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128 Cards in this Set
- Front
- Back
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top 3 causes of meningitis over 60
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strep pneumo
gram negative rods listeria |
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what group of genes is responsible for skeletal development
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HOX genes
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what is the hallmark of a brainstem lesion?
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contralateral long tract involvement and ipso cranial nerve involvement
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what distinguishes lateral from medial brainstem lesions?
what distinguishes PICA from AICA? (CNs) |
if lose pain and temperature- is lateral (unless have hypoglossal involvement, then is medial medulla)
if lose hearing/tinnitus = AICA (cochlear nucleus, CN VIII at pons) if hoarse/lose gag reflex (nucleus acuumbens for IX), PICA/wallenburg syndrome/lateral medullary syndrome note that there is only 1 P in either PICA-lateral medullary/wallenberg syndrome, and AICA-Lateral Pontine syndrome |
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how distinguish wallenburg syndrome?
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among other deficits, will have contralateral body pain and temp loss with hoarseness/gag reflex/difficulty swallowing.
think "Mark WALLENBURG Likes Money (lateral medulla) and is no Pussy (PICA)" |
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what is exception to the pain and temp loss indicating a lateral brainstem lesion?
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medial medullary syndrome, but will have ipso hypoglossal nerve involvement to diagnose
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hemianopsia with macular sparing
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PCA
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blood vessel infarct: CNIII lesion
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posterior communicating artery
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blood vessel infarct: bitemporal hemianopsia
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anterior communicating artery
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stroke lesion:
general sensory and motor dysfunction, aphasia |
anterior circle of willis
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stroke where can cause coma
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posterior circle of willis (as well as CN deficits, ataxia, neglect)
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locked in syndrome comes from stroke of
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basilar artery
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stroke lesions:
CNIII lesion (strabismus- down and out) vs CNIII lesion and contra hemiparesis |
CNIII only- post. communicating artery (smaller part of PCA)
CNIII and contra hemiparesis- paramedian branches of PCA (Bigger part of PCA) (Weber's) |
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charcot-bouchard aneurysms seen where, in what condition
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in thalamus and basal ganglia, associated with HTN
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atheroscleroic ischemic brain infarct will eventually result in
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cavity with reactive gliosis border
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for stroke, what is use of CT? MRI?
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CT used first to see if hemorrhage (will pick up, if not hemorrhage and less than 3 hours can push tPA. will show ischemia, but only after 1 day)
if want to see ischemia before 1 day, do MRI |
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foramen of monroe
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connects lateral ventricles to 3rd ventricle
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dementia, ataxia, and urinary incontinence in elderly, must rule out
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normal pressure hydrocephalus (stretching corona radiata fibers)
DOES NOT INCREASE SUBARACHNOID SPACE VOLUME |
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young obese female with daily headaches worse in morning, papilledema?
complication? 3 possible drug causes? |
pseudotumor cerebri
(increase in CSF pressure without ventricular dilation) can get vision loss can be caused by vit A, tetracylines, corticosteroid withdrawal |
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marker for lumbar puncture
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anterior superior iliac crest
(at level of L3-L5) |
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MS damages what
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oligodendrocytes (demyelination in CNS and spinal cord, can see periventricular plaques)
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do what to diagnose MS (2)? how treat an acute attack?
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oligoclonal bands, MRI (gold standard) of brain and spinal cord
give acute steroids |
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what gene and product are implicated in ALS?
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superoxide dismutase 1 (SOD1)
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what part of cell is dysfunctional in friedrich's ataxia?
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mitochondria
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5 hereditable causes of ataxia:
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Friedrichs ataxia
hereditable vit.E deficiency ataxia- telngectasia (poor eye following) metachromatic leukodystrophy wilson's disease |
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what brainstem nucleus provides visceral sensory information about taste, barorecetors, gut distention?
what brainstem nuclei innervates pharynx, larynx, upper esophagus? what brainstem nuclei sends autonomic fibers to the heart, GI, and lungs? |
visceral Sensory info- Nucleus Solitarius (VII, IX, X)
motor info to throat- Nucleus ambiguus (IX, X, XI) autonomic stimulation to heart, lungs, GI- Dorsal Motor Nucleus (Misnomer) |
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anterior hip dislocation can damage what nerve?
