uWorld 25 Flashcards

1
Q

what defines a sarcomere

A

the distance between two Z lines

the thin ACTIN filaments in the I BAND (light color surrounding darkest line) are bound to structural proteins at the Z LINE (darkest line on EM)

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2
Q

what part of the sarcomere is always the same length during muscle contraction

A

A band (myosin filaments in the sarcomere)- region contains the overlap of myosin and actin as well as non-overladed myosin

(H band is ONLY MYOSIN)
(M Line is light parallel lines on EM in A band = where myosin anchors to structural elements) in MIDDLE of sarcomere)

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3
Q

what is the most common cause of retinal artery occlusion (cause of acute, painless, monocular vision loss)

A

thromboembolic complications of atherosclerosis in the INTERNAL CAROTID

(retinal artery is branch of ophthalmic artery, which is a branch off the internal carotid)

retinal artery travels with retinal nerve to supply INNER RETINA and the SURFACE of the OPTIC NERVE

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4
Q

4 yr old with recurrent skin and respiratory infections
light skin and silvery hair
horizontal nystagmus
giant cytoplasmic inclusions in neutrophils and monocytes
the fuck he got?

A

CHEDIAK-HIGASHI Snydrome

Autosomal RECESSIVE

neurologic defects: nystagmus, peripheral and cranial neuropathies

defect in neutrophil phagosome lysosome fusion (large CYTOPLASMIC INCLUSIONS)

recurrent PYOGENIC (staph and strep) infections

abnormal MELANIN STOREAGE in melanocytes causes PARTIAL OCULOCUTANEOUS ALBINISM

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5
Q

complete albinism presents how and is due to what

A

lack of TYROSINASE

white hair, blue eyes and pink or white skin

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6
Q

what skin lesions are seen in sarcoidosis, also what part of the liver is fucked up by the granulomas

A

subcutaneous nodules (erythema nodosum), erythematous plaques, macules that are slightly reddened and scaling

PORTAL TRIADS fucked more than lobular parenchyma

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7
Q

when is hepatic centrilobular necrosis seen

A

death of hepatocytes immediately surrounding the terminal hepatic vein

ISCHEMIC INJURY (as in right sided heart failure), drugs, toxins, and fulminant hepatitis

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8
Q

portal hepatic fibrosis is a pathologic finding seen in what

A

CHRONIC viral hepatits

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9
Q

what is the major cause of morbidity in sarcoidosis

A

pulmonary fibrosis, which can progress to COR PULMONALE

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10
Q

what does klebsiella granulomatis cause

A

granuloma inguinale (donovanosis)
painLESS GENITAL papule that eventually ulcerates
lymphadenopathy is UNCOMMON

deeply staining gram-negative intraCYTOPLASMIC cysts (DONOVAN bodies) are diagnostic

base may have GRANULATION TISSUE

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11
Q

how is lymphogrnauloma venereum (LGV) caused by Chlamydia treated

A

DOXY

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12
Q

oral thrush is common in people with what

A
denture wearers
diabetics
immunosuppressed
steroids
antibiotics
chemotherapy

if patient seems normal- proly HIV and immunocompromised

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13
Q

hospice care requires what

A

prognosis of LESS THAN or equal to 6 MONTHS

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14
Q

what is systemic mastocytosis

A

clonal mass cell proliferation occurs in the bone marrow, skin, and other organs

often assisted with mutation in the KIT receptor TYROSINE KINASE

prominent expression of mast cell TYRPTASE

excessive HISTAMINE release mediates symptoms:
syncope, flushing, hypotension, pruritus, urticaria, maculopapular rash
GASTRIC ACID SECRETION- ULCERS and inactivated pancreatic and intestinal enzymes (DIARRHEA)
can also have nausea, vomiting, and cramps

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15
Q

what is special about the bronchial circuit (supplies oxygen and nutrients to pulmonary parenchyma)

A

drains mostly to LEFT ATRIUM as opposed to right atrium

creates a RIGHT-to-LEFT shunt that acts as a partially independent circuit from the pulmonary-systemic circuit

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16
Q

what balance is necessary to maintain continuous blood flow through the body (and exists at both rest and during exercise)

A

volume of output of the left ventricle must closely match the output of the right ventricle

(blood flow per minute in systemic circulation should be the same as pulmonary)

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17
Q

what change in the post-synaptic cell most likely explains myasthenia gravis

A

decreased ability of acetylcholine to bind and open post synaptic cation channels, thereby DECREASING the END-PLATE POTENTIAL and preventing the formation of muscular action potentials

(also see a reduction in compound action potential with repeated excitation)

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18
Q

what drugs are used to reduce the side effects caused by acetylcholinesterase inhibitors in myasthenia gravis

A

SCAPOLAMINE (anti muscarinic so it stops acetylcholine actions at M receptors but leaves the NMJ nicotinic receptors needed for treatment alone)

HYOSCYAMIN

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19
Q

what does the frontal eye field do

A

Brodmann areas 6 and 8
found near the caudal end of the middle frontal gyrus anterior to the pre central sulcus

damage causes EYES to DEVIATE to the IPSILATERAL SIDE

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20
Q

what is the lymph drainage of the male genitals

A

testis: para-aortic

glans penis (and superficial nodes): deep inguinal nodes (drain to external iliac nodes)

scrotum: superficial inguinal nodes

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21
Q

the inferior mesenteric nodes receive lymph form where

A

descending and sigmoid colon
upper rectum

(efferents drain into the pre-aortic nodes)

22
Q

what passes through the inferior orbital fissure but do not enter orbit

A

V2 (maxillary branch)
infraorbital vessels
branches of sphenopalatine ganglion

23
Q

the foramen rotunda transmits what

A

maxillary division (V2) from the skull to the pterygopalatine fossa

from there it courses through the inferior orbital tissue to appear on the face at the infraorbital foramen as the infraorbital nerve

24
Q

what foramen is occluded by cartilage

A

foramen lacerum

internal carotid courses just superior to foramen lacerum in the lacerum portion of the carotid canal

25
Q

what passes through the foramen ovale

A

V3 (mandibular branch)

26
Q

what goes through the foramen spinosum

A

middle meningeal artery

27
Q

what is seen in Treacher-Collins Syndrome (TCS)

A

fucked up 1st and 2nd pharyngeal arches

often get airway compromise and feeding difficulties from craniofacial abnormalities (mandibular, maxillary, and zygomatic bone hypoplaisa; muscles of mastication and facial muscle loss)

also have CONDUCTIVE hearing loss form absent or abnormal ossicles (incus, malleus, stapes)

28
Q

where are the neuritic plaques found in alzhemiers

A

medial temporal lobe (hippocampus, amygdala, entorhinal cortex)

central amyloid beta core surrounded by dystrophic neuritis

the neurofibrillary tangles are in the neuronal cytoplasm (HYPERPHOSPHORYLATED TAU)

29
Q

what is the difference between ADHD and a learning disorder

A

ADHD has to show inattention and/or hyperactivity/impulsivity across at LEAST 2 SETTINGS (multiple subjects, at home and school)

learning disorders can present with anxiety, inattention, or hyperactivity when under stress- like doing the subject they struggle in

30
Q

what are the levels of cholesterol, bile acids, and phosphatidylcholine in patients with cholesterol gallstones (echogenic foci on ultrasound)

A

cholesterol: ↑
bile salts (or acids): ↓
phosphatidylcholine: ↓

(high levels of bile salts and phosphatidylcholine increase cholesterol solubility and decrease the risk of gallstones)

31
Q

what is the rate limiting step of bile acid synthesis

A

cholesterol 7alpha-hydroxylase
starts series of chemical reactions that covers cholesterol into chalice and chenodeoxycholic acids

bile acids conjugated to GLYCINE or TUARINE to create bile slides

32
Q

what change in MITRAL valve STENOSIS indicates a more SEVERE murmur (most reliable indicator of degree of stenosis)

A

if the opening snap is closer to A2 (time interval decreases)

done via mean transvalvular pressure gradients via 2-D Doppler echocardiography

33
Q

if pre-systolic accentuation (due to left-atrial contraction) of the mitral valve stenosis disappears what does that indicate

A

the mitral valve stenosis has become bad enough to precipitate ATRAIL FIB

34
Q

reddish color urine that darkens on standing is seen in what

A

acute PORPHYRIES

ari and light and air exposure oxidize the excess PBG (porphobilinogen)

35
Q

what is seen in acute intermittent porphyria (what causes it)

A

AD deficiency in PORPHOBILINOGEN (PBG) DEAMINASE

accumulation of: porphobilinogen and delta-ALA, corporphobilinogen (urine)

