Upper Body Flashcards

(171 cards)

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
How does the **mass action effect** facilitate the reformation of _creatine phosphate_ in muscle during rest after exercise?
depends on [products/substrates] in cell log of ratio \< 1 = negative delta G
26
Hexokinase Features Product? Cofactor?
Phosphorylation by use of ATP traps glucose in cell forming **Glucose-6-P** ATP high energy and G6P low energy = irreversible Cofactor is **Mg2+**
27
Phosphofructokinase features product?
Phosphorylates Fructose-6-P ⇒ Fructose-1,6-biphosphate using ATP is the rate-determining step of glycolysis irreversible
28
What is the rate-determing step of glycolysis?
Fructose-6-phosphate ⇒ Fructose-1,6-biphosphate **Phosphofructokinase** irreversible
29
Features of Glyceraldehyde-3-P what is the coenzyme?
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
30
What is NAD+ derived from?
niacin
31
Phosphoglycerate Kinase features?
1,3-Biphosphoglycerate ⇒ 3-Phosphoglycerate 1st site of ATP production; 2 ATP substrate-level phosphorylation
32
What enzyme is responsible for the 1st site of ATP production in Glycolysis?
Phosphoglycerate Kinase
33
Pyruvate kinase features?
Phosphoenolpyruvate ⇒ Pyruvate 2nd site of ATP production; 2 ATP substrate-level phosphorylation end of glycolysis
34
How is NAD+ regenerated anaerobicaly in glycolysis? what enzyme is it feeding?
Pyruvate ⇒ Lactate (lactate dehydrogenase) NADH + H+ ⇒ NAD+ **glyceraldehyde-3-P dehydrogenase**
35
Niacin defiecieny name? characterized by 4 D's
**Pellagra** * diarrhea* * dermatitis* * dementia* * death*
36
Outline the pathway of glycogenesis
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*)
37
What is the principal, regulated enzyme of glycogenesis?
**glycogen synthase** regulated by phosphorylation to hormonal signals UDP-glucose ⇒ glucose-branched
38
Outline the path of glycogenolysis
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
39
the principal enzyme of glycogenolysis?
**glycogen phosphorylase**
40
what is the principal enzyme of glycogenolysis? what is its cofactor?
**glycogen phosphorylase** pyridoxal phosphate
41
Overview of Fatty Acid Degradation
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
42
How many times does the 16-carbon palmitoyl CoA cycle through in the Beta-oxidation pathway?
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
43
How is **Hexokinase** allosterically regulated? Why is this advantageous?
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
44
What are the allosteric regulators of Phosphofructokinase-1 (PFK)?
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
45
Activator of Phosphofructokinase
AMP
46
Inhibitors of Phosphofructokinase
ATP H+
47
Inhibitor of Fructose-1,6-bisphosphatase
AMP
48
What is AMP a signal of in the cell?
Low Energy
49
Overall why is Fructose-1,6-BisPhosphatase activated in the cell?
reverse glycolysis to provide G-6-P for the replenishment of glycogen stores from circulating lactate.
50
How does Epinephrine increase glucose?
GPCR → cAMP → PKA → Phosphorylase kinase**-P** → Glycogen phosphorylase **-P** PKA → Glycogen synthase**-P** (inactive)
51
What is an allosteric activator of Phosphorylase kinase?
Ca2+
52
What is an allosteric activator of Glycogen Phosphorylase? What other pathway does this signal substrate work on? Why?
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
53
Besides inhibiting Hexokinase, G-6-P can inhibit and activate which substrates in Epi pathway?
Inhibit ⇒ Glycogen Phosphorylase**-P** Activate ⇒ Glycogen Synthase**-P** (inactive)
54
How does insulin reverse the cyclic AMP-mediated cascade? What phosphatase does it activate?
Phosphodiesterase = cAMP ⇒ AMP inactivates PKA activates **protein phosphatase** (removes **P** from phosphorylase kinase and glycogen phosphorylase to inactivate)
55
How does G-6-P inhibit glycogenolysis and activate glycogenesis?
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)
56
E1 for pyruvate dehydrogenase complex cofactors? classification (coenzyme, prosthetic)? vitamin source? function? Deficiency leads to what?
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.
57
E2 for pyruvate dehydrogenase complex cofactors? classification (coenzyme, prosthetic)? vitamin source? function? Deficiency leads to what?
