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200 Cards in this Set
- Front
- Back
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lesion
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any pathologic abnormality in a cell, tissue or organ
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structural lesion
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morphologically detectible
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functional lesion
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biochemically detectable
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which lesion generally precedes the other?
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functional lesions precede structural
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2 types of intrinsic etiologies
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inherited - germ cell mutations
developmental defects - somatic cell mutations |
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most common cause of cell and tissue injury
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hypoxia
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adapted cell
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exists in altered homeostasis
new levels of certain metabolic activities, changes in concentrations of metabolites not in danger of dying |
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morphologic changes that can corespond to adaptation or functional change
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atrophy
hypertrophy hyperplasia metaplasia change in #/size of intracellular organelles |
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example of ultrastructural changes in hepatocytes, in response to toxin
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increased amounts of smooth ER
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are morphological changes in adapted cells reversible or irreversible?
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reversible
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injured cell
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unable to maintain a normal or adapted homeostatic state
in danger of dying |
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morphologic changes indicative of injured cells include...
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cell swelling (vacuolar or hydropic degeneration) - reversible
fatty change (steatosis) - reversible necrosis - irreversible |
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what morphological change is considered a harbinger of cell death?
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severe steatosis
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G1 precedes what process?
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DNA synthesis
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G2 precedes what process?
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mitosis
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labile cells
definition 3 examples |
continuously renewable cells
continuous turnover, short lifespan hematopoietic cells mucosal epithelium epidermis |
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stable/quiescent cells
definition 3 examples |
do not continue to multiply once they are fully differentiated, but retain capacity to do so
parenchymal cells of most visceral organs/gands mesenchymal cells endothelial cells |
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permanent cells
definition 3 examples |
lose capacity to multiply once they are fully differentiated (i.e.: terminally differentially)
neurons cardiac myocytes skeletal muscle |
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hyperplasia
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only occurs with labile or stable cells
controlled, orderly proliferation reversible if stimulus for proliferation is removed |
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3 mechanisms of hyperplasia
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increased local production of GFs by effector cells
increased levels of GF receptors on target cells increased activation of intracellular signaling pathways |
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2 types of physiologic hyperplasia
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hormonal
conpensatory (i.e.: increased functional demand) |
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example of hormonal physiologic hyperplasia
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proliferation of glandular epithelium in female breasts at puberty and during pregnancy
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compensatory physiologic hyperplasia occurs in response to...
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tissue damage or loss
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example of compensatory physiologic hyperplasia
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liver regeneration/hepatocellular hyperplasia
response of remaiing kidney following unilateral nephrectomy |
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4 types of pathologic hyperplasia
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excessive hormonal stimulation
chronic irritation or injury viral infection precancerous hyperplastic lesions |
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2 examples of hormonal PATHOLOGIC hyperplasia
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endometrial hyperplasia in response to estrogen-progesterone imbalance
benign prostatic hyperplasia in response to excess androgens |
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example of pathologic hyperplasia in response to chronic irritation
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wound healing - hyperplasia of CT and vascular endothelium
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example of viral infection related hyperplasia
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papillomavirus -induced cutaneous warts or mucosal polyps
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endometrial hyperplasia is a RF for what?
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cancer
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2 definitions of hypertrophy
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increased size of an organ due to increase in cell size
increased number and size or organelles, increased size of nucleus |
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example of genetic basis of hyperplasia in skeletal muscle
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switch from alpha- to beta- form of myosin heavy chain in myocardial cells --> more energy-efficient contraction
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2 examples of physiologic hypertrophy
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breast hypertrophy during pregnancy
exercising skeletal or cardiac muscle |
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2 examples of pathologic hypertrophy
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Cushing disease
myocardial hypertrophy in response to valvular insufficiency or vascular disease |
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Cushing disease
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adrenocortical hypertrophy and hyperplasia in response to ACTH-secreting pituitary gland adenoma
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hypoplasia
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small tissue or organ that never attained normal size, i.e.: underdeveloped
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aplasia
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aka: agenesis
complete failure of a tissue or organ to develop |
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atrophy
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decreased size of a tissue or organ that had previously been of normal size
decreased individual cell size |
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functional and ultrastructual changes accompanying cell atrophy
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decreased protein synthesis (less GER, fewer ribosomes)
fewer mitochondria loss of specialized functions, e.g.: fewere secretory granules |
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2 protein degradation pathways upregulated in atrophy
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ubiquitin-proteasome pathway activated in a variety of catabolic conditions (eg: CA)
increased numbers of autophagic vacuoles or residual bodies containing fragmented cellular components (eg: lipofuscin granules) |
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6 mechanisms of atrophy
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decreased functional workload
decreased nutrient supply decreased neural stimulation decreased hormonal stimulation pressure aging |
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disuse atrophy
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atrophy due to decreased workload
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cause of decreased nutrient atrophy
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dminished bloodflow
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2 conditions causing primary nutrient deficiency
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marasmus (protein-calorie malnutrition)
cachexia - marked skeletal mm wasting (may be secondary to chronic ds, inflammation, CA) |
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loss of estrogen stimulation at menopause causes atrophy of...
