UWorld 2 Flashcards
Part of brain responsible for
(a) Pupillary light reflex
(b) Oculocephalic reflex
(a) Pupillary light reflex mediated by upper midbrain. CN II brings signal to pretectal nuclei, communicates w/ Edinger-WEstphal nucleus to shoot out CN III fibers
- midbrain
(b) Oculocephalic (Doll’s eye) reflex mediated by horizontal eye center of the pons
Part of brain responsible for
(a) Gag reflex
(b) Corneal reflex
(a) Gag reflex: CN IX and CN X both in the medulla
(b) Cornel reflex: CN V and VII both in the pons
Part of brain that contains the majority of
(a) Dopaminergic neurons
(b) Serotonergic neurons
(a) Dopaminergic neurons in the substantia nigra
- involved in Parkinsons
(b) Serotonergic neurons (aka neurons that release serotonin) primarily located in the Raphe nuclei
Involvement in disease
(a) Caudate nucleus
(b) Locus ceruleus
(a) Caudate nucleus is part of the striatum (caudate plus putamen = striatum). Loss of ACh and GABA in the striatum = Huntingtons
(b) Locus ceruleus = contains NE-releasing neurons, potentially overactive in anxiety
Involvement in disease
(a) Nucleus basalis of Meynert
(b) Raphe nuclei
(a) Nucleus basalis of Meynert hold the cell bodies of cholinergic neurons which undersecrete ACh in Alzheimers
(b) Raphe nuclei houses serotonergic neurons which may undersecrete 5-HT in depression/anxiety
3 mechanism of actions of anti-emetics used for chemo-induced nausea
- 5-HT3 inhibitors = Onadestron
- Dopamine receptor inhibitors = Metocloprmaide
- Neurokinin 1 (NK1) inhibitor = Aprepitant, Fosaprepitant
The following are major virulence factors of what organisms?
(a) Polyribosylribitol phosphate
(b) Lecithinase
(a) PRP = virulence factor on the capsule of H. influenzae B (think epiglottitis)
- this PRP is conjugated to the toxoid vaccine = HiB vaccine
(b) Lecithinase (also called alpha toxin or phospholipase C) is the virulence factor of C. perfinges (gas gangrene)
Two bacteria whose toxins inhibit EF-2
Both Diptheria toxin and pseudomonas toxin ribosylate (and therefore inhibit) elongation factor 2 to kill cells
Explain why rocuronium is a better paralytic than succinylcholine in burn victims
Succinylcholine (depolarizing blockade) binds to nicotinic ACh receptors to depolarize the motor end plate, acts continuously b/c not degraded by ACh-ase. However this n-AChR are upregulated in burn victims (and crush victims) and are non-selective cation channels => along w/ Na+ outflux they can allow a dangerous outflux of K+ => hyperkalemia and lethal arrhythmias
So due to risk of hyperkalemia w/ succinylcholine, use rocuronium (non-depolarizing agent) in burn, crush, and denervating injury victims
27 yo M w/ foot pain after stepping on a nail
- imaging shows gas in the tissues
- Cx shows G pos rods
Mechanism of the toxin causing his pain
G pos rods causing gas gangrene = C. perfinges
C. perfinges toxin = lecithinase (also called alpha toxin or phospholipase C) that catalyzes splitting of phospholipids to cause cell lysis
Which class I antiarrhythmic is specifically helpful on ischemic myocardium
IB (Lidocaine, Mexiletine, Tocainide) is more selective for ischemic myocardium -IB has the lowest dependence of the class I, and ischemic myocardium spends the most amount of time in the inactivated state so that IB has time to bind
What class of antiarrhythmic:
(a) Flecainide
(b) Disopyramide
(c) Quinidine
(d Lidocaine
(e) Tocainide
(f) Propafenone
(g) Procainamdide
(h) Mexiletine
Recall: IC > IA > IB
(a) Flecainide = IC
(b) Disopyramide = IA
(c) Quindine = IA
(d) Lidocaine = IB
(e) Tocainide = IB
(f) Propafenone = IC
(g) Procainamide = IA
(h) Mexiletine = IB
Antiinflammatory cytokine
IL-10 = antiinflammatory cytokine
- inhibits Th1 cytokines
- reduces MHC II expression
- suppresses activated macrophages and dendritic cells
Main fxn of
(a) IL-1
(b) IL-5
(c) TNF-alpha
Main fxn
(a) IL-1- proinflammatory and fever induction
(b) IL-5 (by Th2 cells)- stimulates B cells and eosinophils
(c) TNF-alpha- promotes leukocyte recruitment and increases adhesion molecule expression on endothelium
Main fxn of
(a) IL-12
(b) IL-10
Main fxn
(a) IL-12 = secreted by macrophages to induce differentiate of Th1 and activate NK cells
(b) IL-10 = antiinflammatory that inhibits Th1 cytokines
Mode of inheritance
(a) Rett syndrome
(b) Hemophilia B
(c) Classic galatosemia
(a) Rett syndrome = X linked dominant
- no males b/c lethal for males in utero
(b) Hemophilia B (factor IX deficiency) = X linked recessive
(c) Classic galatosemia (absence of galatose-1-phosphate uridyl transferase) = autosomal recessive
Which fatty acids cannot be metabolized if there is a peroxisome defect?
Very long chain fatty acids or fatty acids w/ branching points at odd-number carbons cannot undergo mitochondrial beta-oxidation => metabolized by a special reaction in peroxisomes
So inborn error of metabolism of dysfunctional peroxisomes => neurologic defects from improper CNS myelination
4 lactose fermenters
Klebsiella
E. Coli
Enterobacter
Serratia
Pink colonies on MacConkey agar
How to differentiate the lactose non-fermenting, oxidase negative gram negative rods
Gram negative rods
Lactose fermenters: Klebsiella, E. Coli, Enterobacter, Serratia
Then non-lactose fermenters (white colones on MacConkey agar), split by oxidase test
- oxidase positive = pseudomonas
- oxidase negative dif by TSI agar
- -no H2S production = Shigella
- -H2S production (black color) = Salmonella and Proteus
Lactose-fermenting, indole positive gram negative rods
E. coliiiiiiii
Indole positive = can convert tryptophan to indole
-distinguishes from Enterobacter cloacae
2 MC clinical side effects of Lithium toxicity
- nephrogenic diabetes insipidus
2. hypothyroidism: pt p/w constipation, hair loss, wt gain, fatigue
Describe the histologic change from bronchi to bronchioles
At terminal bronchioles airway epithelium changes from pseudostratified ciliated columnar to ciliated simple cuboidal
Differentiate the location of the
(a) Cilia
(b) Goblet and mucous glands
(c) Cartilage
(b,c) Submucosal mucus and serous glands travel within cartilage, all of which terminate at the smallest bronchi => no goblet cells, glands, or cartilage in the bronchioles
(a) While cilia go down into bronchioles, terminate so not in alveolar ducts or alveoli
- presence of cilia beyond most distal mucus-producing cells prevents bronchiolar mucus accumulation and airflow obstruction
45 yo construction worker p/w fatigue, constipation x4 mo
-microcytic anemia w/ normal ferritin and serum iron
(a) Dx
(b) Peripheral blood smear finding
(a) Lead poisoning, Pb inhibits ALA dehydratase and ferrochelatase in heme synthesis pathway causing microcytic, hypochromic anemia
(b) Basophilic stiplling on peripheral blood smear