Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Pathophys > Cardio Patho > Flashcards

Cardio Patho Flashcards

1
Q

How much blood does the heart pump per day

A

6000L

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

How thick is the Right and left ventricle

A

R=0.3cm-0.5cm

L=1.3-1.5cm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

how is cardiomegaly defined

A

inc in cardiac weight(hypertrophy) or size(dilation) or both

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

what is the concentration of mitochondria in the cardiac myocytes compared to skeletal muscle

A

cardiac=23% (heart needs more O2)

skeletal= 2%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

how are myocytes arranged

A

cirumferentially in a spiral orientation to allow for maximal ejection fraction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

what are cytoplasmic electron dense granules

A

found in the atria and contain ANP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

what is the significance of intercalated discs with gap junctions

A

allow atria or ventricles to function as a unit and contract together

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

what are the 3 types of pathologic changes that can occur in heart valves and what is their effect

A

collagen damage=prolapse
nodular calcification=stenosis
fibrotic thickening= stenosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

how does Rheumatic heart dz affect the heart

A

The body forms antibodies to group A strep. These antibodies then attack the heart valves causing fibrotic thickening

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

what is the likely effect from a bicuspid aortic valve

A

causes early stenosis(40-60yo) bc one valve takes the brunt of the pressure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

what is the blood supply to the 1)SA node 2)AV node 3) Bundle of His

A

1)55%RCA 45% circumflex
2)70% RCA(Right dom)
20% circumflex (Left dom)
10% Codominant
3) RCA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Can a heart convert from R dominant to L dominant

A

a heart can convert to codominant only with chronic ischemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

A occlusion to which cardiac wall is the most concerning in regards to rate control

A

Inf wall MI bc a R dom heart will have infarct to the SA and AV node

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

how much necrosis is considered not viable to life in the L ventricle

A

40% or more

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

how much necrosis is considered not viable to life in the R ventricle

A

90% or more

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

what are the branches of the circumflex

A

obtuse marginals

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

what are the branches of the L ant descending artery

A

diagonals and septal perforators

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

with a infarct, where are the myocytes located that typically die 1st?

A

the endocardial surface

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

how long does it take for irreversible damage(necrosis) to occure from ischemia

A

20-30min

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

where are common locations of stenosing plaques?

A

First several cm of LAD
First several cm of circum flex
Entire length of RCA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

are most cases of ischemic heart Dz single or multivessel

A

90% are multivessel

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

what % of a coronary artery must be obstructed for Sx to occur on exertion

A

> 75%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

what % of a coronary artery must be obstructed for Sx to occur at rest

A

> 90%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

what % of obstruction to a coronary artery would indicate PCI and what percent would indicate medical treatment?

A

PCI at >70% occlusion but still medically treat those with >50% occlusion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

what % of acute ischemia is caused from vessels with <70% occlusion

A

2/3 of events happen in <70%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

what type of patients are likely to have silent angina pectoris

A

DM, Alcoholics

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

what are the 3 biochemical components of IHD

A

1) Hypoxia=dec contractility
2) insufficient metabolic substrates(glucose)
3) accumulation of metabolic waste (lactic acid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

how does lactic acid affect cardiac myocytes

A

it blocks the actin/myosin crossbridge= dec contractility

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

what is done prior to surgery to negate the hypotensive effect of anesthesia

A

IV bolus to inc fluids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

How does volume overload affect those with IHD

A

inc ventricular volume= inc actin/myosin crossbridge overlap= inc O2 demand

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

what is ashen

A

grey appearance from severe cyanosis and vasoconstriction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What is the mechanism for IHD causing pallor

A

vasoconstriction from

1) dec CO= shunting of blood to central organs
2) Pain activates sympathetics

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

what is the mechanism for IHD causing diaphoresis

A

pain activates sympathetics= activation of diaphoresis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Ischemia to which part of the heart will dec CO the most and how does the heart respond

A

blocking the free wall(anterior) of the LV will dec CO the most bc it is unable to expand= dec CO= inc HR= tachy arrhythmias

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What is a important consideration when CP is accompanied with N/V

A

This type of discomfort is typically from the phrenic nerve which indicates inf infarct= RCA blockage= possible arrhythmias.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

how do nitrates relieve CP

A

Vasodilate the periphery= dec afterload and dec preload= heart works less

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

what three terms is unstable angina AKA

A

preinfarction, crescendo, impending MI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

what is prinzmetal angina

A

spasm of epicardial artery causing transmural ischemia(ST elevation)

39
Q

when does prinzmetal angina occur

A

its unpredictable and can occur at rest

40
Q

what causes prinzmetal angina

A

may be due to inc SNS, inc Ca++, TXA2/PGI2 imbalance

41
Q

how do you diagnose prinzmetal angina

A

ergonovine maleate is used to induce a spasm to confirm diagnosis

42
Q

how is Thallium 201 used in radioisotope imaging

A

only enters cells by Na/K pump so it indicates cells that are alive making it a hot isotope

43
Q

what do the different grades IHD indicate

A

grade1=up to 25% occlusion
grade2= 25-50
grade3= 50-75
grade 4= 75-100

44
Q

how do you dec O2 demand in the heart

A

Bed rest
Preload reduction
Afterload reduction
(Beta/Ca++ blockers, nitrates)

45
Q

how do you inc O2 supply to the heart

A

MONA, rate reduction(Beta/Ca++ blockers)

46
Q

when is morphine typically used in IHD

A

only for MI (rarely for stable angina)

47
Q

what is paclitaxel (taxol)

A

Chemo agent combined with stents which disrupts tubular dynamics necessary for endothelial cell division

48
Q

what is sirolimus(rapamycin)

A

immunosupressant combined with stents to dec inflammation= dec endothelialization

49
Q

what meds are typically given after stents are put in

A

ASA and plavix are usually given for 6-9m to prevent clots

50
Q

when is CABG typically performed

A

if more than 2 vessels occluded

51
Q

what is the definition of a MI

A

persistent occlusion resulting in death of the heart muscle

52
Q

what are key features of necrosis

A

membrane disruption, cardiac enzymes are released

53
Q

what is the WHO criteria for MI

A

2 or more of the following

  • prolonged ischemic type chest discomfort
  • serial ECG changes
  • Rise and fall of serum cardiac markers
54
Q

what typically causes global hypotension and what type of MI does it cause

A

caused from anesthesia causing dec blood flow in all coronary arteries=circumferential subendocardial infarct

55
Q

what type of MI would DIC cause

A

small intramural vessel obstructions=microinfarcts= subendocardial infarct

56
Q

what is stunned myocardium

A

located in periphery of infarcted area-edematous and dysfunctional that is not yet dead and may be recovered

57
Q

what factors determine the extent of structural or functional changes after infarction

A

Location, severity and rate of development
Size of vascular bed perfused by obstructed vessel
Duration of occlusion
Metabolic/oxygen needs of myocardium at risk
Extent of collateral blood vessels
Presence, site, and severity of vessel spasm
Other factors: HR, rhythm, and blood oxygenation

58
Q

what information do collateral coronary blood vessels give you

A

most hearts have collaterals but they are only noticeable if there is a chronic obstruction

59
Q

what determines how beneficial reperfusion therapy will be

A

Rapidity of alleviating obstruction

Extent of correction

60
Q

what causes reperfusion injury

A

oxidative stress
calcium overload
inflammation and lactic acid build up distal to clot

61
Q

how does reperfusion injury cause arrhythmias

A

inc necrotic tissue= inc extracellular K+=raise resting membrane potential= inc excitability= arrhythmias

62
Q

what is the most common type of reperfusion injury

A

hemorrhage d/t inflammation

63
Q

what causes a Q wave

A

necrotic tissue becoming fibrotic. (Typically from transmural infarct)

64
Q

how specific and sensitive is ST elevation

A
  • specificity of 91%

- sensitivity of 46%

65
Q

In regards to ST elevation, how do you determine the severity of a infartion

A

the higher the elevation and the more leads involved, the larger the infarction and greater mortality

66
Q

when does troponin I begin to rise, peak, and disappear after MI

A

rises 2-4 hrs, peaks 48hrs, and lasts up to to weeks

67
Q

what is acute organic brain syndrome

A

Confusion/ disorientation usually caused by dec perfusion to brain

68
Q

when is greatest risk for ventricular wall rupture post MI

A

usually 4-7 days post transmural MI

69
Q

what has dec risk for cardiogenic shock post MI

A

intra aortic balloon pump perfusing the coronary and brain arteries

70
Q

what are common complications of transmural anterior wall MI

A

thrombi or rupture(tamponade)

71
Q

what are common complications of transmural post wall MI

A

conduction block d/t AV node involvement

72
Q

poor prognosis post MI are associated with what

A

female
DM
age
hx of prev MI

73
Q

what is sudden cardiac death

A

Unexpected death from cardiac causes in individuals without symptomatic heart disease. Usually from lethal arrhythmias

74
Q

what is often the first clinical manifestation of IHD

A

sudden cardiac death

75
Q

what are heritable conditions associated with SCD

A

channelopathies (long QT syndrome) causing overlap of depolarization and repolarization= inc risk for arrhythmias

76
Q

what is the effect of chronic ischemic heart dz with heart failure

A

Left vent hypertrophy and dilation

77
Q

what is the hearts adaptive mechanism to heart failure

A

Frank-Starling mechanism

Myocardial hypertrophy with or without dilation (ventricular remodeling)

78
Q

how are catecholamines related to heart failure

A

dec CO= inc SNS= inc HR and TPR= heart working harder

Deleterious effects: apoptosis of myocytes, down regulation of adrenergic receptors, arrhythmias

79
Q

how is Angiotension II related to heart failure

A

dec kidney perfusion= inc Ang II release
Deleterious effects: inc fluid retention
fibroblast remodeling stimulation
-hypertrophy from mitogen activated protein kinase

80
Q

how is arginine vasopressin(ADH) related to heart failure

A

inc ADH= peripheral vasoconstriction(to inc kidney perfusion) and fluid retention
Deleterious effect= exacerbation of hyponatremia and edema

81
Q

how is natriuretic(ANP, BNP) peptides related to heart failure

A

inc natriuretic= dec preload/afterload

82
Q

how are endothelial hormones related to heart failure

A

Endothelin is a potent vasoconstrictor and associated with a poor prognosis in individuals with CHF. It is also a growth factor for myocytes.

83
Q

how are endotoxins related to heart failure

A

Linked to myocyte apoptosis and release of tumor necrosis factor and interleukins.
Endotoxins are from gram neg bacteria so typically only problematic in sepsis pts.

84
Q

how is TNF-alpha related to heart failure

A

Elevated in CHF and contributes to myocardial remodeling
Down-regulates the synthesis of nitric oxide=vasoconstriction
Induces myocyte apoptosis
Contributes to weight loss and weakness

85
Q

how do ACE/ARB affect heart failure

A

diuretic= dec preload, dec afterload

prevent remodeling

86
Q

what is meant when the heart is in fetal production mode

A

BNP usually not produced on a daily basis except in fetuses. Fetal mode indicates the ventricles are producing BNP on daily basis. This occurs during heart failure

87
Q

what is characteristic of hypertrophic myocytes

A

contain increased mitochondria and have enlarged nuclei (Increase DNA ploidy-DNA replication in absence of cell division))

88
Q

what is concentric hypertrophy

A

inc in thickness more than dilation

89
Q

what is essentric hypertrophy

A

inc in diameter of ventricle

90
Q

how are sarcomeres assembled in pressure overload hypertrophy

A

assembled in parallel to long axis of cells forming concentric inc in wall thickness

91
Q

how are sarcomeres assembled in volume overload hypertrophy

A

assembled in series with existing sarcomeres forming essentric hypertrophy

92
Q

how does myocardial hypertrophy affect the vascular bed

A

decreased capillary density
increased intercapillary distance
deposition of fibrous tissue

93
Q

what is the effect of diastolic failure

A

CO preserved at rest

During exertion: “flash pulmonary edema”

Pathophys (15 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions