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552 Pathophysiology > Cell pathology > Flashcards

Cell pathology Flashcards

(77 cards)

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1
Q

Insult/stress

A

stimulus that upsets normal homeostasis

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2
Q

compensation

A

body’s attempt to maintain normal homeostasis under stress

i.e. shivering and “white hands” when its cold, increased HR upon standing, etc

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3
Q

Cell injury

A

result of a stimulus in excess of a cell’s immediate adaptive response
i.e. hypothermia/frost bite

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4
Q

Reversible cell injury

A

injury which does not kill the cell
i.e. muscles getting bigger when working out
Anything that doesn’t kill me makes me stronger (takes some time to adapt)

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5
Q

Irreversible cell injury/ cell death

A

injury that results in cell death

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6
Q

Apoptosis

A

clean, controlled cell death

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7
Q

Necrosis

A

messy uncontrolled cell death

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8
Q

Cellular adaptation

A

compensation that occurs on the cellular level

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9
Q

Atrophy

A

decrease in the size of cells

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10
Q

Hypertrophy

A

increase in the SIZE of cells

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11
Q

Hyperplasia

A

increase in the NUMBER of cells

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12
Q

Metaplasia

A 
change of cell from one type to another
can be normal or abnormal
result of a stressor:
i.e. smokers, GERD
metaplastic tissue can become dysplastic
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13
Q

Dysplasia

A

abnormal cells that are not necessarily cancer
these cells are not a legitimate cell type
“pre-cancerous”

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14
Q

Neoplasia

A

abnormal disorganized growth: tumor
can be cancer
e.g. warts

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15
Q

T/F all neoplasia is cancer.

A

False

BUT: all cancer results in neoplasia

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16
Q

T/F myocardial cells can undergo hyperplasia and hypertrophy

A

F: only hypertrophy

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17
Q

If a cell is injured by a stressor but doesn’t die, what happens?

A

it prepares for for another (similar) insult

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18
Q

ATP depletion

A

oxygen deficiency greatly decreases ATP production
i.e. MI, stroke
lack of ATP prevents fx of Na+/K ATPase, etc
Na flows in, water follows, cell swells

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19
Q

Free radicals & reactive oxygen species (ROS)

A

cause oxidation of membranes and other structures

particularly problematic w/ reperfusion

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20
Q

Increase in intracellular Ca2+

A

low ATP and Na gradient prevent removal of Ca &
release of Ca from mitochondria and ER
CA activates many enzymes
@ very high levels: signals apoptosis

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21
Q

Defects in plasma membrane

A

loss of Na gradient, activation of proteases & phospholipases
permeable plasma membrane prevents normal cell fx

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22
Q

Reversible cell injury

A 
DNA clumping, lysosome appearance
generalized cell swelling
blebs
ER swelling
small densities
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23
Q

Irreversible cell injury

A 
rupture of lysosomes (autolysis)
 defects in cell membrane (lose Na gradient, Ca rushes in)
lose integrity of cell
karyolysis (chopping up nucleus)
mitochondrial cell swelling
lysis of ER
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24
Q

hypoxia

A

low tissue O2 level

caused by hypoxemia, or Hb problems (anemia)

