Brainscape's Knowledge GenomeTM

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


See full index

patho final > Functional cardiac disorders > Flashcards

Functional cardiac disorders Flashcards

1
Q

what is CAD

A

atherosclerosis of coronary arteries- disease of the intima (inner lining)

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

what kind of disorder is CAD and how does it start

A

it is chronic and progressive

inflammation starts the process

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

what is the first stage of the CAD patho chain

A

inflammation-> endothelium damage-> lipids deposited-> lipids are oxidized and attract macrophages-> monocytes enter intima-> become macrophages which ingest LDL-> transformed into foam cells-> foam cells release cytokines-> cause inflammation and injury

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

what is the second stage of CAD patho

A

fatty streak starts causing narrowing

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

what is a fatty streak

A

yellow, lipid filled smooth muscle cell- an organized collection of foam cells

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

what is the third stage of CAD patho

A

fibrous plaque causes further narrowing

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

what is fibrous plaque

A

fatty streak + collagen + elastic fibers

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

what is the fourth stage of CAD patho

A

complicated (advanced) lesion hemorrhages causes clot formation and obstruction

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

what is complicated (advanced lesion

A

fibrous plaque (all the before things) hemorrhages

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

what is the incidence of CAD

A

1 killer in us and other developed counteries

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

what are the 3 most dangerous risk factors for CAD

A

smoking
HTN
hyperlipidemia

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

what are the other risk factors for hyperlipidemia in CAD

A

age,
male gender under 60,
genetic predisposition (under 35),
hyper lipidemia

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

what causes hyperlipidemia in CAD

A
  1. increase in dietary fat intake
  2. diabetes and genetics
  3. lipoproteins (lipids, phospholipids, cholesterol and triglycerides bound to carrier proteins
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

what are found in a blood lipid profile

A

total cholesterol
triglycerides
LDL
HDL

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

why does type 1 affect CAD

A

increased blood glucose accelerates CAD

2x men, 4x women

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

why does htn affect CAD

A

increased peripheral vascular resistances increases workload of heart and accelerates process of atherosclerosis

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

why does smoking affect CAD

A
  1. nicotine- causes release of epi and increases hr and vasoconstriction
  2. increased platelet adhesiveness- increases clot formation
  3. CO- attaches to Hgb
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

women and CAD

A 
women have a higher morality rate after acute MI
#1 killer of women all cancers together
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

how does cocaine and meth affect CAD

A

increases BP hr and causes vasoconstriction of coronary arteries

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

how does hyperhomocysteinemia affect CAD

A

causes injury to arterial walls

treat/prevent with folic acid (folate)

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

what is homocysteine

A

an amino acid from animal protein normally broken down in the liver with help of vitamin b6 b12 and folic acid.. increased amount CAD

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

how do we measure what is the role of inflammation in the development of CAD

A

c reactive protein– high sensitivity– increases measures inflammation

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

what is myocardial ischemia

A

local and temporary deficiency of blood supply due to obstruction of coronary circulation

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

how does CAD lead to angina

A

CAD-> myocardial ischemia after 10 seconds-> angina from lactic acid production during anaerobic respiration

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

what are the classical (transient) signs of myocardial ischemia

A

3-20 mins
pain- substernal pain, discomfort, heaviness, pressure, tightening, squeezing or aching
may radiate to neck, left arm, jaw, teeth, back

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

what are the non classical signs of myocardial ischemia

A

indigestion
upper back pain
jaw pain ONLY
increasing fatigue

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

what are the types of angina

A

stable

unstable

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

describe stable angina

A

predictable
similar events initiate attack (stress activity)
similar type of sensation with each attack
relief WITH REST and nitrates

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

describe acute coronary syndrome

A

sudden coronary artery obstruction due to thrombus formation over atherosclerotic plaque

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

what kind of angina is with acute coronary syndrome

A

unstable- unpredicable sensation often OCCURES WITH REST

indicates advanced CAD

31
Q

what is an MI

A

CAD that leads to myocaridal ischemia which leads to irreversible hypoxia and cellular death

32
Q

what is the cause of MI

A

narrowed coronary artery and clot formation with 100% of coronary artery occluded

33
Q

describe cellular injury in MI

A
  1. first 30-60 seconds of hypoxia with EKG changes

2. cells without o2 and nutrients lose contractility

34
Q

describe cellular death (myocyte death) with MI

A

after 20 minutes (irreversible hypoxia injury)

death and necrosis

35
Q

describe remidelng with MI

A

scar formation and loss of function of cardiac cells leads to thin poorly contracting ventricular walls

36
Q

what is cell membranes rupturing mean with cellular death for MI

A

intracellular enzymes spill out into blood stream

37
Q

what is the zone of ischemia in MI

A

outside ring

colateral circulation causes healing

38
Q

what is the zone of injury in MI

A

middle ring

colateral circulation causes healing

39
Q

what is the zone of infarction in mi

A

inner ring

doesn’t heal and becomes scar tissue

40
Q

describe the scar formation of an mi

A

zone of infarction–

  1. weak and mushy 10-14 days post MI
  2. strong scar 6 weeks but does NOT contract/pump
41
Q

clinical mani of classical MI

A
  1. substernal pain an discomfort, heaviness, pressure, tightening, squeezing, aching
  2. may radiate to neck, left arm, jaw, teeth, back
  3. indigestion, nausea, vomiting
  4. diaphoresis
  5. cool clammy skin
  6. change in BP or HR and rhythm
    NO RELIEF WITH NITRATES
42
Q

what lab data is collected to diagnose an MI

A
  1. enzyme increase of CK- MB (creatinine phosphokinase) is released when cells die
  2. Tropinin increase- protein in cardiac cell ‘’
  3. WBC increase- reflects inflammatory response
  4. glucose increased- elevates with stress
43
Q

what does a 12 lead EKG do

A

identifies if and where a MI occurred

44
Q

what are the post MI complications

A
  1. heart failure/ cardiogenic shock

2. arrhythmias/dysrhythmias

45
Q

why is heart failure/ cariogenic shock a post MI complication

A

decreased ejection fraction- % of blood the left ventricle ejects
normal is 50-60%

46
Q

why is arrhythmias/dys a post MI complication

A

disturbance of cardiac rhythm occurs with 80-90% of MIs

47
Q

what is heart failure

A

inability of heart to maintain adequate cardiac output to support body functions (heart fails as a pump)

48
Q

what is the ejection fraction of heart failure

A

less than 40% (60-80 norm)

49
Q

what does the 40% ejection fraction of heart failure lead to

A

results in ventricular remodeling where the heart chamber walls become thin, dilated and poorly contract

50
Q

what is preload

A

amt of blood coming into the heart LV

51
Q

what is afterload

A

load against which the heart must pump against

52
Q

what is the incidence of heart failure

A

increased incidence because people are surviving MI

53
Q

what are the four compensatory mechanisms in heart failure

A

ventricular hypertrophy
SNS stimulation
ADH
Renin release

54
Q

how does ventricular hypertrophy not help HF

A

heart enlarges to increase CO which increased the workload of the heart

55
Q

how does SNS stimulated not help HF

A

increases HR and SV which increases workload of the heart

56
Q

how does ADH not help HF

A

water is retained increasing BV and increases the workload of the heart

57
Q

how does RENIN release not help HF

A

release of angio II leads to vasoconstriction and increases workload on the heart

58
Q

left sided HF turns into what also

A

right sided HF

59
Q

left sides was also called

A

congestive HF

60
Q

what are the causes of LVHF

A
  1. MI- no contractility area
  2. hypertension- increase in SVR (vascular resistance)
  3. aortic stenosis or incompetence- increase in SVR
61
Q

what is backward effect in LVHF

A

decreased emptying of the left ventricle-> increases volume preload in left ventricle-> increaded volume preload in left atrium-> increased volume in pulmonary veins-> increased volume in pulmonary cap beds-> movement of fluid from caps to alveoli activation-> rapid filling of alveolar spaces-> pulmonary edema-> RVF (right ventricle failure)

62
Q

what is the forward effect in LVHF

A

decreased cardiac output-> decreased perfusion of tissues of body-> decreased BP-> decreased glomerular filtration rate-> decreased urine output-> renin activation-> sodium and water retention

63
Q

what are the mani of LVHF

A
  1. decreased BP
  2. dyspnea
  3. lung crackles (rales)
  4. frothy sputum
  5. fatigue, exercise intolerance
64
Q

what are the two causes of RVHF

A
  1. pulmonary artery hypertension (COPD, pulmonary emboli)

2. LVHF (most common)

65
Q

what is the backward efffects of RVHF

A

decreased emptying of RV-> increased volume preload in the RV-> increased volume preload in the right atrium-> increased volume in the vena cava-> increased volume in the systemic venous circulation-> increased volume in the distensible organs (liver, spleen)-> increased cap pressure-> peripheral, dependent edema

66
Q

what is the forward effects of RVHF

A

decreased volume from the RV to the lungs-> decreased return to left atrium and decreased left ventricular cardiac output-> all the forward effects of LVHF

67
Q

what are the clinical mani of RVHF

A
  1. jugular venous distension
  2. increased central venous pressure
  3. peripheral edema
  4. abd. distention from liver and spleen
  5. wt gain
  6. fatigue, exercise intolerance
68
Q

p wave

A

impulse from SA (normal pacemaker) through atria and atrial contraction (atrial depolarization)

69
Q

PR interval

A

beginning of P to beginning of QRS (impulse from SA through AV)

70
Q

QRS

A

impulse through ventricles (v depolarize causing v contraction)

71
Q

ST segment

A

end of s to beginning of t wave (time between depolarization and repolarization of ventricles)

72
Q

t wave

A

depolarization of ventricles

73
Q

what are the clinical non classical of MI

A
  1. weakness
  2. fatigue
  3. dyspnea
  4. upper back pain
  5. no symptoms

patho final (3 decks)

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