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Pathohysiology > Cardio Disorders > Flashcards

Cardio Disorders Flashcards

1
Q

cardiovascular/heart disease

A

disease of the heart and/or blood vessels

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2
Q

heart disease is considered a consequence of

A

atherosclerosis

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3
Q

what are the effects of atherosclerosis?

A

thickening and hardening in the artery wall

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4
Q

what causes the effects of atherosclerosis?

A

thickening and hardening is caused by an accumulation of lipid-laden macrophages in the arterial wall.
increased inflammation signals

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5
Q

atherosclerosis is a consequence and cause of

A

increased blood pressure

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6
Q

atherosclerosis increases risk of

A

cardiovascular infarction

cerebrovascular infarction

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7
Q

atherosclerosis is thought to stem from

A

cholesterol

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8
Q

what does high blood pressure cause?

A

tearing of endothelium and therefore inflammation.

turbulent flow in a blood vessel

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9
Q

where is turbulent flow most apparent?

A

in areas of branching or constriction of the blood vessel

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10
Q

turbulent flow damages:

A

endothelium

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11
Q

A type LDL cholesterol is

A

large and less dense

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12
Q

B type LDL cholesterol is

A

Small and more dense

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13
Q

what are the risk factors for pattern B LDL cholesterol

A

Genetic
oral contraceptives
diet

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14
Q

what can increase your levels of patten B LDL cholesterol?

A

a very low fat high carb diet

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15
Q

dietary cholesterol has ____ impact on blood cholesterol

A

little

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16
Q

increased consumption leads to ____ absorption

A

reduced

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17
Q

where does most circulating cholesterol come from?

A

it is synthesized de novo

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18
Q

where is cholesterol synthesized?

A

80% in the liver
10% in intestine
5% in skin

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19
Q

what is the most potent activator of de novo cholesterol synthesis?

A

insulin

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20
Q

what is related to increased cholesterol synthesis?

A

increased fasting insulin.

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21
Q

what increases cholesterol synthesis from the liver?

A

insulin-stimulating meals

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22
Q

what are the most widely prescribed drug in the world?

A

statins

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23
Q

HMG-CoA reductase inhibitors

A

statins

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24
Q

what do HMG-CoA reductase do?

A

they play a role in synthesizing cholesterol in the liver.

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25
Q

which group of people do statins help the most?

A

people with previous history of cardiovascular event. They don’t really help other people

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26
Q

what are some of the side effects of statins?

A

increased risk of diabetes (T2)
kidney failure
liver failure
muscle pain (muscle break down)

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27
Q

what is normal blood pressure

A

systolic: 90-119
diastolic: 60-79

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28
Q

what is prehypertension BP?

A

systolic: 120-139
Diastolic: 80-89

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29
Q

What is stage one (primary) hypertension BP?

A

systolic: 140-159
Diastolic: 90-99

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30
Q

what is stage 2 (secondary) hypertension BP?

A

Systolic: eq > 160
diastolic: eq > 100

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31
Q

primary hypertension

A

“essential” hypertension
affects 90-95% of individuals with hypertension
results from weight gain
associated with insulin resistance
there are genetic and environmental factors

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32
Q

Secondary hypertension results from

A

a structural, renal or endocrine problem

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33
Q

what reduces BP in hypertensives?

A

carb restriction

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34
Q

who does salt sensitivity affect the most?

A

people who are insulin resistant

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35
Q

in RAAS dysfunction, _____ is increased in obesity

A

Plasma Sodium content

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36
Q

what induces prolonged sodium retention in RAAs dysfunction?

A

CHO ingestion

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37
Q

insulin increases_____ in RAAS dysfunction

A

kidney sodium reabsorption

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38
Q

urinary sodium excretion ___ with insulin injection

A

decreases

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39
Q

insulin increases ____ secretion

A

aldosterone

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40
Q

in RAAS dysfunction, what is capable of eliciting an antidiuretic effect?

A

a very slight increase in plasma insulin

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41
Q

what reduces BP in hypertensives?

