Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Step 1 > Musculoskeletal UWorld > Flashcards

Musculoskeletal UWorld Flashcards

1
Q

Which sarcomere bands remain the same and which change over the course of muscle contraction?

A

The A-band (myosin filaments) stays the same.
The H-band (area where myosin does not overlap actin) and I-band (area where actin does not overlap myosin) decrease during contraction. “An Interesting Zoo Must Have Mammals” = Actin in the I-band attaches to the Z-line. Myosin in the H-band attaches to the M-line.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Sensitivity

A

Probability a diseased person will test positive

TP / (TP + FN)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Specificity

A

Probability a non-diseased person will test negative

TN / (TN + FP)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Positive predictive value

A

Probability disease is present given a positive result

TP / (TP +FP)
*affected by prevalence and pre-test probability

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Negative predictive value

A

Probability disease is absent given a negative result

TN / (TN + FN)
*affected by prevalence and pre-test probability

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Positive likelihood ratio

A

Likelihood of having the disease given a positive result

Sensitivity / (1 - Specificity)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Negative likelihood ratio

A

Likelihood of not having the disease given a negative result

(1 - Specificity) / Sensitivity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

A child is born with flaccid leg paralysis, dorsiflexed foot contractures and urinary incontinence. Physical exam reveals anal atresia. What condition did the mother likely have during pregnancy?

A

Poorly controlled maternal diabetes can result in caudal regression syndrome.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Sensorimotor innervation of the peroneal nerve

A

Superficial: sensation to dorsum of foot and innervation to lateral compartment (eversion)

Deep: sensation to 1st webbed space and motor to anterior compartment (dorsiflexion)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Numbness/pain on sole of foot vs medial foot.

A

Sole = tarsal tunnel compression of tibial nerve.

Medial foot = compression of saphenous nerve

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

HLA class II antigens

A

DR, DP and DQ

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Rotator cuff muscle origins, insertions, innervation and function

A

Supraspinatus: originates at supraspinous fossa, inserts at greater tuberosity, innervated by suprascapular nerve, abducts arm.

Infraspinatous: originates at infraspinous fossa, inserts at greater tuberosity, innervated by suprascapular nerve, externally rotates arm.

Teres minor: originates at lateral border of scapula, inserts at greater tuberosity, innervated by axillary nerve, externally rotates arm.

Subscapularis: originates at sub scapular fossa, inserts at lesser tuberosity, innervated by upper and lower subscapular nerves, adducts and internally rotates arm.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Function of free ribosomes

A

Synthesis of proteins in the cytosol, nucleosol, peroxisome matrix and nuclear-encoded mitochondrial proteins.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Function of rER ribosomes

A

Synthesis of secretory proteins, membrane proteins and proteins within the rER, golgi and lysosomes.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

How do ribosomes end up on the rER?

A

The 60S subunit binds translocon on the rER.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

In which organelle does steroid hormone synthesis take place?

A

sER

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What is responsible for skin wrinkling as people age?

A

Reduced collagen fibril production leads to a net decrease in dermal collagen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What histones make up the nucleosome core?

A

H2A, H2B, H3 and H4. H1 is located outside of the core and binds to DNA of adjacent nucleosomes, resulting in more efficient DNA packing.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Epigenetic process involved in genomic imprinting

A

DNA methylation by DNA methyltransferases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

B. anthracis toxins

A

Edema factor: acts as adenylate cyclase, increases cAMP, increasing edema and causing phagocyte dysfunction.

Lethal factor: zinc-dependent protease that inhibits MAP-K signaling, resulting in apoptosis

Protective antigen: gets LF and EF intracellular

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

B. pertussis toxins

A

Pertussis toxin: Gi ribosylation results in disinhibition of adenylate cyclase -> increased cAMP, edema and phagocyte dysfunction.

Adenylate cyclase toxin: functions as adenylate cyclase, increasing cAMP, edema and phagocyte dysfunction.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

C. botulinum toxin

A

Blocks pre-synaptic release of ACh

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

C. difficile toxin

A

A: recruits and activates PMNs

B: induces actin depolymerization leading to cell death, necrosis and pseudomembrane formation.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

S. dysenteriae toxin

A

Shiga toxin: disables 60S subunit, reducing protein synthesis and inducing cell death

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

S. pyogenes toxins

A

Pyrogenic exotoxin: superantigen, scarlet fever

Streptolysin O & S: damages erythrocyte membranes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Viral DNA/RNA recombination mechanism

A

Genetic exchange via crossing over on homologous regions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Viral DNA/RNA reassortment mechanism

A

2 segmented viruses exchange whole genome segments (“BOAR”: bunyavirus, orthomyxovirus, arenavirus, reovirus”

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Viral phenotypic mixing mechanism

A

Co-infection of a host cell and incorporation into DNA results in a capsid from one virus and genome from the other virus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Why is there reduced complement levels in patients with SLE?

A

Immune-complex deposition results in complement activation.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What determines to natural progression of leprosy in patients infected by M. leprae?

A

Tuberculoid: least severe, skin hypopigmentation, plaques and decreased sensation due to intact cell-mediated immune response (Th1)

Lepromatous: most severe, weak cell mediated response (Th2) results in disseminated disease,

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

How does vitamin B6 result in a microcytic hypochromic anemia? Pellagra? Hypercoaguability?

A

A) It is necessary for the enzyme ALA synthase to function in generation of porphyrins for heme synthesis, deficiency = sideroblastic anemia.

B) B6 is needed in the synthesis of niacin. Also needed to synthesize DA, histamine, 5-HT and GABA.

C) Needed for cystathione synthase conversion to cysteine. Absence = homocysteinemia.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Southern blot
Northern blot
Western blot
Southwestern blot

A 
Southern = DNA
Northern = mRNA
Western = protein
Southwestern = DNA-bound protein
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Structures contained within the carpal tunnel

A

FDP, FDS, median nerve and FPL

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Common meds to avoid in older adults (Beers criteria)

A 
Anticholinergics
Alpha-blockers (orthostasis)
TCAs (sedation)
Sulfonylureas (hypoglycemia)
Muscle relaxants (sedation)
35
Q

1st line drug for acute gout flare

A

NSAIDs. PMNs phagocytose crystals and release inflammatory mediators that recruit more PMNs, resulting in a vicious cycle that can be broken by NSAID-mediated inhibition of prostaglandin synthesis and reduced PMN activation.

36
Q

Preferred therapy for gout prophylaxis

A

Xanthine oxidase inhibitors: allopurinol or febuxostat. Probenecid would be second line

37
Q

Bisphosphonate mechanism of action

A

Pyrophosphate analogue that attaches to hydroxyapatite binding sites on bone. Osteoclast uptake of bisphosphonates prevents further bone resorption, induce osteoclast apoptosis and reduce osteoclast recruitment and activation.

38
Q

Second line drugs for osteoporosis in patients who cannot tolerate bisphosphonates?

A

Raloxifen (SERM)
Teripartide (rPTH)
Denosumab (RANK-L monoclonal antibody)

39
Q

Characteristics of drugs that largely undergo hepatic metabolism prior to renal excretion

A

Highly lipophilic drugs (lipophilic drugs escape renal tubules easily) with a high volume of distribution.

40
Q

Drug efficacy

A

Maximum pharmacodynamic effect achievable with a given drug (loops are always more efficacious than thiazides, regardless of dose)

41
Q

Drug potency

A

Dose of drug required for desired effect. Drugs with better potency penetrate to target tissue well and have high affinity for the target receptor.

42
Q

Water soluble vitamin functions and signs of deficiency

A

B1 - decarboxylates alpha-keto acids in carbohydrate metabolism (pyruvate -> acetyl CoA and alpha-ketoglutarate -> succinyl CoA). Deficiency = beriberi (CHF, neuropathy) and Wernicke-Korsakoff syndrome.

B2 (riboflavin) - carries H+ in mitochondria (FAD, FMN). Deficiency = angular chelosis, stomatitis, glossitis and normocytic anemia

B3 (niacin) - H+ acceptor (NAD+). Deficiency = pellagra

B6 (pyridoxine) - transamination, decarboxylation and deamination of amino acids in amino acid synthesis. Deficiency = cheilosis, stomatitis, glossitis, seborrheic dermatitis, neuropathy.

B7 (biotin) - cofactor for all 4 carboxylase enzymes

B9 - hydroxymethyl/formyl carrier in purine and thymine synthesis. Deficiency = megaloblastic anemia and neural tube defects.

B12 - isomerase and methyltransferase cofactor in DNA and methionine synthesis. Deficiency = megaloblastic anemia and neurologic side effects

Ascorbic acid - hydroxylation of proline and lysine residues in collagen synthesis. Deficiency = scurvy.

