UWorld Pics Flashcards
Name the 4 muscles of the rotator cuff
SITS
- supraspinatus
- infraspinatus
- teres minor
- subscapularis
Activity of opoid analgesia
- inhibits intracellular Ca2+ influx at presynaptic neuron
- stimulates K+ efflux at postsynaptic neuron
Differentiate type of virally-acquired resistance:
reassortment vs. recombination
Recombination = crossing over and homologous recombination btwn genes on chromosomes
Reassortment = when segmented viral segments exchange entire segments
Name mechanism by which a drug can exert chronotropic w/o inotropic effects (target which ion transporter)
Drug that can change HR (chronotropy) w/o altering contractility (inotropy) works at the nodal pacemaker cells and not at the ventricular cells
- so need to work on the If (funny current) of phase IV (present in nodal action potential and not ventricular action potential)
- b/c both use L-type Ca2+ channels during phase 2 and K+ rectifier in stage 3
- ventricular cells use rapid Na channels in phase 0
Differentiate structure injured in anterolateral vs. anteromedial humeral fracture
Anterolateral humeral fracture causes injury to the radial nerve
Anteriomedial humeral fracture causes injury to either (or both) brachial artery and median nerve
What structures do you cut thru for a surgical airway?
Cut thru the superficial cervical fascia and the cricothyroid membrane
-not any platysma or thyroid or cartilage (kinda the hole point is to find the place btwn the thyroid cartilage and cricoid cartilage to make the easiest incision)
Name the branches of the external carotid artery
From inferior to superior
Posteriorly: ascending pharyngeal, occipital, posterior auricular
Anteriorly: superior thyroid, lingual, facial, maxillary
Explain the role of fibronectin
(a) Role in malignancy
Fibronectin = part of the cellular adhesion complex
-integrin is a transmembrane protein that binds to intracellular matrix proteins (ex: actin) then connects outside cell to proteins such as fibronectin or laminin
Then fibronectin or laminin connect to ECM collagen
(a) Different integrins can lose ability to bind to fibronectin properly, giving cells malignant potential
What enzyme is responsible for
(a) Green discoloration of few day old bruises
(b) Conjugating bilirubin
(a) Heme –> (heme oxygenase) –> biliverdin
Biliverdin is green in color, so heme oxidase is responsible for greenish hue
Then biliverdin –> biliverdin reductase (in macrophages) –> unconjugated bilirubin
(b) UCB –> UGT (glucuronyl transferase) –> conjugated bilirubin
Then this conjugated bilirubin is excreted into intestinal lumen where bacteria act on it, creating urobilinogen which colors stool and urine
Name the structure that Meckel diverticulum arises from
Meckel diverticulum (true diverticulum containing all 3 layers of the abdominal wall) is 2/2 incomplete obliteration of the omphalomesenteric (also called vitelline) duct
-vitelline duct connects midgut lumen and yolk sac in early embryo
What enzyme catalyzes the first step of base excision repair?
(a) The third?
- Glycosylase cleaves altered base
- Endonuclease cleaves 5’ end
(a) 3. Lyase cleaves 3’ end - DNA polymerase fills single nucleotide gap
- Ligaseseals nick
BP, K+ status seen in
(a) 11-beta hydroxylase deficiency
(b) 21-hydroxylase deficiency
(c) 17-alpha hydroxylase deficiency
(a) 11-beta hydroxylase deficiency => deficient aldo and cortiso, but build up of deoxycorticosterone which is a weak mineralocorticoid => hypertension, hypokalemia, ambiguous genitalia
(b) 21-hydroxylase deficiency: no aldo or cortisol, no aldo deoxycorticosterone => hypotension, hyperkalemia, ambiguous genitalia
- mineralocorticoid deficiency predominates
(c) 17-alpha deficiency = aldo excess => hypertension, hypokalemia
Name key histologic feature of Graves disease
“Scalloping of colloid” materal: see pink material in the lumen not firmly up against follicular cells (see white btwn colloid and follicular cells)
-excess colloid in the lumen scallops up against follicular cells