A

carb restriction

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42
Q

who does salt sensitivity affect the most?

A

people who are insulin resistant

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43
Q

in RAAS dysfunction, _____ is increased in obesity

A

Plasma Sodium content

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44
Q

what induces prolonged sodium retention in RAAs dysfunction?

A

CHO ingestion

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45
Q

Which neuro transmitter of the sympathetic nervous system is affected by primary hypertension due to insulin resistance and how?

A

insulin causes a dose-related increase in norepinephrine release. which then increases pulse and blood pressure.

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46
Q

urinary sodium excretion ___ with insulin injection

A

decreases

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47
Q

insulin increases ____ secretion

A

aldosterone

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48
Q

in RAAS dysfunction, what is capable of eliciting an antidiuretic effect?

A

a very slight increase in plasma insulin

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49
Q

primary hypertension due to insulin resistance enhances _____ activtiy

A

growth factor

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50
Q

there are receptors for ____ and ___ in capillary endothelial cells which causes vascular cells to be responsive to insulin

A

IGF-1 and insulin

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51
Q

enhanced growth factor activity causes ___ of the vascular wall

A

hypertrophy

-narrowing of vascular wall due to thickening of the wall. Narrower opening.

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52
Q

Primary hypertension due to insulin resistance affects the ____ nervouse system

A

sympathetic

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53
Q

Which neuro transmitter of the sympathetic nervous system is affected by primary hypertension due to insulin resistance and how?

A

insulin causes a dose-related increase in norepinephrine release. which then increases pulse and blood pressure.

54
Q

how does insulin resistance induced primary hypertension affect nitric oxide.

A

Normally, insulin increases the production of endothelium derived NO which is a potent vasodilator.
But, insulin resistant endothelial cells can’t release NO so then NO can’t be produce to cause vasodilation

55
Q

what is NO made from?

A

L-arginine

56
Q

what improves blood pressure more than restricting salt and fat?

A

restricting carbs and weight loss

57
Q

sodium has ___ effect on hypertension onset

A

no effect

58
Q

preeclampsia

A

pregnancy induces hypertension

59
Q

what is the leading cause of maternal death?

A

preeclampsia

60
Q

what is going on in preeclampsia?

A

reduced kidney function leads to chronic excessive increased blood pressure.

61
Q

what is eeclampsia?

A

toxin accumulation
seizures
death

62
Q

what are some drug treatments for hypertension?

A 
alpha blockers
beta blockers
diuretics
ACE inhibitors
metformin
63
Q

what do alpha blockers do?

A

they reduce SNS activity which slows heart rate and stroke vol

64
Q

what do beta blockers do?

A

reduce heart contractility

65
Q

what is an aneurysm?

A

a local dilation or outpouching of a vessel wall or cardiac chamber

66
Q

true aneurysm

A

involve all three layers of the arterial wall

67
Q

false aneurysm

A

do not have distension of all three layers of the arterial wall.

68
Q

thrombus

A

blood clot that remains attached to the vessel wall

69
Q

thromboembolus

A

a clot (thrombus) that breaks free

70
Q

thrombophlebitis

A

swelling of the veins cause by a thrombus

71
Q

why are arterial thrombi so rare?

A

bc of the pressure in the arteries. Thrombi that are formed here are usually pushed out into the veins and become venous thrombi

72
Q

embolism

A 
bolus of matter in circulation in the blood stream 
this can include:
dislodges thrombus
air bubble 
aggregate of fat 
bacteria
cancer cells
or a foreign substance
73
Q

what is a common feature of peripheral artery disease?

A

intermittent claudication

74
Q

what is intermittent claudication?

A

obstruction of arterial blood flow in the iliofemoral vessels resulting in pain with movement

75
Q

what are thromboangitis obliterans?

A

buerger disease
lesions to the endothelial lining caused by inflammation.
obliterates the small and medium sized artering in perfusion. So you can’t get blood out as well.