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25
anoxia
very low tissue O2; no O2
26
hypoxemia
low blood oxygen tension (decreased O2-saturation) PaO2 | caused by: poor air exchange, difficulty breathing, HF, suffocation
27
ischemia
insufficient blood supply to tissue or organ (constriction)
28
infarction
ischemia w/ necrosis
29
reperfusion
restoration of blood supply that had been cut off
30
thrombus
fixed in 1 place and blocks artery blood supply cut d/t size get rid of thrombus and restore bld flow when bld flow is restored, harm is caused w/ free radicals
31
emobolism
moving; breaks off and gets stuck somewhere bld supply cut when blood supply is restored; harm is caused w/ ROS (reactive O2 species)
32
Free radical
molecule w/ unpaired electron (indicated w/ little dot) oxygen: gaines e- H: loses e- O2-, H2O2, OH H2O2: not a free radical but acts like one
33
ROS
highly reactive molecule that contains Oxygen (some overlap btw free radicals & ROS) extremely reactive w/ anything it comes in contact with
34
superoxide dismutase (SOD)
converts superoxide ion (O2-) to H2O2
35
H2O2
hydrogen peroxide not free radical reactive oxygen species beneficial in killing bacterial
36
catalase
converts H2O2 to H2O
37
hydroxyl radical
OH w/ a dot (free radical)
38
glutathione peroxidase
OH is made into H2O2
39
necrosis
irreversible damage contents spill out causes inflammatory response
40
apoptosis
controlled cell death eaten by phagocytes, contents of cell never exposed to outside no inflammatory response
41
Coagulative necrosis
tissue left maintains normal architecture after death usually result of infarction (except in brain) causes: chromatin clumping, organeller swelling, eventual membrane damage
42
Liquefactive necrosis
tissue is dissolved by digestive enzymes loses normal appearance i.e. brain infarction: brain will have holes & tissue will be replaced by fluid; abscesses (fungal abscess)
43
Caseous necrosis
yellow-white and cheesy (queso) | Specific to Tuberculosis
44
Fat necrosis
typically seen in pancreatitis | enzymes released: proteases eat tissue; fat eaten by lipases: create free fatty acids which bind to Ca
45
dry gangrene
occurs in dry tissue, eg feet of diabetic | often involves clostridium infections exposed to air
46
wet gangrene
occurs in moist tissue, eg internal organs and bed sores | numerous bacteria involved, but C. perfringens most common
47
Gas gangrene
similar to wet gangrene w/ addition of gas production | medical ER: can spread quickly resulting in sepsis and death
48
Telomeres
don't code for anything DNA caps @ ends of chromosomes every time a cell replicates, the end isn't copied completely: lose a bit of the telomere each time when enough is lost, cell doesn't replicate anymore (replicative senescence) Theory behind cancer and aging
49
Sodium
increased w/ dehydration | decreased w/ H2O overload
50
Potassium
kidney failure | diuretics
51
Chloride
increased in response to a decrease in HCO3 (anion gap)
52
standard HCO3
acid-base
53
Blood urea nitrogen
elevated: think kidney problem; also reflects diet
54
Creatinine
elevated: think kidney failure; also changes w/ muscle mass
55
Fasting glucose
diabetes
56
Anion gap
used to determine source of metabolic acidosis Na - (Cl + HCO3) High: addition of acid Normal: loss of bicarb w/ increase in Cl-
57
Phosphorous
inorganic (Pi) | dietary intake, GI, renal handling, cellular shift (high: acidosis; low: alkalosis, insulin)
58
Uric acid
gout
59
ALT; AST
liver damage
60
Alkaline phosphate
biliary duct system or bone
61
direct bilirubin (conjugated)
elevated: can conjugate it, but can't get rid of it end result of heme breakdown that we can't recycle unconjugated heme is not water soluble liver takes water insoluble molecule and conjugates it
62
total bilirubin
making bilirubin too fast or liver malfunction
63
unconjugated bilirubin
Total-direct | increased in liver failure; can't conjugate bilirubin
64
albumin
most plentiful protein | liver will make as much as needed
65
total protein
all protein in plasma decreased: (in conjunction w/ low albumin) indicates liver problem; could result from loss of protein in kidney normal/elevated: (in conjunction w/ low albumin) something else is making too much protein (liver will make less albumin)
66
LDH: lactate dehydrogenase
nonspecific; something is leaking used in cell to convert pyruvate to lactate when too much glycolysis but not enough O2 if cell dies, LDH leaks out 5 different isoenzymes
67
GGT
biliary duct damage
68
What is probably the issue if alkaline phosphate is elevated but GGT is not
probably not a biliary duct problem & liver is ok; probably a bone problem
69
What will happen if a blood draw is bad (poor phlebotomy)?
``` hemolysis: plasma will be pink/red LDH will be very high total protein will increase albumin will be normal bilirubin will be normal (heme not broken down yet) K will be high ```
70
what will happen if a bad blood sample is allowed to sit around a while?
macrophages will convert Hb to bilirubin
71
what will happen to a blood sample if there is poor handling and poor phlebotomy?
increase in unconjugated bilirubin
72
Reticulocytes
baby RBCs from marrow average RBC life span is 100 days, change from reticulocyte after 1st day (t/f it is a reticulocyte for 1% of its life span) will tell you if RBCs are dying early or bone marrow problem
73
mean corpuscle volume (MCV)
average RBC size: what kind of anemia? low: microcytic normal: normocyctic high: macrocyctic
74
INR
ratio of patient blood clotting time to how long it takes normal person to clot <1: patient is quicker to clot
75
PT
extrinsic pathway something else is needed to clot used to measure coumadin and vitamin K status
76
APTT
intrinsic pathway | measures heparin therapy
77
bleeding time
cut and blot blood until bleeding stops Ivy method: 10mm x 1mm cut duke method: finger or earlobe stick not used very often, but easy

552 Pathophysiology (5 decks)

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