Pathophysiology Exam 2 Flashcards

1
Q

a protective response by the body to tissue damage from a variety of causes (traumatic, toxic, allergic, infectious).

A

Inflammation

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2
Q

Inflammation is an incredibly complex biochemical process involving what?

A

numerous types of cells, plasma proteins, and chemicals

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3
Q

Inflammation can what?

A

involve any organ and be localized, regional, or diffuse

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4
Q

“itis”

A

denotes inflammation of an organ/structure

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5
Q

What is necessary for inflammation to occur?

A

adequate blood supply

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6
Q

inflammation is a prerequisite for what?

A

tissue repair and wound healing

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7
Q

Anything that impairs inflammation also impairs what?

A

tissue repair and wound healing

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8
Q

a rapid onset and typically lasts for 2-10 days

A

acute inflammation

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9
Q

acute inflammation is characterized by the following findings, known as the 5 cardinal signs of inflammation:

A

redness, heat, swelling, pain, and loss of function

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10
Q

What is initiated when tissue damage occurs?

A

an acute inflammatory response, blood vessels at the site of tissue damage dilate (allows more bloodflow)

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11
Q

Blood flow resulting from blood vessels dilating causes what?

A

redness and heat

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12
Q

What causes the loss of function symptom of acute inflammation?

A

tissue damage

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13
Q

Why is extra blood flow beneficial?

A

many of the cells contributing to the inflammatory response are present in the bloodstream.

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14
Q

What are released from various cell types, causing a local increase in capillary permeability?

A

numerous chemical inflammatory mediators

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15
Q

What produces the pain in an acute inflammatory response?

A

the numerous chemical inflammatory mediators release

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16
Q

What causes swelling or edema?

A

local increase in capillary permeability caused by chemical inflammatory mediator release

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17
Q

Why is local increase in capillary permeability beneficial?

A

It allows leukocytes and platelets to leave the bloodstream and migrate to the site of tissue damage to limit further damage and begin the process of repair and wound healing

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18
Q

a prolonged state of inflammation lasting more than 3 months and can be present for years.

A

Chronic inflammation

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19
Q

Chronic inflammation is characterized by what?

A

reoccurring cycles of tissue damage and repair

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20
Q

is infarction (death) of brain tissue, resulting in an irreversible neurologic deficit. classified as either Ischemic or hemorrhagic

A

Stroke (Cerebrovascular accident or CVA)

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21
Q

accounts for 80-85% of all strokes and is almost always caused by the presence of atherosclerotic plaques in the arteries supplying the brain, causing ischemia (reduced blood flow) to the brain and resulting in cell death.

A

Ischemic stroke

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22
Q

Stroke caused by what would also be considered ischemic?

A

reduction in blood volume, blood flow or reduced cardiac output would also be considered ischemic

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23
Q

Risk factors for ischemic stroke include what?

A

classic cardiovascular risk factors such as diabetes mellitus, smoking, hyperlipidemia/hypercholestrolemia, sedentary lifestyle, high fat diet

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24
Q

accounts for the remaining 15-20% of strokes and is caused by rupture of a blood vessel supplying the brain.

A

Hemorrhagic stroke

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25
Q

Most common risk for hemorrhagic stroke is what?

A

poorly controlled hypertension

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26
Q

The clinical manifestations of stroke depend on what?

A

the location and size of the infarct

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27
Q

A relatively small infarct involving a vital brain region may be what?

A

lethal

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28
Q

whereas a relatively larger infarct involving a non-vital brain region may what?

A

produce milder clinical manifestations

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29
Q

It is also important to understand that strokes can what?

A

progress (the size of the infarct can expand)

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30
Q

In a stroke, there is a central area of infarcted tissue that is what?

A

irreversible

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31
Q

Surrounding that central area is ischemic tissue that is what?

A

reversible

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32
Q

This surrounding ischemic tissue is called what?

A

penumbra

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33
Q

Penumbra is still viable and if timely intervention is implemented, the ischemic tissue can be what?

