Study your flashcards anywhere!

Download the official Cram app for free >

  • Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off

How to study your flashcards.

Right/Left arrow keys: Navigate between flashcards.right arrow keyleft arrow key

Up/Down arrow keys: Flip the card between the front and back.down keyup key

H key: Show hint (3rd side).h key

A key: Read text to speech.a key


Play button


Play button




Click to flip

91 Cards in this Set

  • Front
  • Back
Define disease
Disease = absence of health, deviation from normal, dyshomeostasis, imbalance
Factors that influence occurrence of disease:
Host (7)
External (6)
Host Factors: heredity, age, sex, immunity, nutrition, mental status, species
External Factors: management, climate, microorganisms, chemicals, physical factors, nutrition
Disease outcomes (3)
return to health
ongoing disease
Levels of study (7)
Levels of study:
population – epidemiology
Animal – clinical signs
Organs and tissues – gross path
Cellular – histopath
Chemical – clin path
Molecular – molecular path, DNA
Etiological – cause: genetic, infectious, chemical, nutritional,
Define pathogenesis
pathogenesis = process of initiation and development of disease
Define diagnosis (2)
process to understand a disease

final conclusion made about the disease
cytosol = fluid component of cytoplasm that surrounds cell contents

place of most intermediary metabolism

free ribosomes produce proteins
energy production –oxidative phosphorylation

derived from intracellular prokaryote: Rickettsia prowazekii
Endoplasmic reticulum
membrane bound space continuous with outer nuclear membrane

produces proteins, lipids, and carbohydrates: incorporated into organelles or secreted; sequester into vesicles, bud, fuse

rough: ribosomes that produce proteins, most glycosylated before leaving ER (proteins formed in cytosol are not glycosylated)

smooth: lipid synthesis, detoxification of lipid soluble toxins into water soluble nontoxic substances (biotransformation); abundant in hepatocytes for lipoprotein prod and detox and in muscle for sequestering Ca from cytosol (sarcoplasmic reticulum)
Golgi apparatus
stacks of membrane-bound sacs near nucleus

modifies, packages, sorts, exports products from ER – control center
primary and secondary
membrane bound sacs of enzymes that degrade

primary lysosomes newly formed by budding off golgi
secondary lysosomes - from fusion of primary lysosomes with vesicles, morphologically more variable than primary, content more heterogeneous with hydrolases and substrates
small vesicles with enzymes that conduct oxidative reactions

bud off smooth ER

catalase – converts H2O2 into water

detoxification and breakdown of fatty acids

major site of O2 utilization but don’t produce energy – remnants of organelle that O2 metabolism before mitochondria developed?
shape, org, movement

microfilaments - thin actin and thick myosin

microtubules - tubilin

intermediate filaments

Ca conc regulates assembly/disassembly
location of cellular DNA

nuclear envelope – double membrane of 2 lipid bilayers; outer is continuous with ER; inner has nuclear pores

histones – DNA-binding, regulate folding
1% of mammalian genome is involved in coding for essential proteins

Gene is piece of chromosome

Genome is DNA from all chromosomes

Site of DNA replication and RNA synthesis

Nucleolus – aggregate of DNA
Ectoderm derivatives
Mesoderm derivatives
mesenchyme: connective tissue, fibroblasts, osteoblasts
Kidney (part of it)
Heart and blood
Cell Cycle
G1 phase = growing and priming itself for division
Cell Cycle
S phase = DNA synthesis (doubles DNA content, 2 identical sets of chromosomes)
Cell Cycle
G2 phase = gap between DNA synthesis and cell division
Cell Cycle
M phase = cell division

mitosis is nuclear division
cytokinesis is cytoplasmic division

2 genetically identical cells
Cell Cycle
G0 phase = resting; exited cell cycle and not directing metabolism towards replication
Cell Cycle - complex regulation
Movement between phases controlled by concentrations of ___________________ in cell – proteins that are synthesized at specific times during cycle; mediated thru complexes with ____________-dependent _______________
Movement between phases controlled by concentrations of CYCLINS in cell – proteins that are synthesized at specific times during cycle; mediated thru complexes with CYCLIN-dependent KINASES
Labile cells
Labile cells = always in cell cycle; intestinal epithelium (8hr), bone marrow, epidermis
Stable cells
Stable cells = remain in G0 until stimulated; hepatocytes, fibroblasts
Permanent cells
Permanent cells = highly differentiated and do not divide, do not enter into cell cycle; neurons, cardiac myocytes (?)
Mechanisms for cell aging (3)
alterations in gene expression – cumulative change

