immediate intervention

A

STEMI

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142
Q

smaller infarction are ______ associated with STEMI

A

Not

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143
Q

T/F in NSTEMI myocardium not at risk

A

false

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144
Q

what are clinical manifestations of MI

A

sudden severse chest pain
ECG changes
troponin I: (most specific)
Creatinine phosphokinase-MB (PCK-MB), LDH (lactic acid)
hyperglycemia

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145
Q

why do you have hyperglycemia with MI

A

1-myocardial tissue damages causes catecholamine release (epi, norepi)
2-epi causes liver to turn glycogen to glucose (glyconeogenesis)
3- epi causes pancrease to stop producing insulin

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146
Q

what are MI treatment

A

hospitilization
O2 and ASA
morphine
bed rest
thrombolytics
antithrombotics
vasodilators
PCI
Sx

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147
Q

how long does troponin I elevated with MI

A

2-4 hrs

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148
Q

what is acute pericarditis

A

acute inflammation of the pericardium (bacterial, viral, covid vaccine)

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149
Q

what are s/s pericarditis

A

fever
myalgias
malaise
sudden onset severe chest pain

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150
Q

why is troponin released in MI

A

damage to muscle cells cause troponin release into blood stream

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151
Q

what is treatment for pericarditis

A

rest
salicylates (ASA)
NSAIDS
nonsteroidals and chochicine

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152
Q

what is pericardial effusion

A

cardiac tamponade

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153
Q

what is treatment for pericardial effusion/tamponade

A

pericardiocentesis

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154
Q

T/F there is a natural amount of fluid around heart

A

T 20-50 ccs

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155
Q

if you have pericardial effusion you usually have what kind of HF

A

bilateral HF

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156
Q

what is purpose of fluid around heart

A

lubricant

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157
Q

what is constrictive/restrictive pericarditis

A

Fibrous scarring with occasional calcification of the pericardium causes the visceral and parietal pericardial layers to adhere.

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158
Q

what are s/s restrictive pericarditis

A

exercise intolerance
dyspnea on exertion
fatigue
anorexia

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159
Q

what is treatment of pericarditis

A

dietary sodium restriction
digitalic glycosides
diuretics

160
Q

what are sx treatments of MI

A

1-CABG (vein from leg (saphenous) sutures into block and then aorta. multiple blocks or posterior)
2-LIMA (left internal mammary artery suture branches and then put it into block. these work best on LAD)
3-PCI- stents

161
Q

what do you do if medical treatments for restrictive pericarditis are not successful

A

surgical excision of scaring

162
Q

What is cardiomyopathy?

A

neurohumoral response to ischemic heart disease or HTN on the heart muscle cause remodeling

163
Q

T/F many cases of cardiomyopathy are iopathic

A

true

164
Q

what is dilated/congestive cardiomyopathy

A

Impaired systolic function, leads to increased intracardiac volume, ventricular dilation, and systolic heart failure

165
Q

how does ventricle wall appear in dilated/congestive cardiomyopathy

A

thin

166
Q

what are causes of dilated/congested heart failure

A

CONDUCTIVE ISSUES (over filling)

MI
DM
alcohol
niacin deficiency
vit D deficiency
selenium deficiecy
hyperthyroidism

167
Q

what are s/s congestive heart failure

A

dyspnea, fatigue

bradycardias

168
Q

what rhythm is common with dilated cardiomyopathy

A

a fib

169
Q

what are treatments for congestive HF

A

salt restriction

vasodilators

diuretics

inotropes

anticoagulants

pacemakers

170
Q

what are two kinds of hypertrophic/asymmetric cardiomyopathy

A

hypertrophic obstructive cardiomyopathy
hypertensive or valvular hypertrophic cardiomyopathy

171
Q

what CO do we need

A

5L/min

172
Q

anything that causes the heart to work harder would lead to

A

hypertrophic cardiomyopathy

173
Q

what is hypertrophic obstructive cardiomyopathy

A

common inherited (genetic) heart defect of a thick septal wall

174
Q

what causes young athletes to die during aport/event

A

hypertrophic obstructive cardiomyopathy

175
Q

what are s/s hypertrophic obstructive cardiomyopathy

A

angina
syncope
palpitations

176
Q

what is treatment of hypertrophic obstructive cardiomyopathy

A

-beta blockers/verapamil to slow HR
-surgical resection of hypertrophied myocardium
-septal ablation (cut off the excess muscle)
-prophylactic placement of ICDs