43
Q

3 phases of wound healing

A

Inflammation: PMNs in 1st day, macrophages in 2-3 days for phagocytosis of necrotic debris

Proliferative: fibroblasts and endothelial vascular cells form granulation tissue with new vessels from days 3-5.

Maturation: fibroblasts synthesize collagen and elastin to form a scar by 6-8 weeks that increases in tensile strength (initially ~30%) over months

44
Q

What drug could you give a patient to augment the anti-inflammatory effects of azathioprine?

A

Xanthine oxidase inhibitor (allopurinol). This results in blockade of the inactivating pathway of azathioprine metabolism. Metabolized azathioprine instead goes the HGPRT route and serum levels of 6-TG increase, increasing its effects without increasing the dose.

45
Q

A mother notes that the urine in the toilet from her 2-year old turned black after sitting there for a while. He also has a bluish-black coloring to his ears, nose and cheeks. What enzyme deficiency could be causing his condition?

A

Homogentistic acid dioxygenase.

46
Q

Amino acids elevated in MSUD

A

Leu, Ile and Val

47
Q

Amino acid change associated with sickle cell anemia

A

Glu -> Val substitution

48
Q

What links osteocyte to osteocyte in mature bone?

A

Canaliculus. This is a gap junction and an extension of their plasma membranes that allow for signal transduction, solute absorption and solute excretion.

49
Q

Cyclosporine mechanism of action

A

Inhibits NFAT from entering the nucleus and impairs the production and release of IL-2

50
Q

Why use calcipotriol for psoriasis?

A

It activates the vitamin D receptor, which promotes keratinocyte differentiation and limits proliferation.

51
Q

Biologics used in treatment of psoriasis

A

Etanercept (anti-TNF-alpha) and ustekinumab (anti-IL-12 and IL-23, limits proliferation of CD4+ T-cells and Th17 cells)

52
Q

How does PTH stimulate bone resorption

A

It binds to osteoblasts, causes them to release RANK-L and M-CSF, which activates osteoclasts and increases production of osteoclasts.

It also reduces production of OPG, which competitively inhibits RANK-L binding to the osteoclastic receptor. Note that estrogen increases OPG levels, decreasing osteoclast activation.

53
Q

Hypothesized pathogenesis of SLE

A

Normally T-cells express a Fas receptor and undergo apoptosis in the presence of constant stimulation by self antigens. Normally Fas-L binds Fas-R -> initiator caspase activation (8 & 10) -> executioner caspase activation (3 & 6) -> karyorrhexis, organelle autophagy and membrane blebbing. Any disruption in this process can result in accumulation of excess T-cells that respond to self.

54
Q

Costimulatory molecules necessary for T-cell activation

A

CD28 on T-cell

B7 and APC

55
Q

Costimulatory molecules necessary for B-cell class switching to occur

A

CD40 on activated B-cell

CD40L on activated T-cell with subsequent cytokine release

56
Q

Viruses with segmented genomes

A

Orthomyxoviruses and rotavirues

57
Q

Universal start codon

A

AUG -> methionine

58
Q

Stop codons

A

UAG, UGA and UAA stimulate releasing factor binding to ribosome and release of the amino acid chain

59
Q

Oocyte progression through puberty and menstruation

A

By 5 months gestation, the full store of oocysts are determined and are arrested in prophase of meiosis I as primary oocytes (46, 4N) until puberty.

At puberty, FSH causes a handful of oocytes to complete meiosis I and become secondary oocytes (23, 2N) and polar bodies. The polar body degenerates and the secondary oocyte progresses to metaphase of meiosis II.

At fertilization, meiosis II completes with the paternal DNA and the second polar body degenerates.

60
Q

How does S. aureus avoid opsonization and phagocytosis?

A

Protein A binds IgG at the complement binding site in the Fc region, preventing production of C3b necessary for opsonization.

61
Q

Why are COX-2 inhibitors associated with higher likelihood of stroke/MI?

A

They block production of PGI2, which normally causes vasodilation and inhibits platelet aggregation. COX-1 activity is also preserved with increased Tx-A2 activity, vasoconstriction and platelet aggregation.