Symptoms: 5 P's
Painful abdomen
Port wine-colored URINE
Polyneuropathy
Psychological disturbances
Precipitated by drugs (CYp450 inducers), alcohol, and starvation

TX: GLUCOSE (or dextrose) and HEME (both INHIBIT ALA SYNTHASE)

36
Q

how does botulism toxin work

A

prevents pre-synaptic release of acetylcholine

37
Q

acute GI hemorrhage or diarrhea would cause what kind of fluid loss

A

ISOSMOTIC VOLUEM CONTRACTION
isotonic loss of ECF volume
no effects on osmolarity or ICF volume

38
Q

what happens to the fluid compartment levels in adrenal insufficiency

A

HYPOSMOTIC VOLUME CONTRACTION (hypertonic loss of NaCl with some extracellular volume loss)
low osmolarity of ECF results in SHIFTING of free water into the ICF compartment, causing ICF expansion

39
Q

what does infusion of large amounts of hypertonic saline do to the ECF and ICF (volume and osmolality)

A

HYPERTONIC VOLUME EXPANSION
both the volume and osmolarity of ECF are increased
high osmolarity of ECF leads to SHIFTING of water from from the ICF, further INCREASING the ECF volume

40
Q

primary polydipsia does what to ECF and ICF (volume and osmolarity)

A

HYPOOSMOTIC VOLUME EXPANSION
expansion of both ECF and ICF compartments and decrease in the osmolarity of both

apparently also seen in SIADH but that should be euvolemic hypernatremia

41
Q

prolonged use of NSAIDs can cause CHRONIC INTERSTITIAL NEPHRITIS, what is seen histologically

A

NSAIDs concentrate in renal medulla along the medullary osmotic gradient, with higher levels in the papillae

fibrosis
tubular atrophy
papillary necrosis and scarring
caliceal architecture distortion (calcifications)

NSAID also decrease prostaglandin synthesis, causing constriction of medullary vasa recta and ISCHEMIC PAPILLARY NECROSIS

42
Q

GH binds what receptor

A

JAK/STAT pathway
(non receptor tyrosine kinase (JAK) with docking sites for signal transducer and activator of transcript (STAT))

in this case (with GH) STAT dimerizes and translocates into nucleus where it activates IGF-1 gene transcription by binding the promoter site

(cytokines like interferon and hematopoietic growth factors like erythropoietin and G-CSF use JAK-STAT pathway too)

43
Q

what antibiotic has good coverage of ORAL ANAEROBES and covers Strep Pneumo too (good for lung abscess in alcoholic or seizure person)

A

CLINDAMYCIN (antibiotic of choice for lung abscess)

covers oral anaerobes: Bactericides, Prevotella, Fuscobacterium, Peptostreptococcus)
also covers AEROBIC bacteria

44
Q

what is seen in McCune-Albright syndrome

A
cafe-au-alit spots (unilateral)
endocrine abnormalities (precious puberty, hyperthyroidism)
fibrous dysplasia (multiple osteolytic-appearing lesions of hip and pelvis)- from activation of fibroblast, IL-6 and osteoclasts

mosaic somatic mutation in GNAS gene encoding the stimulatory ALPHA SUBUNIT of G PROTEIN

constitutive ACTIVATION of ADENYLATE CYCLSE leads to OVERPRODUCTION of several hormones

45
Q

what is Legg-Calve-PErthes disease

A

disease of young children that results in ISOLATED IDIOPATHIC OSTEONECROSIS of the HIP

46
Q

what is omalizumab

A

monoclonal antibody (IgG1) to IgE

47
Q

what is bortezomib

A

proteasome inhibitor

used to treat MULTIPLE MYELOMA and Waldenstrom macroglobulinemia

48
Q

left circumflex occlusion would be seen in what leads

A

V6 and V6 (possibly I and aVL)

49
Q

LAD occlusion is seen in what leads

A

V1 and V2 for interventricular septum

V3 and V4 for anterior left ventricular wall

50
Q

rightt coronary occlusions are seen in what leads

A

II, III and aVF

51
Q

supplementation with what can reduce erythroid precursor cell apoptosis in things with folic acid deprivation

A

THYMIDINE (can use the salvage pathway using thymidine kinase to partially compensate)

folate is necessary for THYMIDYLATE SYNTHETASE (THF + dUMP = DHF + dTMP)

52
Q

what are homocysteine levels like in folate defieicency

A

elevated (can be reduced by folate deficiency)