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552 Pathophysiology > Cell pathology > Flashcards

Cell pathology Flashcards

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
Q

anoxia

A

very low tissue O2; no O2

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26
Q

hypoxemia

A

low blood oxygen tension (decreased O2-saturation) PaO2

caused by: poor air exchange, difficulty breathing, HF, suffocation

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27
Q

ischemia

A

insufficient blood supply to tissue or organ (constriction)

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28
Q

infarction

A

ischemia w/ necrosis

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29
Q

reperfusion

A

restoration of blood supply that had been cut off

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30
Q

thrombus

A

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

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31
Q

emobolism

A

moving; breaks off and gets stuck somewhere
bld supply cut
when blood supply is restored; harm is caused w/ ROS (reactive O2 species)

32
Q

Free radical

A

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
Q

ROS

A

highly reactive molecule that contains Oxygen
(some overlap btw free radicals & ROS)
extremely reactive w/ anything it comes in contact with

34
Q

superoxide dismutase (SOD)

A

converts superoxide ion (O2-) to H2O2

35
Q

H2O2

A

hydrogen peroxide
not free radical
reactive oxygen species
beneficial in killing bacterial

36
Q

catalase

A

converts H2O2 to H2O

37
Q

hydroxyl radical

A

OH w/ a dot (free radical)

38
Q

glutathione peroxidase

A

OH is made into H2O2

39
Q

necrosis

A

irreversible damage
contents spill out
causes inflammatory response

40
Q

apoptosis

A

controlled cell death
eaten by phagocytes, contents of cell never exposed to outside
no inflammatory response

41
Q

Coagulative necrosis

A

tissue left maintains normal architecture after death
usually result of infarction (except in brain)
causes: chromatin clumping, organeller swelling, eventual membrane damage

42
Q

Liquefactive necrosis

A

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
Q

Caseous necrosis

A

yellow-white and cheesy (queso)

Specific to Tuberculosis

44
Q

Fat necrosis

A

typically seen in pancreatitis

enzymes released: proteases eat tissue; fat eaten by lipases: create free fatty acids which bind to Ca

45
Q

dry gangrene

A

occurs in dry tissue, eg feet of diabetic

often involves clostridium infections exposed to air

46
Q

wet gangrene

A

occurs in moist tissue, eg internal organs and bed sores

numerous bacteria involved, but C. perfringens most common

47
Q

Gas gangrene

A

similar to wet gangrene w/ addition of gas production

medical ER: can spread quickly resulting in sepsis and death

48
Q

Telomeres

A

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
Q

Sodium

A

increased w/ dehydration

decreased w/ H2O overload

50
Q

Potassium

A

kidney failure

diuretics

51
Q

Chloride

A

increased in response to a decrease in HCO3 (anion gap)

52
Q

standard HCO3

A

acid-base

53
Q

Blood urea nitrogen

A

elevated: think kidney problem; also reflects diet

54
Q

Creatinine

A

elevated: think kidney failure; also changes w/ muscle mass

55
Q

Fasting glucose

A

diabetes

56
Q

Anion gap

A

used to determine source of metabolic acidosis
Na - (Cl + HCO3)
High: addition of acid
Normal: loss of bicarb w/ increase in Cl-

57
Q

Phosphorous

A

inorganic (Pi)

dietary intake, GI, renal handling, cellular shift (high: acidosis; low: alkalosis, insulin)

58
Q

Uric acid

A

gout

59
Q

ALT; AST

A

liver damage

60
Q

Alkaline phosphate

A

biliary duct system or bone

61
Q

direct bilirubin (conjugated)

A

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
Q

total bilirubin

A

making bilirubin too fast or liver malfunction

63
Q

unconjugated bilirubin

A

Total-direct

increased in liver failure; can’t conjugate bilirubin

64
Q

albumin

A

most plentiful protein

liver will make as much as needed

65
Q

total protein

A

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
Q

LDH: lactate dehydrogenase

A

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
Q

GGT

A

biliary duct damage

68
Q

What is probably the issue if alkaline phosphate is elevated but GGT is not

A

probably not a biliary duct problem & liver is ok; probably a bone problem

69
Q

What will happen if a blood draw is bad (poor phlebotomy)?

A 
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
Q

what will happen if a bad blood sample is allowed to sit around a while?

A

macrophages will convert Hb to bilirubin

71
Q

what will happen to a blood sample if there is poor handling and poor phlebotomy?

A

increase in unconjugated bilirubin

72
Q

Reticulocytes

A

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
Q

mean corpuscle volume (MCV)

A

average RBC size: what kind of anemia?

low: microcytic
normal: normocyctic
high: macrocyctic

74
Q

INR

A

ratio of patient blood clotting time to how long it takes normal person to clot
<1: patient is quicker to clot

75
Q

PT

A

extrinsic pathway
something else is needed to clot
used to measure coumadin and vitamin K status

76
Q

APTT

A

intrinsic pathway

measures heparin therapy

77
Q

bleeding time

A

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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