62
Q

A patient presents with:
1) Sensory deficit on medial thigh and inability to adduct the thigh
2) Sensory deficit on anterior thigh and medial leg with poor thigh flexion and leg extension
3) Sensory deficit on lateral leg with poor foot eversion, dorsiflexion and toe extension
4) Sensory deficit on bottom of foot with poor foot inversion, plantar flexion and toe flexion
5)

A

1) L2-L4 obturator
2) L2-L4 femoral
3) L4-S2 common peroneal
4) L4-S3 tibial

63
Q

Pathogenesis of acne vulgaris

A

1) Follicular epidermal hyperplasia with keratin plug that blocks sebum secretion (mechanism of steroid-related acne)
2) Hypertrophy of sebaceous gland (mechanism of steroid-related acne)
3) Gland colonization with propionibacterium acnes
4) Bacteria hydrolyzes TGs in sebum and inflammatory fatty acids are released

64
Q

Merocrine vs. Holocrine vs. Apocrine glands

A

Merocrine: exocytosis, salivary, eccrine sweat and apocrine sweat glands

Apocrine: vesicles, mammary glands

Holocrine: cell lysis, sebaceous and meibomian gland

65
Q

How does the splicesome work?

A

snRNPs bind to the 5’ donor site and the branch point on the intron. The 5’ end is cleaved and joins the branch point. Finally, the 3’ end is cleaved and the two ends of the exon on joined by a phosphodiester linkage.

66
Q

Disease with anti-snRNP antibodies

A

Mixed connective tissue disease

67
Q

Latissimus dorsi innervation

A

Thoracodorsal nerve

68
Q

Enzyme that forms pre-mRNA from DNA template

A

RNA polymerase II

69
Q

Post-transcriptional processing of pre-mRNA

A

7-methyl-guanosine cap is added to the 5’ end
Poly-A polymerase adds poly A tail after the segment AAUAAA
Introns are removed by splicesome

70
Q

How is collagen able to form a tight triple helix?

A

It has a simple amino acid sequence of Gly-X-Y that gets repeated and allows for tight coiling. Many of the X and Y’s are Pro because it allows for bending of the helix.

71
Q

How does allergic contact dermatitis occur?

A

Lagerhans cells take the antigen to the lymph node and present it to naive CD4+ T-cells. CD4+ T-cells migrate from lymph node to dermis and induce an inflammatory reaction within 24 hours of antigen re-exposure.

72
Q

Epidermal acanthosis

A

Expansion of the stratum spinosum

73
Q

Epidermal hyperparakeratosis

A

Nucleus remains in apical portion of epithelium, seen in actinic keratosis and psoriasis

74
Q

Essential cofactor needed for transaminases

A

B6

75
Q

Superficial infantile red compressible hemangioma with sharp borders that grows rapidly during the first 1 to 2 years of life and regress by age 5-8.

A

Strawberry capillary hemangioma

76
Q

Small bright red cutaneous papules that consist of dilated capillaries in adults

A

Cherry hemangioma

77
Q

Anti-histidyl-tRNA synthetase antibodies

A

Anti-Jo-1 antibodies present in most cases of polymyositis (biopsy will show endomysial inflammation as opposed to perimysial inflammation seen in dermatomyositis)

78
Q

Largest ion contributing to the resting membrane potential

A

K+, it has the highest conductance (permeability). Since there is some membrane permeability to Na+, the membrane potential is slightly more positive than the equilibrium potential of K+ by itself.

79
Q

c-Jun and c-Fos

A

Nuclear transcription factors coded for by a proto-oncogene that directly bind DNA via the leucine zipper motif.

80
Q

How to calculate serum drug concentration

A

Dose / Volume of Distribution

81
Q

Mechanism of development of wound contractures

A

MMPs degrade collagen and extracellular matrix. When there is excessive degradation and myofibroblast contraction, wound contractures can occur.

82
Q

A patient presents with fever, pruritic rash and arthralgias 1 week after receiving monoclonal antibody therapy for AIHA. Skin biopsy reveals small vessel vasculitis with fibrinoid necrosis and PMN infiltrate. What labs would you expect to see?

A

This patient has serum sickness (type III hypersensitivity). Labs would show decreased C3 secondary to deposition of complement fixing antibodies.

83
Q

Mechanism of urushiol contact dermatitis

A

Type IV hypersensitivity.
Langerhans cells phagocytose antigen and take it to regional lymph node and present it to CD4+ and CD8+ T-cells. This causes activation and clonal expansion over 10-14 days. 2-3 days after the second hapten exposure, the CD8+ T-cells that have migrated peripherally and induce apoptosis.

84
Q

Most common location in bone to see hematogenously seeded osteomyelitis in kids?

A

Metaphysis of long bones due to slow flowing vasculature through sinusoids. Note that the vertebral body is the most common location in adults.

Step 1 (14 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions