Exam 2 Flashcards
Simple squamous epithelium
thin, flat layer of cells
found in endothelium of blood vessels, mesothelium that lines body cavities, alveoli, Bowman’s capsule, & loop of Henle
Simple cuboidal epithelium
single layer of square-shaped cells
found in kidney/renal tubules, rete testis, small ducts of exocrine glands, surface of ovary, bronchioles
Simple columnar epithelium
single layer of tall rectangular cells, can be ciliated
found in stomach, small intestine, gall bladder
ciliated in fallopian tubes
Stratified squamous epithelium
multiple layers of thin flat cells, keratinized (skin) or non-keratinized (esophagus, lining of oral cavity, epiglottis, anus, cervix, vagina, vulva, glans penis, cornea)
Stratified cuboidal epithelium
multiple layers of square-shaped cells
found in larger ducts of exocrine glands
Stratified columnar epithelium
multiple layers of tall rectangular cells
found in large ducts of glands
Pseudostratified columnar epithelium
layers of cells that are all attached at basal lamina but may not reach the surface/lumen/apex
ciliated
found in respiratory tract including nose, sinuses, trachea
Transitional epithelium
urothelium
similar to pseudostratified
found in urinary tract (renal pelvis, ureters, bladder, urethra)
Simple glandular epithelium
found in colon, stomach, eccrine sweat glands
Compound glandular epithelium
found in sebaceous sweat gland, Brunner’s glands of duodenum, small salivary glands, breast, prostate
Exocrine glands (solid organs)
major salivary glands, liver, pancreas (acinar)
Endocrine glands (solid organs)
thyroid, anterior pituitary, adrenal, pancreas
Epithelial polarity - apical domain
exposed to lumen or external environment
specialization - cilia (move mucous and fluid out, sperm motility), microvilli (increased surface area/absorption), stereocilia (inner ear, epididymis; sense changes in position orientation/pitch)
Epithelial polarity - lateral domain
facing neighboring cells, linked together by junctional complexes and cell adhesion molecules
Epithelial polarity - basal domain
associated with basal lamina and connective tissue
basement membrane
Functions of epithelia
protection (skin), absorption (intestines), secretion (glands), excretion (kidney), gas exchange (lung), gliding between surfaces (mesothelium)
Endocrine vs. exocrine glands
endocrine glands release products directly into the blood
exocrine glands release their products onto the surface
Simple vs. compound (branched) glands
simple glands have ducts that do not branch, can still have glandular portions that do branch
compound (branched) glands have ductal structures that do branch
Serous secretions
secreting cells have large spherical nucleus, basal region in which rough ER predominates, and apical region with red-stained zymogen granules (secretory vesicles with enzyme precursors)
Serous secreting glands
secreting cells have large spherical nucleus, basal region in which rough ER predominates, and apical region with red-stained zymogen granules (secretory vesicles with enzyme precursors)
Mucous secreting glands
glands often pail staining due to high content glycoproteins and glycolipids, nuclei flattened against basal portion of secretory cells
Merocrine secretion
secretory vesicle approaches apical domain of epithelial cell, vesicular membrane fuses with plasma membrane to release its contents into ECM, fused plasma membrane can be taken back into cell by endocytosis and recycled
Apocrine secretion
some of apical cytoplasm is pinched off with contained secretions
Holocrine secretion
cell produces and accumulates secretory product in cytoplasm (such as sebum in sebaceous glands) then disintegrates to release secretory material
Adaptive cellular changes
experienced by cells in response to physiological or pathological stimuli
Non-adaptive cellular changes
random
including genetic drift, mutation, and recombination
Metaplasia
changing differentiation of cell type (phenotype & function)
ex: normal mucosal epithelium of pseudostratified columnar w/ cilia to stratified squamous w/ no cilia in response to irritation from smoke inhalation
ex: vitamin A deficiency in geckos causing lacrimal gland to secrete keratin instead of tears causing blindness
Ubiquitin-proteasome pathway
molecular pathway involved in cellular atrophy
proteins enter proteasome and get chewed up into peptides that are recycled
causes cells to shrink from loss of proteins & cell membrane
lipofuscin
“ultimate recycling pathway”
Disuse atrophy
relatively slow
ex: osteoarthritis, lameness
Neurogenic atrophy
rapid onset
ex: mass in brain compressing cranial nerve
Two basic pathways for hepatic lipidosis
overload of cells (metabolic alterations) - fat/energy mobilized to liver causing build-up
decreased function of cells (especially lysosomes) - cell injury, diabetes
Intravascular hemolysis
breakdown occurs in circulation
hemoglobin filtered out in kidneys before macrophages can detect
hemoglobinuria is major clinical sign
ex: copper toxicosis in small ruminants, bacterial toxemia, sepsis
Extravascular hemolysis
breakdown occurs in macrophages
hemoglobin breaks down to hemosiderin and bilirubin (yellow/brown pigment)
icterus (jaundice) is major clinical sign
ex: IMHA, trauma
Icterus formation
phagocytosis of RBCs by macrophages releases hemoglobin that gets broken down into heme and iron to form bilirubin and hemosiderin to be secreted and absorbed by tissues
bilirubin = yellow = jaundice/icterus
implies severe extravascular hemolysis
Lysosomal storage disease
lysosomes incapable of breaking down protein/lipid/carbohydrate causing build-up of partially digested metabolites in cells and eventually cell death
brain/liver/muscle primarily affected due to rapid turnover of organelles and high energy demand
Primary amyloidosis
overproduction of light chain of immunoglobulins
defect in plasma cell production
rare in veterinary medicine
Secondary amyloidosis
overproduction of serum amyloid A (SAA) produced in liver
upregulated during inflammation
Islet cell amyloid
IAPP produced by pancreatic beta-cells
common in cats
How hepatic amyloidosis interferes with liver function
amyloid build-up in liver blocks hepatocytes from being able to “filter” blood
hepatocytes atrophy and entire liver looks grossly big because of amyloid accumulations
results in liver failure
Dystrophic calcification/mineralization
local deposition of calcium in injured/dying/dead tissue
unrelated to serum Ca:PO4 balance
can be anywhere in body where there are dead cells, old abscesses/granulomas, dead parasites
Metastatic calcification/mineralization
systemic deposition of calcium in connective tissues and basement membranes
when there is hypercalcemia or hyperphosphatemia, and solubility product of Ca:PO4 is exceeded
etiologies: kidney disease, vitamin D toxicosis, parathyroid disorders, neoplasia
can be located in stomach, lungs, heart, kidney, parietal pleura
Karyolysis
nuclear fading
chromatin dissolution due to action of DNAases and RNAases
Pyknosis
nuclear shrinkage
DNA condenses into shrunken basophilic mass
Karyorrhexis
nuclear fragmentation
pyknotic nuclei membrane ruptures and nucleus undergoes fragmentation
Why is cellular eosinophilia a sign of cell injury/death?
hematoxylin stains nucleic acid (RNA, ribosomes) blue
injured cells appear pinker due to denatured protein (lost ribosomes) and loss of blue staining
Apoptosis
orderly cell death
“clean”
no inflammation
Necrosis
disorderly, sloppy death
leaks a lot of inflammatory molecules resulting in secondary inflammation
Reversible cell injury
some cells may develop “fatty change”
usually occurs in liver and muscle cell
apoptosis
Irreversible cell injury/cell death
necrosis
cell size enlarges and plasma membrane/organelles/nucleus break down
leakage of contents attracts neutrophils = inflammation
Coagulative necrosis
maintains overall shape of organ
pallor, shrunken
may still look similar in shape, function is decreased/absent
commonly identified in ischemic, metabolic, or toxic injury
Liquefactive necrosis
pus
loss of tissue architecture
tissue is liquified or paste-like
commonly identified in extracellular bacteria (neutrophils)
Caseous necrosis
“cheese crumbles”
loss of tissue architecture
dry and crumbly
commonly identified in intracellular bacteria (macrophages)
Fat necrosis/saponification
specific to coagulative necrosis of adipocytes
fat within cells are saponified (precipitated with calcium soaps)
2 ways to initiate apoptosis
extrinsic - activation of cell death receptors
intrinsic - injury to mitochondria
culminates in common “execution” pathway
What enzymes mediate apoptosis?
caspases - activated by calcium release, catalyze all aspects of apoptosis
results in cleavage of membranes, DNA, proteins, etc.
cell falls apart but remains membrane bound
Reperfusion injury
tissue damage caused when blood supply returns to tissue after period of ischemia
lots of calcium/potassium/lactic acid build up suddenly gets dumped into circulation
ex: great dane with GDV, equine colic
Embryonic connective tissue
fills spaces between developing tissues and organs
large number of stellate multi-potential mesenchymal stem cells
develops into connective tissues
Adult loose (areolar) tissue
supports epithelia, mucosa (gut), stroma of organs, surrounds blood vessels and nerves
contain collagen bundles and elastin fibers
Adult dense irregular tissue
many fibers arranged randomly
dermis of skin, capsules of organs, sheaths of nerves and muscle
Adult dense regular tissue
collagen fibers regularly arranged/running in same direction
tightly bundled, cells squished
tendon and ligament
Specialized connective tissue
adipose, cartilage, bone, hematopoietic tissue (bone marrow)
Cells found in connective tissue
Fibroblast - ECM
Macrophage - phagocytic, turn over old ECM
Mast cell - histamine
Plasma cell - antibodies
Collagen type I
major fibrillar collagen that provides tensile strength
found in bone, tendon, ligament, skin
(90% of body collagen)
Collagen type II
cartilage collagen
thinner fibrils than type I