Key urinalysis finding of primary hyperparathyroidism
Primary hyperparathyroidism: increased urinary cAMP
- PTH receptor medicated by Gs which activates adenylate cyclase (catalyzes ATP –> cAMP)
- so excess PTH effect on kidney = excess cAMP in renal tubules cells that gets excreted out in urine
3 layers of the adrenal cortex and what they produce
‘GFR’- “deeper you go the sweeter it gets”
Zona Glomerulosa- mineralocorticoid (aldo)
Zona Fasciculata- glucocorticoid (cortisol)
Zona reticulata- androgens
Distinguish which enzyme works on pyruvate when O2 is vs. is not present
O2 present: pyruvate makes the most ATP by conversion into acetyl coA by pyruvate dehydrogenase
O2 not present (ex: mesenteric ischemia): intracellular NADH accumulates and inhibits pyruvate dehydrogenase, pyruvate then shunted to make lactate by lactate dehydrogenase, regenerating more NADH
Distinguish microscopic appearance of the following types of kidney stones
(a) Calcium oxalate
(b) Triple phosphate
(c) Uric Acid
(d) Cystine
Microscopic apperance (in order of descending frequency of type of stone)
(a) Calcium oxalate: octahedron: diamoid w/ ‘X’ shape in middle
(b) Triple phosphate (Magnesium ammonia phosphate) stone: rectangular prism, “coffin lid” appearance
(c) Uric acid stones: yellow or red/brown, diamoid or rhomboid
(d) Cystine: flat, yellow hexagon
Actvity of glucokinase
Glucokinase phosphorylates Glucose –> G-6-P
- acts as glucose sensor, b/c has lower affinity for glucose than hexokinase so only takes glucose into pancreatic islet cell when serum glucose is high enough
- once serum insulin high enough, glucose taken into pancreatic islet by GLUT2 then converted into G6P by glucokinase so it stays inside the cell (G6P trapped inside cell while glucose is not)
Activity of pyruvate carboxylase
Pyruvate carboxylase catalyzes pyruvate –> oxaloacetate inside the mitochondria as a key step of gluconeogenesis
Differentiate the histologic features of inflammation seen in UC vs. Crohn Disease
UC: inflammation manifests as crypt abscesses = see neutrophils in the crypts of the SI (crypts are the downward protruding parts)
Crohn disease: lymphoid aggregates w/ non-caseating granuloma formation
Differentiate the gross pathologic features of UC vs. Crohn Disease
UC: ulcers are by definition mucosal and submucosal (not full thickness)- get pseudopolps (bumps from healing ulcers) and ‘lead pipe’ appearance on imaging 2/2 loss of haustra in the colon
Crohn: transmural, so then myofibroblasts come in to repair. Get cobblestoning (scars), creeping fat (myofibroblasts have contractile properties), and strictures (2/2 full wall thickness)
Spinal cord tract damaged in tabes dorsalis
Tabes dorsalis = manifestation of neurosyphilis
-get sharp shooting pains in extremities, loss of proprioception (positive Rombergs), parasthesias
Spirochetes damage the dorsal columns
What is the arcuate fasciculus?
Arcuate fasciculus attaches Broca’s and Wernicke’s area, so Wernicke’s area heps you understand the language, then you can respond w/ fluent language w/ help of Broca’s area
-injury to arcuate fasciculus =pt unable to repeat phrases, speech is fluent and comprehension is intact b/c Broca’s and Wernicke’s areas respectively are not impacted
Differentiate the two proteins used for retrograde vs. anterograde axonal transport
Dynein is used for retrograde transport- aka how HSV-1 gets from skin to the trigeminal sensory ganglia where it lays dormant
Then kinesin molecule transports the virus anterograde for reactivation
(a) Name the cell type
(b) What cell stimulates their formation?
(c) Seen in what conditions
(a) Langhans giant cells = multinucleated large cells w/ nuclei arranged in horseshoe-pattern in the periphery
(c) Seen in granulomas, ex: Tb
(b) CD4+ Th1 lymphocytes stimulate macrophages
Diagnose the type of leukemia
Auer rods = linear purple-red inclusions w/in blasts (immaure myeloid precursors)
Dx = AML = acute myelogenous leukemia
4 yo boy p/w elbow extended and forearm pronated, which ligament is injured?
