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Boards II > Biochem > Flashcards

Biochem Flashcards

1
Q

pre-pro sequence degradation

  • when is pre degraded: what is it replaced
  • when is pro degraded; function
  • when is pro not degraded, what is its pro?
  • how to send protein to lysosome; what happens w/o
A
  • after protein enters RER -> will add cysteine on end
  • after protein enters Golgi -> helps with folding and packaging
  • insulin, it is c-peptide
  • add mannose 6 phosphate, protein will get exocytosed
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2
Q

I cell disease

  • what happens
  • mutation
  • sxs
  • prognosis
  • looks like, dx
A
  • mannose 6 phosphate
  • AR, deficiency of GLC-NAC phosphotransferase
  • coarse facial feature, hepatomegaly, splenomegaly, club foot, growth retardation
  • die by 10 yrs of age
  • hurlers, aminoassay
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3
Q

How to send something to Mito

- accompanied by

A
  • add short end terminal sequence

- heat shock protein 70

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4
Q

Recptors

  • alpha 1
  • alpha 2
  • B1
  • B2
  • V1
  • V2
A
  • SM contraction, Gq
  • decrease pre-synaptic release of NE; Gi
  • in crease CO, HR, stroke vol, increase Renin from JG cells; Gs
  • SM relaxation; Gs
  • vasoconstriction
  • Aquoporin II channels
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5
Q

G- alpha- s pathway

- enzyme needed

A
  • AC-> cAMP -> PKA

- mg

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6
Q

cGMP

  • ligand
  • pathway
A
  • NO

- activate GC -> cGMP -> PKG -> SM relaxation -> vasodilation

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7
Q

Ca as second messenger

  • IP3- DAG: pathway ; used in
  • Ca-Calmoduin
  • Ca
A
  • galpha -> PLC -> PIP2 -> Ip3 -> binds to SR and releases Ca and DAG -> PKS ; all hypothalamic hormones except CRH, and SM contraction w/ Nor-epi / epi
  • SM contraction by distention
  • 2nd messenger for gastrin
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8
Q

Ca-Calmodulin

  • pathway
  • how is it activated
A
  • Ca binds to calmodulin -> activates MLCK -> myosin ATPase active -> cross bridging
  • stretch; in uterus will be by vol of baby
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9
Q

Tyrosine Kinase

  • used as
  • needs
  • what med inhibits
A
  • 2nd messenger for all growth factors
  • mg
  • ematinib (ALL, CML, GIST)
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10
Q

Phosphodiesterase

  • what is it
  • what happens when blocked
  • popular drug that does this: other actions
  • platelet
  • penis: what happens, meds, not allowed to take
A
  • degrades cAMP and cGMP
  • increased cAMP and cGMP -> vasodilation
  • caffeine; also blocks adenosine receptors to prevent drowsiness which causes increase in Epi which causes increase in symp, which causes increase in dopamine and causes euphoria
  • PDE is on platelets and can therefore be used to prevent platelet aggregation
  • PDE5 found in corpus cavernosum and when blocked allows for dilation for erection ; sildenafil and tadalafil; nitro
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11
Q

Collagen

  • what is it
  • SCAB
  • what is needed
  • synthesis
  • most common AA in collagen
  • wound contraction
  • simple scarring
  • desmoplasia; desmoblast
  • keloid: what is it, seen in, sequelae; tx
A
  • most abundant protein in body
  • skint, CT, arteries, BM
  • vit C for hydroxylation of proline and lysine
  • synthesis of pre-pro alpha chain-> pro alpha chain is made -> hydroxylation of proline and lysine -> glycosylation of hydroxylysine -> 3 pro-alpha chains linked by hydrogen bonds -> triple helix is packaged into vessicle and secreted out -> procollagen peptidase cleaves ends -> collagen goes into fibril -> mult fibrils used
  • guanine (every 3rd AA) and proline (responsbile for kinks/ bends)
  • myofibrils
  • fibroblasts
  • process that produces scar tissue; benign tumor made up of desmoblast
  • excessive collagen deposition post insult; african, asian, hispanic; if try to remove will grow back even bigger; excise it and then inject steroids to reduce the scarring OR remove and take straight for radiation on area
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12
Q

Ehler- Danlos

  • mutation
  • what happens
  • sxs
A
  • AD or AR caused by def of lysyl hydroxylase or pro-collagen peptidase (more common)
  • faulty collagen synthesis leads to highly stretchable skin
  • hyper elastic skin, hypermobile joints, easy bruising (bc decreased strength and support of vasc)
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13
Q

Osteo Imperfecta

  • mutation
  • sxs
A
  • AD, lysine replaced with bulky AA

- thin skin, brittle bones, blue sclera can see choroidal v

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14
Q

Collagen Vasc Dx

  • CREST
  • Scleroderma
  • Progressive systemic sclerosis
  • Lupus
  • RA
A
  • anti centromere
  • anti-SCL7
  • anti scl7
  • anti - DsDNA, anto-smith, anti phospholipid antibody
  • anti- CCP
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15
Q

Keratin

  • what does it do
  • contains lots of
  • seen in
  • bonds
  • stain for
A
  • tensile strength
  • cysteine
  • outer layer of skin, hair, nails, cornea
  • disulfide, easily broken w/ heat
  • tumor of epi origin
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16
Q

Elastin

  • used for
  • contains
  • protein and links
  • lysyl oxidase
  • main Dx
A
  • stretch and recoiling
  • hydroxy proline
  • tropoelastin linked by desmosine and isodesmosine
  • reaction that links tropoelastin need Copper
  • Marfan Dx, FBN1 -> fibrillin
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17
Q

Elastase

  • what is it
  • protects from
A
  • enzyme that destroys elastin

- a- 1- antitrypsin protects lungs and liver from elastase

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18
Q

AA

  • glycine: size, function in CNS
  • aromatic AA: 3, recognized by
  • basic AA: 2; structure, recognized by
  • acidic AA: 2; function; structure
  • sulfur containing: 2; function, hormones
  • AA that form N bonds: 3
  • AA in O bonds: 3; contain
  • branched chain AA: 3, pathology, converted into
  • tryptophan: precursor for, drug
  • tyrosine: function, made from
  • ketogenic
  • glucogenic: function, 7 not
  • gluco and keto: PITTT
  • essential: PVT TIM HALL
A
  • smallest; inhibitory NT of SC (opens up cl channels in cells hyper-polarizing it)
  • phenylalanine, tryptophan, tyrosine, recognized by chymotrypsin
  • lys, arg -> contain extra NH3 that is positively charge making them want to go to negative charge; recognized by trypsin
  • aspartic a and glutamic a; stimulate NMDA; have extra neg charge and will more towards positive
  • cysteine and methionine; help form di-sulfide bonds (hormones: prolactin, inhibin, growth hormone, insulin)
  • asparagine and glutamine
  • serine, threonine, tyrosine; contain hydroxy groups on side chains
  • leucine, isoleucine, valine; Maple Syrup Urine Dx; acetyl CoA or succinyl CoA -> can be used for energy
  • niacin and serotonin; sumatriptan -> used for migraines
  • makes dopamine -> NE -> epi; phenylalanine;
  • leucine and lysine; will be turned into ketone bodies via ketogenesis when there is extreme starvation
  • can be converted into glucose via gluconeogenesis;
  • phenylalanine, isoleucine, tryptphan, tyrosine, threonine
  • phenylalanine, valine, threonine, tryptohpan, isoleucine, methionine, histidine, arginine, lysine, leucine
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19
Q

AA related

  • PKU
  • Albinism
  • Alcaptonuria
  • maple syrup urine dx
  • cystinuria
A
  • def of phenylalanine hydroxylase; accumulation of phenylalanine and cant convert to tyrosine
  • deficiency of tyrosinase; cant turn DOPA into melanin
  • homo1-2 doxygenase; cant break down phenylalanine or tyrosine
  • deficiency of branched-chain alpha-keto acid dehydrogenase; cant break down leucine, isoleucine, valine
  • SLC3A1 and SLC7A9; cannot reabsorb Cysteine, Ornithine, lysine, arginine (COLA)
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20
Q

Anabolic vs Catabolism

  • occurs
  • 3 pathways occur in both
A
  • A: cytoplasm, C: mito

- gluconeogenesis, urea cycle, heme

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21
Q

Source of energy

  • glucose
  • protein/fat
  • how many calories
A
  • 40% energy
  • 30 % each
  • glucose and protein are 4 cal per gram and fat is 9 calories per gram
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22
Q