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endometrium, breast epithelium, vaginal epithelium
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3 causes of pressure atrophy
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expanding mass (neoplasm, abcess)
fluid accumulation (hydrocephalus) extracellular substances, e.g: amyloid |
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most likely underlying mechanism of pressure atrophy
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decreased nutrient supply
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which organs are most affected by aging/senile atrophy
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organs with permanent cells (brain heart)
reproductive organs skeletal mm bone |
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metaplasia
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substitution of one type of fully differentiated cell with another fully differentiated cell type not normally found in that tissue
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what type of metaplasia occurs in response to smoking?
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squamous metaplasia in resp tract
response to chronic irritation |
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what other morphological change is metaplasia often associated with?
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hyperplasia
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2 causes of metaplasia
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chronic irritation (mechanical or inflammatory)
nutritional deficiencies |
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stones in salivary, pancreatic or bile ducts --> _____ metaplasia?
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squamous
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GERD ----> _____ metaplasia in esophagous
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columnar
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vitamin A deficiency ---> ___ metaplasia in the ____ tract
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squamous metaplasia in the respiratory tract
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4 key events in cell injury
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ATP depletion
accumulation of intracellular Ca2+ accumulation of oxygen-derived free radicals cell membrane damage |
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most common cause of ATP depletion
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oxygen deprivation
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2 causes of oxygen deprivation
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hypoxia - oxygen deficiency in cells or tissues
(inadequate O2-carrying capacity of blood from cardioresp failure or anemia) ischemia - loss of blood supply to cells or tissues b/c of arterial blockage or impaired venous drainage |
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O2-deficiency pathway leading to cell swelling
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O2-deficiency --> decreased aerogic respiration in mito --> decreased ATP production
decreased ATP --> reduced activity of energy-dependent Na+-K+ ATPase plasma membrane pump --> influx of Na+ & efflux of K+ water follows Na+ into cell --> swelling |
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during cell swelling, where does water accumulate?
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in ER and mitochondria
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effects if anaerobic glycolysis as compensation for ATP deficiency
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glycogen stores depleted
lactic acid accumulates intracellularly intracellular pH decreases --> decreased activity of many enzymes & increased activity of lysosomal hydrolases, which break down cell components |
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how does depletion of ATP result in protein synthesis disruption
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detachment of ribosomes from GER
dissocation of polysomes proteins become misfolded |
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reperfusion injury
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injury resulting from bloodflow to area following ischemia
reoxygenation --> formation of more ROS attract inflammatory cells to reperfused tissues activation of complement |
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what maintains Ca2+ homeostasis within a cell?
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Ca2+-Mg2+ ATPases
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3 examples of ROS
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superoxide anion
hydrogen peroxide hydroxyl ion |
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2 effects of ROS
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lipid peroxidation in cell membranes
oxidative damage to proteins and DNA |
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2 cellular systems that prevent oxidative stress
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anti-oxidants
Fe- and Cu-binding proteins |
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anti-oxidant function
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block free radical formation (initiation) or scavenge free radicals (and terminate autocatalytic process)
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4 anti-oxidants
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glutathione system - peroxidase and reductase enzymes
vitamins A, C, E catalase: in peroxisomes superoxide dismutases |
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which superoxide dismutase (SOD) is found in mitochondria?
in cytosol? |
mito - Mn-SOD
cytosol - Cu-Zn-SOD |
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which two cations can contribute to formation of free radicals?
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Fe2+
Cu2+ |
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2 key events leading imminently to cell death
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irreversible mitochondria dysfunction
severe membrane hyperpermeability |
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effects of severe membrane hyperpermeability
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leakage of lysosomal enzymes intracellularly --> degradation of cellular componenets
leadkage of lysosomal enzymes extracellularly --> tissue damage |
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increased CK or troponin in peripheral blood indicates what?
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cardiac muscle injury
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increased liver transanimases (AST, ALT) in peripheral blood indicates what?
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hepatocellular injury
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cell swelling reflects loss of...
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ionic and volume homeostasis across plasmalemma
due to ATP depletion or direct membrane damage |
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first LM manifestation of reversible cell injury
... & LM appearance |
cell swelling
cytoplasm stains paler than normal nucleus is essentially normal |
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cloudy swelling
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cytoplasm is only slightly paler than normal
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hydropic degeration
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cytoplasm appears to contain indistinctily bordered, clear vacuoles
indicative of cell swelling |
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vacuolar degeneration
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cytoplasm appears to contain rather distinctly bordered clear vacuoles
indicative of cell swelling |
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does degeneration imply irreversible or reversible injury?
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reversible
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6 ultrastructural changes consistent with cell swelling
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dilation of ER
dissociation of ribosomes from ER disaggregation of polysomes dilation of mitochondria increased lucency of cytoplasm plasmalemma alterations |
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gross changes corresponding to cell swelling
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if entire organ involved, organ may be enlarged and paler than normal
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morphologic changes with necrosis are the result of ...
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denaturation of intracellular proteins and enzymatic digestion of all cellular components
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enzymatic digestion by lysosomal enzymes of dead cells themselves =
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autolysis
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enzymatic digestion by lysosomal enzymes of infiltrating WBCs =
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heterolysis
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histological appearance of necrosis
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increased cytoplasmic eosinophilia b/c of increased eosin binding by denatured proteins & decreased basophilia from dispersal of ribosomes in cytoplasm
nuclear changes: pyknosis karyorrhexis karyolysis |
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pyknosis
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shrunken, intensely basophilic nucleus, with condensed chromatin
earliest LM manifestation of cell death |
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karyorrhexis
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fragmented nucleus
loss of nuclear membrane |
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karyolysis
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dissolution of nucleus
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5 types of necrosis
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coagulative necrosis
liquefactive necrosis gangrenous necrosis caseous necrosis enzymatic fat necrosis |
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coagulative necrosis
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histologically, cell borders & tissue architecture preserved
often seen initially w/ ischemia or hypoxia low intracellular pH denatures structural proteins and proteolytic enzymes (blocking proteolysis) grossly, area of necrosis paler & softer than normal |
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liquefactive necrosis
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histo - loss of cell & tissue; inflitration of inflamm cells
associated with bacterial infection grossly, area of necrosis is fluid, opque and purulent typeically seen in the brain b/c of high brain lipid content |
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gangrenous necrosis
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not really a distinct pattern of necrosis
usu. refers to necrosis in limb s/ blood supply if compounded by bac infxn, = "wet" gangrene |
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caseous necrosis
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gross, cheese-like consistency of area (dry, pasty)
histo, loss of cellular and tissue architecture (amorphous, granular, eosinophilic debri) with a rim of inflamm cells (mostly Mf's) most common in chronic microbial infxns |
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enzymatic fat necrosis
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specifically refers to necrosis of adipose tissue as a result of lipase activity
chalky, opaque, white, firm histo, normally transparent adipocytes have pale basophilic or eosinophilic cytoplasm |
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etiology of enzymatic fat necrosis
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TGs in adipocytes are broken down to FAs and glycerol
FAs + Ca2+ --> soaps may be seen in abdominal fat wiht pancreatititis |
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steatosis
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abnormal accumulation of TGs in injured parenchymal cells
most commonly seen in hepatocytes, but also in cardiac myocytes, skeletal mm, and renal epithelium |
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3 fates of FFAs in hepatocytes
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esterification to TGs
converted to Chl or phospholipids oxidized to KBs |
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4 mechanisms of steatosis
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alcoholism
increased mobilization of FAs from adipose tissue decreased FA oxidation decreased protein synthesis |
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effect of alcoholism on fatty change
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increased mobilization of FAs from adipose tissue
metabolism of EtOH in cytosol and is derivative, acetylaldehyde, in mito, leads to high NADH:NAD+ ratio --> increased TG synthesis decreased FA ox. in mito impaired transport of lipoproteins from the liver |
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3 examples of conditions that cause increased mobilitzation of FAs from adipose tissue
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starvation
DM anorexia |
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condition associated with decreased FA oxidation
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hypoxia
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gross morphology of steatosis for
liver |
enlarged, rounded lobe edges
paler than normal to yellow possibly greasy and soft |
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gorss morphology of steatosis for
heart |
linear streaks of pale yellow myocardium with prolonged moderate hypoxia
or more uniform pale appearance w/ prolonged, severe hypoxia |
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LM appearance of steatosis
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discrete, round, clear, intracytoplasmic vacuoles
signet ring appearance - lipid vacuoles displace nucleus to cell periphery lipid vacuolation diff. to distinguish from intracell. accum. of H2O or glycogen |
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stain used for glycogen
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periodic acid-Schiff
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stain used for lipid
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frozen sections stained with Oil Red O or Sudan IV
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pathologic glycogen accumulation a sign of
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problems with glucose and/or glycogen metabolism
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impaired glucose utlization by cells -->
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hyperglycemia and intracellular storage of glycogen
accumulates in hepatocytes, renal tubular epithelium, cardiac myocytes, pancreatic islet beta cells |
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ground glass appearance of cells suggests...
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glycogen accumulation
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glycogen accumulation is only associated with cell INJURY if...
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present in large amounts
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4 possible causes of protein accumulation in cells
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resorption by proximal renal tubular epithelium in conditions associated with proteinuria
excessive synthesis of secretory proteins (eg: Ig's) virus infection (accum of viral proteins) defective protein folding --> defective intracell transport/secretion --> accum |
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hyaline change
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homogenous, eosinophilic appearance in H&E
implies protein, but not specific protein |
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2 examples of hyaline change
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hyaline droplets in renal tubular epithelium
CT hyalin may be found in scars or blood vessel walls thickened by arteriosclerosis amyloid can be described as hyaline |
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do dead apoptotic cells excite an inflammatory response?
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no
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do dead necrotic cells excite an inflammatory response?
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yes
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3 examples of apoptosis in PATHOLOGIC conditions
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death of virus-infeted and neoplastic cells by CTLs
elimination of cells damaged by radition or chemotherapeutic drugs, if DNA repair is not possible atrophy of parenchymal organs after duct obstruction |
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morphology of apoptosis
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cell shrinkage w/ separation from adjacent cells - cytoplasm may stain more intensely
nuclear chromatin condensation fomration of apoptotic bodies - membrane-bound blebs of cytoplasm break off the cell phagocytosis of apoptotic bodies or cells by macrophages |
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initiation phase of apoptosis
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activation of caspases
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extrinsic pathway of apoptosis
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death receptor mediated
cell surface receptors (members of TNF family) Fas - FasL --> apoptotic signals |
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intrinsic pathway of apoptosis
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mitochondrial
increased mitochondrial permeability leads to leadage of pro-apop molecules (eg: cytC) into cytoplasm |
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3 phases of apoptosis
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initiation
execution cell removal |
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execution phase of apoptosis
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caspase cascade
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cell removal phase of apoptosis
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in early stages of apoptosis, dying cells secrete soluble factors that recruit phagocytes
macrophages have receptors for apoptotic cells and secrete substances that opsonize cells for phagocytosis |
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exogenous pigements
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dust particles - inhaled carbon, siliac, asbestos, etc.
found in lungs and LNs draining resp tract |
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antrhacosis
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condition of inhaled carbon or coal dust
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pneumoconiosis
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general term for condition associated with any inhaled dust
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what cell type are dusts generally found in?
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macrophages
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4 endogenous pigments
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melanin
lipofuscin hemosiderin bilirubin |
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lipofuscin
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wear&tear or aging pigment
accumulates in lysosomes as cells age, in chronically injured cells and in cells undergoing atrophy esp. common in hepatocytes and cardiac myocytes nondegradable material derived from cell component breakdown |
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lipfuscin is a sign of what?
histological? |
sign of free radical injury
histo - light brown or yellow, intracytoplasmic granules |
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hemosiderin
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yellow brown granule pigment, derived from iron in Hb
when iron in excess, ferritin molecules aggregate to form hemosiderin found in PMNs and hepatocytes |
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conditions associated with hemosiderin
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excessive RBC breakdown:
prolonged congestion hemorrhage primary hemolysis (hemolytic anemia) |
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are lipofuscin or hemosiderin themselves damaging to cells?
