10/6 Histology Flashcards
how do plica increase surface area
3 fold by increasing the folds in the epithelium, present in colon, added to with villi in the small intestine, and even with folds in the submucosa in the small intestine
how are lipids handled in the lumen of the small intestines?
lipids will be emulsified by the bile acids, and difuse into the enterocytes and then made into triglyceride plus protein cover structure called chylomicron that is then diffused out of the cell and into the lymphatic capillary.
describe the epithelium of the small intestines
the epithelium cover villi and the surface and have a brush border of the microvilli, covering a columnar layer of enterocytes (absorptive columnar cells) also have goblet cells, Enteroendocrine cells, and paneth’s cells
what is the general feature of the small intestine surface?
villus sticking out that increase the surface area by 10 fold, covered by microvilli that will increase the surface are by 20-fold.
what does celiac disease do to the villi
leads to the shrinkage or loss of the villus (now it looks like a colon)
what are the absorptive columnar cells called?
enterocytes
describe the enterocytes
include: brush border, tight junctions, zonula adherens (terminal bar); desminsome; meidesmisome; gap junctions; Na,K-ATPase pump; K channel; AA carrier channels etc.
the cells at the base of the villi that are full of peptide that have anti-bacterial activities and maintain normal level of gut bacteria
the bright orange staining paneth cells at the base of the villi
associated with the stem cells and regulate the stem cells to keep them in the pathway of stem cells
paneth cells
stimulates HCO3 and H2O secretion by the pancreas and bile ducts
Secretin
stimulates pancreatic acinaar cell secretion and smooth muscle contraction by gall bladder. signal immediate satiety to the brain
CCK
stimulates the insulin secretion by beta cells in pancreas
GIP (glucose-dependent insulinotropic hormone)
signals long term satiety to the brain
peptide YY
a cell that releases secretin or CCK or GIP or peptide YY
enteroendocrine cells
under the epithelium cells, containing the plasma cells that are making anti-bodies
lamina propria
extensive blood supply, lymphatic and immune cells and smooth muscles that move these things around to pump thing around and stir things up are found here, just under the epithelium
lamina propria
thin band of smooth muscle just deep to the lamina propria and just deep to the deep glands of the small intestine
muscularis mucosae
the layer under the muscluaris mucosa
the submucosa, then the muscularis externa, and the adventita or serosa
cells in the duodenum that only make a pretective mucus
brunner’s glands
the largest number of the plica circularis or extensions of the glands into the lumen
in the jejunum
pathches that are full of lymphocytes that appear after birth and peak around 30 and lose these
peyer’s patches
where are peyer’s patches located?
in the ileum – look like little pyrimides of lymphatic cells that have no villi!
specialized cells in the peyer’s patches that have immune responsibilities
M or microfold cells that are specialized in bringing antogens from the lumen to the imune cells in layer under the endothelium
a general term for the lymphatic assiciated tissue in the intestines that helps mediate the immune response in the epithelium of the gut
MALT (mucosal associated lymphatic tissue) – called GALT (gut associated lymphatic tissue)
how do we get the immune response into the lumen of the gut?
IgA is taken up by the enteriocytes and transported across the epithelium and into the lumen.
area where max triglyceride and iron are absorbed
early in the duodenum
where are vitamin and B12 and GIF and bile salts absorbed?
Late, and in the ileum
where do digestive enzymes come form?
most from the exocrine pancreas, and from absorptive columnar cells containing a set of hydrolases on the brush border involved in end-stage digestion: disaccharidase, dipeptidase, etc.
found near the base of the glands unlike the stomach where they are near the top of glands
stem cells
control muscularis externa, if damaged motility is disrupted and swelling occures (hischsprung disease)
Myenteric plexi (auerbach’s plexi)
regulate muscularis mucosae and DNES cells
submucosal (meissner’s) plexi
describe the colon
has an epithelium and a lamina propria and none of the long villi that are in the small intestines
long section of the smooth muscle in the colon below the lamina propria these are non-uniform patches of smooth muscle!
taeniae coli – unique to the colon
a pouch off of the cecum
vermiform appendix
vermiform appendix
doesn’t have a taeniae coli, therefore has very uniform smooth muscle layers
lots more of these type of cells in the colon to provide more protection and less absorption
goblet cells
why is there such a potential for diarrhea?
there is such a large flow of water accross the colon normally! about 50L/d
involves the disruption of the homeostatic interactions between mucosal epithelium, ummune system, and bacteria
inflammatory bowel disease
aggregates of multi-nucleated cells in the sub-mucosa or lamina propria
granuloma formation
what does a granuloma formation mean?
a longterm inflammatory response in the bowl
what would indicated extensive damage in a tissue (such as the appendix?)
eroded epithelium, hemorrhaging of blood where it shouldn’t be, and lots of lymphocytes
where is the brush border?
in the enterocytes or the absorpative columnar cells
how does AA get into and out of the enterocytes?
Na+/AA co transporter in. AA Carrier out
what are the components of the terminal bar?
tight junctions/zonula occludens and zonula adherens
what are the general layers of the intestine from the lumen down…
- Enterocytes, goblet cells, paneth cells, and enteroendocrine cells
- Lamina propria
- Muscularis Mucosae
(1-3 are all the Mucosa) - Submucosa
- muscularis externa
- Adventitia or serosa
Describe white adipose tissue
unilocular (one fat drop) white fat that is abundant, about 20% of weight (higher in women), localizes as you age.
Describe brown adipose tissue
present at birth (5% of weight), decreases with age, multiocular brown fat
where does brown adipose come from?
arises form embryonic precursors that also give rise to skeletal muscle (paraxial mesoderm), express Myf5…this is the classic location brown fat in infants
where does white fat come from?
arise from the division of pericyte-like cells (Myf5 - negative cells) from the division of the pericyte-like cells.
generates heat
brown fat
one fat globular vs. multi blobs of fat
unilicular vs. multilocular
what are pericytes?
they are cells that are associated with small blood vessels
where does beige fat come from?
found in white fat and can be induced by adrenergic stimulation; (Myf5- negative)
what is adrenergic stimulation?
epinephrin and neuroepinephrin
describe brown fat
they have multiple lipid stores and lots of mitochondria to produce heat, by allowing protons to move through the membrane of the mitochondria without making ATP (uncoupling) and this produces heat.
why do babies have brown fat in the neck?
to heat blood to the brain
what do beige adipocytes do?
they get stimulated by cold and/or adrenal stimulation from white adipocytes and start to burn energy up like brown adipocytes.
how could we possibly lead to the production of brown fat (beige fat cells) from white fat
Cold
epinephrin/neuroepinephrin
exercise may also convert it to brown fat via hormone irisin (possibily)
what is cachexia
a wasting that occurs in cancer patients, that may be due to the production of cytokines like IL6 that can convert white fat to beige fat cells.
the functions of white adipose tissue
store lipids, buffer plasma lipids (remove excess chylomicrons from the blood), and secrete hormones (endocrine activities)
Explain the general cycle of fatty acids between adipocytes and capillaries
lipoprotein lipase causes the release of chylo. and VLDL in the form of free fatty acids to the adipocytes that generate triglyceride. then the hormone sensitive lipase can break the triglyceride down to release free fatty acids and fre glycerol phosphate back to the capillaries to be transported by albumin in the blood (transport free fatty acids)
the liver version of a chylomicron
VLDL
how do we get lipoprotein lipase in the capillary?
produced by adipocyte, secreted, transcytosed, and bound to the endothelial cell surface.
what would stimulate the synthesis and delivery of lipoprotein lipase to the capillary to absorb more fat?
insulin
endocrine function proteins from the adipocytes
Leptin, and Adiponectin
what does leptin do?
macronutrient homeostasi (food intake and energy expenditure) It lowers appitite and increase activity
where does the leptin act to reduce apitite and increase activity?
hypothalamus
what does adiponectin do?
it is a insulin sensitizing adipokine; decrease lipid accumulaiton and increase glucose uptake in muscles; avoid fat buildup in the liver; lots of other great effects! (anitdiabetic, anti-atherogenic, anti-inflammatory and cadioprotective porperties!)
Leptin:
communicates information on sufficiency of energy supply;
secretion increases as fat stores increase
involved in energy homeostatsis
also interacts with immune system, hematopoiesis, angiogenesis, bone development
Adiponectin:
modulates several metabolic processess
secretion decreases as fat stores increase
enhances insulin sensitivity of the liver
stimulates fatty acid and glucose utilization in muscle
Inhibits macrophage activity, stimulates angiogenesis
imparied ability to stimulate peripheral glucose uptake and suppress hepatic glucose output
insulin resistence!
what happens to mice that have no white adipose tissue?
they quickly become insulin resistance and type two diabetes. Therefore, if you have too much or too little white adipose tissue then you get type two diabetes.
how could white adipose help prevent diabetes?
by acting as a lipid buffer to the blood. if you don’t buffer it out then you get a build up of lipid in the muscle and the liver
what if you have lots of lipid in the muscle?
triggers signaling cascade that inhibits insulin-stimulated translocation of GLUT4 to the surface, reducing glucose uptake and therefore leaving lots of reactive glucose in the blood
what if lots of fat in the liver?
inhibits insulin-stimulated glycogen synthesis and reduces insulin-suppression of gluconeogenesis.
how can the expansion of adipose tissue lead to damage and insulin resistance?
Obesity leads to enlarged adipocytes that down lipid buffering capacity - ectopic fat deposit and insulin resisitence
-or-
enlarge adipocytes - increase hypoxia and death and down TAG (triAcyl Glycerol) clearence - ectopic fat and insulin resisitence
-or-
increase in hypoxia - can’t secrete the right cytokines or adipokines - death of adipocytes - increase macrophage infiltration and ectopic fat deposition and - insulin resistance
