Week 1 Flashcards
innervation to the submandibular gland
superior salivatory nucleus facial nerve chorda tympani, trigeminal nerve's lingual nerve submandibular ganglion.
innervation to the parotid
Inferior salvitory nucleus to glossopharyngeal to tympanic to lesser petrosal to otic ganglion to auriculotemporal (branch of the mandibular)
innervation to sublingual gland
chorda tympani off of facial nerve
lingual nerve
submandibular ganglion
white adipose tissue role in metabolism of sugars
Ferments glucose to glycerol 3-phosphate, the backbone for triacylglycerol synthesis.
why do you have high insulin in a hypercatabolic state
you need a little insulin around for protein synthesis
amylose
a bunch of glucose linked (1,4)
amylopectin
chains of glucose in 1,4 linkages that are linked to other chains (1,6)
chemically similar to glycogen, but not as branched
four enzymes at the brush border of the gut epithelial cells
breakdown di and tri saccharides into mono
maltase-glucoamylase. An exoglycosidase - cleaves a 1-4 bond of maltose to form two molecules of glucose - it is the exoglycosidase version of alpha-amylase - activity is highest in illium - lysosomal alpha1,4-glucosidase (acid maltase) is defective in pompe disease (pompe trashes the pump - heart liver muscle)
sucrase/isomaltase complex - two extracellular domains with different substrate specificities - the isomaltase activity cuts the 1,6 bonds in amylopectin, the sucrose domain cuts sucrose - activity is highest in jejunum (in the liver, deficiency of the 1,6 debranching enzyme is cori disease (milder form of von girke with no increase in blood lactate))
trehalase - cleaves trehalose - disaccharide of glucose (1,1)
beta-glycosidase complex - b-glycosidase complex is a glycophosphatidylinositol (GPI) glycan anchored protein with two catalytic domains.
Glucosyl ceramide domain: Cuts glucose and galactose from glucosylceramide and galatosylceramide
Lactase domain: Splits the 1,4 bond in lactose to make galactose and glucose. (loss of beta-glucosidase in lysosomes –> gauchers!!)
endoglycosylase
e.g. amylase
cuts carbohydrates into di and tri saccharides `
amylase activity is highest in this part of the gi tract
duodenum
why did i get diarrhea when i ate a whole tub of cottage cheese that one time
Without lactase, bacteria ferment lactose to lactic acid. Water enters the lumen of the gut to balance difference in proton concentration, causing diarrhea.
sucrase
cleaves sucrose to fructose and glucose
its how high fructose corn syrup is made ya dingus
in hypercatabolism, what hormone causes muscle protein breakdown
cortisol
How does Epinepherine cause the “ebb” phase in hypercatabolism
it activate hormone sensitive lipase, which moves fatty acids out of the adipose
Most important hormone for storage in fed state
Most important enzyme for catabolism
Insulin
Glucagon (when glucose in gone)
What are Insulin’s actions intracellularly?
Tyrosine kinase transmembrane protein, leads to inactivation of Glycogen phosphorylase and activation of glycogen synthase.
where do preganglionic sympathetic neurons lie in the spinal chord
intermediolateral cell column
in the thoracolumbar (t1 to l2)
what are the names for the nerves that leave the intermediolateral cell column and go straight to the organs without going into the prevertebral ganglia
splanchnic
the go to peripheral ganglia
pregangionic parasympathetic origins for the gut
vagus and S2,3,4
what does the vagus “turn into” below the level of the trachial bifurcation
the esophageal plexus
nerve that supplies motor to the diaphragm
phrenic
what part of the colon does the vagus supply
the midgut and foregut derived parts
transverse colon, proximal colon
BASICALLY IT STOPS AT THE SPLENIC FLEXURE SHE SAID
which part of the vagus - anterior or posterior - supplies the greater curvature of the stomach
posterior supplies greater
what supplies the posterior and lower portions of the colon with parasympathetic activity
pelvic splanchnic
(cell bodies in s234)
they leave the motor neurons they were traveling with and enter the inferior hypogastric plexus
then they follow the inferior hypogastric plexus to the organs right there, or they can travel all the way up to the superior hypogastric plexus (which is near the inferior mesenteric artery) and ride with that to innervate sections of the hindgut
pudendal nerve
from s234
carrying sensation and voluntary motor to the external urinary and anal sphincter
Odynophagia vs dysphagia
Odynophagia - pain on swallowing
vs