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obturator
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tibial nerve can be damaged by trauma to what?
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knee trauma
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polio can damage what lower extremity nerve?
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superior gluteal
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tibial branch of sciatic nerve (upper leg) does what?
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innervates hamstrings- hip extension and knee flexion (biceps femoris, semitendinous, semimebranous)
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sacral plexus has what motor function?
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lateral rotation of thigh (inferior gluteal nerve does same)
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if weber test is more loud on patient's right, 2 possibilities
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Conduction hearing loss ON RIGHT (will be louder! rhine will have greater bone conduction)
sensorineural hearing loss ON LEFT |
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what is pretectal nucleus function in pupillary reflex?
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recieves info from optic tract, splits and delivers to both edingerwestphal nuclei (which output to parasymp. fibers in oculomotor nerve) for bilateral response
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pt shines light in left eye, produces bilat constriction. pt shines light in right eye, bilateral pupillary dilation. defect where?
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afferent pupillary defect (marcus gunn pupil)
optic nerve damage or retinal detachment |
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sudden onset of flashing lights indicates
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retinal detachment (can result in degeneration of photoreceptors--> vision loss)
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fast vs. slow macular degeneration cause
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slow ("dry")- fat deposits in retina
fast ("wet")- neovascularization |
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glaucoma vision loss
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starts peripherally, moves inward
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dementia associated with frequent falls and/or syncope?
hallucinations? |
lewy body dementia for both
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what is dark pigment in substantia nigra and locus ceruleus
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melanin
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where are hirano bodies seen?
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rod-like structures seen in hippocampus of Alzheimer's patients
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filamentous neural inclusions that stain with silver
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Pick bodies
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filamentous neural inclusions that stain with PAS and ubiquitin
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Lewy Bodies
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guillain barre CSF findings
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increased protein (AIDP and others) with normal cell count
causes papilledema |
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what viral brain disorder can occur after viral infection or vaccination?
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acute disseminated encephalomyelitis
-perivenular inflammation and demyelination |
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which seizure drugs are teratogens
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valproic acid
carmbazepine phenytoin |
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phenytoin mech and side effects
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na channel blocker
grows hair, gums, and fucked up baby (fetal hydrantoin syndrome) also SLE and steven-johnsons |
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what are the common side effects of all antiepileptics?
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diplopia, ataxia, sedation, dizziness, nystagmus
(because slows down CNS) |
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what seizure drugs can produce steven johnsons (along with sulfas and cillins and allopurinol)
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carbamazepine
lamotrigine phenobarbitol phenytoin ethosuxamide |
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what seizure drugs induce p450 (think of Queen Barb pneumonic
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phenobarbitol
phenytoin carbamazepine |
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2 hepatotoxic seizure drugs
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valproic acid (fulminant liver failure), carbamazepine
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which seizure drugs na channel blockers, calcium channel blockers, GABA potentiators?
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look at venn diagram p 431
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why do benzos cause poor sleep?
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decrease REM and stage 4 sleep
(so can be used for night terrors, sleep walking) |
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benzo, barb, etoh action site
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bind GABA(a)-R in allosteric site to open cloride channel
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what is first line for trigeminal neuralgia?
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carbamazepine (because pretty much seuzure of trigeminal nerve- shooting pain triggered by light touch)
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sumatriptan mech
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serotonin (5-HT) agonist
Sumotriptan-Serotonin (2 S's) cluster or migraines |
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women with migraine with aura, make sure they ARE NOT ON
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OCPs (thrombotic stroke)
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what is first line treatment for cluster headaches
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02 (oxygen)
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uncal herniation could compress what vessel?
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PCA (producing CONTRATERAL homomynous hemianopsia)
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which of these are ring enhancing, uniformly enhancing:
toxoplasma neurocysticercosis metastases lymphoma AIDS lymphoma abscess |
ring-enhancing:
toxoplasma abscess neurocysticercosis AIDS lymphoma metastases Uniformly enhancing lesion: -lymphomas -meningioma |
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1st line for myoclonic seizures
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valproic acid
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first line for peripheral neuropathy (a seizure drug)
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gabapentin
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vertigo, tinnitis, hearing loss, think of what?
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triad for meniere's disease
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what is mechanism of opioid receptor?