MC from FOOSH, annular ligament gets trapped btwn radial head and distal humerus
- common in children b/c annular ligament isn’t fully strengthened yet
- hurts upon movement (fine at rest)
Histologic finding of gardenerella vaginalis infection
When normal vaginal flora (lactobacillus) replaced by overgrowth of gram negative gardenerella vaginalis
- pH of vaginal secretions increases to above 4.5
- get fishy-smelling white discharge
- Histologically (pap smear finding): squamous cell covered w/ bacteria
Histologic finding of HPV infection
Koilocyte = HPV infected squamous cell w/ dense irregular staining cytoplasm and perinuclear staining
- raisinoid-appearance of nucleus, halo-like clearing of cytoplasm
- dense than normal chromatin (dark nucleus)
Explain the serologic test findings of a pt w/ resolved Hep B
Recovered from past infection and now immune:
Negative: HBsAg (first marker to appear of acute infection), neg IgM anti-HBc (first Ab to arrive)
Positive total Anti-HBc (IgG), positive anti-HBs (confers immunity), positive anti-HBe w/ negative HBeAg suggesting subsided viral activity (no active viral replication)
Explain the serologic difference btwn pt w/ resolved Hep B and chronic Hep B carrier
Hep B resolved: negative HBsAg, negative HBeAg (marker of viral replication). Positive anti-HBc, anti-HBs (lifelong immunity)
While chronic carrier will have anti-HBc (in response to presence of antigen), however HBsAg will remain positive and HBeAg remains positive suggestive of active viral replication
Chronic infection: pt never develops anti-HbS
How to differentiate a pt who was infected and cleared HepB vs. vaccinzed pt
Vaccinated pt: positive anti-HBs w/o positive anti-HBc
While pt who was infected will have both anti-HBs and anti-HBc
Give the MC location of origin for type A vs. type B aortic dissection
Type A aortic dissection (involving ascending aorta) usually originates at the sinotubular junction (where aortic sinuses end and the aorta becomes a tubular structure)
Type B aortic dissections (only descending) usually originate near the origin of the left subclavian artery
Explain how class I antiarrhtymics interact w/ the voltage activated Na channel in its different states
(a) Concept of dependence
Voltage activated Na channel has 3 states
- Closed (resting) where the drug is released/dissociated
- Open- Na+ getting thru to cause depolarization
- Inactivated- where the drug binds readily
(a) Dependence meaning the more the cardiac myocyte is depolarizing, the more effect a class I antiarrhtyhmic can have
- more depolarization = less time in closed (resting) state = less time where drug gets kicked off the channel
Distinguish the 3 subgroups of class I antiarrthymics by their dependence
IC > IA > IB
- IC (Propafenone, Flecainde) has the slowest dissociation from the channel => blockage effect accumulates w/ beats and is the strongest
- IA (DIsopyramide, Quinidine, Procainamide) intermediate
- IB (Lidocaine, Mexiletine, Tocainide) has the lowest affinity => least dependence
Clinical presentation of classic galatosemia
Newborns present w/in days of birth w/ jaundice, vomiting, and hepatomegaly
- autosomal recessive
- absence of galatose-1-phosphate uridyl transferase
Cross-shaped intraerythrocytic inclusions- dx?
Maltese cross = cross-shaped intraerythrocytic inclusions
Dx = babesiosis
-transmitted by Ixodes tick (same tick as Lyme disease)
Differentiate histologic findings (and transmission) of babesiosis and malaria
Babesiosis- both ring and cross-shaped intraerytroblastic inclusions
-transmitted by Ixodes tick (same tick that transmits Lyme)
Malaria (plasmodium falciparum has just the ring-shaped intraerythroblastic inclusions
-transmitted by mosquito
Dietary supplementation of what molecule helps in PKU?