A

preserved

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34
Q

If intervention is not implemented or implemented too late then what can happen?

A

the ischemic tissue may progress to infarction, thereby increasing the size of the infarct

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35
Q

defined by the American Heart Association and the American Stroke association as “a transient episode of neurologic dysfunction caused by focal brain, spinal cord or retinal ischemia without acute infarction”

A

Transient Ischemic Attack (TIA)

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36
Q

TIAs produce what?

A

reversible neurologic deficits

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37
Q

Most TIAs last less than what?

A

an hour (often less than 30 minutes, but they may be more prolonged)

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38
Q

Signs/ symptoms frequently resolve before what?

A

presentation to a clinician

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39
Q

Neurologic manifestations vary depending on what?

A

the site of the TIA

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40
Q

TIAs are occasionally precursors to what?

A

ischemic stroke

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41
Q

A patient with a history of TIAs has what?

A

an increased risk for having an ischemic stroke

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42
Q

ADH

A

anti-diuretic hormone

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43
Q

What does ADH cause?

A

water retention via decreased urine output
- causes increase BV -> increase BP
Vasoconstriction
- increase SVR -> increase BP

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44
Q

More ADH is produced than needed; excess ADH

A

Syndrome of inappropriate ADH (SIADH)

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45
Q

SIADH causes what?

A

Too much water retention
- causes increase BV -> increase BP
- ECF becomes Hypotonic -> cells swell
- More dilute ECF -> hyponatremia

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46
Q

How to treat SIADH?

A

Treat underlying cause

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47
Q

No ADH or deficient response to ADH; ADH “deficiency”

A

Diabetes Insipidus (DI)

48
Q

No ADH; absolute ADH deficiency

A

Central diabetes insipidus (CDI)

49
Q

Normal/high ADH levels; impaired kidney response to ADH

A

Nephrogenic diabetes insipidus (NDI)

50
Q

Diabetes insipidus patients urine output is often what?

A

10-14 L; normal = 2L

51
Q

Diabetes insipidus have _ blood volume

A

very low

52
Q

Diabetes insipidus causes what?

A

Increased urine output
- decreased BV -> decreased BP
- ECF becomes hypertonic -> cells shrink
- Less dilute ECF -> hypernatremia

53
Q

No ADH in blood

A

Central diabetes insipidus

54
Q

Normal/ high ADH levels in blood

A

nephrogenic diabetes insipidus

55
Q

too much thyroid hormone

A

hyperthyroidism

56
Q

hyperthyroidism effects

A

Increased sensitivity to sympathetic nervous system (fight or flight)
- hypertensive
- increased metabolic rate

57
Q

problem with thyroid gland (high)

A

primary hyperthyroidism

58
Q

problem with anterior pituitary (high)

A

secondary hyperthyroidism

59
Q

TH levels high & TSH levels low

A

primary hyperthyroidism

60
Q

TH levels high & TSH levels high

A

secondary hyperthyroidism

61
Q

primary hyperthyroidism treatment

A

radiation thyroid ablation

62
Q

secondary hyperthyroidism treatment

A

tumor resection

63
Q

TSH levels are low. What are the possible disorders.

A
  • primary hyperthyroidism
  • secondary hypothyroidism
64
Q

Thyroid hormone replacement therapy

A

Radiation treatment and then synthroid (treat hypothyroidism caused by radiation)

65
Q

TH deficiency

A

hypothyroidism

66
Q

problem with thyroid gland (low)

A

primary hypothyroidism

67
Q

Problem with anterior pituitary (low)

A

secondary hypothyroidism

68
Q

TH low and TSH high

A

primary hypothyroidism

69
Q

TH low and TSH low

A

secondary hypothyroidism

70
Q

Cortisol effects

A
  • increased blood glucose
  • catabolic (break-down)
  • anti-inflammatory
71
Q

Cushings syndrome

A

hypercortisolism

72
Q

too much cortisol

A

hypercortisolism (cushing’s syndrome)

73
Q

Endogenous

A

primary and secondary hypercortisolism

74
Q

caused by abnormal adrenal cortex production (tumor)

A

primary hypercortisolism

75
Q

cushing’s disease

A

secondary hypercortisolism

76
Q

caused by excess ACTH

A

secondary hypercortisolism (cushing’s disease)

77
Q

cortisol high and ACTH low

A

primary hypercortisolism

78
Q

cortisol high and ACTH high

A

secondary hypercortisolism (cushing’s disease)

79
Q

Exogenous hypercortisolism cause

A

steroid administration

80
Q

Why do steroids lower cortisol and ACTH levels?

