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uWorld 27 Flashcards

1
Q

what is the motor and sensory innervation of the tibial nerve

A

Motor:
foot PLANTAR FLEXION (gastrocnemius, soleus, planters muscles)
INVERION (tibialis posterior muscle)
TOE FLEXION (flexor digitorum longs, flexor hallucis longus muscles)

sensory: plantar foot
lateral 4 toes (posterior tibial nerve)

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2
Q

how does tibial nerve injury (at the popliteal fossa- deep penetrating trauma, knee surgery) often present

A

calcaneovalgus position (dorsiflexed and everted)

if tarsal tunnel may cause sensory loss over the sole with intrinsic foot muscle weakness (plantar flexion and inversion remain intact)

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3
Q

the femoral nerve dos what motor and sensort

A

motor:
leg flexion at the hip
leg extension at the knee

sensory:
medial leg (saphenous nerve)
anterior thigh (femoral nerve)
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4
Q

the superficial peroneal nerve does what motor and sensory

A

motor:
foot EVERSION

sensory:
dorsal surface (top) of foot
anterolateral leg

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5
Q

the deep peroneal nerve dos what motor and sensory

A

motor:
foot dorsiflexion
toe extension

sensory:
between first and second toes

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6
Q

what is the T LOOP of the tRNA

A

contents T(psi)C sequence that is necessary for BINDING of tRNA to RIBOSOMES

refers to the presence of ribothymidine, pseudouridine, and cytidine residues

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7
Q

what is the D LOOP of tRNA

A

facilitates correct tRNA recognition by the proper AMINOACYL tRNA SYNTEHTASE (with the acceptor stem and anticodon loop)

contains dihydrouridine residues (modified bases)

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8
Q

what is the ANTICODON loop of tRNA

A

contains sequences that are complementary to the mRNA codon

during translation, the RIBOSOME complex SELECTS the proper tRNA based SOLEY on its ANTICODON SEQUENCE

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9
Q

what is the ACCEPTOR STEM of tRNA

A

created through the base parking of the 5’-terminal nucleotides with the 3’terminal nucleotides

has the CCA at the 3’ end, with the amino acid bound to the 3’ terminal hydroxyl group

helps mediate correct tRNA recognition by the proper aminoacyl tRNA synthetase

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10
Q

if a patient has decreased breath sounds, hemithroax opacification on one side (right), and deviation of the trachea toward the opacified side are suggestive of what

A

COLLAPSED LUNG due to BRONCHIAL OBSTRUCTION

complete collapse of a lung usually occurs following obstruction of a MAINSTEM BRONCHUS (central lung tumors in smokers)

alveolar collapse (atelectasis) which causes TRACHEA to DEVIATE TOWARD SIDE of LESION

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11
Q

when does one see COMPLETELY OPACIFIED HEMITHROAX w/ tracheal deviation TOWARD the effected lung

A

mainstream bronchus lesion causing ATELECTEASIS

loss of radiolucent air combined with shifting of organs into the hemithroax

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12
Q

bilateral fluffy appearing infiltrates in the lungs are typically seen when

A

pulmonary edema (fluid in alveolar species)

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13
Q

when does one see COMPLETELY OPACIFIED HEMITHROAX w/ tracheal deviation AWAY FROM the effected lung

A

large pleural effusion

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14
Q

what are the two main enzymes of the non oxidative reaction of the HMP shunt

A

transketolase (two carbon group transfer) w/ TPP substrate
transaldolase (three carbon transfer)

can synthesize ribose from fructose-6-phosphate

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15
Q

what does the HMP shunt produce from one molecule of glucose

A

five-carbon sugar, two molecules of NADPH and CO2

two reactions:
oxidative (irreversible)
non-oxidative (reversible)

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16
Q

the oxidative portion of the HMP shunt primarily occurs where

A

tissues active in reductive biosynthesis
fatty avid and steroid synthesis
CYP450 pathway
generation fo superoxide in phagocytes

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17
Q

what enzymes are necessary for the oxidative part of the HMP shunt

A

GLUCOSE-6-PHOSPHATE DEHYDROGENASE (RATE LIMITING): glucose-6-phosphate to 6-phosphogluconate

6-phosphogluconate dehydrogenase: 6-phosphogluconate to ribulose-5-phosphate

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18
Q

what does enolase do

A

convers 2-phosphoglycerate to phosphoenolpyruvate in glycolysis

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19
Q

why does aconite do

A

catalyzes isomerization of citrate to isocitrate in the TCA cycle

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20
Q

what treatment is being researched for AR SCID

A

RETROVIRAL VECTORS to “INFECT” patient STEM CELL with the GENE CODING for ADENOSINE DEAMINASE

