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MSS Gun Show > Upper Body > Flashcards

Upper Body Flashcards

1
Q
A
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4
Q

Pronator Teres

Orgin

Insertion

Innervation

action

A

Medial Epicondyle - Humerus and Ulnar Head

Middle lateral surface of radius

Median n.

Pronates forearm and hand; flexes forearm

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5
Q

Flexor carpi radialis

orgin

insertion

innervation

A

Medial epicondyle - humerus

Base of 2nd metacarpal

Median n

Flexes and abducts hand

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6
Q

Palmaris longus

orgin

insertion

innervation

action

A

Medial epicondyle - humerus

Flexor retinaculum and palmar aponeurosis

Median n.

Flexes hand and tenses palmar aponeurosis

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7
Q

Flexor carpi ulnaris

orgin

insertion

innervation

action

A

Humeral head - Medial epicondyle and Ulnar head - Olecrannon process (medial edge)

Pisiform, hook of hamate and 5th metacarpal

Ulnar n.

Flexes and adducts hand

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8
Q

Flexor digitorum superficialis

orgin

insertion

innervation

action

A

Humeroulnar head and Radial head

Middle phalanges of 4 fingers

Median n.

Flexes PIP, MCP of 4 fingers and wrists

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9
Q

Flexor digitorum profundus

orgin

insertion

innervation

action

A

Anterior ulna and interosseous membrane

Distal phalanges of 4 fingers

Anterior interosseous br. of median for radial half

ulnar n. for ulnar half

Flexes DIP, MCP, PIP of 4 fingers; flexes wrists

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10
Q

Flexor pollicis longus

orgin

insertion

innervation

action

A

Anterior radius and interosseous membrane

Distal phalanx of thumb

Anterior interosseous br. of median n.

Flexes thumb MCP and carpometacarpal joints

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11
Q

Brachioradialis

orgin

insertion

innervation

action

A

Lateral supracondylar ridge of humerus

lateral surface of distal radius

Radial n.

flexes forearm

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12
Q

Extensor carpi radialis longus

orgin

insertion

innervation

action

A

Lateral supracondylar ridge of humerus

Base of 2nd metacarpal

Radial n.

Extends and abducts hand

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13
Q

Extensor carpi radialis brevis

orgin

insertion

innervation

action

A

Lateral epicondyle

Base of 3rd metacarpal

Deep radial n./Post. interosseous n.

Extends and abducts hand

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14
Q

Extensor digitorum

orgin

insertion

innervation

action

A

Lateral epicondyle

Dorsal surface of the distal and middle phalanges of 4 fingers

Deep radial n./Post. interosseous n.

Extends fingers at MCP and interphalangeal joints

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15
Q

Extensor carpi ulnaris

orgin

insertion

innervation

action

A

Lateral epicondyle and posterior ulna

Base of 5th metacarpal

Deep radial n./Post. interosseous n.

Extends and adducts hand

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16
Q

Supinator

orgin

insertion

innervation

action

A

Lateral epidondyle, radial collateral and annular ligaments, post. ulna

Lateral, anterior/posterior radius

Deep radial n./Post. interosseous n.

Supinates forearm

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17
Q

Abductor pollicis longus

orgin

insertion

innervation

action

A

Posterior ulna, interosseous membrane and post. radius

Base of 1st metacarpal

Deep radial n./Post. interosseous n.

Abducts and extends thumb

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18
Q

Extensor pollicis brevis

orgin

insertion

innervation

action

A

Posterior radius and interosseous membrane

Base of proximal phalanx of thumb

Deep radial n./Post. interosseous n.

Extends thumb at MCP and CM joints

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19
Q

Extensor pollicis longus

orgin

insertion

innervation

action

A

Posterior ulna and interosseous membrane

Base of distal phalanx of thumb

Deep radial n./Post. interosseous n.

Extends thumb at IP, MCP and CM joints

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20
Q

boundaries of the ‘anatomical snuff box’ (medial, lateral, floor)

What nerve passes through it?

A

Extensor pollicis longus (EPL) tendon - medially

Extensor pollicis brevis (EPB) tendon - laterally

Abductor pollicis longus (APL) tendon - laterally

floor - scaphoid (most frequent fractured carpal) and trapezium

radial artery

superficial radial n.

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21
Q

Carpal tunnel

What are its contents?

A

flexor retinaculum spans the lateral-most and medial-most carpal bones of the proximal and distal rows

  • 4 Flexor digitorum superficialis tendons

- 4 Flexor digitorum profundus tendons

- Flexor pollicis longus tendon

- Median nerve

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22
Q

What is high-energy phosphate transfer potential?

name 1 example

A

Breaking the terminal phosphate bond of ATP releases energy –> drives rxns in the cell

example: phosphocreatine and ATP reaction; phosphocreatine

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23
Q

The creation of ATP without oxygen is called?

A

substrate-level phosphorylation

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24
Q

High energy compounds found in the Glycolytic pathway that have high-energy phosphate transfer potential? (4)

A

Phosphoenolpyruvate >> phosphocreatine (creatine phosphate) > 1,3-bisphosphoglycerate >> ATP (gamma-phosphate)

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25
Q

How does the mass action effect facilitate the reformation of creatine phosphate in muscle during rest after exercise?

A

depends on [products/substrates] in cell

log of ratio < 1 = negative delta G

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26
Q

Hexokinase Features

Product?

Cofactor?

A

Phosphorylation by use of ATP traps glucose in cell forming Glucose-6-P

ATP high energy and G6P low energy = irreversible

Cofactor is Mg2+

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27
Q

Phosphofructokinase features

product?

A

Phosphorylates Fructose-6-P ⇒ Fructose-1,6-biphosphate using ATP

is the rate-determining step of glycolysis

irreversible

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28
Q

What is the rate-determing step of glycolysis?

A

Fructose-6-phosphate ⇒ Fructose-1,6-biphosphate

Phosphofructokinase

irreversible

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29
Q

Features of Glyceraldehyde-3-P

what is the coenzyme?

A

Glyceraldehyde-3-P (1st half glycolysis) ⇒ 1,3-Bisphosphoglycerate

NAD+ is the coenzyme that is reduced to NADH by oxidizing G-3-P; phosphate comes from Pi

NAD+ cofactor must be continuously replenished by oxidizing NADH; otherwise glycolysis will stop

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30
Q

What is NAD+ derived from?

A

niacin

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31
Q

Phosphoglycerate Kinase features?

A

1,3-Biphosphoglycerate ⇒ 3-Phosphoglycerate

1st site of ATP production; 2 ATP

substrate-level phosphorylation

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32
Q

What enzyme is responsible for the 1st site of ATP production in Glycolysis?

A

Phosphoglycerate Kinase

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33
Q

Pyruvate kinase features?

A

Phosphoenolpyruvate ⇒ Pyruvate

2nd site of ATP production; 2 ATP

substrate-level phosphorylation

end of glycolysis

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34
Q

How is NAD+ regenerated anaerobicaly in glycolysis?

what enzyme is it feeding?

A

Pyruvate ⇒ Lactate (lactate dehydrogenase)

NADH + H+ ⇒ NAD+

glyceraldehyde-3-P dehydrogenase

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35
Q

Niacin defiecieny name?

characterized by 4 D’s

A

Pellagra

  • diarrhea*
  • dermatitis*
  • dementia*
  • death*
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36
Q

Outline the pathway of glycogenesis

A

Glucose ⇒ G-6-P (hexokinase; ATP)

G-6-P ⇒ G-1-P (phosphoglucomutase)

G-1-P ⇒ UDP-glucose (Glucose-1-P Uridyl-Transferase) (UTP ⇒ PPi)

UDP-glucose ⇒ Glucose-branched (Glycogen synthetase)

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37
Q

What is the principal, regulated enzyme of glycogenesis?

A

glycogen synthase

regulated by phosphorylation to hormonal signals

UDP-glucose ⇒ glucose-branched

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38
Q

Outline the path of glycogenolysis

A

Glycogen ⇒ G-1-P (glycogen phosphorylase)

G-1-P ⇒ G-6-P (phosphoglucomutase)

G-6-P ⇒ Pyruvate (glycolysis)

w/o O2 ⇒ lactate (lactate dehydrogenase)

w/ O2 Pyruvate ⇒ Acetyl-CoA ⇒ CO2

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39
Q

the principal enzyme of glycogenolysis?

A

glycogen phosphorylase

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40
Q

what is the principal enzyme of glycogenolysis?

what is its cofactor?

A

glycogen phosphorylase

pyridoxal phosphate

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41
Q

Overview of Fatty Acid Degradation

A

FFA into muscle cell (albumin) ⇒ fatty-acyl-CoA (acyl CoA synthetase)

fatty-acyl-CoA (Palmitate) cant be transported to mit. matrix directly ⇒ carnitine transporter ⇒ palmitoyl CoA

Thru oxidation/hydration steps ⇒ FADH2 (2 ATP) and NADH (3 ATP) via respiratory chain

Product = acetyl CoA and a fatty acyl CoA molecule that is two carbons shorter; in this case a 14-carbon fatty acyl CoA

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42
Q

How many times does the 16-carbon palmitoyl CoA cycle through in the Beta-oxidation pathway?

A

7 times

to produce 8 molecules of acetyl CoA from palmitoyl CoA.

each cycle produces FADH2 and NADH, which are then oxidized in the respiratory chain, forming ATP

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43
Q

How is Hexokinase allosterically regulated?

Why is this advantageous?

A

The product, G-6-P will inhibit Hexokinase if the cell has too much glucose.

excessive glycolytic intermediates ⇒ limit free Pi for synthesis of ATP

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44
Q

What are the allosteric regulators of Phosphofructokinase-1 (PFK)?

A

PFK is a physiologically irreversible rxn (rate-determining step)

under certain conditions (exercise), a phosphatase (fructose-1,6-biphosphatase) will provide glucose-6-P for glycogen stores

High ATP inhibits PFK

High [H+] (high metabolic activity) inhibits PFK

High AMP activates PFK; inhibits fructose-1,6-BP

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45
Q

Activator of Phosphofructokinase

A

AMP

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46
Q

Inhibitors of Phosphofructokinase

A

ATP

H+

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47
Q

Inhibitor of Fructose-1,6-bisphosphatase

A

AMP

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48
Q

What is AMP a signal of in the cell?

A

Low Energy

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49
Q

Overall why is Fructose-1,6-BisPhosphatase activated in the cell?

A

reverse glycolysis to provide G-6-P for the replenishment of glycogen stores from circulating lactate.

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50
Q

How does Epinephrine increase glucose?

A

GPCR → cAMP → PKA → Phosphorylase kinase-P → Glycogen phosphorylase -P

PKA → Glycogen synthase-P (inactive)

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51
Q

What is an allosteric activator of Phosphorylase kinase?

A

Ca2+

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52
Q

What is an allosteric activator of Glycogen Phosphorylase?

What other pathway does this signal substrate work on?

Why?

A

AMP

(Glycogen Phosphorylase: tense to relaxed form)

AMP signals the cell to mobilize more glucose, and at the same time, stimulates phosphofructokinase to catalyze the reaction of fructose-6–P to fructose- 1,6–bisphosphate (advancing to the next steps of glycolysis to produce more energy).

mobolize glucose

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53
Q

Besides inhibiting Hexokinase, G-6-P can inhibit and activate which substrates in Epi pathway?

A

Inhibit ⇒ Glycogen Phosphorylase-P

Activate ⇒ Glycogen Synthase-P (inactive)

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54
Q

How does insulin reverse the cyclic AMP-mediated cascade?

What phosphatase does it activate?

A

Phosphodiesterase = cAMP ⇒ AMP

inactivates PKA

activates protein phosphatase (removes P from phosphorylase kinase and glycogen phosphorylase to inactivate)

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55
Q

How does G-6-P inhibit glycogenolysis and activate glycogenesis?

A

Inhibits phosphorylase kinase

Turns glycogen phosphorylase to its tense (inactive) state. In this state glycogenolysis is inhibited

allosteric activator to glycogen synthase-d, allowing override of hormonal input. Glycogen synthase may be inactive - d form (phosphorylated)

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56
Q

E1 for pyruvate dehydrogenase complex

cofactors?

classification (coenzyme, prosthetic)?

vitamin source?

function?

Deficiency leads to what?

A

Cofactor: thiamine diphosphate

Type: Prosthetic group

Vitamin source: Thiamine

Function: carries acetate carbons to E2

Deficiency: leads to Beri Beri and is associated with muscle weakness, heart failure. Insufficient energy production.

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57
Q

E2 for pyruvate dehydrogenase complex

cofactors?

classification (coenzyme, prosthetic)?

vitamin source?

function?

Deficiency leads to what?

A

Coenzyme A

Cosubstrate

Pantothenic acid

Activates acetate group

Lipamide

Prosthetic group

none, dietary

Oxidizes product from E1

Cofactor for alpha-ketoglutarate dehydrogenase.

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58
Q

E3 for pyruvate dehydrogenase complex

cofactors?

classification (coenzyme, prosthetic)?

vitamin source?

function?

Deficiency leads to what?

A

Cofactor: FAD

Type: Prosthetic group

Vitamin source: riboflavin

Function: Reoxidizes lipoate

Cofactor: NAD+
Type: Co-substrate

Dietary source: niacin

Function: Reoxidizes FAD

Deficiency: Niacin deficiency (pellagra) is characterized by the 4 Ds: diarrhea, dermatitis, dementia, and death.

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59
Q

How is the pyruvate dehydrogenase complex regulated allosterically?

A

Acetyl CoA ⇒ E2

NADH ⇒ E3

Remember: these are products; pool of NAD+ is limited; do not want to waste energy

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60
Q

How is the pyruvate dehydrogenase complex regulated via phosphorylation of E1?

A

Phosphorylation of E1 deactivates the enzyme

Pyruvate Dehydrogenase Kinase (PDH Kinase) is activated by Acetyl-CoA and NADH

PDH Kinase is inhibited by Pyruvate, NAD+, CoA-SH

PDH phosphatase works on E1 = activation

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61
Q

isocitrate → alpha-ketoglutarate

enzyme?

cofactors?

A

Isocitrate dehydrogenase

NAD+ → NADH

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62
Q

alpha-ketoglutarate → Succinyl CoA

enzyme?

cofactors?

A

alpha-ketoglutarate dehydrogenase

CoA, NAD+ → NADH, CO2

cofactors:

NAD+ = cosubstrate

FAD = Prosthetic group

Lipoic acid = prosthetic

thiamine diphosphatase

CoA-CO = substrate

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63
Q

Succinyl CoA → Succinate

enzyme?

cofactors?

A

Succinyl CoA Synthetase

GDP → GTP → ADP → ATP + GDP

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64
Q

Succinate → Fumarate

enzyme?

A

succinate dehydrogenase (attached to membrane)

FAD → FADH2

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65
Q

Malate → Oxaloacetate

enzyme?

A

Malate dehydrogenase

NADH → NAD+

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66
Q

What does NADH inhibit in the Citric Acid Cycle?

A

the 2 enzymes that produce it

alpha-ketoglutarate

isocitrate dehydrogenase

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67
Q

What inhibits alpha-ketoglutarate dehydrogenase?

A

NADH (product)

succinyl CoA (product)

ATP, GTP (do not need more energy)

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68
Q

What signals low cellular energy levels that activates isocitrate dehydrogenase?

A

ADP

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69
Q

What is preemptive analgesia?

A

pre-incisional local anesthesia will help block pain impulses

70
Q

Why do we use multiple levels of analgesia for pain management?

A

to facilitate rehabilitation and a return to normal function.

Accomplished by reducing pain and inflammation at both the central and the peripheral nerve levels.

71
Q

phenanthrene alkaloids opiods

A

morphine

codeine

72
Q

semisynthetic opioids

A

hydrocodone

oxycodone

73
Q

synthetic opioids

A

meperidine

fentanyl

sufentanil

methadone

74
Q

advantage of opioids

A

act both centrally and peripherally

75
Q

Opioids mechanism of action

A

mimic endogenous opioid peptides (enkephalins and endorphins)

mu-GPCRi

  1. inhibit voltage gated Ca2+ channels
  2. open K+ channels → neuronal hyperpolarization
76
Q

Where do opioids work in general?

A

mu GPCRi in the brainstem on GABA neurons resulting in disinhibition to “turn-on” neurons resulting in activation of the descending brainstem pain inhibition pathways as well as activation of dopamine cells in the VTA to release dopamine in the nucleus accumbens resulting in rewarding behavior

77
Q

How are opioids best used for treatment?

A

PCA machine (Patient-Controlled Analgesia)

Scheduled dose regimen

acute- used for moderate-severe; fracture, soft-tissue injury

chronic - cancer, inflammatory arthritis

78
Q

Opioid adverse effects?

A

CNS depression

sedation

urinary retention

constipation

nausea

vomitting

Reversible w/ naloxone

79
Q

advantages of NSAIDs

A

used perioperatively, combined w/ opioids, they tend to decrease narcotic consumption

fewer adverse SE’s

80
Q

NSAID mechanism of action

A

prevent enzyme cyclooxygenase from contributing to prostaglandin production

81
Q

Issues w/ NSAID use?

A

COX-1 constitutionally expressed in GI tract = ulcers

COX-2 is induced by cytokines, GF’s and endotoxins = cardiovascular issues

decrease in bone healing time (osteoblast/-clast effect)

82
Q

Actetaminophen

What does it do?

A

CNS

increase pain threshold

central inhibiton of prostaglandin production

83
Q

Tramadol (tapentadol) is a synthetic analogue of what?

What is its mechanism of action?

A

codeine

acts centrally w/ weak affinity for mu opioid receptors

inhibitor of NE and serotonin re-uptake

84
Q

Why is tramadol and NSAIDs used together?

Where are they normally used?

A

Combination: rapid analgesia from acetaminophen, longer duration from tramadol

regional neural blockade for mild-moderate pain

85
Q

What is used for regional anesthetic nerve blocks and neuraxial anesthesia?

A

Local anesthetics

lidocaine (3-4 hrs)

bupivacaine (4-6 hrs)

ropivacaine (less cardiotoxicity than bupivacaine)

86
Q

How do Regional Anesthetics work?

A

local anesthetic injected around the peripheral nerves from region involved in surgery to the CNS.