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no
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bilirubin
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derived from non-Fe-containing porphoryin ring of heme in Hb
major pigment in bile conditions causing byperbilirubinemia lead to jaundice, in which CT are stained yellow by bilirubin |
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2 types of pathologic calcification
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dystrophic calcification
metastatic calcification |
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dystrophic calcification
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calcium salt deposition in areas of cellular injury
blood [Ca2+] normal histo - intensely basophilic, sometimes amorphous or granular, sometimes crystalline common in atheromas in advanced atherosclerosis or in aged/damaged heart valves |
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metastatic calcification
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Ca2+ deposition in uninjured, normal interstitial CT, in association w/ hypercalcemia
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4 major causes of hypercalcemia
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increased PTH secretion --> increased Ca2+ resorption from bone
direct destruction of bone vit D related disorders renal failure --> retention of PO4 --> 2* hyperparathyroidism |
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2increased PTH secretion is assoicated with...
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parathyroid neoplasms or other malignant neoplasms that secrete PTH-related protein
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2 vit D related disorders
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intoxication (oversupplmentation)
sarcoidosis (Mf's activated vit D precursor) |
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common sites of Ca2+ deposition
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gastric mucosa
kidneys lungs systemic aa pulmonary vv |
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purposes of inflammation
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containment of injury
elimination of offending agent repair of damaged tissue |
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harmful effects of inflammation
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tissue damage by WBC enzymes, reactive oxygen metabolites, etc
fibrosis or scarring - disfigurement, limited mobility, functional compromise |
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timing of arteriolar dilation in inflammation
begins.. duration |
begins by 5 minutes
lasts up to 1-2 hours |
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arterioloar dilation is mediated by vasoactive amines like...
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histamine and NO
(also PGs, LTs and platelet-activating factor) |
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what chemical is the primary mediator of vascular permeability in inflammation?
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histamine
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vasoactive substances
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serotonin
complement factors (C3a, C5a) PGs LTs PAF substance P |
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primary mechanism of vascular permeability
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endothelial cell contraction
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which vessels act in vascular permeability?
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venules
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which chemicals mediate the delayed prolonged phase of inflammation?
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cytokines (IL-1, TNF, IFN-gamma)
kinins LTs (LTC4, LTD4, LTE4) |
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timing of delayed prolonged phase of inflammation
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begins after dealy of 2-12 hours and may last several hours to days
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immediate and sustained pattern of inflammation
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caused by direct endothelial injury
severe burns, certain bacterial toxins lasts several hours to days arterioles, capillaries, venules are involved |
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fluid exudate into tissue in inflammation
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due to increased vascular permeability
rich in protein and cells includes fibrin |
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protein concentration in fluid exudate of inflammation "inflammatory edema"
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> 3 g protein/dL
specific gravity (SG) > 1.012 |
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fibrin in inflammation
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found in fluid exudate during ACUTE inflammation
derived from plasma protein, fibrinogen functions: blood clotting isolation/confinement of inflammatory agent chemotactic for PMNs scaffold for healing |
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sequence of leukocytic events in inflammation
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margination - altered blood flow leads to peripheralization of WBCs
sticking - WBCs adhere to vascular walls rolling emigration chemotaxis |
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mechanism of adherence in WBC sticking
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binding of complementary adhesion molecules
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families of adhesion molecules
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selectins
Ig superfamily integrins cytoadhesion family |
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selectins in sticking of WBCs to vascular endothelium
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E-selectin (endothelial cells)
P-selectin (endothelial cells) L-selectin (PMNs, other WBCs) |
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Ig superfamily examples
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ICAM (endothelial cells & WBCs)
VCAM (endothelial cells) PECAM (endothelial cells, lymphocytes) Ig superfamily serve as ligands for integrins |
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integrins
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transmembrane glycoproteins
bind to ligands on endothelial cells , WBCs and ECM beta1 & beta2 involved in sticking |
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mediators such as ____, ____ & ____ stimulate redistribution of stored ____ in endothelial cells to cell surfaces
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mediators such as HISTAMINE, THROMBIN and PAF stimulate redistribution of stored P-selectin in endothelial cells to cell surfaces
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rolling of WBCs is mediated by
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selectins and then integrins on both cell types
under influence of TNF, IL-1, IL-2, PDGF |
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molecules that mediate emigration
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beta-integrins
Ig adhesion molecules |
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2 phages of emigration
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immediate phase
delayed phase |
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immediate phase of WBC emigration
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begins within 1 hour and lasts several hours
PMNs predominate |
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delayed phase of WBC emigration
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begins after several hours and may last days or weeks if stimulus for inflammation persists
mononuclear cells, lymphocytes, plasma cells |
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all WBC emigrate through which structures?
