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Unit 2: SIGS > Week 2 > Flashcards

Week 2 Flashcards

1
Q

Describe the clinical presentation of discogenic low back pain

A
  • pain radiation to the buttocks or proximal posterior thigh and increased pain with prolonged sitting, coughing, sneezing, or a Valsalva maneuver.
  • Disk herniations typically cause mechanical or chemical irritation of a nerve root (or both) with corresponding radicular symptoms of numbness, tingling, or weakness.
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2
Q

Acute back pain

  • how long does it last?
  • how do you fix it?
  • how is it caused?
A
  • lasts a few days to a few weeks
  • resolve on its own with self-care and there is no residual loss of function.
  • mechanical in nature, disruption in the way the components of the back (the spine, muscle, intervertebral discs, and nerves) fit together and move.
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3
Q

Subacute low back pain

A

pain that lasts between 4 and 12 weeks.

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4
Q

Chronic back pain

  • how long?
  • how many people?
  • does it go away?
A
  • pain that persists for 12 weeks or longer, even after an initial injury or underlying cause of acute low back pain has been treated.
  • 20 percent of people affected by acute low back pain develop chronic low back pain
  • pain can persist despite medical and surgical treatment.
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5
Q

Sprains

A

caused by overstretching or tearing ligaments

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6
Q

Strains

A

tears in tendon or muscle

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7
Q

Intervertebral disc degeneration

A

discs lose integrity as a normal process of aging

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8
Q

Herniated or ruptured discs

A

when the intervertebral discs become compressed and bulge outward (herniation) or rupture,

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9
Q

Radiculopathy

  • what is it?
  • what does it feel like?
  • how is it caused?
A
  • compression, inflammation and/or injury to a spinal nerve root
  • results in pain, numbness, or a tingling sensation that travels or radiates to other areas of the body that are served by that nerve
  • spinal stenosis or herniated/ruptured disk
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10
Q

Sciatica

A
  • form of radiculopathy caused by compression of the sciatic nerve
  • causes shock-like or burning low back pain combined with pain through the buttocks and down one leg, occasionally reaching the foot
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11
Q

Spondylolisthesis

A

condition in which a vertebra of the lower spine slips out of place, pinching the nerves exiting the spinal column

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12
Q

Spinal stenosis

A

narrowing of the spinal column that puts pressure on the spinal cord and nerves

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13
Q

Infection causing back pain

A
  • osteomyelitis: infection of vertebrae
  • discitis: infection of intervertebral discs
  • sacroilitis: infection of sacrum and illiac bones
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14
Q

Cauda equina syndrome

A

serious but rare complication of a ruptured disc. It occurs when disc material is pushed into the spinal canal and compresses the bundle of lumbar and sacral nerve roots, causing loss of bladder and bowel control. Permanent neurological damage may result if this syndrome is left untreated.

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15
Q

Osteoporosis

A

-metabolic bone disease marked by a progressive decrease in bone density and strength, which can lead to painful fractures of the vertebrae

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16
Q

Kidney stones

A

can cause sharp pain in the lower back, usually on one side

17
Q

Abdominal aortic aneurysms

A

large blood vessel that supplies blood to the abdomen, pelvis, and legs becomes abnormally enlarged. Back pain can be a sign that the aneurysm is becoming larger and that the risk of rupture should be assessed.

18
Q

utility of NSAIDs for acute mild low back pain

A
  • relieve pain and inflammation
  • inhibit Cox1 and Cox2 which prevents arachadonic acid from being made into prostaglandins, thromboxane, and prostacyclin–stops increased inflammation
19
Q

Side effects of NSAIDs

A
  • stomach irritation, ulcers, heartburn, diarrhea, fluid retention, kidney dysfunction and cardiovascular disease
20
Q

Ketorolac

A
  • inhibition of COX-1 and COX-2
  • indirect analgesic effect by inhibiting prostaglandins E and F
  • bio availability is 100% orally
21
Q

Ibuprofen

A
  • inhibition of COX-1 and COX-2
  • indirect analgesic effect by inhibiting prostaglandins E and F
  • bio availability is 80% orally
22
Q

DOCSIFY the straight leg test

  • name
  • use
  • how performed
  • positive
  • negative
A
  • Name: Lasegue’s Supine Straight-Leg-Raising Test.
  • Use: Checks for radiculopathy and impingement of the nerves
  • Steps to Perform Test: The patient lies supine with legs extended. The examiner places one hand under the heel of the affected side and the other hand is placed on the knee to prevent the knee from bending. With the limb extended, the examiner flexes the thigh on the pelvis to the point of pain, keeping the knee straight.
  • Positive: maneuver is markedly limited by pain, suggests sciatica/ radiculopathy (usually caused by herniation)
  • Negative: limb extended to almost 90° without pain.
23
Q