telomere shortening – short DNA sequences at ends of chromosomes maintained by telomerase, telomerase is not in somatic cells

progressive metabolic injury – oxidative processes damage membranes; lipofuscin is wear and tear pigment
Morphology of aging cells (4)
irregular nuclei
vacuolated mitochondria
lipofuscin accumulation
abnormal metabolic products
def and sig
apoptosis = physiological cell death; programmed

damage to the cell makes it a liability, remove damaged cells

maintains homeostatic balance
Major components of ECM (3)
structural: collagen and elastin

absorptive: glycosaminoglycans and proteoglycans

adhesive: fibronectin and laminin
Cell's major responses to injury (3)
sublethal damage (injured)
Major causes of cell injury (4)
changes in stimulation or demands – hormone stimulation, functional demands

changes in nutrients available – too few (O2), too many (glucose)

genetic alterations

injury – reversible (metaplasia) or irreversible non-lethal injury, lethal injury (necrosis)
Define hyperplasia
increase in number of cells
define physiologic hyperplasia
physiologic hyperplasia = replicate to fulfill functional responsibilities; transient stimuli; cell numbers return to normal

endometrium during pregnancy
mammary while lactating
fibroblast during healing
define pathologic hyperplasia
pathologic hyperplasia = replicate in response to persistent, excessive, or inappropriate stimuli; detrimental; response often normal but result contributes to damage; stimuli and hyperplasia long-term and persistent; enlarged tissue or organ

parathyroid hyperplasia secondary to renal disease
define hypertrophy
hypertrophy = increase in size of a cell; sometimes with hyperplasia, stimuli the same
define physiologic hypertrophy
physiologic hypertrophy = enlarge to fulfill functional responsibilities; transient stimuli; return to normal size

uterine smooth muscle during pregnancy
mammary during lactation
define pathologic hypertrophy
pathologic hypertrophy = enlarge due to persistent, excessive, or inappropriate stimuli; cell response contributes to disease instead of maintaining homeostasis; long-term and persistent; enlarged organ or tissue

cardiac myocyte in failing heart contribute to abnormal flow
define atrophy
atrophy = decrease in size of cell, also decrease in number of cells; cell is smaller
define physiologic atrophy
physiologic atrophy = shrink b/c decreased stimulation or decreased demand; termination of physiologic event and atrophy returns cell/tissue to its normal resting state


endometrium after parturition
myocytes when stop training
define pathologic atrophy
pathologic atrophy = shrink b/c inappropriate loss of stimuli or detrimental events; long-term or permanent; shrunken tissue/organ; small cells with otherwise normal appearance

muscle after denervation due to trauma
define metaplasia

most common
metaplasia = replacement of one mature cell type with another; local stem cells change pattern of differentiation; occurs in tissue; response to irritation/injury

columnar/cuboidal to squamous epithelium
3 major mechanisms of cell injury
loss of membrane integrity
loss of ability to produce energy
genetic damage
3 major pathways to loss of membrane integrity
free-radical induced injury
phospolipase-induced injury
direct membrane damage
Protective mech against free radicals
vit E, A, C
iron and copper binding proteins
superoxide dismutase
phospholipase activation (losing membrane integrity)
decreased energy -->
membrane pumps can't maintain gradients -->
cytoplasmic Ca increases -->
phospholipase activated
Major changes in cells depleted of energy
failure of energy-dependent pumps
cell swelling
decreased intracellular pH
decreased protein synthesis
degradation of cytoskeleton
membrane degradation
leakage organelle contents
organelle dysfunction
3 major morphologic features of sublethal cell injury
cell swelling
fatty change
intracellular accumulations
define mutation
mutation = permanent change in DNA from damage that is not repaired
4 categories of genes that are commonly affected in cells that undergo neoplastic transformation
(genes involved in major life events)
genes that:
promote cell growth
inhibit cell growth
regulate apoptosis
regulate DNA repair
define pleomorphism
variable cell size and shape

feature of neoplastic cells
2 pathways of cell death
Apoptosis requires _____
apoptosis does not have _____
apoptosis requires energy
apoptosis does not have tissue damage/inflammation
final pathway of apoptosis mediated by ________-ases
final pathway of apoptosis mediated by caspases
end point of apoptosis
membrane-bound vesicles/apoptotic bodies that are removed by phagocytosis
morphologic features of necrosis
disruption of membranes
degeneration of nucleus
mitochondrial swelling
"ground glass" smooth homogenous cytoplasm