A

because the body no longer needs to make it

81
Q

Universal symptoms of hypercotisolism

A

moon face, buffalo hump, chicken legs

82
Q

Addison’s disease

A

hypocortisolism

83
Q

primary adrenal cortex insufficiency; decrease cortisol & aldosterone

A

hypocortisolism (addison’s disease)

84
Q

low cortisol and high ACTH

A

hypocortisolism (addison’s disease)

85
Q

aldosterone effects

A

increase blood Na+ (retention)
- water retention -> increase BV/BP
decrease blood K+ (excretion)

86
Q

aldosterone deficient

A

hypoaldosteronism

87
Q

hypoaldosteronism causes

A

hyperkalemia
- increase NM
- heart risk (slows)
- decrease BV/BP (less water retention)

88
Q

too much aldosterone

A

hyperaldosteronism

89
Q

adrenal cortex problem

A

primary hyperaldosteronism (Conn’s disease)

90
Q

Conn’s disease

A

primary hyperaldosteronism

91
Q

primary hyperaldosteronism causes what?

A

increase Na retention
- increase water retention -> increase BV/BP (hypertension)
increase K+ excretion
- hypokalemia -> decrease NM
decrease Renin

92
Q

caused by increased renin

A

secondary hyperaldosteronism

93
Q

secondary hyperaldosteronism causes what?

A

increase Na retention
- increase water retention -> increase BV/BP (hypertension)
increase K+ excretion
- hypokalemia -> decrease NM
increase Renin

94
Q

R.A.A.P. pathway

A

angiotensinogen -(renin)-> A1 -(ACE)-> A2 -> increase aldosterone & vasoconstriction

95
Q

Diabetes refers to what?

A

increase urine output

96
Q

hyperglycemia

A

diabetes mellitus (DM)

97
Q

increase urine output

A

polyuria

98
Q

increase thirst

A

polydipsia

99
Q

increase hunger

A

polyphagia

100
Q

what causes polydipsia?

A

polyuria

101
Q

Polydipsia is associated with what kind of ECF?

A

hypertonic

102
Q

absolute insulin deficiency; beta cell destruction

A

Type I diabetes mellitus

103
Q

Type I diabetes mellitus treatment

A

insulin

104
Q

Type I diabetes mellitus acute complication

A

DKA

105
Q

“relative” insulin deficiency & tissue resistance to insulin

A

Type II diabetes mellitus

106
Q

Type II diabetes mellitus treatment

A

Insulin (some), insulin sensitizers

107
Q

Type II diabetes mellitus acute complication

A

HHNKS

108
Q

Are chronic complications of diabetes mellitus type specific?

A

No

109
Q

atherosclerotic plaque formation

A

Macrovascular chronic complications

110
Q

atherosclerotic plaque formation may cause what?

A

Coronary artery disease (CAD)
- MI (heart attack)
Cerebral vascular disease (CVD)
- Ischemic stroke
Peripheral arterial disease
- amputation

111
Q

Result of poor glucose control

A

microvascular chronic complications

112
Q

microvascular chronic complications include

A
  • nephropathy (kidneys)
  • neuroopathy (sensory)
  • retinopathy
113
Q

Diagnostic criteria for diabetes mellitus

A
  • A1C >/= 6.5% on 2 separate tests
  • Fasting blood glucose >/= 126 on 2 separate tests
114
Q

Hgb A1C

A

glycated (glycosylated Hgb)

115
Q

increase blood sugar

A

increase glycosylated hemoglobin