76
Q

what are the effects of thromboangiitis obliterans?

A 
pain 
tenderness
hair loss in the affected area
gangrenous lesion 
loss of oxygen to the tissues
77
Q

what are some symptoms of thromboangiitis obliteran?

A

slow and sluggish blood flow

78
Q

raynaud phenomenon /disease

A

episodic vasospasm in arteries and arterioles of the fingers, less commonly the toes
(where the fingers are whit or like green)
usually triggered by cold or stress

79
Q

which diseases is raynaud phenomenon secondary to?

A

collagen vascular disease (scleroderma)
smoking
pulmonary hypertension

80
Q

Deep vein thrombosis (DVT)

A

obstruction of venous flow leading to increased venous pressure

81
Q

what are factors that increase your risk of DVT?

A

venous stasis
venous endothelial damage
hypercoagulable states

82
Q

Myocardial ischemia

A

heart is not getting blood

83
Q

temporary myocardial ischemia

A

deprivation of the coronary blood supply

result in angina pectoris

84
Q

angina pectoris

A

chest pain from coronary ischemia

85
Q

stable angina

A

recurrent pain from chronic coronary artery obstruction during effort

86
Q

unstable angina

A

result of reversible ischemia

sign of possible future attacks

87
Q

sustained ischemia

A

prolonged blockage of coronary artery

leads to myocardial infarction

88
Q

myocardial infarction

A

myocardial inflammation and necrosis

89
Q

myocardial infarction

A

sustained and complete obstruction of the myocardial blood supply

90
Q

subendocardial infarction

A

affects only the inner 1/3 to 1/2 of the heart wall.

91
Q

Why is the inner wall more affected in subendocardial infarction?

A

because blood supply goes first to outer wall.

92
Q

transmural infarction

A

affects more than 1/2 of the heart wall

more serious

93
Q

stent

A

a treatment for myocardial infarction that pushes plaque out of the way so that blood can pass. doesn’t clear plaque

94
Q

___ can induce ischemia in predisposed individuals

A

stress

95
Q

insulin resistance increases risk of which cardiomyopathies?

A

dilated

hypertrophic

96
Q

dilated cardiomyopathy

A

congestive cardiomyopathy

rounder than it should be

97
Q

hypertrophic cardiomyopathy

A

when heart muscle gets thicker and it doesn’t allow the chambers to fill up
hypertension is the leading cause

98
Q

restrictive cardiomyopathy

A

deposition of material in myocardium

it has normal dimensions but doesn’t move as it should.

99
Q

systolic heart failure

A

inability of the heart to generate adequate cardiac output to perfuse tissues
the heart is just not able to generate enough force and its not able to it blood around the body

100
Q

diastolic heart failure

A

pulmonary congestion

101
Q

what is the cause of pulmonary congestion due to diastolic heart failure?

A

LV stiffening

102
Q

why does diastolic heart failure cause pulmonary congestion?

A

is the left side isn’t working well, it’s having a hard time getting blood out so its having a hard time getting blood in from the lungs which then causes the lungs to get congested.

103
Q

right heart failure

A

harder time getting blood to the lungs

causes by hypoxic pulmonary disease

104
Q

what can result from an increase in left ventricular filling pressure that is reflected back into the pulmonary circulation

A

right heart failure

105
Q

high output failure

A

inability of the heart to supply the body with blood borne nutrients despite adequate blood volume and normal or elevated myocardial contractiloty

106
Q

valvular stenosis

A

narrowing of valves

107
Q

what are types of valvular stenosis?

A

aortic stenosis

mitral stenosis

108
Q

valvular regurgitation

A

leakage of valves

109
Q

what are types of valvular reguritation?

A

aortic regurgitation

mitral regurgitation

110
Q

mitral valve prolapse syndrome

A

when the valve is ballooning up into the atrium

111
Q

aortic valve stenosis

A

stiffening and narrowing of the aortic valve
blood has difficulty exiting the heart
prolonged ejection sound

112
Q

what are clinical manifestations of aortic valve stenosis?

A

crescendo-decrescendo systolic hear sound during systole
decrease in stroke volume
increased LV pressure (not getting all the blood out)
decreased systolic BP
decreased HR
hypertrophy of left ventricle resulting in ischemia, left heart failure

113
Q

what does aortic valve stenosis cause a decrease HR?

A

the heart is trying to maintain function so it will reduce heart rate to not get too full

114
Q

aortic regurgitation

A

failure of the aortic valve to properly close

blood leaks back into the ventricle after ventricular contraction

115
Q

what are clinical manifestations of aortic regurgitation?

A

diastolic murmur (blowing sound) of high pitch over the left ventricle
dysrhythmia
hypertrophy of left ventricle
left heart failure
doppler echocardigram reveals blood flow back through aortic valve

116
Q

mitral stenosis

A

narrowing or stiffening of the mitral valve
has a hard time opening
blood flow into the ventricle during diastole

117
Q

what are clinical manifestations of mitral stenosis?

A 
subtle crescendo diastolic murmur (rumbling) 
decreased blood flow from left atrium to left ventricle 
increased left atrial pressure 
hypertrophy and dilation of left atrium 
atrial dysrhythmias 
increases pulmonary blood pressure 
pulmonary edema 
right heart failure
118
Q

mitral regurgitation

A

failure of the mitral valve (left AV valve) to properly close
blood passing into atrium from ventricle during contraction

119
Q

what are clinical manifestations of mitral regurgitation?

A 
systolic murmur 
dilated hypertrophied left ventricle 
dilated left atrium 
left heart failure 
pulmonary hypertension and edema 
right heart failure 
doppler cardiography reveals blood flow back through mitral valve
120
Q

Which side of the heart is dominant in utero?

A

the right ride because they don’t need their lungs since mom is providing all the oxygen

121
Q

what are the changes in dynamic that take place with a baby’s first breath?

A

decreased pulmonary pressure and increased systemic vascular resistance

122
Q

which structures go away with the baby’s first breath?

A

ductus arteriosus

foramen ovale

123
Q

what are some prenatal, environmental, and genetic risk factors for infant congenital heart defects?

A 
maternal rubella
insulin-dependent diabetes
alcoholism 
hypercalcemia
come prescription drugs
chromosome aberrations
124
Q

what are some complications that may occur with congestive heart failure?

A

congestive heart failure

hypoxemia (which leads to cyanosis)

125
Q

Patent ductus arteriosus

A

increases pulmonary blood flow
failure of the ductus arteriosus to close
blood moves from the aorta to the PA
blood that just got to the heart from the lungs is going back into the lungs.

126
Q

atrial septal defect

A

increases pulmonary blood flow
abnormal communication between the atria
there is a communications between the atris so blood will leak from the left side to the right side and will then go back to the lungs where it had just come from.

127
Q

ventricular septal defect

A

increases pulmonary blood flow
abnormal communication between the ventricles
most common type of congenital heart defect
less consequences the closer the defect is to the apex

128
Q

atrioventricular canal defect

A

increases pulmonary heart flow results from nonfusion of the endocardinal cushions
the atrium and the ventricles are connected

129
Q

tetralogy of fallot

A 
decreases pulmonary blood flow 
a mix of four syndromes:
ventricular septal defect 
overriding aorta (aorta literally moved to left)
pulmonary valve stenosis 
right ventricle hypertrophy 
sending less blood to the lungs and increasing the amount of unoxygenated blood to the body 
hypoxia
130
Q

tricuspid atresia

A

imperforate tricuspid valve (lack of communication between the right atrium and left ventricle

131
Q

coaractation of the aorta

A

narrowing of the lumen of the aorta that impedes blood flow

obstructive defect

132
Q

hypoplastic left heart syndrome

A

obstructive defect
abnormal development of the left sided cardiac structures
requires a patent ductus arteriosis or a septal defect to move blood into systemic circulation

Pathohysiology (16 decks)

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