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Spring 2023 > Pathophysiology Exam 3 > Flashcards

Pathophysiology Exam 3 Flashcards

1
Q

BP =

A

CO x SVR

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2
Q

MAP

A

mean arterial pressure

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3
Q

MAP =

A

DBP + 1/3 (SBP-DBP)

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4
Q

Pulse pressure

A

SBP-DBP

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5
Q

Minimum MAP

A

60 mmHg

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6
Q

Vasodilation

A

decrease SVR

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7
Q

Vasoconstriction

A

increase SVR

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8
Q

CO =

A

SV x HR

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9
Q

What influences SV?

A

BV & contractility

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10
Q

low BP

A

hypotension

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11
Q

Hypotension parameters

A

BP < 90/60 mm

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12
Q

Only treat hypotension if it is what?

A

symptomatic

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13
Q

In Cardiogenic hypotension what is impacted?

A

Cardiac output (CO)

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14
Q

How is cardiogenic hypotension treated?

A

increase CO
- Epi/dobutamine

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15
Q

Epi/dobutamine are what?

A

(+) inotropes

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16
Q

(+) inotropes do what?

A

increase contractility

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17
Q

drug that raises blood pressure
- many are vasoconstrictors

A

pressor agent

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18
Q

Hypotension caused by Sepsis

A

vasodilation (decreases SVR)

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19
Q

How is sepsis hypotension treated?

A

Increase SVR
- NE/Vasopressin (ADH)/Epi/Phenylephrine

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20
Q

NE/Vasopressing (ADH)/Epi/Phenylephrine are all what?

A

vasoconstrictors (pressor agents)

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21
Q

Hypovolemia

A

decrease BV

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22
Q

How to treat hypotension caused by hypovalemia

A

increase IV fluids -> increase BV -> increase SV -> increase CO

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23
Q

high BP

A

hypertension (HTN)

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24
Q

Stage 1 hypertension

A
  • systolic 130-139
    OR
  • diastolic 80-89
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25
Q

Stage 2 hypertension

A
  • systolic >/= 140
    OR
  • diastolic >/= 90
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26
Q

Resistance heart pumping against

A

afterload

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27
Q

hypertension caused by what?

A

increased heart workload

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28
Q

effect of heart having to pump against increase resistance (effect of HTN)

A

ventricular hypertrophy.

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29
Q

ventricular hypertrophy

A

ventricular layer thickens
- ventricle holds less blood & pumps less blood

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30
Q

How to treat hypertension

A

decrease CO, decrease SVR or both

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31
Q

how to decrease CO

A

decrease SV by either decreasing BV or contractility

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32
Q

how to decrease SVR

A

vasodilation

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33
Q

Drugs that decrease CO

A
  • diuretics (thiazide - HCTZ)
  • Beta blockers
  • ACE inhibitors/ARBs/Renin inhibitors
  • Calcium channel blockers (CCBs)
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34
Q

Drugs that decrease SVR (vasodilators)

A
  • ACE inhibitors/ ARBs/ Renin inhibitors
  • CAlcium channel blockers
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35
Q

Drugs that are (-) inotropes and (-) chronotropes

A

Beta blockers & Calcium channel blockers. (CCBs)

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36
Q

Vasodilations decreases SVR and what?

A

LV afterload

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37
Q

atherosclerotic plaque

A

Coronary artery disease

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38
Q

chest pain caused by myocardial ischemia

A

Angina pectoris

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39
Q

angina with exertion; relieved with rest
- increase demand (exertion)
- decrease demand (at rest)

A

Stable Angina

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40
Q

Angina at rest
- decrease supply

A

Unstable Angina

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41
Q

CAD -> Myocardial ischemia -> ?

A

Myocardial Infarction (MI) = heart attack

42
Q
  • Unstable angina
  • MI
A

Acute Coronary Syndrome (ACS)

43
Q

MI’s can be _ or _

A

STEMI or non- STEMI

44
Q

Immediate compensatory response for MI

A

increase SNS activity (bororeceptor reflex)
- heart: increase HR & CTX -> increase CO
- Blood Vessels: Vasoconstriction -> increase SVR

45
Q

Slower compensatory response for MI

A

increase fluid retention -> increase BP

46
Q

Cardiac enzymes (MI markers)

A

Troponins ( not detected till 3 hrs after MI)

47
Q

CO inadequate to meet metabolic demand

A

Congestive heart failure (CHF)

48
Q

Compensatory responses:
- increased preload caused by fluid retention
- increased afterload caused by increase SNS activity
Overall, increases myocardial workload

A

Congestive heart failure

49
Q

“stretch” on ventricle wall

A

preload

50
Q

“Resistance” ventricle must pump against

A

afterload

51
Q

A failing heart _ than a non failing heart

A

works harder

52
Q

decrease CO below normal

A

low output failure

53
Q

loss of contractility

A

systolic

54
Q

filling problem - small, “stiff” ventricle

A

Diastolic

55
Q
  • increase myocardial workload
  • increase preload
  • increase afterload
  • dilated heart
A

systolic CHF

56
Q

Systolic CHF treatment

A
  • increase contraction with (+) inotropes
  • decrease workload with beta blockers
  • decrease preload with diuretics (decrease BV)
  • decrease afterload with vasodilators (ARBs, Renin inhibitors, ACE inhibitors)
57
Q

Dilated heart =

A

cardiomegaly

58
Q

decrease SNS effect
- (-) inotropes
- (-) chronotropes
- used to decrease workload

A

beta blockers

59
Q
  • often caused by poorly controlled HTN
  • increase afterload
A

Diastolic CHF

60
Q

Diastolic CHF treatment

A
  • increase ventricle filling time by decreases HR with CCBs
  • decrease workload with CCBs
61
Q

Heart failure with reduced ejection fraction (HFrEF)

A

Systolic failure

62
Q

Heart failure with preserved ejection fraction (HFpEF)

A

Diastolic factor

63
Q

Ejection factor (EF) =

A

SV (stroke volume) /EDV (end diastolic volume)

64
Q

normal EF

A

50-60%

65
Q

normal SV

A

70 mL

66
Q

normal EDV

A

120 mL

67
Q

Ejection fraction is not the same as what?

A

CO

68
Q

LV failure ->

A

pulmonary edema -> increased pulmonary hydrostatic pressure -> fluid retention -> increased BV

69
Q

low RBC count or low Hgb or low hematocrit

A

Anemia

70
Q

% of blood that is RBC

A

hematocrit

71
Q

What do you rule out first with Anemia?

A

blood loss

72
Q

What do you rule out next with Anemia?

A
  • decreased RBC production (bone marrow)
  • increased RBC destruction (sickle cell anemia, hemolytic anemia)
73
Q

What is the typical presentation of Anemia?

A
  • fatigue (less O2 transport)
  • pallor
74
Q

more pale than normal

A

Pallor

75
Q

Whats the anemia test?

A

H/H test = hemoglobin/hematocrit

76
Q

Normal RBC size

A

80-100 fL

77
Q

RBC may indicate what?

A

cause of anemia

78
Q

micrositic anemia

A

<80 fL
- iron deficiency / Hgb deficiency

79
Q

macrositic anemia

A

> 100 fL
- B12 deficiency

80
Q

high WBCs (>10,000)

A

leukocytosis

81
Q

Normal WBC count

A

5k-10k / uL

82
Q

Potential causes of a WBC count of 15k

A
  • infection present (rule out 1st)
  • inflammation
83
Q

Potential cause of a WBC count of 100k

A

Leukemia
- WBC are not function -> increased infection risk

84
Q

low WBCs

A

Leukocytopenia or Leukopenia

85
Q

WBC count of 1k has an increased what?

A

infection risk

86
Q

low platelet count

A

thrombocytopenia

87
Q

Normal platelet count

A

150k - 400k

88
Q

Platelet count of 30k

A

increased bleeding risk

89
Q

Platelet count of 15k

A

severe - may bleed spontaneously

90
Q

Thrombosis

A

Deep vein thrombosis (DVT)

91
Q

clot that has detached from the wall; now in circulation

A

thromboembolus

92
Q

DVT -> thromboembolus ->

A

pulmonary embolus -> circulatory collapse

93
Q

Virchow’s triad

A

3 risk factors for DVT

94
Q

What are Virchow’s triad?

A

1) Hypercoaguability - blood clots easier
- pregnancy/OC (birth control)/cancer

2) Venous stasis - slow venous blood flow
- immobility/A-fib

3) Vessel wall damage (endothelial injury)
- smoking/ HTN

95
Q
  • life threatening
  • cellular/tissue hypoxia
  • If caught early, reversible
  • If allowed to rapidly progress, irreversible
  • most common presentation = hypotension
A

Circulatory shock

96
Q

4 types of circulatory shock

A
  1. Distributive
  2. Cardiogenic
  3. Hypovolemia
  4. Obstructive
97
Q

severe peripheral vasodilation
- septic, anaphylactic, neurogenic, toxic shock

A

Distributive circulatory shock

98
Q

intracardiac cause of pump failure
- MI, CHF

A

cardiogenic circulatory shock

99
Q

Low BV
- hemorrhagic vs non-hemorrhagic

A

Hypovalemia circulatory shock

100
Q

extracardiac cause of pump failure
- PE

A

Obstructive circulatory shock

101
Q

circulatory shock can lead to what?

A

Multiple Organ failure (MOF)

Spring 2023 (10 decks)

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