Cell pathology Flashcards
Insult/stress
stimulus that upsets normal homeostasis
compensation
body’s attempt to maintain normal homeostasis under stress
i.e. shivering and “white hands” when its cold, increased HR upon standing, etc
Cell injury
result of a stimulus in excess of a cell’s immediate adaptive response
i.e. hypothermia/frost bite
Reversible cell injury
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)
Irreversible cell injury/ cell death
injury that results in cell death
Apoptosis
clean, controlled cell death
Necrosis
messy uncontrolled cell death
Cellular adaptation
compensation that occurs on the cellular level
Atrophy
decrease in the size of cells
Hypertrophy
increase in the SIZE of cells
Hyperplasia
increase in the NUMBER of cells
Metaplasia
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
Dysplasia
abnormal cells that are not necessarily cancer
these cells are not a legitimate cell type
“pre-cancerous”
Neoplasia
abnormal disorganized growth: tumor
can be cancer
e.g. warts
T/F all neoplasia is cancer.
False
BUT: all cancer results in neoplasia
T/F myocardial cells can undergo hyperplasia and hypertrophy
F: only hypertrophy
If a cell is injured by a stressor but doesn’t die, what happens?
it prepares for for another (similar) insult
ATP depletion
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
Free radicals & reactive oxygen species (ROS)
cause oxidation of membranes and other structures
particularly problematic w/ reperfusion
Increase in intracellular Ca2+
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
Defects in plasma membrane
loss of Na gradient, activation of proteases & phospholipases
permeable plasma membrane prevents normal cell fx
Reversible cell injury
DNA clumping, lysosome appearance generalized cell swelling blebs ER swelling small densities
Irreversible cell injury
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
hypoxia
low tissue O2 level
caused by hypoxemia, or Hb problems (anemia)
anoxia
very low tissue O2; no O2
hypoxemia
low blood oxygen tension (decreased O2-saturation) PaO2
caused by: poor air exchange, difficulty breathing, HF, suffocation
ischemia
insufficient blood supply to tissue or organ (constriction)
infarction
ischemia w/ necrosis
reperfusion
restoration of blood supply that had been cut off
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
emobolism
moving; breaks off and gets stuck somewhere
bld supply cut
when blood supply is restored; harm is caused w/ ROS (reactive O2 species)
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
ROS
highly reactive molecule that contains Oxygen
(some overlap btw free radicals & ROS)
extremely reactive w/ anything it comes in contact with
superoxide dismutase (SOD)
converts superoxide ion (O2-) to H2O2
H2O2
hydrogen peroxide
not free radical
reactive oxygen species
beneficial in killing bacterial
catalase
converts H2O2 to H2O
hydroxyl radical
OH w/ a dot (free radical)
glutathione peroxidase
OH is made into H2O2
necrosis
irreversible damage
contents spill out
causes inflammatory response
apoptosis
controlled cell death
eaten by phagocytes, contents of cell never exposed to outside
no inflammatory response
Coagulative necrosis
tissue left maintains normal architecture after death
usually result of infarction (except in brain)
causes: chromatin clumping, organeller swelling, eventual membrane damage
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)
Caseous necrosis
yellow-white and cheesy (queso)
Specific to Tuberculosis
Fat necrosis
typically seen in pancreatitis
enzymes released: proteases eat tissue; fat eaten by lipases: create free fatty acids which bind to Ca
dry gangrene
occurs in dry tissue, eg feet of diabetic
often involves clostridium infections exposed to air
wet gangrene
occurs in moist tissue, eg internal organs and bed sores
numerous bacteria involved, but C. perfringens most common
Gas gangrene
similar to wet gangrene w/ addition of gas production
medical ER: can spread quickly resulting in sepsis and death
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
Sodium
increased w/ dehydration
decreased w/ H2O overload
Potassium
kidney failure
diuretics
Chloride
increased in response to a decrease in HCO3 (anion gap)
standard HCO3
acid-base
Blood urea nitrogen
elevated: think kidney problem; also reflects diet
Creatinine
elevated: think kidney failure; also changes w/ muscle mass
Fasting glucose
diabetes
Anion gap
used to determine source of metabolic acidosis
Na - (Cl + HCO3)
High: addition of acid
Normal: loss of bicarb w/ increase in Cl-
Phosphorous
inorganic (Pi)
dietary intake, GI, renal handling, cellular shift (high: acidosis; low: alkalosis, insulin)
Uric acid
gout
ALT; AST
liver damage
Alkaline phosphate
biliary duct system or bone
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
total bilirubin
making bilirubin too fast or liver malfunction
unconjugated bilirubin
Total-direct
increased in liver failure; can’t conjugate bilirubin
albumin
most plentiful protein
liver will make as much as needed
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)
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
GGT
biliary duct damage
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
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
what will happen if a bad blood sample is allowed to sit around a while?
macrophages will convert Hb to bilirubin
what will happen to a blood sample if there is poor handling and poor phlebotomy?
increase in unconjugated bilirubin
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
mean corpuscle volume (MCV)
average RBC size: what kind of anemia?
low: microcytic
normal: normocyctic
high: macrocyctic
INR
ratio of patient blood clotting time to how long it takes normal person to clot
<1: patient is quicker to clot
PT
extrinsic pathway
something else is needed to clot
used to measure coumadin and vitamin K status
APTT
intrinsic pathway
measures heparin therapy
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
