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Spring 2023 > Pathophysiology Exam 2 > Flashcards

Pathophysiology Exam 2 Flashcards

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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
Most common risk for hemorrhagic stroke is what?
poorly controlled hypertension
26
The clinical manifestations of stroke depend on what?
the location and size of the infarct
27
A relatively small infarct involving a vital brain region may be what?
lethal
28
whereas a relatively larger infarct involving a non-vital brain region may what?
produce milder clinical manifestations
29
It is also important to understand that strokes can what?
progress (the size of the infarct can expand)
30
In a stroke, there is a central area of infarcted tissue that is what?
irreversible
31
Surrounding that central area is ischemic tissue that is what?
reversible
32
This surrounding ischemic tissue is called what?
penumbra
33
Penumbra is still viable and if timely intervention is implemented, the ischemic tissue can be what?
preserved
34
If intervention is not implemented or implemented too late then what can happen?
the ischemic tissue may progress to infarction, thereby increasing the size of the infarct
35
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"
Transient Ischemic Attack (TIA)
36
TIAs produce what?
reversible neurologic deficits
37
Most TIAs last less than what?
an hour (often less than 30 minutes, but they may be more prolonged)
38
Signs/ symptoms frequently resolve before what?
presentation to a clinician
39
Neurologic manifestations vary depending on what?
the site of the TIA
40
TIAs are occasionally precursors to what?
ischemic stroke
41
A patient with a history of TIAs has what?
an increased risk for having an ischemic stroke
42
ADH
anti-diuretic hormone
43
What does ADH cause?
water retention via decreased urine output - causes increase BV -> increase BP Vasoconstriction - increase SVR -> increase BP
44
More ADH is produced than needed; excess ADH
Syndrome of inappropriate ADH (SIADH)
45
SIADH causes what?
Too much water retention - causes increase BV -> increase BP - ECF becomes Hypotonic -> cells swell - More dilute ECF -> hyponatremia
46
How to treat SIADH?
Treat underlying cause
47
No ADH or deficient response to ADH; ADH "deficiency"
Diabetes Insipidus (DI)
48
No ADH; absolute ADH deficiency
Central diabetes insipidus (CDI)
49
Normal/high ADH levels; impaired kidney response to ADH
Nephrogenic diabetes insipidus (NDI)
50
Diabetes insipidus patients urine output is often what?
10-14 L; normal = 2L
51
Diabetes insipidus have _ blood volume
very low
52
Diabetes insipidus causes what?
Increased urine output - decreased BV -> decreased BP - ECF becomes hypertonic -> cells shrink - Less dilute ECF -> hypernatremia
53
No ADH in blood
Central diabetes insipidus
54
Normal/ high ADH levels in blood
nephrogenic diabetes insipidus
55
too much thyroid hormone
hyperthyroidism
56
hyperthyroidism effects
Increased sensitivity to sympathetic nervous system (fight or flight) - hypertensive - increased metabolic rate
57
problem with thyroid gland (high)
primary hyperthyroidism
58
problem with anterior pituitary (high)
secondary hyperthyroidism
59
TH levels high & TSH levels low
primary hyperthyroidism
60
TH levels high & TSH levels high
secondary hyperthyroidism
61
primary hyperthyroidism treatment
radiation thyroid ablation
62
secondary hyperthyroidism treatment
tumor resection
63
TSH levels are low. What are the possible disorders.
- primary hyperthyroidism - secondary hypothyroidism
64
Thyroid hormone replacement therapy
Radiation treatment and then synthroid (treat hypothyroidism caused by radiation)
65
TH deficiency
hypothyroidism
66
problem with thyroid gland (low)
primary hypothyroidism
67
Problem with anterior pituitary (low)
secondary hypothyroidism
68
TH low and TSH high
primary hypothyroidism
69
TH low and TSH low
secondary hypothyroidism
70
Cortisol effects
- increased blood glucose - catabolic (break-down) - anti-inflammatory
71
Cushings syndrome
hypercortisolism
72
too much cortisol
hypercortisolism (cushing's syndrome)
73
Endogenous
primary and secondary hypercortisolism
74
caused by abnormal adrenal cortex production (tumor)
primary hypercortisolism
75
cushing's disease
secondary hypercortisolism
76
caused by excess ACTH
secondary hypercortisolism (cushing's disease)
77
cortisol high and ACTH low
primary hypercortisolism
78
cortisol high and ACTH high
secondary hypercortisolism (cushing's disease)
79
Exogenous hypercortisolism cause
steroid administration
80
Why do steroids lower cortisol and ACTH levels?
because the body no longer needs to make it
81
Universal symptoms of hypercotisolism
moon face, buffalo hump, chicken legs
82
Addison's disease
hypocortisolism
83
primary adrenal cortex insufficiency; decrease cortisol & aldosterone
hypocortisolism (addison's disease)
84
low cortisol and high ACTH
hypocortisolism (addison's disease)
85
aldosterone effects
increase blood Na+ (retention) - water retention -> increase BV/BP decrease blood K+ (excretion)
86
aldosterone deficient
hypoaldosteronism
87
hypoaldosteronism causes
hyperkalemia - increase NM - heart risk (slows) - decrease BV/BP (less water retention)
88
too much aldosterone
hyperaldosteronism
89
adrenal cortex problem
primary hyperaldosteronism (Conn's disease)
90
Conn's disease
primary hyperaldosteronism
91
primary hyperaldosteronism causes what?
increase Na retention - increase water retention -> increase BV/BP (hypertension) increase K+ excretion - hypokalemia -> decrease NM decrease Renin
92
caused by increased renin
secondary hyperaldosteronism
93
secondary hyperaldosteronism causes what?
increase Na retention - increase water retention -> increase BV/BP (hypertension) increase K+ excretion - hypokalemia -> decrease NM increase Renin
94
R.A.A.P. pathway
angiotensinogen -(renin)-> A1 -(ACE)-> A2 -> increase aldosterone & vasoconstriction
95
Diabetes refers to what?
increase urine output
96
hyperglycemia
diabetes mellitus (DM)
97
increase urine output
polyuria
98
increase thirst
polydipsia
99
increase hunger
polyphagia
100
what causes polydipsia?
polyuria
101
Polydipsia is associated with what kind of ECF?
hypertonic
102
absolute insulin deficiency; beta cell destruction
Type I diabetes mellitus
103
Type I diabetes mellitus treatment
insulin
104
Type I diabetes mellitus acute complication
DKA
105
"relative" insulin deficiency & tissue resistance to insulin
Type II diabetes mellitus
106
Type II diabetes mellitus treatment
Insulin (some), insulin sensitizers
107
Type II diabetes mellitus acute complication
HHNKS
108
Are chronic complications of diabetes mellitus type specific?
No
109
atherosclerotic plaque formation
Macrovascular chronic complications
110
atherosclerotic plaque formation may cause what?
Coronary artery disease (CAD) - MI (heart attack) Cerebral vascular disease (CVD) - Ischemic stroke Peripheral arterial disease - amputation
111
Result of poor glucose control
microvascular chronic complications
112
microvascular chronic complications include
- nephropathy (kidneys) - neuroopathy (sensory) - retinopathy
113
Diagnostic criteria for diabetes mellitus
- A1C >/= 6.5% on 2 separate tests - Fasting blood glucose >/= 126 on 2 separate tests
114
Hgb A1C
glycated (glycosylated Hgb)
115
increase blood sugar
increase glycosylated hemoglobin

Spring 2023 (10 decks)

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