Energy Use: normal, stressful, extreme stress

  • brain
  • heart
  • muscle
  • RBC
A
  • glucose, glucose, ketone
  • FFA
  • glucose, FFA, FFA
  • glucose
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23
Q

How long will energy last

  • plasma gluc
  • liver glycogen
  • proteolysis
  • lipolysis
  • ketogenesis
A
  • 2-4 hours
  • 24-48 hrs
  • start at 36 hours
  • start at 36 hrs
  • after 36 hrs
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24
Q

glut transporters

  • 1
  • 2
  • 3
  • 4
  • 5
A
  • RBC/ CNS; responsible for basal glucose transport
  • in hepatocytes and pancreatic beat cells; reg release of insulin
  • kidney, brain, placenta
  • adipocytes and skeletal muscle
  • fructose transport; GI and spermatocytes
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25
Q

Glycolysis

  • ATP
  • NADH
  • pyruvate
  • occurs in
  • F6P to F-1,6 BP/ rate limiting eznyme;
  • what happens when there is increased activity
A
  • 2
  • 2
  • 2
  • cytoplasm
  • enzyme used is PFK1 (RLE); PFK1 is activated by AMP and build up of citrate inhibits;
  • PFK1 doesnt work fast enough and there becomes build up of F6P which is turned into F-2,6- BP by PFK2 (activated by insulin) which will increase the amount of PFK 1 made so that more F6P can be turned into F- 16- BP
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26
Q

Creation of 2,3 - BPG

  • what happens
  • when
  • sequelae
A
  • shunt G -1,3- BP to 2,3 BPG instead of it being made into phosphoglycerate
  • during ischemia
  • increase O2 delivery to tissue by decreasing affinity of hemoglobin for O2; will fix hypoxia and allows for G-1,3- BP to go back to phosphoglycerate
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27
Q

Gluconeogenesis

  • location
  • controlled by
  • irreversible steps: PEP
  • irreversible steps: F 1,6 BP
  • irreversible steps: G6P
  • what else can DHAP make
  • other source of pyruvate
  • metformin: MOA, SE
A
  • liver, adrenal medulla
  • epi and glucagon
  • PEP to pyruvate, pyruvate must be turned into OAA in mitochondria and OAA goes back into cytoplasm to be made back into PEP by PEP carboxylase
  • F - 1,6 - BP back into F-6-P by Fructose 1-6- biphosphatase
  • G6p to glucose with G- 6- phosphatase
  • glycerol, used in tri- glyceride; so glycerol can be made back into DHAP for gluconeogenesis if needed
  • alanine, glutamate
  • inhibits pyruvate carboxylase -> cannot turn pyruvate to OAA -> inhibit hepatic production of glucose; lactic acidosis
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28
Q

Cori Cycle

  • how does it work
  • ATP
  • what happens w/ contd low O2
A
  • 2 lactate -> 2 pyruvate -> glucose -> to muscle -> glucose -> 2 pyruvate -> no O2 causes -> 2 lactate -> back to liver
  • loss of 4 ATP
  • will be made into lactate and go into lactic acidosis
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29
Q

Conversion of OAA to leave mito

  • PEP: enzyme
  • aspartate: enzyme, shunt, needs
  • malate: enzyme; what else happens; what happens in cytoplasm
A
  • mito PEPCK; goes back into gluconeogenesis
  • aspartate transaminase; leaves through malate- aspartate shunt but needs glutamate and alpha KG
  • malate DH; NADH to NAD; oxidized back in cytoplasm
30
Q

Galactose Metabolism

  • how does it work
  • galactosuria: deficiency of, sxs, not bad bc
  • galactosemia: deficiency of; bad bc; management
A
  • galactose to galactose 1 phosphate (galactokinase) to glucose 1 phosphate (G1P uridyl transferase) to Glucose 6 phosphate
  • galactokinase def; pyuria, polyuria, polydipsia; filled in by hexokinase
  • def G1P uridyl transferase; will be converted to sorbitol or galacticol -> causes nerve damage and cataracts; switch to soy milk
31
Q

Fructose Metab

  • pathway
  • RLE
  • Fructosuria: deficient, sxs, not bad bc
  • Fructosemia: deficient, what happens, how different from galactose
A
  • fuctose to F1P -> GAP and DHAP -> into glycolysis
  • aldolase B from F1P to GAP and DHAP
  • def fructokinase -> fructose spills into urine; hexokinase fills in
  • def aldolase B; accumulation of F1P; 6 mnths or later when fruits introduced
32
Q

Lactic Acid

  • how is it made
  • hyoxia induced
  • iso enzyme: LDH1, 2/3, 4/5
A
  • pyruvate
  • no O2 so lactic acid is made and then have hyper ventilation so 2 acidoses on top of eachother
  • cardiac, RBC/muscle, lungs/liver/kidney
33
Q

Pyruvate Dehydrogenase

  • E1
  • E2
  • E3
  • 5 factors needed
A
  • TPP (decarboxylate),
  • Lipoic Acid (accepts 2 carbon unit -> becomes reduced and adds to Actyl CoA)
  • FAD and NAD -> needed for redox of lipoic acid so it can be reused
  • TPP (thiamine), Lipoic Acid (vit B4), CoA (Vit B5), FAD (B2), NAD (B3)
34
Q

Alcohol and pyruvate

  • deficient in -> sequelae
  • what happens instead
A
  • thiamine -> no TTP -> no E1

- pyruvate cannot be turned into acetyl CoA -> instead turned into lactic acid

35
Q

Alcohol metabolism

  • cycle
  • side product produced; what happens
  • sxs; caused by
  • disulfram: MOA, other meds cause similar effects
  • methanol: metabolized into, causes
  • ehtylene glycol: metabolized into, causes
  • Tx of methanol poisoning: med vs drip
A
  • ethanol -> acetylaldehyde -> acetate
  • NADH; helps to convert pyrvate to lactic acid, or can be used as reducing agent in FA synthesis (make more fat)
  • acetylaldehyde is gastric irritant and will cause n/v
  • blocks acetylaldehyde DH and causes build up of acetylaldehye-> EtOH deterant (metronidazole)
  • metabolized into formic acid; snow storm vision and then will be blind
  • metabolized into glycoxylate; kidney stones
  • Fomepizole: antagonizes alcohol dehydrogenase OR ethanol drip bc it has higher affinity than methanol and ethylene glycol
36
Q

B def and seuelae

  • B1
  • B2
  • B3
A
  • dry beri beri (nerve damage and nystagmus), wet beri beri (dry + heart failure), wernicke (beri beri, + short term memory loss) and kosakoff (antero and retorgrade amnesia, confabulation)
  • angular cheilitis
  • pellagra
37
Q

Pyruvate to Alanine

  • when
  • via
A
  • occurs anaerobically

- ALT

38
Q

Citric Acid Cycle

  • used to
  • RLE
A
  • make 3 NADH and 1 FADH2 to be reduction power in ETC

- isocitrate DH; iso citrate to alpha ketoglutarate

39
Q

NADH in cytoplasm

  • cant
  • how to get in
  • malate- asp shuttle
A
  • get into mito
  • malate-asparta of G3P shuttle
  • OAA + NADH into malate then into mito -> malate into OAA + NADH -> NADH to ETC and OAA + glutamate into alpha KG
  • glutamate will be turned into Aspartate and go back into cytoplasm and alpha KG go back into cytoplasm -> aspartate and alpha KG meet up and turned back into OAA and glutamate
40
Q

G3P shuttle

  • needs
  • how does it work
  • when is it used
A
  • 2 ATP
  • NADH + DHAP -> NAD + G3P -> G3P + FAD -> FADH2 + DHAP -> FADH2 goes into mito and DHAP is reused
  • during growth spurt or puberty -> when we need extra NADH
41
Q

Methylmalonic Acidemina

  • cycle
  • BCAA def
  • Vit B12 def
A
  • isoleucine and valine -> proprionyl CoA -> methomalonyl CoA -> Succinyl CoA (needs B12) -> TCA
  • cant turn isoleucine and caline into proprionyl CoA
  • cant turn methylmalonyl CoA into succinyl CoA and back up damages the dorsal tract causing nerve sxs
42
Q