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open K+ channels and close calcium channels
inhibit release of NE, ACh, 5-HT, glutamate, substance P |
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2 causes of neuronal death in huntington's
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NMDA-R binding and glutamate toxicity
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butorphanol mech
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partial opioid agonist (like buprenorphine)
for pain with less addictive potential, but can cause withdrawal if on other opioids |
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tramadol mech
possible complication |
weak opioid agonist, NE and serotonin uptake inhbitor ("tram it all" in)
for pain decreases seizure threshold |
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which IV anesthetic causes decreased cerebral blood flow?
increased cerebral blood flow? |
decreased- thiopental (think decreased brain activity)
increased- ketamine (makes you hallucinate and dream- increased brain activity) |
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propofol mech for anesthesia induction
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potentiates GABA
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what is order of nerve fibers local anesthetics affect?
small/large, unmyelinated/myelinated |
pain goes first, then temp, then touch, then pressure
likes myelinated and small small myelinated, small unmyelinated, large myelinated, large unmyelinated |
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what is non-psychotic use of haloperidol
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huntington's
(dopamine receptor antagonist) |
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what is the endogenous receptor for the opioid receptors:
mu delta kappa |
mu- morphine
delta- enkephalin kappa- dynorphin |
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diphenoxylate is used for what?
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diarrhea (is opioid like loperamide)
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opioid commonly used in heart failure
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morphine (decreases pulmonary edema)
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what inhaled anesthetic produces nephrotoxicity
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methoxyflurane (meth, neph sound similar)
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long term use of propofol can cause
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pancreatitis (has high TG content)
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pramipexole, ropinerol, pergolide are
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dopamine agonists for parkinsons
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SAM:
main fxn made from what cofactors needed helps produce what 3 things |
give methyl groups (SAM is the METHYL donor man)
made from ATP and methionine cofactors needed- B12, THF 1. turned into homocysteine when gets rid of CH3 group 2. used to make phosphocreatine 3. turns NE--> Epi |
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what is activated carrier for:
a carbon group? CH3 group? CO2 group? aldehyde? |
1 carbon- THF
CH3 group- SAM CO2 group- biotin aldehyde- TPP |
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hexokinase vs glucokinase:
what is Km, Vmax for each? which is expressed in liver and beta islet cells? |
hexokinase (everywhere)
low Km (high affinity) low Vmax glucokinase (liver, beta islet cells) high Km High Vmax (for storage) |
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how does Glucagon effect levels of fructose-2,6-bisphosphate, and what is the overall effect
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Glucagon stimulates cAMP, which causes stimulates PKA. PKA phosphorylates fructobisphosphatase-2/phosphofructokinase-2 complex, which activates the fructosebisphosphatase-2 component. This decreases levels of fructose-2,6-bisphosphatase. that inhibits glycolysis by inhibiting phosphofructokinase-1 (the rate limiting enzyme for glycolysis), and stimulates gluconeogenesis
insulin does opposite (decreases cAMP) |
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what are the three main enzymes in glycolysis?
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hexokinase/glucokinase
phosphofructokinase pyruvate kinase |
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what metabolic disorder causes hemolytic anemia?
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pyruvate kinase deficiency, because RBCs cant operate Na/K ATPase, swell and lyse
(most succeptable to glucose decrease damage) |
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what enzymes does gluconeogenesis use to overcome:
pyruvate kinase? phosphofructokinase-1? glucokinase/hexokinase? |
pryuvate kinase:
-pyruvate carboxylase (using biotin) -PEP carboxykinase phosphofructokinase: -fructose-1,6-bisphosphatase glucokinase: -glucose-6-phosphatase |
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can both odd and even chain fatty acids serve as a glucose source?
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NO!
only odd-chain fatty acids (can go to propionyl-CoA and become succinyl-CoA) |
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3 places gluconeogensis can happen
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liver (main place)
kidney intestinal epithelium have gluconeogenic enzymes |
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what are the three main enzymes in glycolysis?
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hexokinase/glucokinase
phosphofructokinase pyruvate kinase |
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what metabolic disorder causes hemolytic anemia?