dysphagia - symptom resulting from the failure to move a food bolus from the mouth to the stomach
esophageal dysphagia
solids only - intermittent
solids only - progressive
solids/liquids - intermittent
solids/liquids - progressive
solids only - intermittent - lower esophageal ring
solids only - progressive - peptic stricture or cancer (esp. if >50)
solids/liquids - intermittent - diffuse spasm, NEMD, Nutcracker
solids/liquids - progressive - Achalasia, scleroderma (CREST)
where and what are the names of the four papillae of the tounge
filliform - cover most of the tounge - keratinized and v-shaped
fungiform - larger papilli that are fewer in number and scattered throughout the tounge
circumvallate - large round papillae at the posterior of the tounge
foliate papillae - on the sides
what papilla are keratinized
filliform
what papillae are club shaped
fungiform - they have a expansive lamina propria, non-keratinized
what papillae are supplied by cranial nerve 7
fungiform
what papillae are supplied by the glosopharingeal
circumvallate
smallest type of ducts
intercalated ducts
what gives striated ducts their striated apperance
ER
myoepithelial cells
specialized smooth muscle cells between serous and/or mucous cells and basement membrane
assist in discharge from the secretory cells
what alveoli stain very darkly
serous alveoli, because they have a lot of ER for making protein
what type of epithelium is on the papillae of the tounge
stratified squamous
pyogenic granuloma
polypoid red lesion composed of lobular reactive proliferation of capillaries
usually on the gingiva in children, young adults, pregnant women
what gives leukoplakia its white appearance
hyper or parakeratosis
actinic chelitis
leukoplakic lesion of the lower lip with loss of the distinct demarcation between the lower lip vermilion border and the skin of the lip
actinic keratosis of the bottom lip
hyperkeratosis and connective tissue solar elastosis
adenoid cystic carcinoma
slow growing salivary gland neoplasm
relentless in its growth and can invade the perineurium of nerves around it
Despite surgical resection, 50% disseminate to lungs, bone, liver, and brain, often decades after removal. While 5-year survival rate is 60-70%, survival drops to 30% at 10 years and 15% at 15 years
you see a bunch of eosinophils and neutrophils on an esophageal biopsy
is it eosinophillic esophagitis?
no
in EE you don’t see neutrophils
chondromyxoid stroma and epithelium
what you thinkking
pleomorphic adenoma
patient comes in with pellagra like symptoms and neutral aminoaciduria
hartnup disease, inherited mutations in the B(not) transporter ( SLC6A9 transporter)
failure to absorb tryptophan
(tryptophan is used to synthesize niacin)
cystinuria defect
defect in the B(not)+ (SLC7A9 transporter) gene leads to basic aminoaciduria causing kidney stones
cannot uptake cystine (not cysteine)
structure of glutathione
glycine-cystine-glutamate
glutamate is “rotated” 180 degrees
enzyme that can cleave glutathione
gamma-glutamyl transpeptidase (GGT)
increased in various liver and biliary diseases (just as
ALP can), but not in bone disease; associated
with alcohol use
AMPK role
inhibits protein synthesis by activating TSC1 and 2, which blocks mTORC1
promotes autophagy and catabolism
metformin makes it active, tricking the cell into thinking that it is in an energy deprived state
key cofactors in aminoacid metabolism
pyridoxal phosphate (B6) (PLP) - transaminations (ALT and AST use it), deaminations, carbon chain transfers. Synthesis of cystathionine, heme, niacin, histamine, and neurotransmitters like serotonin, epi, norepi, dopamine, and GABA (def causes - seizures, diarrhea, sideroblastic anemia (impared heme synthesis and iron excess), EEG abnormalities)
tetrahydrofolate (B9) - one carbon transfers (def causes - megaloblastic anemia)
tetrahydrobiopterin - ring hydroxylations (phe -> tyr) (def causes - PKU - seizures, developmental delays, fair skin, eczema, musty body odor) (PKU also can be from Phe hydroxylase def)
what activates lipoprotein lipase
ApoC-II
its in the capillary beds
what hormone causes the pancrease to secrete its enzymes
secretin
what turns triacylglycerols in micelles into 2 fatty acids and a 2-monoacylglycerol
pancreatic lipase
the products can be taken up by gut epithelial cells
nascent chylomicrons vs mature
mature contains Apoc-II, ApoE
both have ApoB-48
what particle functions to distribute fat synthesized from carbohydrates to tissues
VLDL
where is vit A stored in the liver
Stellate cell
what molecule changes shape in you rod cells in the retina to signal to the brain that light is hitting it
cis-retinal gets converted to trans-retinal
cis retinal is bound to opsin. when it becomes trans-retinal, it dissociates and activates a g-protein coupled sodium channel which opens and HYPERpolarizes the rod cell. it is then recycled to cis-retinal
retinoic acid’s effect on b-cells
stimulates them to move to the gut
main functions of vitamin K
carboxylation, coagulation
function of coumadin
blocks vitamin K epoxide reductase, cannot regenerate the hydroquinone version of vitamin K
vitamin D can be synthesized de novo from what
cholesterol
cholesterol gets converted to this form of vitamin D when hit with UV light
cholecalciferol
gets 25-hydroxylated in liver
1-hydroxylase in kidney (active form) (responsive to parathyroid hormone)
TRPV6 function
takes up calcium at the brush border
is upregulated when activated vitamin D does its business as a transcription factor
calbindin function
once calcium gets into the gut epithelial cell, this transports it from the TRPV6 channel to the Ca/ATPase which puts Ca into the blood
how does vit D prevent colorectal cancer
stabilizes beta-catenin
this blocks the action of parathyroid hormone
calcitonin
also it is a medullary thyroid carcinoma tumor marker
function of calmodulin
Carries calcium around the cell
and example he talked about:
If epi or norepi hits a muscle cell, it activates phopholipase C, making IP3, which makes the ER secrete Ca, which binds calmodulin and then:
shuts off glycogen synthase
turns on glycogen phosphorylase
high doses of this can be used to treat hyperphosphatemia secondary to kidney failure
Ca
blocks phosphorous uptake
mutation in thiazide sensitive NaCl transporter
what are your ion disturbances
gitelman syndrome
hypomagnesemia, hypokalemia, hypocalciuria
bacteria breaks down stuff to provide fuel for colonocytes
what is the stuff?
they break down fiber into short chain FA
get uptaken by monocarboxylate transporter
SCFAs effect our immunity how
act as a ligand for GPR43
e.g. in the macrophage inflammatory cytokines go down, IL-10 goes up (antiinflammatory.
GPR43 in adipose
decreased fat storage as TAG, and insulin sensitivity when activated
what does PKB/Akt do
it is a downstream signal of insulin binding.
inactivates glycogen synthase kinase
activates protein phosphatase 1 (PP1), which makes:
- glycogen synthase is DEPHOSPHORYLATED and ACTIVE
- glycogen phosphorylase is DEPHOSPHORYLATED AND INACTIVE.
INSULIN –> DEPHOSPHORYLATION –> SYNTHESIZE GLYCOGEN
what happens to glucagon if you eat a protein rich meal
After eating a protein rich meal, elevated amino acids in the blood increase the secretion of glucagon by pancreatic alpha cells. In this case, excess amino acids are used by the liver for gluconeogenesis
in the fed state, gut epithelial cells use what as their primary fuel
glutamine, aspartate, gluatmate
insulin and glucagon
which for PKA, which for PKB (downstream molecules)
insulin for PI3 –> PKB (think beta cells)
glucagon for cAMP –> PKA (think alpha cells!)
Insulin and glucagon - which one causes a net phosphorylation event? dephosphorylation?
glucagon –> PKA –> phosphorylation
Insulin –> PKB –> dephosphorylation
glucagon as an example:
Glucagon causes:
Glycogen phosphorylase kinase phosphorylation and activation:
Glycogen phosphorylase is subsequently phosphorylated and activated
(remember glycogen phosphorylase breaks down glycogen stores for use)
Also Glycogen synthase is phosphorylated and inactivated by glucagon
what happens to glycogen synthase when it is phosphorylated
it is inactivated
the ATP power to drive gluconeogenesis comes from what source
the FAD2H and NADH reduced by fatty acid beta oxidation
glucose enters the gut epithelial cell from the blood to be used as fuel. how is it used?
What is the primary source of food for the enterocyte in the fasting state\?
it is fermented to pyruvate, which is used as a nitrogen acceptor from glutamate to make alanine, which is exported back into the blood
primary source of food is glutamine, but from the blood, not from the lumen (glutamine is also the primary food source for lymphocytes)
what signalling molecule mobilizes FA from adipose tissue during hypercatabolism
epinephrine activating hormone sensitive lipase
nitrogen balance equation
Nitrogen balance = nitrogen intake – (urinary urea nitrogen + 2)
where is apob-48 made
100?
RNA editing produces ApoB-48 in intestinal epithelial cells. The unedited transcript produces full length ApoB-100 in hepatocytes