Poison to ETC

  • Aspirin, thermogenin (found in brown fat), and 2-3 dinitrophenol (anti-septic and pesticide): main function,
  • Rotenone
  • Antimycin A
  • Cyanide: what happens, sxs, tx
  • carbon monoxide
  • Oligomycin
A
  • uncoupplers -> opening of passive H+ channel between inner and outer mito membrane -> bypasses ATP synthase
  • inhibits e transport of complex 1; pesticide
  • inhibits e transport of complex 3
  • inhibits e transport of complex 4; dizziness, headache, n/v, tachy cardia, tachypnea; hydroxycobalamin (cobalt will bind to cyanide), met-hemoglobin (binds to cyanide)
  • block ETC and binds to myoglobin causing muscle damage; confusion, muscle pain, cherry red skin
  • direct inhibition of ATP synthase
43
Q

AA catabolism

  • when is it used
  • transmainase
  • need
  • how: pyruvate
  • how: AKG
  • how with OAA
  • 3 AA that can be brokwn down and immediately used
A
  • after glucose used up, before fat
  • GGT (in mito), AST, ALT
  • Vit B6
  • AA + pyruvate (ALT) -> alanine + 2c molecule -> 2c molecule into glycolysis or krebb cycle
  • AA + AKG (GGT) -> glutamate and 2c molecule
  • AA+ OAA (AST)-> aspartate + 2c mol
  • alanine -> pyruvate, isoleucine -> acetyl CoA, valine -> succinyl CoA; OAA, fumerate, alpha KG
44
Q

Fat Metoblism

  • how many NADPH do you use
  • how many ATPs do you use
  • what happens with odd number
  • stimulated by
  • Short and medium vs long chain
A
  • number of carbons -2
  • number of carbons -1
  • 3 carbon FA (propionly CoA) turned into 4 carbon molecule that becomes succinyl CoA and dumped into TCA
  • glucagon -> hormone sensitive lipase -> mobilizes FA and sends to liver
  • short and medium corss freely into mito and long need CAT1-2
45
Q

Ketogenesis

  • when
  • how
  • product functions
  • management of ketoacidosis
A
  • synthesized by liver when excess acetyl CoA
  • acetyl coA -> acetoactyl CoA -> -> aetoacetate -> beta hydroxylate and acetone
  • beta hydroxylate -> fuel for brain; acetone will make pts breath smell like nail polish remover
  • hyrdate -> will cause acteone to be peed out then hydroxybuterate will be made into acetoacetate
46
Q

DKA

  • complication
  • making electrolyte correction
  • making glucose correction
  • caused by
A
  • hypovol, hyperkalemia, hypophos, hyponatermia, pain, elevated creatinine, decreased pH, HCO3 and CO2
  • for every 100mg/dL glucose is above 100 then Na is dilute 1.6 meq/ L
  • do not correct glucose more than 100 mg/ dL with insulin
  • infection, people didnt take insulin,
47
Q

Type 1 DM Meds

  • NPH and reg insulin
  • aspartat, lispro
  • glargine
A
  • lasts 12 hrs, peak 16; covers lunch, midnight or bedtime snack; lasts 6 hrs, peaks at 2 hrs; covers breakfast and dinner
  • only last 1 hour
  • steady dose for 24 hours
48
Q

The Samogyi Effect

  • what happens
  • why
A
  • early morning hypoglycemia leads to reactive hyperglyemia late in morning
  • bc leads to stimulation of epi and glucagon
49
Q

dawn phenomenon

  • what is it
  • time
  • manage
A
  • auto induced hyperglycemia caused by normal increase in epi, glucagon, cortisol, and growth hormone
  • 1 at 4 pm and other at 4 am
  • give early morning regular insulin
50
Q

Type 2 DM meds

  • sulfonylurea: MOA; secondary effects; AE; examples
  • biguinide: what is it; MOA; AE
  • alph gluco inhibitor: MOA, examples, AE
  • glitizone: MOA, AE
  • niglitnide: MOA, example, AE
A
  • increase beta cell insulin secretion; decrease haptic glucose output, increase insulin receptor sensitivity, inhibit potassium ATP channel; weight gain; glipizide, glyburide, glimepiride
  • metformin -> decrease hep glucose production, GI absorption and increase peripheral glucose uptake and utilization; lactiic acidosis, GI upset, renal failure and heaptic dysfunction
  • block enzyme that convert starch to sugar; acarbose and niglitol; GI upset
  • increased insulin receptor sensitivity by binding to PPR gamma (transcriptional reg for genes needed for glucose and lipid metabolism); hepato tox, edema
  • bind K channel like sulfonylurea but at different site; repaglinide; GI upset
51
Q