Tyrosine supplementation, b/c allows normal catecholamine production due to intact tyrosine hydroxylase
Explain how a pt w/ PKU can develop hyperprolactinemia
PKU –> tyrosine and tyrosine –> DOPA both require BH4 cofactor, generated by dihydropteridine reductase
Dihydropteridine reductase deficiency can cause PTU w/ hyperprolactinemia b/c w/o DOPA production from tyrosine, no DA which is needed for tonic inhibition of prolactin
(a) Name the finding
(b) Ddx
(a) Basophilic stippling 2/2 RBC inclusions
(b) Lead poisoning, thalassemias, myelodysplastic syndromes
Locate the area postrema
Area postrema- dorsal medulla near 4th ventricle, caudal end of the 4th ventricle
-samples peripheral blood by fenestrated vessels
3 EKG features of Wolff-Parkinson White
- Delta wave = slurred initial upslope of QRS indicating ventricular preexcitation
- Shortened PR interval (b/c less delay btwn ventricular and atrial contraction)
- Widened QRS (b/c ventricular contraction takes longer when not only thru fast pathway)
Differentiate function of LH and FSH in males
- LH stimulates Leydig cells to release testosterone
- FSH stimulates Sertoli cells to release inhibin
Functions of glossopharyngeal nerve
(a) Motor
(b) Parasymp
(c) General sensory
(d) Taste
CN IX = glossopharyngeal nerve
(a) Somatic motor innervation to stylopharyngeus to elevate the larynx during wallowing
(b) Parasymapthetic for parotid gland
(c) Sensory: inner tympanic membrane, posterior 1/3 of the tongue, afferent limb of gag reflex, carotid body and carotid sinus (so afferent limb of carotid massage)
(d) Taste to posterior 1/3 of tongue
Ansa cervicalis
(a) From what spinal nerve roots
(b) Function
Ansa cervicalis
(a) Spinal roots C1,C2,C3
(b) Innervates muscles of the anterior neck
Describe histologic features of irreversible neuronal injury
Red neuron = 12-24 hrs after irreversible injury
- cell body shrinkage, nuclei shrinkage (pyknosis)
- eosinophilia of cytoplasm (hence red)
- loss of Nissl substance (rER)
What are golgi tendon organs?
(a) Location
(b) Sensory fibers
(c) Fxn
Golgi tendon organ = sensory receptors at
(a) The jxn btwn muscle and tendon
(b) Innervated by group Ib sensory axons
(c) To monitor and maintain muscle tension (not length which is done by the spindle system)
So if wt lifter exerts more force than muscle can handle, golgi tendon organ sesnses the tension and immediately uses its inhibitory interneuron to inhibit contraction via alpha motor neuron, causing sudden muscle relaxation to prevent damage to muscle
Ex: Wt lifter immediately drops too heavy a weight
Differentiate sensory axons that mediate stretch vs. tension of muscle
Stretch mediated by muscle spindle system (intra and extrafusal fibers) innervated by group Ia and group II sensory axons
While tension is monitored/mediated by golgi tendon organs (GTOs) which act via group Ib sensory axons to immediately cause muscle relaxation if tension gets too high (to prevent damage to muscle)
Where is the common peroneal nerve susceptible to damage
(a) Motor finding
(b) Sensory finding
Over the fibular neck
(a) Motor: weakness in foot dorsiflexion and eversion
(b) Lateral shin, dorsal foot, and btwn first and second toes
What structures connect the following
(a) Lateral and 3rd ventricles of the brain
(b) 3rd and 4th ventricles
(c) 4th and central canal
(a) Interventricular foramina of Monro connects lateral ventricles to 3rd ventricle
(b) Btwn 3rd and 4th ventricle = cerebral aqueduct
(c) Median foramen of Magendie and lateral foramen of Luscka connect 4th ventricle to central canal
Differentiate train of 4 findings in depolarizing vs. nondepolarizing neuromuscular blockade agents
Depolarizing agent (succinylcholine) has phase I when all 4 twitches constant but diminished (all 4 twitches reduced), then phase II (reversible) when ACh receptors become desensitized, twitches fade
Nondepoliarizing agent (Vecuronium): fade
Mechanism of this finding
(a) MC in what organs
Free radical injury and lipid peroxidation forms lipofuscin = yellow-brown intracytoplasmic granules
- seen over time (aka in elderly)
(a) MC in heart and liver
What sequence of the target gene needs to be known to do PCR
Know the nucleotide sequence of the region flanking the exon
-thats where the primers attach to start extending
Differentiate mechanism of tacrolimus and sirolimus
Both inhibit IL-2 and therefore lymphocyte proliferation but in different ways
- tacrolimus (calcineurin inhibitor) inhibits NFAT to block IL-2 transcription
- Sirolimus inhibits mTOR signaling pathway to block IL-2 signal transduction
Location of CN nuclei
Midbrain: CN I, II, III, IV
Pons: V-VII
VIII kinda just btwn pons and medulla
Medulla: IX-XI
Label
A = red nucleus
B = hippocampus
C = substantia nigra
D = insular cortex
E = thalamus
Location of ulnar and median nerve off brachial plexus
Median: C5-T1
Ulnar: C8-T1