177
Q

what is hypertensive or valvular hypertrophic cardiomyopathy

A

hypertrophy of myocytes: attempting to compensate for increased work load

178
Q

what are s/s hypertensive or valvular hypertrophic cardiomyopathy

A

asymptomatic OR
angina, syncope, dyspnea, palpitations

179
Q

what causes increased workload of valvular dysfucntions

A

increased afterload leads to decreased CO, so heart increases HR , this leads to hypertrophy

180
Q

what are s/s restricive cardiomyopathy

A

R sided HF occurs with systemic venous congestion

181
Q

restrictive cardiomyopathy is a ________ in contractility

A

decrease

182
Q

what are the two kinds of restrictive cardiomyopathy

A

amyloidosis
sarcoidosis

183
Q

What is restrictive cardiomyopathy?

A

myocardium becomes rigid and noncompliant, impeding ventricular filling and raising filling pressures during diastole

184
Q

what is treatment for restrictive cardiomyopathy

A

correct underlying cause

185
Q

what are disorders of endocardium

A

dysfunction of the heart valves

186
Q

what determines CO

A

HR
contractility
preload
afterload

187
Q

what does valvular dysfunction lead to

A

chamber dilation and/or myocardial hypertrophy

188
Q

what is treatment for valvular dysfunction

A

Careful fluid management. Valvular repair or valve replacement with a prosthetic valve, followed by long-term anticoagulation therapy and life-long antibiotic prophylaxis before invasive procedures.

189
Q

what valves have stenosis

A

aortic and mitral

190
Q

what valves have regurge (leak)

A

aortic, mitral, tricuspid

191
Q

what is subaortic stenosis

A

hypertrophic obstructive cardiomyopathy

192
Q

What is aortic stenosis?

A

narrowing of the aortic valve so decreased blood flow from LV into aorta

193
Q

what are causes aortic stenosis

A

bicuspid valve
dystrophic calcification

194
Q

what are S/S aortic stenosis

A

angina, syncope (decreased O2 to brain), HF

195
Q

what is treatment of aortic stenosis

A

valve replacement/repair, long term anticoag therapy
transcatheter aortic valve implantation

196
Q

what is mitral stenosis

A

narrowing of the mitral valve, so decreased flow from LA to LV

197
Q

what is the most common cause of mitral stenosis

A

acute rheumatic fever

198
Q

What are the s/s of mitral stenosis?

A

opening snap

199
Q

what are treatments of mitral stenosis

A

surgical repair, valve replacement

200
Q

normal EF is greater than

A

55%

201
Q

T/F every mitral stenosis requires valve replacement

A

F, has to be very severe, gravity alone allows enough volume to pass through

202
Q

What is aortic regurgitation?

A

inability of the aortic valve leaflets to close properly during diastole

203
Q

What are the s/s of aortic regurgitation?

A

widened pulse pressure from increased stroke volume and diastolic back flow

204
Q

what is treatment for aortic regurgitation

A

valve replacement but can be delayed with with use of vasodilators and inotropic agents

205
Q

what is most common cause of mitral regurgitation

A

mitral valve prolapse and rheumatic heart disease

206
Q

What is mitral regurgitation?

A

Reflux of blood from left ventricle into left atrium during systole

207
Q

what is treatment for mitral regurgitation

A

Surgical repair or valve replacement

208
Q

what does rheumatic fever lead to

A

inflammation of the joints, skin, nervous system, and heart

209
Q

What is rheumatic fever?

A
  1. it is an inflammatory disease that may develop after an infection with beta-hemolytic streptococcus bacteria
    a febrile illness
210
Q

if left untreated what does rheumatic fever lead to

A

rheumatic heart disease

211
Q

What causes rheumatic fever?