Blocks peripheral nerves for 6-8 hrs

use Ultrasound-guided regional anesthesia

87
Q

Most efficacious way to administor opioids for Neuraxial blocks?

A

intrathecal

epidural

88
Q

TCA’s used to treat chronic pain

A

amitriptyline

nortriptyline

desipramine

89
Q

SSRI’s used to treat chronic pain

A

sertraline

paroxetine

fluoxetine

90
Q

Anti-epileptics used to treat chronic pain

A

gabapentin

pregabalin

carbamazepine

lamotrigine

91
Q

Most common Corticosteroid used to treat chronic pain?

A

Prednisolone

92
Q

What Nociceptor fiber detects pain 1st?

Wht stimuli does this fiber detect?

A

A-delta (med. diameter, thinly myelinated)

detect noxious, mechanical and thermal stimuli

93
Q

What type of stimuli do C-fibers detect?

A

noxious mechanical, thermal and Chemical stimuli

94
Q

Trapezius

orgin

insertion

innervation

action

A

superior nuchal line

Ext. occipital protuberance

Ligamentum nuchae

Spinous processes C7-T12

Lateral clavicle

Acromion

Spine of scapula

Accessory n.

Elevates, depresses/retracts scapula

tilts glenoid upwards in abduction of arm

95
Q

Levator scapulae

orgin

insertion

innervation

action

A

transverse processess C1-C4

Upper part of medial border of scapula

Dorsal scapular n.

Elevates scapula

tilts glenoid downward

96
Q

Rhombodieus major and minor

orgin

insertion

innervation

action

A

Minor: spinous processes C7-T1

Major: Spinous processes of T2-T5

Vertebral border of scapula

Dorsal scapular n.

Retract and elevate scapula

tilts glenoid downward in adduction of arm against resistance

97
Q

Serratus anterior

orgin

insertion

innervation

action

A

ribs 1-8

Anterior surface of medial border of scapula

Long thoracic n.

Protracts scapula

rotates glenoid upward

holds scapula against thorax

98
Q

Pectoralis minor

orgin

insertion

innervation

action

A

Coracoid process

Ribs 3-5

Medial and Lateral pectoral n.

Protracts and depresses scapula

99
Q

Subscapularis

orgin

insertion

innervation

action

A

subscapular fossa

lesser tubercle

upper and lower subscapular n.

medially rotates arm

stabilizes shoulder joints

100
Q

Supraspinatus

orgin

insertion

innervation

action

A

Supraspinous fossa

greater tubercle (highest facet)

Suprascapular n.

Abducts arm (initiates abduction)

stabalizes shoulder joint

101
Q

infraspinatus

orgin

insertion

innervation

action

A

infraspinous fossa

greater tubercle (middle facet)

suprascapular n.

Laterally rotates arm

stabalizes shoulder joint

102
Q

Teres Minor

orgin

insertion

innervation

action

A

Lateral border of scapula

Greater tubercle (lowest facet)

Axillary n.

Laterally rotates arm

stabilizes shoulder joint

103
Q

Latissimus dorsi

orgin

insertion

innervation

action

A

spinous processes T7-T12

Thoracolumbar fascia

lumbar spinous processes, iliac crest, lower ribs

Intertubercular groove

Thoracodorsal n.

Adducts

Extends

Medially rotates arm

104
Q

Teres major

orgin

insertion

innervation

action

A

inferior angle of scapula

intertubercular groove

Lower subscapular n.

Adducts

extends

medially rotates arm

105
Q

Pectoralis Major

orgin

insertion

innervation

action

A

clavicle, sternum, costal cartilages, ext oblique aponeurosis

intertubercular groove

lateral pectoral n.

Adducts and medially rotates humerus

upper fibers flex arm

lower fibers extend arm from flexes position

106
Q

Deltoideus

orgin

insertion

innervation

action

A

spine of scapula, acromion process, clavicle

deltoid tuberosity

Axillary n.

Flexes, abducts, extends arm

107
Q

Triceps brachii

orgin

insertion

innervation

action

A

long head - infraglenoid tubercle of scapula

lateral head - posterolateral humeral shaft

medial head - posteromedial humeral shaft

Olecrannon process

Radial n.

Extends arm and forearm

108
Q

Biceps brachii

orgin

insertion

innervation

action

A

short head - coracoid process

long head - supraglenoid tubercle of scapula

Radial tuberosity

Musculocutaneous n.

Primarily supinates and flexes forearm

109
Q

Coracobrachialis

orgin

insertion

innervation

action

A

Coracoid process

humeral shaft

musculocutaneous n.

Flexes and adducts arm

110
Q

Brachialis

orgin

insertion

innervation

action

A

humeral shaft

ulnar tuberosity

musculocutaneous n.

flexes and adducts arm

111
Q

Brachialis

orgin

insertion

innervation

action

A

humeral shaft

ulnar tuberosity

musculocutaneous n. and radial n.

Flexes forearm

112
Q

What are the boundaries of the Triangular space?

contents?

(black dashes)

A

teres minor (axillary edge of scapula)

teres major

triceps brachii - long head

contents: circumflex scapular a.

113
Q

Boundaries of Quadrangular space?

Contents?

(white dashes)

A

teres minor

teres major

triceps brachii - long head

humerus

contents: axillary n.

posterior circumflex humeral a.

114
Q

Boundaries of Suprascapular notch

(gray circle)

contents?

A

suprascapular notch

superior transverse scapular ligament

contents: suprascapular n. (suprascapular a. passes above notch)

115
Q

Deltopectoral triangle boundaries?

contents?

A

deltoid, pectoralis major, clavicle

contents: cephalic vein
br. of thoracoacromial artery

lateral pectoral n.

116
Q

How does coordinated motion of the scapula and humerus result in full ROM of shoulder abduction

A

As the humerus abducts, the greater tubercle hits the acromion. This limits range of motion.

trapezius - retracts scapula; superiorly rotates glenoid fossa

serratus anterior - protracts scapula; superiorly rotates glenoid fossa

teres minor/infraspinatus externally rotate humerus

deltoid/suprspinatus abduct humerus

117
Q

Explain the sequence of movement from 0-180º

A

0-60º: deltoid/supraspinatus abduct humerus

60-120º: trapezius/serratus ant. rotate glenoid superiorly

deltoid/supraspinatus abduct humerus

around 90º - teres minor/ infraspinatus laterally rotate humerus clearing greater tubercle form acromion

120-180º: deltoid/supraspinatus abduct humerus

118
Q

What are chronic pain conditions where there is evidence to treat with acupuncture?

A

low back pain

knee osteoarthritis

migraine headaches

labor pain

119
Q

What aspects of yoga have an effect in management of chronic pain?

A

Asana - posture

lower stress levels (leads to muscle spasms)

improves sleep (poor sleep worsens pain)

breathing → PNS

120
Q

what are the mind-body medicine modalities used to treat chronic pain?

A

meditation and mindfulness

Cognitive Behavioral Therapy

Hypnosis

Relaxation (training to relax)

121
Q

internal validity

A

the study design performance at measuring differences, if they exist, between groups, i.e. intervention and control, that are due only to the hypothesized effect.

122
Q

Critical appraisal

A

The process of assessing and interpreting evidence systematically, considering its validity, results, and relevance.

123
Q

Randomized Controlled Trial

A

Essentially an experiment in which individuals are randomly allocated to receive or not receive an experimental preventive, therapeutic, or diagnostic procedure and then followed to determine the effect of the intervention.

124
Q

Eligibility criteria

Exclusion criteria

A

the set of criteria used to determine who can participate in a study

factors that exclude patients from participating in a study

125
Q

What are the fundamental characteristics of the RCT within a scientific article?

A

Patients randomly assigned to control or study treatment using an outside source

Study participants and caregivers do not know which group the patient belongs to

126
Q

Explain why concealment is important for Internal Validity

A

If the patient knows which group he/she belongs to, then this will bias their thinking towards the effectiveness of the treatment and may skew the results (the brain is very powerful and can influence the effectiveness of treatment)

Concealment attempts to remove a confounding factor, i.e. knowledge of received treatment, in order to more accurately assess whether or not the treatment works.

127
Q

Demonstrate a general understanding of how Internal Validity is presented and discussed in a Journal Club setting

A

Examine sample size, single/double blindedness, how the procedures or drugs were given (to indicate if they may be able to tell the difference between them), and whether or not the study went back to prove that patients didn’t know which treatment they were receiving.

Also examine if safety committees/review committees were involved to approve the study and to monitor its progress.

128
Q

What is the function of the Palamar Aponerurosis

A

Creates compartments

anchors flexed tendons

protection

129
Q

nerve that innervates Thenar compartment

A

Reccurent branch of median n.

130
Q

How would I perform a sensory test to localize carpel tunnel syndrome?

muscular test?

A

palmar branch good

numbness over cutaneous lateral 3.5 digits

opposition test (opponens pollicis)

131
Q

Guyon’s canal

A

b/w pisiform and hook of hamate

where ulnar n. enters

132
Q

Handlebar Neuropathy

A

causes: cysts

clot in ulnar a.

fracture of hamate

arthritis of wrist

pressure from pussy bicycle = “handlebar palsy”

= decreased feeling in medial 5th digit and weakness in hand muscles

133
Q

What is the optimal position of the wrist for gripping objects?

