Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

Clinical Pathophysiology > Module 1 Cell Injury, Aging, and Death > Flashcards

Module 1 Cell Injury, Aging, and Death Flashcards

(91 cards)

Start Studying
1
Q

Cellular response to stress

A
  • atrophy
  • hypertrophy
  • hyperplasia
  • metaplasia
  • dysplasia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Atrophy

A

decrease in size
- may decrease function

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

Hypertrophy

A

increase in cell size
- increased protein
- heart increase in workload

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

Hyperplasia

A

increase in cell number

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

Metaplasia

A

reversible replacement of one mature cell type by another less mature cell type

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

Dysplasia

A

abnormal change in size, shape, organization
- called atypical hyperplasia

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

Atrophied cells

A

-less ER (endoplasmic reticulum)
- fewer mitchocondria
- decreased O2 consumption

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

Hypertrophy signaled by

A

mechanical stretch, growth factors, hormones, and vasoactive agents

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

Compensatory

A

liver cells

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

Hormonal

A

estrogen dependent such as breast and uterus

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

Pathologic

A

uterus and prostate

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

Dysplasia can be

A
  • cervical dysplasia, respiratory, and breast tissue
  • pre- cancer
    *oftenr eversible with removal of stimulus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Causes of Cell injury

A
  • physical
  • mechanical
  • thermal
  • chemical (toxins, endogenous, exogenous)
  • deficit injury (free radical injuries)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Types of cellular death

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

Hypoxia

A

lack of oxygen within a cell

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

Ischemia

A

lack of blood supply to the cell

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

Two things happen on a cellular level with an ischemic injury

A
  • decrease in mitochondria oxygenation
  • decrease in ATP
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Hyperplasia relations with menstrual cycle

A

estrogen in her body during her period signals hyperplasia, which results in the addition of more cells to the lining to get ready for the chance of pregnancy

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

Apoptosis

A

programmed cell death
- killed by suicide
- killed by T cell

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

Necrosis

A

cell death where cell membrane ruptures, triggering inflammation
- occurs bc of ischemia or toxic injury

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

Coagulative necrosis

A

tissue death caused by lack of blood supply (ischemia) and protein denaturation
- gelatinous, opaque substance

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

Liquefactive necrosis

A

cell death caused from ischemic injury to neurons and glial cells in the brain
- soft and liquified

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

Caseous necrosis

A

cell death from pulmonary tuberculosis or infection
- cheese like

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

Fat necrosis

A

fatty tissue in the breast become damaged or injured caused by lipase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Gangrenous Necrosis
Death of tissue from severe hypoxic injury from the blockage of major arterial vessels
26
Nutritional Injury
may result from - poor intake - altered absorption - impaired distribution by circulatory system - inefficient cellular uptake
27
Nutritional injuries common causes
- poverty - chronic alcoholism - chronic illness etc.
28
Cellular aging
- progressive decline in proliferation and reparative capacity - exposure to environmental factors that cause damage
29
Cellular aging responsible mechanisms
- dna damage - reduced proliferation capacity of stem cells - metabolic damage - telomere shrink
30
Physiologic causes of cellular aging
- age related decrease in functional reserve - inability to adapt to environmental demand
31
Somatic Death
death of entire organism
32
Total body water
water is 60% of body weight - intracellular fluid - intravascular fluid
33
Net filtration
pushing out fluid in intravascular space to tissue
34
Capillary hydrostatic pressure
pushing pressure - pushing out against the wall
35
Interstitial oncotic pressure
pulling pressure - water pulling - keeping fluid outside of cell
36
Reabsorption
pulling fluid back into intravascular space
37
Plasma oncotic pressure
water pulling - inside blood vessels (protein) holding onto water
38
interstitial hydrostatic pressure
pressure against the walls
39
Net filtration
forces favoring filtration - forces opposing filtration = net filtration - where the water is going
40
At arterial end of capillary
- hydrostatic pressure is higher than oncotic - fluid moves into the interstitial space
41
At venous end of capillary
- oncotic pressure is higher than hydrostatic - fluid moves back into circulation
42
Edema
accumulation of fluid within the interstitial spaces
43
Edema causes
increase in blood pressure increase in sodium retention tight clothing lymph obstructions
44
water balance hormones
ADH Aldosterone
45
ADH
tells cell to hold onto water - high pressure
46
thirst perception
Osmolality receptors
47
Osmolality receptors
detect increase concentration causes thirst perception and ADH release
48
Fluid loss- baroreceptors
baroreceptors receptors know volume is low so they hold onto water and release ADH
49
Sodium
Primary ECF cation (positive) - regulates water - pulls on water
50
Chloride
primary ECF anion (negative) - provides electroneutrality
51
Sodium and chloride off balance
kidneys excrete sodium then there is a decrease in concentration - aldosterone increase reabsorption of sodium
52
Afferent arterioles
contain cells that release renin
53
Renin
promotes aldosterone - turning 1 into 2
54
Natriuretic hormones
promotes excretion of sodium and water to decrease BP
55
Atrial natriuretic hormone
produces in heart to control and reduce BP
56
Isotonic alterations
- in balance of water and electrolytes
57
Isotonic fluid excess
too much fluids causes BP increase
58
Hypertonic alterations
more electrolytes than water
59
Hypernatremia
excess sodium in the blood - water leaving the cell
60
Intracellular increase of sodium
decrease in membrane potential - easier to make action potential happen
61
hyperchloremia
excess chloride caused by Na or to litle bicarbonate
62
Hyponatremia
decreased osmolality (concentration goes down)
63
hypertonic hyponatremia
excess lipids, protien, and sugar can displace sodium causing it
64
SIADH
stop excreting water - cancer cells produce ADH
65
Hypochloremia
result of hypotremia or elevated bicarbonate concentration (to balance)
66
cystic fibrosis
disease of chloride (lack of chloride) - mucus becomes thick
67
Potassium
major intracellular cation - maintained by Na/K pump - on outside trying to get in
68
Potassium levels
changes in pH affect K+ balance
69
Acidosis
decrease in ICF potassium means decrease in K secretion means hyperkal
70
Alkalosis
decrease in H ICF means K increase = hypokal
71
Aldosterone
increase plasma K means increase aldosterone = release of K
72
Insulin
stimulates Na/K pump = moving into cell = hypokalemia
73
hypokalemia
not enough potassium - membrane becomes hyperpolarized
74
hyperkalemia
greater potassium levels
75
calciutonin
hormone causing it to move into bones - causing muscle contraction in heart
76
hypercalcemia
break down bone
77
hypocalcemia
body is not absorbing calcium
78
Phosphate
works opposite of calcium
79
hypophosphatemia
not enough phospate
80
hyperphosphatemia
too much phosphate
81
pH
H+ high in number = low pH H- low in number = high pH
82
pH balance
H+ must be neutralized or excreted - bones, lungs, and kidneys are involved in regulation
83
types of acid
- volatile - nonvolatile
84
buffering systems
most important are carbonic acid bicarbonate system and hemoglobin
85
Carbonic acid bicarbonate pair
ratio of 20:1 must be maintianed
86
Acidosis
increase in H+ concentration
87
Alkalosis
decrease in H+ concentration
88
respiratory acidosis
increase of pCO2 from ventilation depression
89
respiratory alkalosis
decrease of pCO2 from alveolar hypervent
90
metabolic acidosis
decrease of HCO2- or increase in noncarbonic acid
91
metaboloic acidiosis
increase of HCO3- form loss of metabolic acids

Clinical Pathophysiology (1 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions