biochem test 2 2011
Quiz yourself by thinking what should be in
each of the black spaces below before clicking
on it to display the answer.
Help!
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| Is triglyceride synthesis a fed or fasted state occurance? | Fed
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| What are 3 lipases we discussed involved in triglyceride lipolysis? Which are fed state, fasted state? | Pancreatic Lipase fed Lipoprotein lipase fed Adipose lipase fasted
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| When triglycerides cross membranes they do it as fatty acids, what happens to the glycerol backbone? | Always goes to the liver. The liver is also the only place it can be rephosphorylated to G 3-P because it has glycerol kinase
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| Where does the glycerol 3 P come from in the fed state to synthesize triglycerides? | DHAP
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| When mobilizing triglycerides from adipose in a fasted state, how is transport different? | Adipose lipase does not convert to triglycerides for transport, that requires energy, it is easier to bind it to Albumin and transport as fatty acids
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| How is pancreatic lipase regulated? | Food ingestion regulates its secretion
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| Adipose lipase is under hormonal control, which one(s)? | Glucagon and Epinephrine, phosporylation activates it.
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| What other lipase is under hormonal influence? | Lipoprotein lipase. activated by insulin
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| What happens to glycerol 3 phosphate in the fed vs fasted state? | Fed, catabolized via glycolysis used for hepatic triglyceride synth. Fasted, convert to glucose via gluconeogenisis
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| What happens to the albumin bound fatty acids mobilized earlier by the Adipose lipase? | enter mitochindria of beta oxidizing cells and catabolized to acetyl CoA, NADH, FADH2
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| Where does beta ox take place? | all mitochondria except in brain cells
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| Is beta ox fed or fasted occurance? | Fasted, getting energy from oxidizing fatty acids.
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| What is the most prevalent type of neuron? | Interneuron, it is multipolar
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| What are examples of excitatory NT's | ACh, Glutamine, seratonin
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| What are examples of inhibitory NT's? | GABA and glycine
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| How do paralytics, like curari and its various clinically relevant derivatives, work? | block ACh receptors so Ach cant bind and AP can't propogate
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| What are the 2 motor proteins involved in axonal transport, which goes what direction? | Kinesin=anterograde
Dynein=retrograde
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| Why does nerve damage take so long heal? | relies in anterograde transport which is very slow, .2mm-4mm p/day
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| Schwann cells produce myelin in the PNS. What is the somewhat analagous cell in the CNS | oligodendrocytes, only they myelinate multiple axons
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| Glioblastoma multiforma is the most common and most aggresive brain tumor in adults. What type of glial cell is this associated with? | Astrocytes. GBM is an advanced astrocytoma
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| Herpes simplex virus hijacks the _______________axonal transporter? | retrograde, permanently sequesters it.
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| What are the layers of CT in a peripheral nerve? | small to large
endoneurium
perineurium
epineurium
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| What type of supporting nerve cells produce CSF? | ependymal cells, with adjacent capillaries they form the Choroid plexus
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| Whats missing in somebody with Herchsprung's? | entire nerves in sections of the colon. due to a failure of the neural crest cells to migrate there. (neonatal intestinal obstruction) gonna nead a colostomy bag.
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| How do nerve cells in the PNS respond to injury? | schwann cells line up to form a tube and release growth factor
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| Why does nerve repair in the CNS suck? | Oligodendrocytes have to still be in contact with their axons or they go through apoptosis
BBB limits macrophage entry to do the clean up
Astrocytes respond to injury by forming a scar
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| Never let monkeys eat bananas? | cells in blood based on prevelance, in decreasing order
Neutrophils 60%
Leukocytes 30%
Monocytes 6%
Eosinophils 4%
Basophils 1%
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| How is blood a type of CT? | cells, ECM, from mesenchyme
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| Some of bloods function? | transporter of nutrients, gases, hormones, immune cells,waste, and helps regulate body temp
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| 45% of blood is formed elements. What are they? | RBC's, WBC's, platelets
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| What is plasma made up of? | 90% water
10% dissolved stuff (ions, gases, waste,nutrients, enzymes, plasma proteins)
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| Of the plaasma proteins Albumin is the most abindant (60%) What is a major role of it in relation to blood? | contributes to blood colloid osmotic pressure. the ability of blood to "hold on to water" If you have liver damage and low albumin levels your blood loses this ability and water goes into the tisseu causing edema
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| What are two other plasma proteins | globulins
fibrinogens
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| What is saltatory conduction and what part of the schwann cell is directly involved? | AP "jump" from one Node of Ranvier to another, the nodes are not myelinated on the end where the signal transmission takes place
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| Where does hemopoiesis take place in adults? In kids? | Adults=proximal humerus and femur, iliac crest and sternum
Kids=liver, spleen and pretty much all spongy bone
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| What does hematocrit measure and what are the normal ranges? | measures % of RBC's in whole blood
Males=39%-50%
Females=35%-45%
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| If you have anemia you hematocrit would be? How about polycythemia? | Anemia= low
polycythemia = high
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| What are reticulocytes? | immature RBC's . Normal range is <1%. problematic if elevated.
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| Granuloctyes | neutrophils, eosinophils, and basophils
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| Agranulocytes | monocytes, and lymphocytes
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| Elevated levels of which specific cell (granulocyte) would indicate a bacterial infection? What about a parasitic infection? | neutrophil = bacterial
eosinophil= parasitic, also mediate allergic reactions and respond to chronic inflamation
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| Eosinophils also counteract histimines released during an allergic reaction, which cells release histimine? | basophils
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| What are the two agranulocytes and what do the do? | Monocytes circulate and when they leave the blood turn into macrophages
Lymphocytes (like T cells and B cells) are involved in immune response...but you'll hear about that later.
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| What layer of the heart has a serosa and contains arterie, vessels and nerves? | Epicardium
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| What component of the myocardium helps with coordinated contraction? | the desmosomes and gap junctions
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| Which node is the "pacemaker" of the heart? | SA node, then to AV node, bundle of his, purkinje fibers, spread to apex(bottom) of heart, for a bottom up squeeze
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| What part of the heart allows for electrical isolation the atria and the ventricles? | fibrous skeleton
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| The heart is innervated by the ANS. which part of the ANS would speed up heart rate? | Sypathetic=fight or flight (tachycardia)
Parasympathetic="rest and digest" would slow it down
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| How does the heart respond to increased blood volume? | When the heart muscle cells stretch they release diuretic and vasodilating hormones which increase urine production, relaxes capillary sphincters thereby decreasing blood volume
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| What layer of the heart would you find chordae tendonae and atrioventricular valves? | endocardium
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| The heart is innervated by the ANS. Which part of the ANS would speed up heart rate | sympathetic. fight or flight tachycardia
parasympathetic= rest and relax
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| Some vessels are large enough to require their own nerves and bllods supply, what are these called? And where would you find them? | nervi vasorum and vaso vasorum. in the tunica adventitia
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| Where would you find the internal elastic lamina? | tunica intima
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| Where would you find the external elastic lamina? | tunica media
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| What type of capilaries would you expect to find in the kidneys? | fennestrated. controlled diffusion. small holes on endothelium but intact basal lamina
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| In most places you would find_______________capilaries? | continuous. gas and nutrient exchange. tight junctions
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| Where do you find pericytes? and what do they do? | capilaries. myofibroblasts that aid in wound healing
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| In the liver you would find________________capilaries? | sinusoidal. dumping large volume
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| What are arteriovenous anastamoses? | shunt that helps control whether bllod goes through the capillaries or bypasses them. If you were trying to decrease blood volume you would close the shunt making the blood go through the capillaries
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| How do endothelial cells control their environment? | -secrete vasoconstrictors and vasodialtors
-express signals to prevent or stimulate clotting
-moderate neutrophil and macrophage migration out of blood
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| Lymph vessels carry "junk" like fluid, proteins, fats , etc form the EC space. They also have valves to make sure the lymph travels to the lymph nodes. Where do they rejoin the blood stream? | subclavian veins
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| An aneurysm is caused by a weakness in which layer of a vessel? | tunica media
associated with atherosclerosis, syphylis, and CT disorders like Ehlers-Danlos and Marfans
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| Restonosis? | proliferation of smooth muscle in the tunica media, can block lumen
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| How are macrophages implicated in atherosclerosis? | cholesterol deposits on the tunica intima and the macrophages engulf and cause further inflamation.
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| Arterial clots can cause | strokes and MI's
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| Venous clots, DVT's can cause? | pulmonary embolisms. always get up and walk around the plane.
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| What stimulates carbamoyl phosohate synthase 1 (CPS1)? | NAG allosterically activates it, it is made from acetyl CoA and glutamine, which are both present whether fasted or fed
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| The urea cycl eis feed forward activated by ammonia. T/F? | True
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| What does BUN reflect? | BUN = blood urea nitrogen, urea concentration in blood.
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| Predict the whether your BUN levels would be high or low depending on the following Kidney failure, high protein diet, liver failure, Malnutrition, overhydration, water retention | Kidney failure high, high protein diet high, liver failure low, malnutrition high or low, overhydration, water retention low
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| Hyperammonemia is a condition where you have elevated blood levels of ammonia. What can this affect, what are some symptoms? | Affects the CNS. Symptoms are tremors aggitation, slurring,blurred vision, hypotonia, seizures, mental retardation, cerebral edema and coma.
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| where in the cell are the first two enzymes if the Urea cylcle located? What are they? is either one of them the rate limiting step? | Located in mitochondria 1. CPS1, carbamoyl phosphate synthase 1 2. OTC, ornithine transcarbamoylase ***CPS1 is the enzyme at the rate limiting step
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| What amino acid is produced in the Urea cycle and also required for growth? | Arginine
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| What are the three AA's that carry nitrogen to the liver to enter the urea cycle? What can they be transamitated to and from? | Alanine--------->pyruvate glutamate and glutamine------>a-ketoglutarate ***glutamine can carry two ammonia molecules
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| Why is alanine a good way to transport ammonia? | transaminated from pyruvate which is abundant, esp in muscles, then it is recycled to pyruvate in the liver
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| Glucogenic AA's are degraded to? | pyruvate or other TCA intermediates from a-ketoglutarate and later.
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| Ketogenic AA's are degraded to ? | acetyl CoA or acetoacetate
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| What cofactor is required in transaminase reaction like the one catalyzed by AST and ALT? | PLP, pyridoxal phosphate, form vit B6
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| PVT TIM HALL the mnemonic for the 10 essential amino acids, ie the ones we can't synthesize. What are they? | phenylalanine valine tryptophan threonine isoleucine methionine histidine arginine leucine lysine
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| Would increased levels of ammonia increase or decrease pH? | increase, which can alter redox balance, denature proteins, and inhibit ox phos by screwing proton gradient
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| would a pregnant woman be more likely to have a positive or negative nitrogen balance? | positive, input>output. She would be using more nitrogen than normal therefore breaking less down
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| What is a hypercatabolic state? | increased fuel usage possibly causes could be
surgery, infection, trauma,
neg N balance and you will be mobilizing stored energy(fat, protein, carbs) to mount a defense
Cortisol important mediator in this response
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| a-ketoacid dehydrogenase is an important enzyme for what process? | breaking down the branched chain amino acids (valine, leucine, isoleucine)
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| What does PEP carboxykinase do? | enzme involved in OAA becoming PEP in the gluconeogenisis pathway.
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| Why would a high protein and high carb meal not stimulate both urea cycle activity and glucose import via GLUT 4 in the liver? | GLUT 4 is a glucose transporter in adipose and muscle tissue, not the liver (GLUT 2)
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| In a fasted state, a patient’s myocardial cells use acetyl CoA from ketone bodies for? | TCA Cycle activity
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| What role does carnitine play in FA metabolism? | Carnitine binds the fatty acyl groups of long chain FA's to get them into the mitochondria for B-oxidation
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| Can your heart use ketone bodies for energy? | Yes, so can your kidneys and skeletal muscle. your brain can too, but its suboptimal and more of a survival mode occurance
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| How is glucose 6 phospahte dehydrogenase connected to fatty acid synthesis? | G6PD is the rate limiting step in the PPP. This is one place that the NADPH comes from that is required for FA synthesis (malic enzyme is the other)
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| What are some sources of citrate for FA synthesis? | Lots. AA's, Ethanol, lactate and glucose can be converted to pyruvate---->Acetyl CoA or OAA, and on to citrate.
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| FA synthesis is highly regulated, generally where are the 5 regulation poitns? | 1. glycolysis via insulin effects on enzymes 2. TCA cylcle via high NADH downreg isocit DH 3. Hormonal control of FA synthesis enzymes 4. Feedback and allosteric control of FA synth (enzymes,substrates,products) regulation of lip. lipase via insulin
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| Is acetyl CoA carboxylase activated by substrate or inhibited by product? | Both, activated by citrate and inactivated by palmitoyl CoA
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| Would increased levels of malonyl CoA activate or inhibit carnitine transport of FA's? | Malonyl CoA would inhibit carnitine transport because you dont want carnitine to transprt the FA's you just made to the mitochondria to get beta oxidized
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| The major regulator of cholesterol synthesis is? | HMG CoA reductase, its activity is dependent on levels of cholesterol and other sterols, (but not affected by cholesterol esters)
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| What effect does high cholesterol levels have on the lypolysis of HMG CoA reductase? | The more you have the less you need to make, so it would increase the lypolysis as you don't need it.
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| What do you use to esterify cholesterol? | ACAT in cells LCAT in lipoproteins
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| What are the primary conjugated bile salt? the secondary? | primary conj taurocholic, taurochenocolic, glycocholi, glycochenocholic secondary. deoxycholic, deoxychenocholic, lithocholic, lithochenocolic
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| What does apoCII do? Where does it come from? | apoCII activates lipoprotein lipase*** It comes form HDL's that transfer it to nascent chylomicrons and VLDL.
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| What do statin drugs target and what effect do they have? | Statins target HMG CoA reductase and downregulate it.
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| PKU, phenylktonuria is the most common disorder of the AA metabolism, what would you look for in the urine of someone you suspected to have PKU | anything starting with "phenyl"
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| PKU is casued by a deficiency in phenylalanine hydroxylase, because of this phenylalanine accumulates and tyrosine os deficient. What are some symptoms? | mental retardation, developmental delay, hyperactivity, tremor, hypopigmentation. treat with restricting phenyalanine in diet and supplement tyrosine
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| An autosomal recessive inheritance of albinism is the worst type. Albinism is due to a deficiency in what? | tyrosinase
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| If you take a urine sample and notice that it changes color, that would be a clue for what? | Alkaptonuria, a deficiency in homogentisate oxidase, you would find homogentisate in the urine as well. Late onset, think arthritis
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| A deficiency in a-ketoacid dehydrogenase will manifest as? | MSUD (amish more affected) BCAA's feeding problems, vomiting, dehdration. detected by presence of leucine in blood if untreated retardation, severe physical disability, death. Treat by limiting BCAA's in diet.
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| Homocystinuria is a metabolic disorder in the methionine and cysteine metabolic pathway. What casues it? | deficiency in cystathione synthase. would see elevated levels of cysteine in urine and blood as well as methionine. symptoms include lens displacement, skeletal abnormalilities, premature arterial disease, and mental retardation.
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| Eicosanoids are derived from? | Arachidonic acid
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| Arachidonic acid is cleaved from phospholipids by? | phospholipase A2 or C through the activity of di and mono-acyl glycerol lipases
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| Phospholipase A2 cleaves the? | sn2 position of a phospholipid
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| Lipoxygenase does what? | converts aracidonic acid to leukotrienes
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| Cyclooxygenase does what? | converts arachidonic acid to prostaglandins
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| What converts arachidonic acid into epoxides? | Cytochrome P450
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| What is the function of prostaglandins? | Prostaglandins function as mediators of inflammation and pain.
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| What type of receptors to prostaglandins bind to? | G protein coupled receptors
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| What is thromboxane? | Thromboxane is synthesized in the platelets and is a potent vasoconstrictor and activator of platelets.
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| What is Prostacyclin? | Protacyclin is synthesized from endothelial cells and is an inhibitor of coagulation.
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| COX-1 is an inducible enzyme. T/F? | False
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| COX-2 is an inducible enzyme. T/F? | True
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| What are Leukotrienes? | Leukotrienes are important regulators in the inflmmatory response and bind to G protein coupled receptors. Leukotrienes are important in Asthma.
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| Isoprostanes are produced when arachidonic acid underoges free radical damage. T/F? | True
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| Isoprostanes are elevated during reperfusion injury. T/F? | True
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| Anadmaide is an eicosanoid that can act as an agonist for which receptor? | The cannabinoid receptor
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| Glucocorticoids inhibit eicosanoid synthesis by blocking? | Phospholipase A2
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| Are elevated VLDL in a fasted serum a positive risk factor for coronary heart disease? | yes, in a fasted state triglycerides will be on VLDL's. In genreal an increase in VLDL will increase IDL which in turn increased LDL
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| What effect would the use of a bile sequestering agent have on the conversion of cholesterol to cholic acid and to chenocholic acid? | Increase the conversion because when you sequester it you end up excreting in feces.
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| How does Cushing’s disease (excess cortisol production) cause polyuria and hyperglycemia? | cortisol stimulates gluconeogenisis, you will break down AA's to get the precusors thereby generating more urea, and more glucose
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| What are the 2 main enzymes in alcohol metabolism? | ADH, alcohol dehydrogenase (mod consumption) ALDH, acetaldehyde dehydrogenase
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| There is another enzyme in alcohol metabolism that kicks in after higher levels of consumption. What is it? | MEOS, microsomal ethanol oxidizing system, it also oxidizes an NADPH, takes place in the ER
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| What enzyme the MEOS system is involved in the oxidation of EtOH and NADPH? | CYP2E1, a cytocrome p450 enzyme. It has a higher Km for EtOH, which makes sense since it only functions when there is a lot around.
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| What can the liver do with the acetate from the alcohol merabolism? | 1. TCA cycle via acetyl CoA +OAA-->Citrate 2. same as above but Citrate--->FA synthesis 3. cholesterol synthesis via acetyl CoA 4. Ketone body synthesis***fasted state***via acetyl CoA
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| Outside the liver, Acetate can be used for....? | TCA cycle activity in heart, kidney and skeletal muscle.
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| How can an increase in NADH cause hypoglycemia? | Hypoglycemia in fasted state b/c more lactate is being made form pyruvate, so there is less pyruvate for gluconeogenisis. And Glucose 3-P is not being converted to DHAP.***less gluconeogenic material***
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| How can an increase in NADH cause hyperglycemia? | Fed state, high NAHD levels decrease glycolysis, so less use and uptake of glucose=more in blood.
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| How is ketoacidosis conected to the high NADH from excess alcohol consumption? | (malnourished, fasted, esp) high NADH decreases TCA so acetyl CoA will build up and ketone body production increases,BUT ketone utilization decreases b/c heart and kidney would rather use the acetate.
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| How does increased NADH cause a fatty liver? | increase triglyceride synthesis b/c availabilty of substrate. Decrease beta oxidation, and you decrease protein synthesis which decreases lipoprotein synth and lpopro. export
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| What causes gout? | high EtOH=high NADH which as we already said increases lactate production form pyruvate. Lacate builds up and competes with , the gout causing, uric acid for excretion.