A

20-30º extension

134
Q

Why is 20-30º wrist extension optimal for gripping objects?

what position are the fingers in?

A

Max tension formed

MAX number of cross-bridges (2-2.2 µm)

wrist in ext./fingers slight flexion

135
Q

What are the motions of the MCPs, IPs when grasping an object?

A

The MCP joints are in slight flexion and the fingers are in flexion (DIP and PIP) to prepare to grasp the object.

136
Q

What are the muscle actions needed to grasp an object?

A

Open the hand: the wrist moves into the functional position via the extensor digitorum muscle. Other extrinsic muscles help to stabilize the wrist.

Shape the hand around the object: The lumbricals activate to flex the MCP and extend the PIPs and DIPs.

Fingers close around the object: lumbricals can flex the MCP, but flexor digitorum superficialis and profundus are needed to flex the DIPs and PIPs. The flexor force from FDS and FDP are stronger than the extension force from the lumbricals and extensor digitorum at the DIPs and PIPs.

137
Q

List the muscles and ligaments that make up the extensor mechanism

A

extensor hood

central tendon of the extensor digitorum tendon

2 lateral bands on each finger of the extensor digitorum tendon

138
Q

How does the extensor mechanism provide coordination of phalangeal motion and coordination of intrinsic and extrinsic muscle action

A

The extensor hood is a fibrous extension of the extensor digitorum tendons. It forms a tent of connective tissue across the proximal phalanx.

The lateral bands and the central tendon extend distally from the extensor hood.

Lumbrical and interosseus muscles attach to the extensor hood, allowing these muscles to have the ability to extend the DIP and PIP while flexing the MCP joint.

139
Q
A

Mallet Finger

rupture of the dorsal attachment to the distal phalanx

  • unable to extend the DIP joint
  • unopposed flexion of DIP joint
140
Q
A

Boutonniere Deformity

unable to extend PIP joint

unopposed flexion of PIP pulls DIP into hyperextension

  • lateral bands slip to ventral side of joint axis
  • rupture of central tendon
141
Q

What is happening at median nerve injury at MCP and IP joints?

A

unable to flex 2nd and 3rd MCP and IP joints

unopposed ext of MCP leads to hyperextension of MCP joints ⇒ pulls PIP and DIP into passive flexion

142
Q
A

Claw hand - ulnar n. injury

MCP hyperextension ⇒ ext. digitorum decreased sarcomere length (ineffective for PIP/DIP)

143
Q
A

Monteggia Fracture

Ulnar fracture w/ radial head dislocation

could bring avascular necrosis of radial head

144
Q
A

Galeazzi Fracture

radial fracture w/ distal ulnar dislocation

145
Q

MUGR

A

Monteggia - Ulnar (fracture)

Galeazzi - Radius (fracture)

146
Q
A

CPPD Arthropathy (Pseudogout)

weakly positive birefringent crystals

Ca2+ pyrophosphate in bone/soft tissue

147
Q
A

Boxer’s Fracture

occurs when punching

transverse fracture of 5th metacarpal

common in young adult males

148
Q
A

Rheumatoid Arthritis

periarticular osteopenia

bilateral and symmetric

joint space destruction

MCP joint subluxation

149
Q
A

Gout

Monosodium Urate Crystals

marginal erosions

overhanging edges

sclerotic borders

joint spaces relatively preserved

ST tophi (soft tissue dense)

150
Q

6 components of the Chronic Care Model

A
  1. Organization of Health Care - commitement to chronic care model
  2. Delivery system design - multiple visits, multiple people helping patient
  3. Decision support - latests guidelines, continual education for physicians
  4. Clinical information systems - can track chronic patients
  5. Patient self management - patient set goals
  6. Community Resources
151
Q

Role of healthcare team in acute care models

role of patient

A

health team: select and conduct therapy

patient: follow orders

152
Q

Role of healthcare team in chronic care models

role of patient

A

health team: Teach/coach/partner

patient: Partner/daily manager

153
Q

What is complex 1 and 3 of the respiratory chain linked by?

A

coenzyme Q

154
Q

Complex I contains?

A

NADH-Q reductase

NADH dehydrogenase

Fp (iron-containing flavoprotein)

155
Q

Contents of Complex III in respiratory chain?

A

cytochrome reductase

b cytochromes

cytochrome c1

156
Q

What are complexes II and III linked by in the respiratory chain?

A

coenzyme Q

157
Q

prosthetic groups of cytochromes?

A

heme irons

158
Q

contents of cytochrome IV?

what type of poisoning occurs here?

A

cytochrome oxidase

cytochrome c

cyt a-a3

<strong>cyanide</strong>

159
Q

What would be seen clinically with respiratory chain defects?

A

Lactic academia (High NADH favors formation of lactate from pyruvate)

High NADH inhibits PDH → blood pyruvate elevated

elevated pyruvate increases production of alanine

160
Q

What happens to ATP production if the ATPase (F1) does not have a proton gradient?

A

ATPase would cleave ATP in the matrix

161
Q

What happens when you inhibit the respiratory chain?

A

Prevents ATP synthesis causing all electron flow to cease. The mitochondrion is unable to pump protons so that mitochondrial respiration and ATP synthesis both cease.

162
Q

How is respiration controlled?

A

ADP increases in the mitochondrial matrix, ADP opens the proton channel.

As protons move thru channel down pH gradient, respiration increases to componsate for the decline in the pH gradient

matrix ADP is low, ATP synthesis ceases, the pH gradient builds up, and oxygen use diminishes.

These events correlate w/ the change in lung respiration during exercise

163
Q

uncoupling of ETC produces?

A

ETC operates at a high rate of respiration becasue protons are pumped out rapidly in an attempt to restore the pH gradient.

Instead energy is released as heat and body temp rises

citric acid cycle and PDH continues at a rapid rate as NADH is maximally oxidized (processes do not get inhibited)

Excessive oxidation of NADH restricts the formation of lactate since NADH is needed to reduce pyruvate to lactate

164
Q

MOA of Oligomycin

A

antibiotic

binds to the F0 component preventing proton flow to the F1-ATPase

proton pumping ceases because size of the pH gradient prohibits the pumping out of additional protons (respiration decreases)

Respiration will decrease even w/ plenty of ADP and phosphate

165
Q

Components of the ATP synthase complex

A

transmembrane component (F0) - proton channel

the stalk

F1-ATPase

166
Q

What causes ‘the stalk’ F0 to open in the ATP synthase complex?

A

increased levels of ADP in the matrix cause it to open

the stalk regulates the proton channel

F1-ATPase catalyzes synthesis of ATP

167
Q

How does the malate-aspartate channel work during respiration?

A

Overall: recycles NADH inside of matrix

  • NADH cant be moved into the mitochondria (made by glycolysis)
  • In the cytoplasm, malate dehydrogenase can reduce oxaloacetate to malate, which also regenrates NAD+ for glycolysis. Malate is shuttled into the matrix via an antiporter with alpha-ketoglutarate (electroneutral transporter).
  • (Matrix) oxaloacetate is regenerated via malate dehydrogenase in the citric acid cycle, which also generates NADH as a product by reducing NAD+.
  • Oxaloacetate is returned to the cytoplasm by moving an amino group onto oxaloacetate from glutamate (aspartate aminotransferase), producing aspartate and alpha-ketoglutarate. Alpha-ketoglutarate is transported out in exchange for malate, as above, and aspartate is transported out in exchange for glutamate. This second translocase iselectrogenic and only operates in one direction.
  • Cytoplasmic aspartate aminotransferase moves the amino group from aspartate to alpha-ketoglutarate, regenerating oxaloacetate (which will be reduced to malate) and glutamate (which will be transported into the matrix in exchange for aspartate).
168
Q

What is electrogenic transport? How does this transport benefit the release of ATP from the mitochondrial matrix?

A

Electrogenic transport relies on charge to move substances across the mitochondrial membrane. For example, an ADP molecule from the intermembrane space (charge —3) is switched with an ATP molecule from the matrix (charge —4); this works because charge is relatively more negative in the matrix than in the membrane space, and the transport has a net movement of —1 to the intermembrane space, which is favored under these conditions. The transports are not reversible because of this.

This type of transport allows ATP to be immediately removed from the mitochondrial matrix. If ATP were left inside, it would be broken back down by ATP Synthase.

169
Q

What is the function of the Complexes of the respiratory chain?

A

NADH dehydrogenase takes electrons from NADH and passes them to the FMN, creating FMNH2. This process pumps hydrogen ions into the intermembrane space.

Electrons are transferred to coenzyme Q, which transfers electrons to cytochrome b and then to c1 (complex III). This process also pumps protons into the intermembrane space.

Cytochromes contain heme prosthetic groups.

Cytochrome c1 passes the electrons to cytochrome c, then to cytochrome a (copper-containing complex IV). Cytochrome a3 accepts electrons from cytochrome a. Transfer through this complex also pumps hydrogen ions into the intermembrane space.

170
Q

What does each complex overall do ?

A

Each complex increases both the pH and charge gradient across the inner mitochondrial membrane.

171
Q
A

MSS Gun Show (2 decks)

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