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interendothelial gaps
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mechanisms of emigration
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filopodia - cytoplasmic processes extend btw interendothelial gaps
assembly, disassembly and reassembly of cytoskeletal proteins cause cell to tumble forward enzymatic digestion of basement membranes and CT matrix integrins help pull cells through |
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which types of cells respond to chemotactic stimuli?
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granulocytes, monocytes, lymphocytes
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exogenous chemokines
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bacterial peptides or lipids
viral proteins foreign materials |
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endogenous chemokines
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complement components (C5a)
leukotrienes (LTB4) many cytokines products released by neoplastic cells |
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what type of receptors are chemokine receptors
|
transmembrane G-rptoein coupled receptors or GPCRs
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3 roles of chemokines
|
migration of leukocytes to focus of inflammation
functional activation of WBCs attachment of WBCs to vascular endothelium during emigration |
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surface receptors involved in phagocyte activation
|
TLRs - bind microbial ligands like bacterial LPS
receptors for chemokines and cytokines receptors for opsonins (e.g.: Fc component of Ig's, C3b, lectins) |
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3 patterns of acute inflammation
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serous inflammation
fibrinous inflammation suppurative or purulent inflammation |
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serous inflammation
|
exudate waterly, serum-like
derived from plasma, through leaky blood vessles or contibutions from meothelial lining cells (peritoneal, pleural or pericardial) |
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fibrinous inflammation
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results with more severe vascular leakage than w/ serous
soluble fibrinogen leaks from plasma & polymerizes to form insoluble fibrin characteristic of actue inflamm in body cavities grossly, fibrin is elastic, tan and peels easily from body surfaces |
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3 possible outcomes of acute inflammation
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complete resolution
healing by CT replacement (repair, fibrosis) progression to chornic inflammation |
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complete resolution of inflammation involves:
|
neutralization/spontaneous decay of mediators
shift from pro-inflamm mediators to anti-inflamm mediators return to normal vascular permeability cessation of WBC infiltration into tissue removal of edema fluid, cellular debris and WBCs |
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healing by CT replacement occurs in tissues with... (3 types)
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tissues with extensive damage
tissues incapable of regeneration (eg: myocardium) tissues or body caviites with abundant fibrinous exudate |
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what three things occur simultaneously during chronic inflammation?
|
active inflammation
tissue damage tissue repair |
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3 major causes of chronic inflammation
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persistant infection
prolonged exposure to toxicants autoimmunity |
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morphologic features of chronic inflammation
|
mononuclear inflammatory cells predominate in tissue
|
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characterization of exudate in chronic inflammation
|
if even mix of mononuclear inflammatory cells present = nonsuppurative exudate
if macrophages predmoinate = granulomatous exudate |
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effects of attempts at healing chronic inflammation by CT replacement
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angiogenesis and fibrosis
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systemic effects of inflammation, aka:
|
actute phase response
systemic inflammatory response syndrome (SIRS) |
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3 characteristics of systemic inflammation
|
fever
increased plasma concentrations of acute phase proteins leukocytosis |
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neutrophilia
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elevated number of mature PMNs in peripheral blood
common in BACTERIAL infections |
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lymphocytosis
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elevated number of lymphocytes in peripheral blood
common in VIRAL infections |
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"left shift" leukocytosis
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elevated number of IMMATURE PMNs in peripheral blood
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leukocytosis
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elevated number of leukocytes in peripheral blood
|
|
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cytokines that accelerate release of cells from bone marrow reserve pool
|
IL-1 and TNF
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|
fever pathway, starting with LPS
|
LPS --> stimulates WBCs to produce IL-1 and TNF --> increase PGs, esp. PGE2 in hypothalamus --> increase cAMP --> reset body temp set-point at higher level
|
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2 acute phase proteins (APPs)
|
C reactive protein (CRP) and serum amyloid A (SAA)
bind to microbial cell walls, act as opsonins |
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most mediators initiate their biolgical effects by ____
but some have _____ activity |
most mediators initiate their biological effects by binding to specific receptors on target cells
but some mediators have direct enzymatic activity or cause oxidative damage to cells and tissues |
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2 factors that allow chemical mediators to be rapidly inactivated
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short half-lives
low systemically circulating concentrations |
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4 types of chemical mediators
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vasoactive substances
chemokines acute phase proteins plasma proteins |
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FLASHCARD CHEMICALS OF INFLAMM RESPONSE LECTURE through page 73
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FLASHCARD CHEMICALS OF INFLAMM RESPONSE LECTURE through page 73
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