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| When you drink too much ALDH can't keep up with all the acetaldehyde that ADH and MEOS are producing, so acetaldehyde builds up. What are the effects of this | 1. Acetaldehyde binds AA's so reduces protein synthesis (ie lipoproteins) 2. it also binds glutathione decreasing it reducing power. 3. The ROS's then oxidize phospholipids (membranes) reduce livers ability to remove VLDL
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| So in general high acetaldehyde wrecks the liver and in an attempt to heal, what happens to the liver? | CT synthesis (esp collagen) is incresed, fibrosis results and eventually the damage is irreversible. cirrhosis
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| The polymorphism of what enzyme has the most profound effect on a persons ability to metabolize alcohol? | ALDH polymorphism, can be culturally linked, and is a common gentic variant. MEOS and CYP2Y1 polymorphism effect it to a lesser degree
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| What would you give to a mother expecting to deliver preterm to help the neonates ability to breathe, why? | glucocorticoids, <35 wks the type II pneumocytes are not secreting surfactant, the glucocorticoids induce this and prevent atalectasis
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| What does sufactant do? | reduces the surface tension in the lungs faciltating exoansion and preventing collapse
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| Which pneumocytes are more abundant? | Type II @ ~60%, but they only cover ~5% of alveolar surface.
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| What part of the type II pneumocyte released surfactant? | lamellar bodies
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| What do bronchiolar exocrine cells do and how are they connected to cystic fibrosis? | secrete GAG's and relesase ions which through osmosis help to thin out mucous. If chloride ion pumps don't work the H2O cant thin out mucous and you get thick mucous which casues problems(^infections and potential asphyxiation)
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| What component of the respiratory system would you target if you were treating someone for asthma. | You would try to relax the smooth muscle that is causing it. via epinephrine, isopreterenol, albuterol...
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| What are the 3 layers of the blood gas barrier (form the oxygen side)? | 1. type I pneumocytes and surfactant layer 2. basal lamina 3. endothelium (inside capillary)
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| Exlplain the metaplasia that can happen from smoking or excessive coughing? What happens of it is chronic? | The respiratory epi undergoes metaplasia to strat squamous b/c it is more abrasion resistant. If it is chronic it will become dysplasia and can be oncogenic
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| What kind of tissue makes up your false vocal fold? | adipose and loose CT
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| What kind of tissue is your true vocal ligament made of? | dense CT
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| What anatomical division are microglial cells a part of? | CNS, macropahges and the only one not from neural crest cells, they are from monocytes
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| What are pericytes? | found in capillaries, myofibroblasts that aid in wound healing
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| What is another structure that does something similar to arteriovenous anastomosis? | precapillary smooth muscle sphincters
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| In a nutshell, what do endothelial cells help control? | prevent/stimuate clotting, mediate immune response (neutrophils and macrophages)
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| Restonosis? | proliferation of smooth muscle in tunica media, can occlude lumen
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| What does apoE do? | Help LDL, LRP receptors recognoze lipoproteins coming to liver
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| Which component of the immune response responds faster? | Innate, the adaptive is slower and more antigen specific
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| What is referred to as the "brain" of the gut? | Enteric component of the ANS. divided into myenteric (Auerbach's) and submucosal (Meisner's) plexii.
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| DiGeorge's syndrome is associated with a partial or complete lack of what organ? | Thymus, presents early with infections invovlving odd organisms, possibly fungal. Sometimes also lack parathyroid= hypercalcemia, cleft pallate
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| What part of the thymus would you find more T cells in. | Cortex. The medulla has reticular cells and Hassal's corpuscles
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| In lymph nodes B cells are predominatly found in the cortex and T cells are found in the paracortex. T/F? | True
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| What happens when you remove the spleen? | Increase in bacterial infections
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| How is the splenic tissue divided? | Red pulp and white pulp.
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| Where in the spleen would you fing most of the lymphoid tissue? | White pulp T cells and B cells. The red pulp is mostly plasma cells, reticular fibers and macrophages.
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| Does the spleen filter lymph? | No, it filters blood= no afferent lymphatics
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| What are PALS? | periarteriolar lymphoid sheaths, part of the white pulp, lots of B cells
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| What is MALT? | mucosa associated lymphoid tissue. found on mucous membranes lining resp, GI, and urogenital tissue (secondary lymphatic tissue)
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| What does independent assortment imply? | One event does not effect a second event, like flipping a coin
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| Complementary mutations are mutations with the same genotype caused by different genes. T/F? | True. ie thalessemia can be from gene encoding alpha or beta
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| A white flower crossed with red flower producing pink flowers is an example of? | semidominance. same phenotypic as gentypic ratios 1:2:1 2 being the blend
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| Codominance? | if heterozygous, neither allele is dominant to the other. ie blood type AB
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| Multiple genes influencing the same trait is______________inheritance? | polygenic. it is the genetic component of multifactoral traits
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| When one gene supresses the phonotype of a totally different gene it is called? | epistasis (can be used to order genes in regulatory pathways)
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| What is a dead giveaway that a trait is x-linked? | Affected grandfather--->unaffected mother--->affected grandson DING
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| How is x-linkage different from sex influenced inheritance? | sex inlfuenced inheritance involves autosomal genes and how thay are expressed differently in males vs females (body hair, fat distribution...)