Coenzyme A Cosubstrate Pantothenic acid Activates acetate group Lipamide Prosthetic group none, dietary Oxidizes product from E1 _Cofactor for alpha-ketoglutarate dehydrogenase._
58
E3 for pyruvate dehydrogenase complex cofactors? classification (coenzyme, prosthetic)? vitamin source? function? Deficiency leads to what?
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.
59
How is the pyruvate dehydrogenase complex regulated allosterically?
Acetyl CoA ⇒ E2 NADH ⇒ E3 Remember: these are products; pool of NAD+ is limited; do not want to waste energy
60
How is the pyruvate dehydrogenase complex regulated via phosphorylation of E1?
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
61
isocitrate → alpha-ketoglutarate enzyme? cofactors?
Isocitrate dehydrogenase NAD+ → NADH
62
alpha-ketoglutarate → Succinyl CoA enzyme? cofactors?
alpha-ketoglutarate dehydrogenase CoA, NAD+ → NADH, CO2 cofactors: NAD+ = cosubstrate FAD = Prosthetic group Lipoic acid = prosthetic thiamine diphosphatase CoA-CO = substrate
63
Succinyl CoA → Succinate enzyme? cofactors?
Succinyl CoA Synthetase GDP → GTP → ADP → ATP + GDP
64
Succinate → Fumarate enzyme?
succinate dehydrogenase (attached to membrane) FAD → FADH2
65
Malate → Oxaloacetate enzyme?
Malate dehydrogenase NADH → NAD+
66
What does NADH inhibit in the Citric Acid Cycle?
the 2 enzymes that produce it **alpha-ketoglutarate** **isocitrate dehydrogenase**
67
What inhibits alpha-ketoglutarate dehydrogenase?
NADH (product) succinyl CoA (product) ATP, GTP (do not need more energy)
68
What signals low cellular energy levels that activates isocitrate dehydrogenase?
ADP
69
What is preemptive analgesia?
_pre-incisional local anesthesia_ will help block pain impulses
70
Why do we use _multiple levels_ of analgesia for pain management?
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
phenanthrene alkaloids opiods
morphine codeine
72
semisynthetic opioids
hydrocodone oxycodone
73
synthetic opioids
meperidine fentanyl sufentanil methadone
74
advantage of opioids
act both centrally and peripherally
75
Opioids mechanism of action
mimic endogenous opioid peptides (enkephalins and endorphins) mu-GPCRi 1. inhibit voltage gated Ca2+ channels 2. open K+ channels → neuronal hyperpolarization
76
Where do opioids work in general?
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
How are opioids best used for treatment?
**PCA machine** (Patient-Controlled Analgesia) **Scheduled dose regimen** acute- used for moderate-severe; fracture, soft-tissue injury chronic - cancer, inflammatory arthritis
78
Opioid adverse effects?
CNS depression sedation urinary retention constipation nausea vomitting Reversible w/ **naloxone**
79
advantages of NSAIDs
used perioperatively, combined w/ opioids, they tend to decrease narcotic consumption fewer adverse SE's
80
NSAID mechanism of action
prevent enzyme cyclooxygenase from contributing to prostaglandin production
81
Issues w/ NSAID use?
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
Actetaminophen What does it do?
CNS increase pain threshold central inhibiton of prostaglandin production
83
Tramadol (tapentadol) is a synthetic analogue of what? What is its mechanism of action?
codeine acts centrally w/ weak affinity for mu opioid receptors inhibitor of NE and serotonin re-uptake
84
Why is tramadol and NSAIDs used together? Where are they normally used?
Combination: rapid analgesia from acetaminophen, longer duration from tramadol regional neural blockade for mild-moderate pain
85
What is used for regional anesthetic nerve blocks and neuraxial anesthesia?
Local anesthetics lidocaine (3-4 hrs) bupivacaine (4-6 hrs) ropivacaine (less cardiotoxicity than bupivacaine)
86
How do Regional Anesthetics work?
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
Most efficacious way to administor opioids for Neuraxial blocks?
intrathecal epidural
88
TCA's used to treat chronic pain
amitriptyline nortriptyline desipramine
89
SSRI's used to treat chronic pain
sertraline paroxetine fluoxetine
90
Anti-epileptics used to treat chronic pain
gabapentin pregabalin carbamazepine lamotrigine
91
Most common Corticosteroid used to treat chronic pain?
Prednisolone
92
What Nociceptor fiber detects pain 1st? Wht stimuli does this fiber detect?
A-delta (med. diameter, thinly myelinated) detect noxious, mechanical and **thermal** stimuli
93
What type of stimuli do C-fibers detect?
noxious mechanical, thermal and _Chemical_ stimuli
94
Trapezius orgin insertion innervation action
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
Levator scapulae orgin insertion innervation action
transverse processess C1-C4 Upper part of medial border of scapula Dorsal scapular n. Elevates scapula tilts glenoid downward
96
Rhombodieus major and minor orgin insertion innervation action
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
Serratus anterior orgin insertion innervation action
ribs 1-8 Anterior surface of medial border of scapula Long thoracic n. Protracts scapula rotates glenoid upward holds scapula against thorax
98
Pectoralis minor orgin insertion innervation action
Coracoid process Ribs 3-5 Medial and Lateral pectoral n. Protracts and depresses scapula
99
Subscapularis orgin insertion innervation action
subscapular fossa lesser tubercle upper and lower subscapular n. medially rotates arm stabilizes shoulder joints
100
Supraspinatus orgin insertion innervation action
Supraspinous fossa greater tubercle (highest facet) Suprascapular n. Abducts arm (initiates abduction) stabalizes shoulder joint
101
infraspinatus orgin insertion innervation action
infraspinous fossa greater tubercle (middle facet) suprascapular n. Laterally rotates arm stabalizes shoulder joint
102
Teres Minor orgin insertion innervation action
Lateral border of scapula Greater tubercle (lowest facet) Axillary n. Laterally rotates arm stabilizes shoulder joint
103
Latissimus dorsi orgin insertion innervation action
spinous processes T7-T12 Thoracolumbar fascia lumbar spinous processes, iliac crest, lower ribs Intertubercular groove Thoracodorsal n. Adducts Extends Medially rotates arm
104
Teres major orgin insertion innervation action
inferior angle of scapula intertubercular groove Lower subscapular n. Adducts extends medially rotates arm
105
Pectoralis Major orgin insertion innervation action
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
Deltoideus orgin insertion innervation action
spine of scapula, acromion process, clavicle deltoid tuberosity Axillary n. Flexes, abducts, extends arm
107
Triceps brachii orgin insertion innervation action
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
Biceps brachii orgin insertion innervation action
short head - coracoid process long head - supraglenoid tubercle of scapula Radial tuberosity Musculocutaneous n. Primarily supinates and flexes forearm
109
Coracobrachialis orgin insertion innervation action
Coracoid process humeral shaft musculocutaneous n. Flexes and adducts arm
110
Brachialis orgin insertion innervation action
humeral shaft ulnar tuberosity musculocutaneous n. flexes and adducts arm
111
Brachialis orgin insertion innervation action
humeral shaft ulnar tuberosity musculocutaneous n. and radial n. Flexes forearm
112
What are the boundaries of the Triangular space? contents? (black dashes)
teres minor (axillary edge of scapula) teres major triceps brachii - long head contents: circumflex scapular a.
113
Boundaries of Quadrangular space? Contents? (white dashes)
teres minor teres major triceps brachii - long head humerus contents: axillary n. posterior circumflex humeral a.
114
Boundaries of Suprascapular notch (gray circle) contents?
suprascapular notch superior transverse scapular ligament contents: suprascapular n. (suprascapular a. passes above notch)
115
Deltopectoral triangle boundaries? contents?
deltoid, pectoralis major, clavicle contents: cephalic vein br. of thoracoacromial artery lateral pectoral n.
116
How does coordinated motion of the scapula and humerus result in full ROM of shoulder abduction
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
Explain the sequence of movement from 0-180º
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
What are chronic pain conditions where there is evidence to treat with acupuncture?
low back pain knee osteoarthritis migraine headaches labor pain
119
What aspects of yoga have an effect in management of chronic pain?
Asana - posture lower stress levels (leads to muscle spasms) improves sleep (poor sleep worsens pain) breathing → PNS
120
what are the mind-body medicine modalities used to treat chronic pain?
meditation and mindfulness Cognitive Behavioral Therapy Hypnosis Relaxation (training to relax)
121
internal validity
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
Critical appraisal
The process of assessing and interpreting evidence systematically, considering its validity, results, and relevance.
123
Randomized Controlled Trial
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
Eligibility criteria Exclusion criteria
the set of criteria used to determine who can participate in a study factors that exclude patients from participating in a study
125
What are the fundamental characteristics of the RCT within a scientific article?