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pyruvate kinase deficiency, because RBCs cant operate Na/K ATPase, swell and lyse
(most succeptable to glucose decrease damage) |
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what enzymes does gluconeogenesis use to overcome:
pyruvate kinase? phosphofructokinase-1? glucokinase/hexokinase? |
pryuvate kinase:
-pyruvate carboxylase (using biotin) -PEP carboxykinase phosphofructokinase: -fructose-1,6-bisphosphatase glucokinase: -glucose-6-phosphatase |
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can both odd and even chain fatty acids serve as a glucose source?
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NO!
only odd-chain fatty acids (can go to propionyl-CoA and become succinyl-CoA) |
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3 places gluconeogensis can happen
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liver (main place)
kidney intestinal epithelium have gluconeogenic enzymes |
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glycogen breakdown problems:
what enzyme breaks down alpha 1,4 linkages in glycogen? deficit produces? what enzyme breaks down alpha 1,6 linkages? defict produces? |
alpha 1,4 - normal glycogen polymers
alpha 1-,6 (sex) - kinky branching glycogen phosphorylase (breaks down alpha 1,4 linkages) - deficit causes McARDLES debranching enzyme (alpha 1,6 glucosidase) - CORI's Disease |
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fasting hypoglycemia, hyerpuricemia, high blood lactate levels, hepatomegaly?
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Von Girke's disease
deficiency of glucose-6-phosphatase, so neither glycogenolysis or gluconeogenesis can occur. hepatomegaly from glycogen in liver |
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fasting hypoglycemia, hepatomegaly, increased glycogen in liver
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Cori's disease
from debranching enzyme deficiency (alpha-1,6-glucosidase, 1,sex for kinky linkages) can do gluconeogensis, but glycogenolysis is partially impaired |
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lysosomal 1,4 glucosidase deficiency causes what
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Pompe's disease
(defiency also called acid maltase) get cardmegaly and early death trashes the heart, liver, muscles |
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painful muscle cramps, myoglobinuria with exercise
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McArdles disease
glycogen phosphorylase deficiency |
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what cofactors are required for pyruvate dehydrogenase?
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TLC for No One
thiamine lipoic acid CoA FAD NAD same for alphaketoglutarate dehydrogenase (to succinyl-coA) |
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what is function of cori cycle?
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takes the Lactate produced in muscle, RBCs, and lactate goes to liver where it is made back into glucose
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what are the two main nitrogen carriers in the blood? what are their non-transportable forms?
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ALANINE CYCLE
glutamate and alanine both undergo transamination reactions to get NH4 to liver for urea cycle glutamate comes from alphaketoglutarate and gets amino group from amino acids alanine comes from pyruvate and gets amino group from glutamate |
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what cofactor must be present for transamination reactions in the alanine cycle?
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B6
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vomiting, rice-water, diarrhea, bad breath indicate poisoning with what? what is cofactor inhibited?
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arsenic
inhibits lipoic acid |
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a pyruvate dehydrogenase deficiency would present with what?
what would be built up? the condition can be congenital, or it can be aquired how? |
lactic acidosis (because can't go to TCA cycle, so alanine and lactate build up)
alcoholics due to B1 deficiency treat with high fats and leucine and lysine (ketogenic AAs) |
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leucine and lysine are used to treat what
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pyruvate dehhydrogenase deficiency
(purely ketogenic amino acids) |
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what is made in TCA cycle in terms of:
NADH FADH2 CO2 GTP ATP equivalents |
per acetyl-coA (so X2 for glucose)
3 NADH 1 FADH2 1 GTP 2 CO2 12 ATP |
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what are the three irreversible steps of TCA cycle
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citrate synthase
isocitrate dehydrogenase (rate limiting) alphaketoglutarate dehydrogenase |
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NADH produces how many ATP, FADH produces how many ATP, why different
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NADH= 3
FADH= 2 because FADH starts farther down ETC |
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2 examples of electron transport inhibitors
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CO
cyanide |
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aspirin toxicity causes hyperthermia how?
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uncouples electron transport chain, releases heat
normally H+ ions trapped in intermembrane space of mitochondria, but aspirin (and thermogeenin for brown fat) uncouple and let back into inner membrane space |
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what are functions of NADH vs NADPH?