A

abnormal immune response to the M proteins - treats it as an allergic response antibodies against betahemolyitc strep also attack the body

212
Q

what are the fibrinoid necrotic deposits from rheumatic fever

A

aschoff bodies- form on heart

213
Q

what sound is associated with mitral valve prolapse

A

click

214
Q

What are s/s of rheumatic fever?

A

carditis: murmur
polyarthritis: large joints maily affected
Chorea: sudde, aimless, irregular, involuntary movements
erythemia: truncal rash

215
Q

what is a murmur

A

leaky valve

216
Q

where is calcium deposited in body

A

kidney, lungs, aortic valve

217
Q

what is treatment for rheumatic fever

A

10 days of antibiotics, NSAIDs, abx for up to 5 years

218
Q

dilated cardiomyopathy is a __________ issue

A

conduction

219
Q

if afterload increase then CO ______________

A

decreases (inverse relationship)

220
Q

in dilated cardiomyopathy afterload is ___________

A

high

221
Q

what medications do we use to treat dilated cardiomyopathy

A

inotropes (digosxin)

222
Q

dilated cardiomyopathy is more common in the ______ side

A

RV

223
Q

what are the two types of hypertrophic cardiomyopathy

A

HTN/Valvular

224
Q

what causes HTN/valvular hypertrophic cardiomyopathy

A

increased workload of heart causes remodeling (thickening) of LV

225
Q

what two conditions lead to aortic stenosis

A

calcium deposits
bicuspid aortic valve

226
Q

how does the heart respond to aortic stenosis

A

increase contractility
increase HR

227
Q

aortic stenosis results in a _________ CO

A

decreased

228
Q

the thickening of the LV in hypertrophic cardiomyopathy results in a ___________ in SV

A

decrease

229
Q

what kind of cardiomyopathy is caused by an enlarged IVS

A

obstructive cardiomyopathy

230
Q

what is another word for obstructive cardiomyopathy

A

sub aortic stenosis

231
Q

what two reasons does aortic stenosis occur

A

bicuspid aortic valv
calcification

232
Q

where does most stenosis occur

A

aoritc and mitral (high prressure)

233
Q

what is infective endocarditis

A

inflammation of the endocardium from infectious agents
-bloodborne microorganism adhere to heart

234
Q

where do microorganisms from infective endocarditis gather in heart

A

on valve leaflets- form vegetations

235
Q

what are clincial manifestations of infective endocarditis

A

fever
murmur
petechial lesions of the skin, conjuctiva, and oral mucosa
Osler nodes-on fingers and toes
Janeway lesions-on palms and soles

236
Q

what is treatment for infective endocarditis

A

high dose antibiotics for 4-6 weeks
surgery to repair affected valve

237
Q

what is HF

A

heart can no longer provide blood to oxygenate body
inadequate perfusion of tissues

238
Q

what are risk factors for HF

A

ischemic heart disease
htn

239
Q

what are signs of RHF

A

peripheral edema
JVD
hepatosplenomegaly

240
Q

what is RHF

A

inability of heart to provide adequate blood flow to pulmonary circulation

241
Q

what are signs of LHF

A

pulmonary edema
dyspnea
orthopnea
cough with frothy sputum

242
Q

what is LHF

A

inability of heart to generate adequate cardiac output to perfuse vital tissues

243
Q

what are dysrythmias

A

disturbances of heart rhythm

244
Q

what causes dysrhthmias

A

can be caused by an abnormal rate of impulse generation or an abnormal impulse conduction

245
Q

in utero what is the openeing between the atria

A

foramen ovale

246
Q

in utero what joins the pulmonary artery to the aorta

A

ductus arteriosus

247
Q

in utero what connects the inferior vena cava to the umbilical vein

A

ductus venosus

248
Q

where does the fetus receive oxygen carrying blood

A

placenta/umbilical vein

249
Q

where does the blood entering the fetus first go

A

liver
portal/hepatic circulation

250
Q

when does the heart form in utero

A

3-7 weeks

251
Q

T/F baby and fetus share blood/circulation

A

F it is separate

252
Q

when does heart get some contractility

A

4 weeks

253
Q

upon entering the fetus how much of the heart is diverted to liver

A

40% (60% to heart )

254
Q

what diverts the blood flow from the liver to the inferior vena cava in fetus

A

ductus venousus

255
Q

where does blood shunted from liver through ductus venosus go next

A

IVC

256
Q

what is blood path through fetal heart

A

enter RA from IVC
shunter through foramen ovale and into LA
to LV
aorta

257
Q

where does less saturated blood from fetus head/neck arms go in fetus

A

from superior vena cava into RA

258
Q

what does the foramen ovale bypass in fetus

A

RV/lungs

259
Q

what two places does blood go out of fetal RV

A

small portion to lungs
most bypasses blood through ductus arterious into descending aorta

260
Q

T/F the mother and fetus have the same blood

A

F, fetus has one blood

261
Q

T/F the lungs of the Fetus are functional

A

false

262
Q

what shunt bypasses the liver

A

ductus venosus

263
Q

blood from descending aorta in fetus goes where

A

returns to placenta through two umbilical arteries

264
Q

blood coming from the umbilical vein bypasses the

A

RV and lungs (goes from RA to LA to LV)

265
Q

what two special structures does fetal blood from umbilicus gothough

A

ductus venousus- bypasses liver to IVC
foramen ovale- bypasses RV and lungs

266
Q

what special structure does fetal blood from head/arms go through

A

from SVC to RA, to RV, some to lungs, most through DUCTUS ARTERIOSUS to descending aorta

267
Q

what are the three special fetal blood systems

A

ductus venous-bypasses liver
ductus ovale-bypasses RV
ductus arteriosus- bypasses lungs

268
Q

what happen with first breath in fetus

A

lungs descend, PA opens, pressure change closes: foramen ovale

269
Q

what does the ductus venosus become

A

round ligament (ligamentum venosus)

270
Q

what does the foramen ovale become

A

fossa ovale

271
Q

What does the ductus arteriosus become?

A

ligamentum arteriosum

272
Q

what is a portal hepatic shunt

A

unclosed ductus venosus bypasses liver

273
Q

what is it called when ductus arteriosus doesn’t heal

A

patent ductus arteriosus

274
Q

what is the leading cause of death in first year of life

A

congenital heart disease (besides premature)

275
Q

what are congenital defects classified by

A

based on blood flow
-increasing pulmonary blood flow
-decreasing pulmonary blood flow
-obstructive lesions
-mixing lesions

276
Q

what are clinical signs of congenital defects

A

poor feedin/sucking
failure to thrive
dyspnea, tachypnea, diaphoresis, grunting, nasal flaring, wheezing, coughing
skin changes like pallor or motling
hepatomegaly
pulmonary overcirculation

277
Q

what is a common condition with congenital birth defects

A

hypoxemia

278
Q

what is eisenmenger syndrom

A

pulmonary vascular resistance increases, exceeds or equals systemic vascular resistance, causes a reversal/shunting of blood

279
Q

what is a VSD

A

Ventricular septal defect-> hole in between ventricles

280
Q

a left to right shunt is okay because

A

still pumping out oxygentated blood

281
Q

a right to left shift is bad because

A

pumping our deoxygenated blood

282
Q

eisenmengers syndrome begins as a

A

1 L to R shunt- forms pulmonary HTN
2 pressure builds on R side, increasing PVR
3 R to L shunt develops
4 aorta pushes out deoxygenated blood

283
Q

T/F eseinmengers is a chronic condition

A

true

284
Q

what defects cause hypoxemia and cyanosis

A

tetralogy of fallot
R to left shunts

285
Q

what is patent ductus arteriousus

A

failure of the ductus arteriosus to close

286
Q

when does the ductus arteriousus usually close

A

15 hours-2 weeks after birth

287
Q

what does the ductus arteriousus connect

A

PA to aorta

288
Q

what are the clinical manifestations of PDA

A

continuous machinery-type murmur (washer machine)

289
Q

what is treatment for PDA

A

surgical closure by ligation by incision, catheter or video-assisted thoracoscopy

290
Q

PDA is a defect of _____________ pulmonary blood flow

A

increasing

291
Q

what is an ASD

A

-atrial septal defect
-hole in the septum b/t the right and left atria that results in increased pulmonary blood flow (left to right shunt)

292
Q

what are the clinical manifestations of murmur

A

often asymptomatic, diagnosed by murmur

293
Q

what are the three major types of ASD defects

A

ostium primum
ostium secundum
sinus venosus

294
Q

what is the treatment for ASD

A

Surgical closure before school age
synthetic patch

295
Q

ASD is a defect of ___________ pulmonary bloodflow

A

increasing

296
Q

what is VSD

A

Ventricular septal defect-> hole in between ventricles
shunting from the high-pressure left side to the low pressure right side

297
Q

what are the types of VSDs

A

perimembranous
muscular
supracristal
AV canal or inlet

298
Q

VSDs is a defect of ___________ pulmonary blood flow

A

increasing

299
Q

what is an atrioventricular canal defect

A

abnormalities in the atrial and ventrical septa and AV valves

300
Q

what are the types of AVC defects

A

complete, partial, and transitional

301
Q

what are clinical manifestations of AVC

A

murmur, HF

302
Q

what is treatment for AVC defect

A

complete repair between 3 and 6 months of life

303
Q

AVC is a defect of _____________ pulmonary blood flow

A

increasing

304
Q

ASD

A
305
Q

PDA

A
306
Q

VSD

A
307
Q

AVC

A
308
Q

what are the 4 aspects of tetralogy of Fallot

A

VSD
Overriding aorta straddles the VSD
Pulmonary valve stenosis
Right Ventricle hypertrophy

309
Q

what are s/s tetralogy of fallot

A

Cyanosis and clubbing
feeding difficulty
squatting

310
Q

what is the cause of clubbing

A

lack of O2 to nailbed

311
Q

what generally occurs with crying an exertion with tetralogy of fallot

A

hypervyanotic spell or tet spell

312
Q

tetralogy of fallot

A
313
Q

tetralogy of fallot is a defect of ___________ pulmonary blood flow

A

decreasing

314
Q

what is tricuspid atresia

A

Complete closure of the tricuspid valve
no communication between RA and RV

315
Q

what defects are found in tricuspid atresia

A

septal defect
hypoplastic or absent RV
enlarged mitral valve and LV
pulmonic stenosis

316
Q

what are clinical manifestations of tricuspid atresia

A

central cyanosis and growth failure
exertional dyspnea
tachypnea
hypoxemia

317
Q

what is treatment of tricuspid atreasia

A

prostaglandin admin
blalock-taussig shunt
rashkind procedure: ballon atrial septostomy
band
closure of septal defects

318
Q

tricuspid atresia is a disease of ____________ pulmonary blood flow

A

decreasing

319
Q

tricuspid atresia

A
320
Q

what is coarctation of the aorta

A

narrowing of the aorta

321
Q

what are clinical signs of coarctation of the aorta

A

CHF : hypotension, acidosis, shock
hypertension in upper extremities
decreases pulses in lower extremities
cool mottled skin
leg cramps during exercise

322
Q

what is treatment for coarctation of the aorta

A

prostaglandin admin
mechanical ventilation
inotropic support
surgery

323
Q

coarctation of the aorta

A
324
Q

tricuspid atresia is a __________ defect

A

obstructive

325
Q

coarctation of the aorta is an _________ defect

A

obstructive

326
Q

What is aortic stenosis?

A

narrowing of the aortic valve

327
Q

what causes aortic stenosis

A

malformation or fusion of the cusps

328
Q

aortic stenosis ___________ the workload of the LV

A

increases

329
Q

what are s/s aortic stenosis

A

often asymptomatic
signs of exercise intolerance in preadolescence
syncope
epigastric pain
exertional chest pain