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| Since females have 2x as many x chromasomes what they they do with the ones they don't need? | X inactivation is inactivation of an x chromasome on each blastomere, they are condensed to Barr Bodies. This phenomenon makes females genetic mosaics, and maybe the reason they sometimes act crazy. Also called Dosage Compensation
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| What is it called when a single gene controls multiple traits? | pleiotropy, cystic fibrosis?
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| Heigth and IQ are examples of what kind of multifactoral trait? | Quantitative. Qualitative miltifactoral traits tend to be all or nothing like MI's psychosis, and cancer
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| What are the assumptions that you have to make when using Hardy-Weinberg? | 1. Pop is at equilibrium. 2. no mutation 3. no genetic drift 4. no migration 5. no natural selection
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| What does 2pq mean? | heterozygous frequency, aka carrier frequency
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| q2 is the affected frequency, it's usally...? | homozygous recessive
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| What is the phenotypic ratio of a dihybrid cross? | 9:3:3:1 Pheno for mono is 3:1
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| What casues independent assortment? | crossing over (meiosis)
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| What are some clues that a pedigree is exhibiting an autosomal recessive inheritance? | tends to skip generations, and horizontal transmission (multiple siblings affected) both parents must be carriers `
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| An pedigree of autosomal dominant inheritance usually do not skip generations, why? | because it is dominant, carriers (heterozygotes) are affected, only need one allele. vertical transmission
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| A pedigree without any distinctive pattern that declines from generation to generation is likely expressing? | multifactorial inheritance
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| What is bile synthesis regulated by? | The 7-a-hydroxycholesterol is feedback inhibited by high levels of bile salts
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| How are dietary cholesterols delivered to adipocytes? | chylomicrons
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| How much of your bile acids to you reabsorb, how would you decrease this? | you reabsorb 95% of them, you could use bile sequestering drugs to decrease amt absorbed thereby increasing the amount of cholesterol you are getting rid of.
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| Who gets dibs on triglycerides before adipose? | skeletal muscle
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| when you break down AA's you get 2 things, what are they? | carbon and nitrogen, use the carbon, lose the nitrogen
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| What is the phenotype for codominance? | 1:2:1 same goes for semidominance. Codominance ex is blood types AB. semidominance is like the pink flower from red and white parents.
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| If you remember one enzyme involved in steroid synhthesis it is? | CYP11A. it is the rate limiting step and happens very early in the pathway so a problem there screws up everything else.
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| A tumor affecting the zona fasciulata of your adrenal gland would impair synthesis of what steroid? | cortisol, glucocorticoid.
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| Aldosterone only has one route to synthesize it, what part of the adrenal gland does this? | zona glomerulosa, think CYP21 and the CYP11B's
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| The other zone, zona reticularis? | DHEA, converted to testosterone and estrogen in the peripheral tissues
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| What all effects cortisol synthesis, besides CYP11A? | ACTH. 4 Neurotransmitters, Ach (up), 5-HT (up), NE(up or down), GABA(down). Stress also induces Cortisol synth. **and Neg feedback to inhibit
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| What does ACTH do? | ACTH induces the adrenal cortex to synthesize glucocorticoids, mineral corticoids and the androgen precursor dehydroepiandrosterone (DHEA).
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| What does ACTH do? | ACTH induces the adrenal cortex to synthesize glucocorticoids, mineral corticoids and the androgen precursor dehydroepiandrosterone (DHEA).