DOCSIFY the Thomas test

A
  • Name: Thomas test
  • Use: measure the flexibility of the hip flexors, which includes the iliopsoas muscle group, the Rectus Femoris, pectineus, gracillus as well as the Tensor Fascia Latae and the sartorius.
  • Steps to Perform Test: patient is supine on the examination table, butt at the end allowing knees to be off and flexed; patient brings both knees to chest then extends one leg, bring one knee towards chest;
  • Positive: If quad is extended while knee is bent and quad is raised off table OR If quad is extended while knee is bent and quad is touching table but knee cant bend more than 70 degrees then rectus femoris tight; If quad is extended and knee is extended and leg is raised off table then iliopsoas tight;
  • Negative: If extended leg is able to lie flat on table and when bent able to bend more than 70 degrees then iliopsoas and rectus femoris not tight
24
Q

strength testing

-levels and what they designate

A
  • 0/5: no contraction
  • 1/5: muscle flicker, but no movement
  • 2/5: movement possible, but not against gravity (test the joint in its horizontal plane)
  • 3/5: movement possible against gravity, but not against resistance by the examiner
  • 4/5: movement possible against some resistance by the examiner (sometimes this category is subdivided further into 4–/5, 4/5, and 4+/5)
  • 5/5: normal strength
25
Q

“red flags” of low back pain

-name and describe (hint*you wont eat this protein)

A
  • T - trauma
  • U - Unexplained weight loss,or decline in general health
  • N - neurologic symptoms or progressive neurologic deficit; Saddle anesthesia, bladder or bowel incontinence, Pain present at night or pain present at rest, Pain lasting more than 1 month or not responding to treatment
  • A - Age (over 50 and under 20)
  • F - fever
  • I - intravenous drug use
  • S- steroid therapy (long term)
  • H - history of cancer
26
Q

importance of the dermatomal distribution of clinical symptoms as it relates to the embryological origin of the spinal column.

A
  • dermatomes derive from somites and innervate all parts of body
  • the CNS can interpret the signaling coming from visceral organ as pain in somatic area that is innervated by the same nerve
27
Q

X-ray for diagnosis of conditions affecting the lumbar spine.

A
  • produces clear pictures of your vertebrae and joints
  • diagnose fractures or broken bones, arthritis, spondylolisthesis, degeneration of the disks, tumors, and abnormalities in the curvature of the spine like kyphosis.
28
Q

MRI for diagnosis of conditions affecting the lumbar spine.

A
  • produces 3-D images of the spinal cord and nerve roots, as well as the disks themselves
  • provides greater images of blood vessel activity, detecting aneurysms/tumors/blocked blood vessels.
  • used for disc herniations, stenosis, Cauda equina, and Myelopathy.
29
Q

Common symptoms seen in patients with Myasthenia Gravis

A
  • ptosis
  • diplopia
  • limb weakness
  • difficulty chewing, swallowing, or talking
  • Weakness worsens as the day progresses
30
Q

function(s) of cranial nerve (CN) III

A
  • enable mostmovements of the eyeand
  • raise the eyelid.
  • contains fibers that innervate the intrinsic eye muscles that enable pupillary constriction and accommodation
31
Q

action of autoantibodies in Myasthenia Gravis

  • overall function
  • mechanisms
A
  • anti-AChR antibodies reduce the number of available AChRs at neuromuscular junctions
  • accelerated turnover of AChRs by cross-linking and causing rapid endocytosis of the receptors;
  • damage to the postsynaptic muscle membrane by the antibody in collaboration with complement;
  • blockade of the active site of the AChR,
32
Q

normal physiology of the neuromuscular junction

  • how AP goes from neuron to muscle
  • how is it terminated
A
  • action potential travels down a motor nerve and reaches nerve terminal, –ACh released from vesicles and combines with AChRs on postsynaptic folds, –AChR opens, permitting entry of sodium, which produces depolarization at end-plate region of muscle fiber–initiates action potential along muscle fiber, triggering muscle contraction.
  • hydrolysis of ACh by acetylcholinesterase (AChE), and diffusion of ACh away from receptor.
33
Q

Tensilon test

  • function
  • how
  • results
A
  • pharmacological test used for the diagnosis of myasthenia gravis by allowing accumulation ofacetylcholine(ACh) in the neuromuscular junctions, and makes more ACh available to the muscle receptors, thereby increasing muscle strength
  • 10mgedrophoniumhydrochloride prepared, 2 mg injected into patient to check for cholinergic crisis, wait 30 seconds, proceed with the rest of 8mg
  • patient with myasthenia gravis experiences increased muscle strength and endurance with repetitive movements/ normal people feel no difference
34
Q

Pyridostigmine

A

inhibits acetylcholinesterase in the synaptic cleft by competing with acetylcholine for attachment to acetylcholinesterase, thus slowing down the hydrolysis of acetylcholine, and thereby increases efficiency of cholinergic transmission in the neuromuscular junction

35
Q

EMG results of healthy patient vs patient with MG

A

Electric shocks are delivered at a rate of two or three per second to the appropriate nerves, and action potentials are recorded from the muscles. In normal individuals, the amplitude of the evoked muscle action potentials does not change at these rates of stimulation. However, in myasthenic patients, there is a rapid reduction of >10–15% in the amplitude of the evoked responses.

36
Q

Identify the support muscles of the head and neck and etiology of postural changes in patients with MG

A

-neck and limb muscles affected in later stages, causing difficulty with holding the head up this can lead to external auditory meatus being anterior in standing postural exam

Unit 2: SIGS (4 decks)

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