330
Q

what is treatment of aortic stenosis

A

balloon aortic valvuloplasty
aortic valvotomy

331
Q

aortic stenosis

A
332
Q

aortic stenosis is an _____________ defect

A

obstructive

333
Q

what is pulmonary stenosis

A

narrowing of the pulmonary valve

334
Q

what is a severs form of pulmonary stenosis

A

pulmonary atresia

335
Q

what are s/s pulmonary stenosis

A

often asymptomatic
exertional dyspnea
murmur
fatigue

336
Q

what is treatment for pulmonary stenosis

A

mild: not treated
severe: balloon angioplasty, pulmonary valvotomy

337
Q

pulmonary stenosis is an __________ defect

A

obstructive

338
Q

pulmonary stenosis

A
339
Q

what is hypoplastic left heart syndrome

A

left side of the heart is underdeveloped
obstruction to blood flow from the left ventricle outflow tract

340
Q

what is underdeveloped in hypoplastic left heart syndrome

A

left ventricle
aorta
aortic arch

341
Q

what two conditions are observed in hypoplastic left heart syndrome

A

mitral atresia
stenosis

342
Q

what happens when ductus closes in hypoplastic left heart syndrome

A

hypoxemia
acidosis
shock

343
Q

what is treatment of hypoplastic left heart syndrome

A

prostaglandins
correction of acidosis
inotropic support for adequate cardiac output
ventilatory manipulation
surgery/transplant

344
Q

what are the three surgical treatments for hypoplastic left heart syndrome

A

norwood
glenn
fontan

345
Q

hypoplastic left heart syndrome

A
346
Q

hypoplastic left heart syndrome is an ____________ defect

A

obstructive

347
Q

what is transposition of the great arteries

A

When aorta arises from the right ventricle and the main pulmonary artery from the left ventricle

348
Q

in transposition of the great arteries unoxygenated blood is circulated through the __________ circulation and oxygenated blood is circulated through the __________ circulation

A

systemic
pulmonary

349
Q

what are s/s transposition of the great arteries

A

worsening cyanosis in first day of birth

350
Q

what is treatment fo transposition of the great arteries

A

surgery to switch the arteries

351
Q

transposition of the great arteries is an example of a ____________ defect

A

mixed

352
Q

transposition of the great arteries

A
353
Q

what is total anomalous pulmonary venous connection (TAPVC)

A

pulmonary veins connect to the right side of the heart, directly or indirectly, through one or more systemic veins that drain in to the ra

354
Q

what are s/s what is total anomalous pulmonary venous connection (TAPVC)

A

cyanosis

355
Q

what is treatment for what is total anomalous pulmonary venous connection (TAPVC)

A

repair obstructive lesions at times of diagnosis
unobstructive lesions are generally repaired during infancy
surgery: anastomosis of the common pulmonary vein to the left atrium, closure of the atrial septal defect

356
Q

what is total anomalous pulmonary venous connection (TAPVC)

A
357
Q

what is total anomalous pulmonary venous connection (TAPVC) is an example of a _____________ defect

A

mixed

358
Q

what is truncus arteriousus

A

failure of the embryonic artery to divide into the pulmonary artery and aorta, trunk straddles an always present VSD

359
Q

what is a type 1 truncus arteriousus

A

most common (60%) the main pulmonary artery arises from the truncus

360
Q

what is a type 2 truncus arteriousus

A

20%, pulmonary arteries arise from the posterior aspect of the truncus

361
Q

what is a type 3 truncus arteriousus

A

10% pulmonary arteries arise from the lateral aspect

362
Q

what is a type 4 truncus arteriousus

A

pseudotruncus: severe form of tetralogy of Fallot with the bronchial arteries arising from the descending aorta to supply the lungs

363
Q

what are s/s truncus arteriousus

A

cyanosis that worsens with activity

364
Q

what is treatment of truncus arteriousus

A

modified Rastelli procedure involving VSD patch closure to divert the blood flow from the left ventricle outflow tract into the truncus
correct pulmonary arteries

365
Q

truncus arteriousus is an example of a __________ defect

A

mixed

366
Q

truncus arteriousus

A
367
Q

what causes systemic htn in children

A

renal disease, coarctation of the aorta

368
Q

what are risk factors for childhood htn

A

race
socioeconomic
lack of health insurance
sedentary lifestyle

369
Q

what is associated with childhood obesity

A

parental obesity

370
Q

what does childhood obesity place child at risk for

A

asthma
sleep apnea
htn
type 2 diabetes
dyslipidemia
cardiovascular disease

371
Q

congenital heart defects come from

A

failure in embryonic failure

372
Q

Define anemia

A

Decrease in number of circulating RBCs or decrease in quality or quantity of hemoglobin