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
Explain why concealment is important for Internal Validity
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
Demonstrate a general understanding of how Internal Validity is presented and discussed in a Journal Club setting
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
What is the function of the Palamar Aponerurosis
Creates compartments anchors flexed tendons protection
129
nerve that innervates Thenar compartment
Reccurent branch of median n.
130
How would I perform a sensory test to localize carpel tunnel syndrome? muscular test?
palmar branch good numbness over cutaneous lateral 3.5 digits opposition test (opponens pollicis)
131
Guyon's canal
b/w pisiform and hook of hamate where ulnar n. enters
132
Handlebar Neuropathy
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
What is the optimal position of the wrist for gripping objects?
20-30º extension
134
Why is 20-30º wrist extension optimal for gripping objects? what position are the fingers in?
Max tension formed MAX number of cross-bridges (2-2.2 µm) wrist in ext./fingers slight flexion
135
What are the **motions** of the MCPs, IPs when grasping an object?
The MCP joints are in slight flexion and the fingers are in flexion (DIP and PIP) to prepare to grasp the object.
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What are the muscle actions needed to grasp an object?
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.
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List the muscles and ligaments that make up the extensor mechanism
extensor hood central tendon of the extensor digitorum tendon 2 lateral bands on each finger of the extensor digitorum tendon
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How does the extensor mechanism provide coordination of phalangeal motion and coordination of intrinsic and extrinsic muscle action
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.
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**Mallet Finger** rupture of the dorsal attachment to the distal phalanx - unable to extend the DIP joint - unopposed flexion of DIP joint
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**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
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What is happening at median nerve injury at MCP and IP joints?
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
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Claw hand - ulnar n. injury MCP hyperextension ⇒ ext. digitorum decreased sarcomere length (ineffective for PIP/DIP)
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**Monteggia Fracture** Ulnar fracture w/ radial head dislocation could bring avascular necrosis of radial head
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**Galeazzi Fracture** radial fracture w/ distal ulnar dislocation
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MUGR
**M**onteggia - Ulnar (fracture) **G**aleazzi - Radius (fracture)
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**CPPD** Arthropathy (Pseudogout) weakly positive birefringent crystals Ca2+ pyrophosphate in bone/soft tissue
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Boxer's Fracture occurs when punching transverse fracture of 5th metacarpal common in young adult males
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**Rheumatoid Arthritis** periarticular osteopenia bilateral and symmetric joint space destruction MCP joint subluxation
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**Gout** Monosodium Urate Crystals marginal erosions overhanging edges sclerotic borders joint spaces relatively preserved ST tophi (soft tissue dense)
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6 components of the Chronic Care Model
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**
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Role of healthcare team in acute care models role of patient
health team: select and conduct therapy patient: follow orders
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Role of healthcare team in chronic care models role of patient
health team: Teach/coach/partner patient: Partner/daily manager
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What is complex 1 and 3 of the respiratory chain linked by?
coenzyme Q
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Complex I contains?
**NADH-Q reductase** NADH dehydrogenase Fp (iron-containing flavoprotein)
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Contents of Complex III in respiratory chain?
**cytochrome reductase** b cytochromes cytochrome c1
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What are complexes II and III linked by in the respiratory chain?
coenzyme Q
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prosthetic groups of cytochromes?
heme irons
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contents of cytochrome IV? what type of poisoning occurs here?
**cytochrome oxidase** cytochrome c cyt a-a3 cyanide
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What would be seen clinically with respiratory chain defects?
Lactic academia (High NADH favors formation of lactate from pyruvate) High NADH inhibits _PDH_ → blood pyruvate elevated elevated pyruvate increases production of _alanine_
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What happens to ATP production if the ATPase (F1) does not have a proton gradient?
ATPase would cleave ATP in the matrix
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What happens when you inhibit the respiratory chain?
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.
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How is respiration controlled?
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
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uncoupling of ETC produces?
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
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MOA of Oligomycin
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
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Components of the ATP synthase complex
transmembrane component (F0) - proton channel the stalk F1-ATPase
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What causes 'the stalk' F0 to open in the ATP synthase complex?
increased levels of ADP in the matrix cause it to open the stalk regulates the proton channel F1-ATPase catalyzes synthesis of ATP
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How does the malate-aspartate channel work during respiration?
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).
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What is electrogenic transport? How does this transport benefit the release of ATP from the mitochondrial matrix?
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.
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What is the function of the Complexes of the respiratory chain?
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.
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What does each complex overall do ?
Each complex increases both the pH and charge gradient across the inner mitochondrial membrane.
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