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| What function does cortisol inhibit? | immune system. lymhocytes, macrophages, monocytes and neutrophils
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| Too much Cortisol causes? Too little cortosol causes? | too much (hypercortisolism) and you get Cushings. too little and you get Addisons
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| What effect do glucocorticoids have on glucose? | Increase gluconeogenisis (prolong effect of glucagon and epi)Increase glycogen synthase. inhibit glucose utilization
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| What would you see in someone with Addison's? | Hypoglycemia, anorexia, nausea, vomitting, hypotension, hyponatremia, *hyperpigmentation* Too much ACTH b/c no cortisol to shut it off.
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| What is StAR? | steroidogenic acute regulatory (StAR) protein. it regulates cholesterol import into the mitochondria.
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| What is yet another way to regulate glucocorticoid synthesis? | regulate transcription of the protein, ie 5 carpenters vs. 20.
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| Mineralocorticoids | Aldosterone, think BP regulation
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| What zone of the adrenal gland does aldosterone come from? | zona granulosa
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| How does primary aldosteronism present? | HYPERtension, fatigue, loss of stamina, weakness, lassitude, polyuria, headaches, HYPOkalemia*
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| The primary control of aldosterone is via rennin/angiotensin. then Na and K. How does too much aldosterone cause hypertension? | High aldosterone means you are retaining too much sodium which leads to fluid retention-->increases ECFV--->increased cardiac output. An increase in Na means more Ca leaving the cell and causing vascular smooth muscle contraction. Also ACTH and Dopamine*
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| With Mineralocorticoid deficiency what would you expect your levels of Na and K to be? | Opposite of priamry aldosteronism. HYPOnatremia and HYPERkalemia. Would also see dehydration, hypotension, acidosis.
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| What is synthesized in the zona reticularis? | DHEA and androstenedione. They are converted to the active androgenic hormones testosterone and dihydrotestosterone in peripheral tissues.
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| Getting from cholesterol to DHEA and adrostenedione uses some shared enzymes, what are they? | CYP17 and 3-beta HSD
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| What are the 2 enzymes used to get androstenedione to the active androgenic hormones? | aromatase and 17 beta HSD
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| What two hormones would a lack of CYP17 directly effect? | cortisol , androstenedione (in turn estradiol and testosterone)
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| congenital adrenal hyperplasia is caused by what? | decreased cortisol and decreased aldosterone. So low cortisol=no control on ACTH, its high. Labs would be consistent with aldosterone deficiency (hyponatremia, hyperkalemia) CYP21 and CYP11B are involved in this pathway
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| In females what peripheral cells are invloved with the sex hormones? | Theca and Stroma cell primarily secrete androgens. Granulosa cells=estrogens. Corpus Luteum=progesterone. These are regulated by FSH via aromatase.
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| Leydig cells do what? | produce testosterone from androstenedione, then send it to the sertoli cells (testicle)Stimulated by LH from ant. pituitary
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| What enzyme is involved in the conversion of cholesterol to pregnenolone? | CYP11A.
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| If you see 17 a-Hydroxysomething... | CYP17 was probably involved.
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| What does LH = | sex steroids*****************
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| Which zones does ACTH regulate? | ACTH primarily regulates the zona fasciculata and the zona reticularis.
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| The enzyme responsible for the conversion of Pregnenolone to Progesterone is: | 3-beta-HSD (3-beta-hydroxysteroid dehydrogenase)
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| The two enzymes that are shared by the synthesis of aldosterone and cortisol synthesis are: | CYP21 (21-alpha-hydroxylase) CYP11B (11-beta-hydroxylase)
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| The enzyme responsible for the conversion of testosterone to Estradiol is: | Aromatase
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| The enzme responsible for the conversion of Pregnenolone to DHEA is: | CYP17 (17-hydroxylase)
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| What organs are involved in vitamin D synthesis? | skin, liver and kidney
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| What regulates Vitamin D synthesis? | PTH
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| The majority of the cholesterol used for steorid synthesis is obtained: | LDL
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| Stress is responsible for activating or inhibiting the HPA axis | Stress is responsible for activating or inhibiting the HPA axis
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