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21
Q

what bug is associated with fever, headache, and diplopia in immunocompromised people and found in DAIRY (milk, soft cheeses, and ice cream) as well as raw fruits and processed meats

A

LISTERIA

significant disease in patients with CELL-MEDIATED immunodeficiency

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22
Q

what happens to 2,3-BPG after chronic high altitude adaptation

A

an organophosphate created in erythrocytes during glycolysis

increase levels of 2,3-BPG decrease hemoglobin O2 affinity , allowing the release of more O2 in the peripheral tissues

curve shifts RIGHT

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23
Q

what happens O2 curve in exercise, severe anemia, and hypoventilation

A

shifts RIGHT

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24
Q

what is a CROSS-SECTIONAL study

A

PREVALENCE STUDY

“SNAPSHOT” design that is inexpensive and easy to perform

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25
Q

what happens to cortisol levels in response to stressful situations (infections, surgery) in patients on chronic glucocorticoid therapy

A

it CANNOT RISE (the adrenal is atrophied)

can result in RELATIVE GLUCOCORTICOID DEFICIENCY even when the patient’s baseline glucocorticoid regime is maintained

can precipitate HYPOTENSION/SHOCK- a higher STRESS DOSE is needed if this happens

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26
Q

what is a rare complication that can happen on first dose of ACE inhibitors

A

FIRST-DOSE HYPOTENSION

happens in patients with high plasma RENIN levels like in VOLUME DEPLETION (from DIURETIC USE) or HEART FAILURE

prevent this by starting therapy at low doses and slowly titrated upward as needed

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27
Q

in a patient with albuminuria why are they started on an ACE inhibitor

A

to treat early diabetic neuropathy

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28
Q

what are the etiologies of hypoxemia in a patient with a NORMAL Aa gradient (5-15 mmHg)

A

HYPOVENTILATION (obesity hypoventialtion syndrome, neuromuscular disorders

LOW INSPIRED FRACTION OF AIR (high altitude)

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29
Q

what are the etiologies of hypoxemia in a patient with a ELEVATED Aa gradient (over 15mmHg)

A

RIGHT-to-LEFT SHUNT (cardiac septal defects, pulmonary edema)

VENTIALTION/PERFUSION MISMATCH (PE, COPD)

IMPAIRED DIFFUSION (interstitial lung disease)

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30
Q

what is seen in OBESITY HYPOVENTILATION SYNDROME

A

increase CO2 production due to increased mass and surface area
sleep-disordered breathing
reduced lung volumes and compliance

chronic fatigue, dyspnea, difficulty concentrating, evidence of hypoventilation (PaCO2 over 45 while awake)

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31
Q

what cells are responsible for synthesizing the structurally important collagen isoforms and extracellular matrix of a atherosclerotic plaque

A

vascular smooth muscle cells (VSMCs)

32
Q

who is renal blood flow calculated

A

first calculate renal PLASMA flow using PAH: RPF = (Urine PAH)*(urine flow rate)/(Plasma PAH)

renal blood flow: RBF = RPF/(1-hematocrit)

33
Q

when placing a chest tube into the 4th or 5th intercostal space in the anterior axillary or MIDAXILLARY line what does the tube traverse

A

SERRATUS ANTERIOR muscle
intercostal (external, internal, innermost) muscles
parietal pleura

34
Q

what does serrates anterior do

A

originated from ribs 1-8 and inserts along the entire length of the medial scapular border
3 parts: superior, intermediate, inferior

infer part of muscle facilitates ARM ELEVATION by PULLING lower end of SCAPULA forward (SCAPULAR ROTATION)

all 3 parts help with respiration by lifting the ribs when the shoulder grille is FIXED

35
Q

what does pectorals major do

A

adduct and internally rotate the humerus

arises from anterior clavicle, sternum, costal cartilages, and aponeurosis of the external oblique muscle
attaches to lateral lip of bicipital groove of the humerus

36
Q

the lateral epicondyle serves as the primary attachment point for what muscles

A

EXTENSOR CARPI RADIALIS BREVIS (ECRB)
EXTENSOR DIGITORUM

both involved in WRIST EXTENSION

lateral epicondylitis aka tennis elbow is pain over the lateral epicondyle of the humerus due to antiofibrotic tendinosis of the ECRB tendon

37
Q

what muscles flex the forearm

A

biceps brachii
brachialis
brachioradialis

38
Q

L2 radiculopathy leads to what

A

sensory loss: upper anteromedial thigh

weakness: hip flexion (ILIOPSOAS)

39
Q

L3 radiculopathy leads to what

A

sensory loss: lower anteromedial thigh

weakness: hip flexion (iliopsoas), hp adduction, knee extension (quads)

40
Q

L4 radiculopathy leads to what

A

sensory loss: lower anterolateral thigh, knee, medial calf and medial foot
weakness: hip adduction, knee extension (quadriceps), PATELLAR REFLEX

41
Q

L5 radiculopathy leads to what

A

sensory loss: buttocks, posterolateral thigh, anterolateral leg, DORSAL FOOT
weakness: foot dorsiflexion and inversion (tibialis anterior), foot eversion (peroneus), toe extension (extensor digitorum brevis)

42
Q

S1 radiculopathy leads to what

A

sensory loss: buttocks, posterior thigh and calf, lateral foot
weakness: hip extension (gluteus maximus), knee flexion (hamstrings), foot plantar flexion (gastrocnemius), ACHILLES REFLEX

43
Q

what are two causes of radiculopathy and how do they differ (if we are talking about say L5-S1 radiculopathy)

A

SPINAL FORAMINA STENOSIS:affects the UPPER nerve root that is actually exiting at that level (since the roots exit below)
- so L5 would be affected if L5-S1 neural foramen were affected

HERNIATED DISC: affects the LOWER nerve root
- so S1 would be affected if L5-S1 disc were to herniate

44
Q

how does Strep Viridans work

A

ADHEREs to tooth enamel and to FIBRIN-PLATELET aggregates on damaged heart valves due to their ability to produce INSOLUBLE EXTRACELLULAR POLYSACCHARIDES (aka DEXTRANS) using sucrose as a substrate

this colonization of host surfaces contributes to their ability to cause infections

45
Q

angiotensin-II, oxytocin, and vascular vasopressin (V1) receptors all work through what mechanism

A

Gq

46
Q

why is oxalate absorption in creased in Crohns

A

calcium normally binds oxalate in the bowel to form insoluble salts that promote oxalate excretion
in Crohns calcium binds LIPIDS instead and cannot complex oxalate
OXALTE ABSORPTION is thus INCREASED, promoting formation of OXALATE KIDNEY STONES (enteric oxaluria)

47
Q

what causes avascular necrosis (osteonecrosis)

A

THOMBOTI/EMBOLIC OCCLUSION (SICKLE CELL, BENDs)
GLUCOCORTICOIDS
vascular inflammation/injury (vasculitis, radiation)
alcohol abuse
traumatic fracture

48
Q

what clinical presentation is seen with osteonecrosis (avascular necrosis)

A

pain on weight bearing
DECREASED RANGE of MOTION

wedge-shaped or geographic zone of necrosis
articular cartilage is viable but may be distorted or detached from underlying bone

necrosis of surrounding adipocytes
dead bony trabecular with empty lacunae

49
Q

prior MI is associated with lower risk of ventricular free wall rupture, why?

A

myocardial fibrosis at the site of infarction

development of collateral circulation

50
Q

what is the TATA box

A

promoter region located 25 bases UPSTREAM from the beginning of the CODING REGION

51
Q

when does gene transcription begin

A

when RNA POLYMERASE II attaches to one of the promoter regions in a process that requires general TRANSCRIPTION FACTORS

52
Q

in eukaryotes translation initiation requires what

A

both ribosomal units (60S and 40S) with their associated rRNA, mRNA, initiation factors, initiator tRNA charged with methionine, and GTP

53
Q

what is adiponectin

A

cytokine secreted by fat tissue that increases the number of insulin-responsive adipocytes and regulates fatty acid oxidation

increased by PPAR-gamma via thiazolidinediones (glitters)

54
Q

what does nedocromil do

A

mast cell degranulation inhibitor (along with CROMOLYN)

55
Q

long term glucocorticoid use stimulates anabolism where and catabolism where

A

anabolism- LIVER (stimulation of GLUCONEOGENESIS and upregulate the synthesis of key gluconeogenic enzymes (PEPCK, G-6-phosphatase), increase in GLYCOGEN RESERVES via expression of glycogen synthase)

catabolism- peripheral in the SKELETAL MSUCLE (antagonizing the action of insulin)- provides substrates for gluconeogenesis and glycogenesis in the liver

can manifest as:
muscle weakness (glucocorticoid myopathy)
lipolytic and antilipolyic, altered fat distribution (central obesity, hypertrophy of dorsocervical fat pad)
increased appetite and caloric intake
HYPERGLYCEMIA (gluconeogenesis and insulin antagonism)

56
Q

what do glucocorticoids do to the skin

A 
inhibition of fibroblast proliferation and collagen formation:
thinning
stria
impaired wound healing
easy bruising
57
Q

how do glucocorticoids decrease bone mass (causing osteoporosis and avascular necrosis)

A

decreased GI calcium absorption
increased renal calcium excretion
direct inhibitor of osteoblast activity

58
Q

high levels of what are rewired for spermatogenesis

A

testosterone

inhibin B

59
Q

how do beta blockers mask hypoglycemia

A

the neurogenic symptoms of hypoglycemia are caused by SYMPATHOADRENAL ACTIVATION and are mediated via norepi/epi and acetylcholine via sympathetic POSTganglionic fibers

symptoms of norepi/epi are tremulousness, palpitations, and anxiety/arousal
cholinergic symptoms: sweating, hunger, paresthesias

NON-SELECTIVE BETA BLOCKERS will block the norepi/epi mediated compensatory reactions leaving the CHOLINERGIC SYMPTOMS UNAFFECTED

blocking beta-2 also stops hepatic gluconeogeneiss, and peripheral glycogenolysis and lipolysis

60
Q

if beta-blocker therapy is needed in a diabetic what is prefered

A

selective beta-1 blockers

beta-blockers with intrinsic sympathomimetic activity (PINDOLOL, ACEBUTOLOL)

61
Q

what causes the hypervitaminosis D in sarcoidosis

A

activated MACROPHAGES expression of 1-alpha-hydroxylase

this causes 1,25-dihydroxyvitamin D to be produced and increased INTESTINAL ABSORPTION of CALCIUM

62
Q

vimentin (an intermediate filament) is a marker for tumors of what origin

A

mesenchymal tissue

63
Q

neuron-specific enolase and chromogranin A are markers for what

A

neuroendocrine tumors

64
Q

what kind of receptor is HER2/neu

A

EPIDERMAL TRANSDUCTION PATHWAY that control EPITHELIAL GROWTH and DIFFERENTIATION

65
Q

what is derived from surface ectoderm

A 
Rathe's pouch (anterior pituitary)
lense and cornea
inner ear sensory organs
olfactory epithelium
nasal and coral epithelial linings
epidermis
salivary, sweat, and mamary glands
66
Q

what is derived form neural tube

A

brain and spinal cord
POSITERIOR PITUITRARY
PINEAL GLAND
RETINA

67
Q

what is derived form the neural crest

A 
autonomic, sensory, celiac ganglia
schwann cells
pia and arachnoid mater
aorticopulmonary septum and endocardial cushions
branchial arches (bones, cartilage)
skull bones
melanocytes
adrenal medulla
68
Q

what is derived from mesoderm

A 
muscles (skeletal, cardiac, smooth), connective tissue, bone, and cartilage
serosa lining (peritoneum)
cardiovascular system
blood
lymphatic system
spleen
internal genitalia
kidney and ureters
adrenal cortex
69
Q

what is derived form the endoderm

A 
GI tract
liver
pancreas
lungs
thymus
parathyroids (???)
thyroid follicular cells (????)
middle ear
bladder and urethra
70
Q

when do the three germ layers form

A

GASTRULATION during week 3 go embryogenesis

initiated by formation of primitive streak (thickening of epiblast cell layer that appears at caudal end of the embryo and grows cranially)

71
Q

what happens 2 days after gastrulation begins

A

some epiblast cells migrate cranially though the primitive node (the cephalic end of the primitive streak) to form a midline cellular cord known as the NOTOCORD

notochord induces overlying ectoderm cells to differentiate into neuroectoderm and form the neural plate

neural plat ogives rise to neural tube and neural crest cells, the rest of the ectoderm becomes the surface ectoderm

72
Q

the notochord becomes what in adults

A

nucleus pulpous of intervertebral discs

73
Q

what is seen in von Hippel-Lindau

A

AD disorder
HEMANGIOBLASTOMAS in the RETINA and/or CEREBELLUM
congenital CYSTS and/or NEOPLASMS of the kidney, liver, and pancreas

increased risk for renal cell carcinoma (BILATERAL)

74
Q

what is seen in Sturge-Weber syndrome (encephalotrigeminal angiomatosis)

A

cutaneous facial angiomas as well as leptomeningeal angiomas
skin involvement in V1 and V2 distributions of the trigeminal nerve

mental retardation
seizures
hemiplegia
skull radiopacies w/ “TRAM TRACK” calcifications

75
Q

what is seen in tuberous sclerosis

A 
AD syndrome
kidney, liver, and pancreatic cysts
cordial and subependymal HAMARTOMAS
cutaneous angiogibromas (adenoma sebaceous)
visceral cysts
varieties of other hamartomas
renal angiomyolipomas
cardiac rhabdomyomas
SEIZURES

uWorld Flashies (62 decks)

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