=tissue damage
postmortem autolysis
postmortem = all cells are affected and all at same stage, no evidence of host response/inflammation
antemortem autolysis (necrosis)
antemortem (necrosis) = groups of affected and non-affected cells, various stages, evidence of host response
basic patterns of disease (6)
coagulative necrosis
coagulative necrosis = cell death due to hypoxia and inability to maintain energy (apoptosis if energy is available); basic outline of cell/tissue retained, not normal but can still recognize, ghost-like
liquefactive necrosis
liquefactive necrosis = infiltration of lots of leukocytes; occurs with infectious agents like bacteria that attract leukocytes; normal tissue replaced with liquefactive debris due to proteolytic activity of leukocyte and dying cells enzymes

pus = area of liquefactive necrosis
caseous necrosis
caseous necrosis = chronic inflammation; infectious agents that cause chronic granulomatous inflammation

a form of coagulative necrosis where necrotic cells have fragmented into amorphous debris mass

original tissue structure gone
gangrenous necrosis
gangrenous necrosis = ischemia

coagulative necrosis with subsequent infection of dead tissue by bacteria and putrefaction, anaerobes

involves large amount of tissue
fat necrosis
fat necrosis = lipase action on adipose tissue; pancreatic necrosis
ways that damaged ECM cause tissue injury
increased destruction of ECM – inflammation/immune responses; lysosomal enzymes

decreased production of ECM –dermatosporaxis; vitaman C deficiencies

excessive production of ECM –healing response for irreversibly damaged tissue; fibrosis forms scar tissue and collagen; permanent damage

deposition of abnormal substances - amyloidosis
what is amyloid
pink, acellular, amorphous material

fibrillar protein
define amyloidosis
Amyloidosis = deposition of amyloid with its B-pleated sheet structure, abnormal folding; 95% consists of fibril proteins; 18 forms of amyloid
2 forms of amyloid
(AL and AA)
Amyloid light chain AL – immunoglobulin light chains, prod by plasma cells

Amyloid associated proteins AA – from serum amyloid-associated protein SAA, produced by liver, acute phase protein in response to inflammation
primary amyloidosis
Primary amyloidosis = immunologic dyshomeostasis and AL protein; plasma cell neoplasmas like multiple myeloma in bone marrow; not common
secondary amyloidosis
Secondary amyloidosis = chronic inflammation and AA protein; often systemic; fairly common; cytokines
2 kinds of calcification
dystrophic calcification
dystrophic calcification = deposition of calcium in necrotic tissue

calcium, phospholipids, and phosphate form microcrystal

indicates tissue damage has occurred

serum calcium normal
metastatic calcification
metastatic calcification = deposition of calcium in normal, viable tissue

calcium dyshomeostatis secondary to hypercalcemia (hyperparathyroidism, vit D dys, bone neoplasia)

form microcrystal like dystrophic

basement membranes, pleura, kidneys

systemic calcium dyshomeostasis (not tissue dysfunction)
major morphologic features of injured tissues (2)
cell injury - necrosis

ECM injury - loss of normal architecture by fibrosis, calcification, amyloidosis
developmental disease:
due to abnormal ________ or postnatal _________
due to abnormal embryogensis or postnatal development
manifested at birth
apparent later in development
developmental disease causes
__% unknown
__% genetic
__% environmental
65% unknown (multifactorial)
70% genetic
30% environmental
autosomal dominant
in every generation but onset later in life
autosomal recessive
not every generation but onset earlier in life
x-linked recessive
asymptomatic females transmit to sons

Mech that result in abnormal development
arrest of inhibition of development
persistence of fetal structures
failure of closure of fetal grooves and fissures
growth in aberrant locations
lack of coordiation of tissue differentiation
limbs absent
limbs partially absent
limbs abnormally contracted, flexed, rotated
lack of coordinated bone and joint development

normal appositional growth
abnormal endochondral growth
thick bone

have hemologic problems because no marrow
absence of brain
hydrocephalus = dilation of lateral ventricles and accumulation of fluid; cerebrum normal but atrophied
hydranencephaly = cerebrum fails to develop properly, absence of cerebral tissue, cerebral hemispheres are cystic cavities; fetal viral infection
major causes of metabolic disease (3)
hormonal regulation
inadequate _____ (3)
inadequate diet: deficiency, excess
inadequate uptake
inadequate absorption