Glycogen Synthesis

  • when does it occur
  • controlled by
  • RLE
  • lasts
  • location for plasma
  • location for self
  • branching enzyme
A
  • well fed
  • insulin
  • glycogen synthetase; adds 8-10 glucose at alpha 1-4
  • 24- 48 hrs
  • liver and kidney
  • muscle
  • change from alpha 1-4 to alpha 1-6
52
Q

Glycogen Breakdown

  • phosphorylase
  • debranching
  • alpha 1-6 glucosidase
A
  • breaks down 1-4 bonds
  • removes alpha 1-6 linkage
  • removed glucoe immediately
53
Q

Glycogen Storage Dx

  • Von Gierke: enzyme, what happens, location, slinical findings
  • Pompe: enzyme, what happens, location, slinical findings
  • Cori: enzyme, what happens, location, slinical findings
  • Anderson: enzyme, what happens, location, slinical findings
  • McArdle: enzyme, what happens, location, slinical findings
  • HER: enzyme, what happens, location, slinical findings
  • Classic form: enzyme, what happens, location, slinical findings
A
  • gluc 6 phosphatase -> turns glucose 6 phosphate into glucose; liver and kidney; hypoglycemia, hyperlipid and urecmeia
  • alpha 1-4 glucosidase -> cant turn glycogen into glucose in lysosome; all organs
  • Debranching enzyme -> short branches and increased amount; liver and muscle; ; similar to von gierke but less severe
  • def of branching enzyme -> can make long branches but cant branch them; spleen and liver; cirrhosis of liver
  • phosphorylase -> muscle, can synthesize but cant break it down; cramping with muscle
  • phosphorylase in liver, increased amount, similar to von gierke
  • phosphofructokinase, muscle, normal strx w/ increased amount, similar to McCardle
  • phosphorylase kinase -> normal strx w/ increased amount, liver, mild hypoglycemia and mild hepatomegaly
54
Q

Pentose Phosphate Pathway (HMP shunt)

  • main function
  • other product
  • when
  • RLE
  • activated by
  • inhibited by
  • oxidative phase
  • non ox phase
A
  • make NADPH
  • ribose - 5- phosphate -> purine and pyrimidine synthesis
  • well fed state, glucose must be high and there must been gycogen synthesis already happening
  • G6P DH, G6p to 6 phospholguconate
  • G6P
  • R5P
  • generated NAPDH
  • gives us R5P and xylose 5 phosphate (4 carbon sugar)
55
Q

AA synthesis

  • when
  • how
  • transamination
A
  • plasma glucose has to be high and all metabolic needs must have been met
  • come from TCA through transamination
  • AA + alpha- keto- acid -> alpha- keto acid + AA; aplpha-keto-acids: pyruvate, OAA, alpha ketogluterate; AA: glutamate (bc carries nitrogenous waste)
56
Q

Transaminases

  • most important
  • AST/ ALT ratio
  • elevated AST and ALT
A
  • AST (cytoplasm and mito), ALT (cytoplasm) GGT (in mito)
  • alcohol -> 2:1, liver dx 1:!
  • hepatocyte injury
57
Q

Fatty Acid Synthesis

  • what is produced
  • saturated vs unaturated
  • omega FA
  • essential
  • what do we use
A
  • palmitic acid -> 16 c
  • no double vs double, all double must be 3 bond away from each other and cannot havy any double bonds after 6th carbon
  • named on location of double bone, omega 3 and 6
  • anything reater than 16 carbons
  • 2 NADPH, each round add 2 carbons, ATP = # carbons - 1
58
Q

Citrate Accumulation in cytoplasm

- what happens

A
  • allosteric inhibition of PFK1, activation of RLE of FA synthesis, gets divided into Acetyl CoA and OAA via lyase -> Acetyl CoA into fatty acid synthesis
59
Q

Formation of arachodonic acid

  • how
  • what is is made into
  • COX1
  • COX2
  • lipoxygenase
A
  • linoleic (omega 6)-> linolenic acid -> arachadonic acid through phospholipase A2
  • COX1, COX2, 5-lipoxygenase
  • homeostatic function
  • inflammation
  • 5- HPETE -> leukotriene -> vasoconstriction, increase vasc permeability, bronchospasm
60
Q

COX pathway

  • thromboxane
  • PGE2/ PGD2
  • PGF2
  • PGI2
A
  • increases vasoconstriction, increases platelet aggregation
  • vasodilates, increases vascular permeability
  • causes vasoconstriction, responsible for painful menstural cramps
  • vasdilation, inhibition of platelet aggregation
61
Q

Aspirin

  • what is it
  • baby
  • 650 or above
  • AE: GI, blood, kids, kidneys
A
  • irreversible blocker of cox pathway through acetylation
  • anti-platelet
  • anti - pyretic, anti- pain
  • GI uleration (bc prostaglandin), thrombocytopenia, cinchonism, reye (liver destruction -> leady to fatty liver), interstitial nephritis (toxic substances can cause damage to interstitium)
62
Q

NSAIDs

  • Indomethacin
  • Ibuprofen
  • Naproxen
A
  • used for gout and to close PDA
  • MC OTC NSAID
  • dysmennorrhea but holds onto Na
63
Q

Other Anti-platelets

  • GpIIb/IIIa inhibitors
  • clopidogrel
  • aspirin
  • dipyridamole
A
  • block GPIIb-IIIa receptor that is used to bind to fibrinogen
  • prevent ADP from binding back on platelet and activating it
  • inactivates COX and prevents ADP and TXA2 from being released and activating platelets
  • inhibits phosphodiesterase from increasing cAMP in platelets and activating COX
64
Q

Steroid

  • MOA
  • what happens
  • examples oral
  • example IV
  • produces surfactant
  • stimulate appetite in CA patients
  • nasal allergies
  • endometriosis
  • mast cell stabilizer: MOA and example
A
  • inhibit phospholipase A
  • kills eosinophils, t cells, macrophage migration, stabilizes mast cells (no histamine) and endothelium (no selectins or intigrins)
  • prednisone
  • methylprednisone
  • beclomethasone and betamethasone
  • megestrol
  • fluticaonse and momeatsone
  • danazol
  • will not degranulate, Cromolyn
65
Q

Leukotriene synthesis

  • MOA
  • MC
A
  • block leukotriene receptor or inhibit lipoxygenase pathway

- montelukast

66
Q

Triglyceride Synthesis

  • what does it do
  • location
  • starts w, add
  • 1 16 chain, 2 16 chains, 3 16 chain
  • modification
A
  • storage of FA chains
  • liver
  • glycerol 3 phosphate, 16 carbon chains
  • lysophosphatidic acid, phosphatidic acid, triacylglycerol
  • serine (phosphatidylserine), choline (phosphatidylcholine), ethanolamine w/ CDP
67
Q

Sphingolipid

  • what is it
  • sphingosine
  • sphingomyelin
  • ceramide
  • break down
A
  • long complex lipid made used by neuronal tissue
  • lipid based signaler
  • part of myelin sheath
  • role in apoptosis; add sugar -> will make cerebroside; + group of sugars -> ganglioside
  • lysosome and phagolysosome
68
Q

Cholesterol

  • component
  • RLE
  • activation
  • inhibition
A
  • membranes
  • HMG CoA reductase
  • HMG CoA
  • Dietary Cholesterol
69
Q

Cholesterol Meds

  • orlistat
  • ezetimibe
  • statins
  • niacin
A
  • block absorption of chol by inhibition of panreatic lipase; steatorrhea
  • decreases chol absorption by inhibiting it from crossing crossing brush border of small intestine; upregulation of LDL receptors and lower circulating levels; steatorrhea
  • most popular and widely used chol meds; inhibit HMG CoA reductase
  • last resort when other meds fail to produce satisfactory results; inhibit VLDL production in liver
70
Q

Urea Cycle

  • when does it occur
  • where
  • RLE
  • activator
  • pathway
  • what happens with liver failure
  • TX for urea with liver failure
A
  • anabolic and catabolic state
  • liver and collecting duct
  • carbamoyl phosphate synthase 1
  • NH4 and N-acetyl glutamate (excessive transamination activates RLE)
  • ammonia + HCO3+ 2 ATP (CPS1) -> Carbamoyl phosphate + ornthine -> citrulline -> out of mito -> argininosuccinate -> fumarate and arginine -> into mito -> back to ornthine to be used again
  • unable to properly partake in urea cycle
  • limit protein intake, and give neomycin (kills off urease positive bacteria to decrease urea); lactulose -> pulls ammonia out from brain and convert to NH4 allowing for excretion through feces

Boards II (20 decks)

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