373
Q

Etiology of anemia

A

Altered RBC production
Blood loss
Increased RBC destruction
Combo of all three

374
Q

Classification of anemias in size

A

“Cytic”

Macrocytic microcytic normocytic

375
Q

Class of anemia by hemoglobin content

A

“Chromic”

Normochromic and hypochromic

376
Q

What is macrocytic normochromic anemia

A

B12 or folate deficiency

377
Q

What is microcytic hypochromic anemia

A

Iron deficiency
Thalassemia

378
Q

Normochromic normocytic anemia

A

Hemorrhage
Hemolytic
Aplastic

379
Q

How does anemia present

A

Hypoxia
Fatigue
Weakness
Angina
Dyspnea

380
Q

How can tissue hypoxia present

A

Ischemia
Weakness
Fatigue
Pallor
Increase RR
Dizziness/fainting

381
Q

What are compensatory mechanisms for tissue hypoxia

A

Increased HR
Increase SV
Dilate capillaries
Increase renin aldosterone
Increase erythropoietin
Increase BPG cells

382
Q

Pathological mechanisms of anemia of chronic disease

A

Decreased erythrocyte life span
Suppressed production of erythropoietin (kidney damage)
Ineffective bone marrow response to erythropoietin
Altered iron metabolism

383
Q

What causes chronic disease anemia

A

Chronic disease or inflammation
Infections
Cancer
Autoimmune diseases

384
Q

What is pancytopenia

A

Reduction of absence of all three types of blood cells
WBC RBC PLT

385
Q

Pathophysiology of aplastic anemia

A

Hypocellular bone marrow that has been replaced with fat

386
Q

What is aplastic anemia caused by

A

Pancytopenia results

Autoimmune disorders due to chemicals drugs physical agents unpredictable exposures, inherited or idiosyncratic cause

387
Q

How does aplastic anemia manifest

A

Hypoxemia
Pallor
Weakness
Fever
Dyspnea
Signs of hemorrhaging if platelets affected

388
Q

what is atherosclerosis

A

intimal lesions atheromas or fibrofatty plaques which protrude into and obstruct vascular lemns and weaken the underlying media

contributes 50% mortality in the western world

389
Q

where does atherosclerosis happen

A

higher pressure vessels/larger vessels often have it

bifurcations

chronic inflammatory problem

390
Q

what are the three principal components

A

cells (macrophages/foam cells, smooth muscle cells, lymphocytes)

macrophages that are engulfed LDL

extracellular matrix (ECM/collagen)

lipid (LDL, oxidized LDL)

391
Q

factors that promote atherogenisis

A

endothelial injury that alters the normal hemostasis of the endothelium
–increased adhesion and permeability
–more procogulant
–formation of vasoactive cytokines and growth factors

continuing inflammatory response

cyclic accumulation of cells and lipids

392
Q

potential consequences of atherosclerosis

A

narrowing of vessels=ischemia

sudden vessel obstruction caused by plaque hemorrhage or rupture

thrombosis leading to embolism

aneurysmal dilation due to weakening of vessel wall (outside of the plaque)

393
Q

define hypertension

A

BP > 140/90

normal is <130/85

394
Q

pathogenesis of HTN

A

increased CO and or SVR
increases afterload
kidneys, RAAS, and SNS all contribute

395
Q

consequences of HTN

A

vessel injury
prolonged vasoconstriction-target organ disease
retinal changes
renal disease
cardiac disease (CAD, CHF)
neuro disease (stroke, dementia, encephalopathy)

396
Q

what are factors that lead to increased Na retention

A

-genetics
-increased SNS
-increased RAAS
-endothelial dysfunction
-dysfunction of natriuretic hormones
-renal glomerular and tubular –inflammation
-obesity
-insulin resistance
-increased dietary intake
-decreased dietary K, Mg, and Ca

397
Q
A

Pathophysiology (3 decks)

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