Biochem Flashcards
(70 cards)
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
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
3
Q
How to send something to Mito
- accompanied by
A
- add short end terminal sequence
- heat shock protein 70
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
5
Q
G- alpha- s pathway
- enzyme needed
A
- AC-> cAMP -> PKA
- mg
6
Q
cGMP
- ligand
- pathway
A
- NO
- activate GC -> cGMP -> PKG -> SM relaxation -> vasodilation
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
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
9
Q
Tyrosine Kinase
- used as
- needs
- what med inhibits
A
- 2nd messenger for all growth factors
- mg
- ematinib (ALL, CML, GIST)
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
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
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)
13
Q
Osteo Imperfecta
- mutation
- sxs
A
- AD, lysine replaced with bulky AA
- thin skin, brittle bones, blue sclera can see choroidal v
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
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
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
17
Q
Elastase
- what is it
- protects from
A
- enzyme that destroys elastin
- a- 1- antitrypsin protects lungs and liver from elastase
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
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)
20
Q
Anabolic vs Catabolism
- occurs
- 3 pathways occur in both
A
- A: cytoplasm, C: mito
- gluconeogenesis, urea cycle, heme
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
22
Q
Energy Use: normal, stressful, extreme stress
- brain
- heart
- muscle
- RBC
A
- glucose, glucose, ketone
- FFA
- glucose, FFA, FFA
- glucose
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
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
25
Glycolysis
- ATP
- NADH
- pyruvate
- occurs in
- F6P to F-1,6 BP/ rate limiting eznyme;
- what happens when there is increased activity
- 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
26
Creation of 2,3 - BPG
- what happens
- when
- sequelae
- 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
27
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
- 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
28
Cori Cycle
- how does it work
- ATP
- what happens w/ contd low O2
- 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
29
Conversion of OAA to leave mito
- PEP: enzyme
- aspartate: enzyme, shunt, needs
- malate: enzyme; what else happens; what happens in cytoplasm
- 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
Galactose Metabolism
- how does it work
- galactosuria: deficiency of, sxs, not bad bc
- galactosemia: deficiency of; bad bc; management
- 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
Fructose Metab
- pathway
- RLE
- Fructosuria: deficient, sxs, not bad bc
- Fructosemia: deficient, what happens, how different from galactose
- 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
Lactic Acid
- how is it made
- hyoxia induced
- iso enzyme: LDH1, 2/3, 4/5
- 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
Pyruvate Dehydrogenase
- E1
- E2
- E3
- 5 factors needed
- 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
Alcohol and pyruvate
- deficient in -> sequelae
- what happens instead
- thiamine -> no TTP -> no E1
| - pyruvate cannot be turned into acetyl CoA -> instead turned into lactic acid
35
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
- 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
B def and seuelae
- B1
- B2
- B3
- 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
Pyruvate to Alanine
- when
- via
- occurs anaerobically
| - ALT
38
Citric Acid Cycle
- used to
- RLE
- make 3 NADH and 1 FADH2 to be reduction power in ETC
| - isocitrate DH; iso citrate to alpha ketoglutarate
39
NADH in cytoplasm
- cant
- how to get in
- malate- asp shuttle
- 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
G3P shuttle
- needs
- how does it work
- when is it used
- 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
Methylmalonic Acidemina
- cycle
- BCAA def
- Vit B12 def
- 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
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
- 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
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
- 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
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
- 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
Ketogenesis
- when
- how
- product functions
- management of ketoacidosis
- 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
DKA
- complication
- making electrolyte correction
- making glucose correction
- caused by
- 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
Type 1 DM Meds
- NPH and reg insulin
- aspartat, lispro
- glargine
- 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
The Samogyi Effect
- what happens
- why
- early morning hypoglycemia leads to reactive hyperglyemia late in morning
- bc leads to stimulation of epi and glucagon
49
dawn phenomenon
- what is it
- time
- manage
- 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
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
- 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
Glycogen Synthesis
- when does it occur
- controlled by
- RLE
- lasts
- location for plasma
- location for self
- branching enzyme
- 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
Glycogen Breakdown
- phosphorylase
- debranching
- alpha 1-6 glucosidase
- breaks down 1-4 bonds
- removes alpha 1-6 linkage
- removed glucoe immediately
53
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
- 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
Pentose Phosphate Pathway (HMP shunt)
- main function
- other product
- when
- RLE
- activated by
- inhibited by
- oxidative phase
- non ox phase
- 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
AA synthesis
- when
- how
- transamination
- 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
Transaminases
- most important
- AST/ ALT ratio
- elevated AST and ALT
- AST (cytoplasm and mito), ALT (cytoplasm) GGT (in mito)
- alcohol -> 2:1, liver dx 1:!
- hepatocyte injury
57
Fatty Acid Synthesis
- what is produced
- saturated vs unaturated
- omega FA
- essential
- what do we use
- 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
Citrate Accumulation in cytoplasm
| - what happens
- 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
Formation of arachodonic acid
- how
- what is is made into
- COX1
- COX2
- lipoxygenase
- 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
COX pathway
- thromboxane
- PGE2/ PGD2
- PGF2
- PGI2
- increases vasoconstriction, increases platelet aggregation
- vasodilates, increases vascular permeability
- causes vasoconstriction, responsible for painful menstural cramps
- vasdilation, inhibition of platelet aggregation
61
Aspirin
- what is it
- baby
- 650 or above
- AE: GI, blood, kids, kidneys
- 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
NSAIDs
- Indomethacin
- Ibuprofen
- Naproxen
- used for gout and to close PDA
- MC OTC NSAID
- dysmennorrhea but holds onto Na
63
Other Anti-platelets
- GpIIb/IIIa inhibitors
- clopidogrel
- aspirin
- dipyridamole
- 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
Steroid
- MOA
- what happens
- examples oral
- example IV
- produces surfactant
- stimulate appetite in CA patients
- nasal allergies
- endometriosis
- mast cell stabilizer: MOA and example
- 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
Leukotriene synthesis
- MOA
- MC
- block leukotriene receptor or inhibit lipoxygenase pathway
| - montelukast
66
Triglyceride Synthesis
- what does it do
- location
- starts w, add
- 1 16 chain, 2 16 chains, 3 16 chain
- modification
- storage of FA chains
- liver
- glycerol 3 phosphate, 16 carbon chains
- lysophosphatidic acid, phosphatidic acid, triacylglycerol
- serine (phosphatidylserine), choline (phosphatidylcholine), ethanolamine w/ CDP
67
Sphingolipid
- what is it
- sphingosine
- sphingomyelin
- ceramide
- break down
- 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
Cholesterol
- component
- RLE
- activation
- inhibition
- membranes
- HMG CoA reductase
- HMG CoA
- Dietary Cholesterol
69
Cholesterol Meds
- orlistat
- ezetimibe
- statins
- niacin
- 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
Urea Cycle
- when does it occur
- where
- RLE
- activator
- pathway
- what happens with liver failure
- TX for urea with liver failure
- 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