(anabolic vs. catabolic) |
NADH- catabolic (used in glycolysis)
NADPH- used in anabolism as a reduction reactions (fatty acid synthesis, steroid synthesis, respiratory burst, p450, glutathione reductase) |
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HMP shunt:
occurs where in cell? how many ATP used/produced? what are products and rate limiting step or oxidative portion? products and rate limiting step of nonoxidative? 4 tissues it takes place |
occurs in cytoplasm, energy neutral! (no ATP needed or produced)
Oxidative: glucose 6 phosphate dehydrogenase produce NADPH and ribulose-5-phosphate Non-oxidative: TRANSKETOLASES ribose-5-phosphate (for nucleotide synthesis takes place in tissue that need reducing agents: -lactating mammary glands (fatty acid synthesis) -liver -RBCs (for glutathione reductase) -adrenal cortex (for steroid synthesis) |
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G6PD deficiency:
inheritance Why do Heinz bodies occur? what capacity is decreased? |
x-linked recessive
Heinz bodies are due to oxidized and aggregated hemoglobin (become bite cells when macrophages remove Heinz bodies) decreased NADPH makes it so that glutathione cannot stay reduced |
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jaundice, hypoglycemia, cirrhosis, vomiting with elevated fructose-1-phosphate level?
deficiency? rx? |
fructose intolerance
ALDOLASE B rx- avoid fructose and sucrose (glucose + fructose) |
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what is deficiency of essential fructosuria?
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fructokinase
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infantile cataracts, failure to track objects and develop a social smile
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galactokinase deficiency
more benign than classic galactosemia, some galacititol is still present but not as much |
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what is difference between lysosomal storage disorder eye problems and classic galactosemia?
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lysosomal storage disorders (Hurler's, scheies, I cell) = corneal clouding
classic galactosemia = infantile cataracts (of lens) |
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failure to thrive, jaundice, infantile cataracts, MR?
deficiency? rx? |
classic galactosemia
galactokinase-1-phosphate uridyltransferase rx- remove galactose, lactose (glucose + galactose) from diet - switch to soy milk formula galactose gets converted to galactitol |
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lactase deficiency: 2 forms
what causes the bloating, gas, abdominal cramping? |
age dependent/hereditary (African Americans, Asians) - loss of brush border enzyme
can also get after gastroenteritis don't break down in gut, bacteria highly ferment it and cause gas, bloating, cramping. diarrhea from osmotic load |
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where in cell is alcohol dehydrogenase? acetylaldehyde dehydrogenase?
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alcohol dehydrogenase- cytosol
acetylaldehyde dehydrogenase- mitochondria |
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alcohol inhibits what metabolic process and stimulates what metabolic process
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inhibits gluconeogensis (high NADH depletes pyruvate and oxaloacetate --> lactate and malate
fatty acid synthesis stimulated |
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excess acetyl-coA from fatty acid metabolism stimulates production of
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ketone bodies
starvation and DKA- oxaloacetate depleted for gluconeogensis alcoholism- NADH shunts oxaloacetate to malate both stall TCA, causing glucose and FFAs to go to ketone bodies |
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is oxidative phosphorylation used in 100 meter sprint?
what is used in a marathon? |
no 1000 meter sprint
100 meter- ATP, creatinine phosphate, anaerobic glycolysis in a marathon, FFAs and glycogen are used, glucose is conserved for the final sprint |
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after last meal, when does:
gluconeogensis begin? FFAs become used? glycogen stores run dry? ketones ramp up? |
in post-absorptive period, body uses glucose from liver and fatty acids from tissues
gluconeogensis starts after 4-6 hours glycogen stores run dry 10-18 hours ketone bodies become major factor 2 days in |
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what is rate limiting step for ketone body synthesis
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HMG-CoA synthase
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KNOW RATE LIMITING ENZYMES
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p 95
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ketone bodies in brain are metabolized to what
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2 molecules of acetyl-CoA
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what is the activated carrier for glucose
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UDP glucose
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how many ATP generated during aerobic metabolism? anaerobic?
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aerobic = 30-32
anaerobic= 2 + lactate |
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is - Gibbs exergonic or endogonic?
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spontaneous= exergonic
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how many days of starvation does the brain switch to dominantly ketones from glucose? muscle?
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brain- about 5 days (though still uses some glucose from the gluconeogenesis from the liver, but most going to RBCs)
muscle- trick question, always uses majority FFAs, but uses some ketones as well |
