Fever, Body Weakness. Easy Fatigability, Pain, Headache, Weight loss, Dyspnea, Cough, Edema Flashcards
an unpleasant sensation localized to a part of the body. It is often described in terms of a penetrating or tissue-destructive process (e.g., stabbing, burning, twisting, tearing, squeezing) and/or of a bodily or emotional reaction (e.g., terrifying, nauseating, sickening)
Pain
These properties illustrate the duality of pain
both sensation and emotion
Peripheral nerve consists of the
axons of three different types of neurons:
primary sensory afferents, motor neurons, and sympathetic postganglionic neurons
The cell bodies of primary sensory afferents
are located in
the dorsal root ganglia
within the vertebral foramina.
The largest diameter afferent fibers, respond maximally to light touch and/or moving stimuli; they are
present primarily in nerves that innervate the skin
A-beta (Aβ)
These fibers are present in nerves to the
skin and to deep somatic and visceral
A-delta (Aδ) and the unmyelinated (C) axons
primary afferent nociceptors (pain receptors)
Innervated only by Aδ and C fiber afferents
Cornea
When intense, repeated, or prolonged stimuli are applied to damaged or inflamed tissues, the threshold for activating primary afferent nociceptors is lowered, and the frequency of firing is higher for
all stimulus intensities
Sensitization
Sensitization occurs at the level of the
peripheral nerve terminal (peripheral sensitization) as well as at the level of the dorsal horn of the spinal cord (central sensitization).
occurs in damaged or inflamed tissues,
when inflammatory mediators activate intracellular signal transduction in nociceptors, prompting an increase in the production, transport, and membrane insertion of chemically gated and voltage-gated ion channels.
These changes increase the excitability of nociceptor
terminals and lower their threshold for activation by mechanical, thermal, and chemical stimuli
Peripheral sensitization
occurs when activity, generated by nociceptors during inflammation, enhances the excitability of nerve cells in the dorsal horn of the spinal cord
Central sensitization
Following injury and resultant sensitization, normally innocuous stimuli can produce pain
Allodynia
increased pain intensity in response to the same noxious stimulus
hyperalgesia
play a significant role in sensitization
Low pH, prostaglandins, leukotrienes
inflammatory mediators such as bradykinin
is released from primary afferent nociceptors and
has multiple biologic activities. It is a potent vasodilator, degranulates mast cells, is a chemoattractant for leukocytes, and increases the production
and release of inflammatory mediators
Substance P
When primary afferents are activated by noxious stimuli, they release neurotransmitters from their terminals that excite the spinal cord neurons. The major
neurotransmitter released is
glutamate
The convergence of sensory inputs to a single spinal pain-transmission neuron is of great importance because it underlies the phenomenon of
referred pain
Inflammation near the central diaphragm
is often reported as
shoulder discomfort.
This spatial displacement of
pain sensation from the site of the injury that produces it is known as
referred pain
causes vasodilation and neurogenic edema with further accumulation of bradykinin (BK).
also causes the release of histamine
(H) from mast cells and serotonin (5HT) from platelets
Substance P
pathway is crucial for pain sensation in humans
The spinothalamic
This projection mediates the purely sensory aspects of pain, i.e., its location, intensity, and quality
somatosensory cortex.
According to this hypothesis, visceral afferent nociceptors converge on the same pain-projection neurons as the afferents from the somatic structures in which the pain is perceived. The brain has no way of knowing the actual source of input and mistakenly “projects” the sensation to the somatic structure
convergence-projection hypothesis of referred
pain
The suggestion that pain will worsen following administration of an inert substance can increase its perceived intensity
(the nocebo effect)
typically has an unusual burning, tingling, or
electric shock like quality and may be triggered by very light touch
Neuropathic pain
a greatly exaggerated pain sensation to innocuous
Hyperpathia
This constellation of spontaneous pain and signs of sympathetic dysfunction following injury has been termed
complex regional pain syndrome (CRPS)
complex regional pain syndrome (CRPS) occurs after an identifiable nerve injury, it is termed
(CRPS) II also known as posttraumatic neuralgia
or, if severe, causalgia
complex regional pain syndrome (CRPS) occurs without obvious nerve injury, it is termed
CRPS type I (also known as reflex sympathetic dystrophy)
Effective for patients with postherpetic neuralgia who have prominent allodynia
topical preparation of 5% lidocaine in patch form
The ideal treatment for any pain is to
remove the cause
Gastric irritation is most severe
with this drug , which may cause erosion and ulceration of the gastric mucosa leading to bleeding or perforation
aspirin
irreversibly acetylates platelet cyclooxygenase and thereby interferes with coagulation of the blood, gastrointestinal bleeding is a particular risk
aspirin
two major classes of COX:
COX-1 is constitutively expressed, and COX-2 is induced in the inflammatory state.
have similar analgesic potency and produce less gastric irritation than the nonselective COX inhibitors
COX-2– selective drugs
COX-2 inhibitors, including celecoxib (Celebrex), are
associated with increased risk of ?
It appears that this is a class effect of NSAIDs, excluding aspirin.
cardiovascular risk
These drugs are contraindicated in patients in the immediate period after coronary artery bypass surgery and should be used with caution in elderly patients and those with a history of or significant risk factors for cardiovascular disease.
Side effects of opiods
Nausea, vomiting, pruritus, and constipation are the most frequent and bothersome side effects.
Respiratory depression is uncommon at standard analgesic doses, but can be life threatening.
Opioid-related side effects can be reversed rapidly with the narcotic antagonist
naloxone
Opioids produce analgesia by actions in
CNS. They activate pain-inhibitory neurons and directly inhibit pain-transmission neurons. Most of the commercially available opioid analgesics act at
the same opioid receptor (μ-receptor)
metabolite of meperidine. At higher doses of meperidine, typically greater than 1 g/d, accumulation
of this drug can produce hyperexcitability and seizures that are not reversible with naloxone. accumulation is
increased in patients with renal failure
normeperidine
The most common error made by physicians in managing severe pain with opioids is to?
Because many patients are reluctant to complain, this practice leads to needless suffering. In the absence of sedation at the expected time of peak effect
prescribe an inadequate dose
Useful for the management of chronic
pain
The tricyclic antidepressants (TCAs), particularly nortriptyline and desipramin
TCAs potentiate opioid analgesia, so they may be useful adjuncts for the treatment of severe persistent pain such as occurs with malignant tumors
TCAs are of particular value in the management of neuropathic pain such as occurs in diabetic neuropathy and postherpetic neuralgia
block both serotonin and norepinephrine reuptake, appear to retain most of the pain-relieving effect of TCAs with a side effect profile more like that of the selective serotonin reuptake inhibitors
These drugs may be particularly useful in patients who cannot tolerate the side effects of TCAs.
nontricyclic antidepressants (SNRI) venlafaxine (Effexor) and duloxetine (Cymbalta),
The most common causes of abdominal pain on admission are
acute appendicitis, nonspecific abdominal pain, pain of urologic origin, and intestinal obstruction.
Pain is steady and aching in character and is located directly over the inflamed area, its exact reference being possible because it is transmitted by somatic nerves
The pain of parietal peritoneal
inflammation
Exposure of blood and urine to the peritoneal cavity may go unnoticed unless it is sudden and massive
Blood is normally only a mild irritant and the response to urine can be bland
Invariably accentuated by pressure or changes in tension of the peritoneum, whether produced by palpation or by movement such as with coughing or sneezing
Characteristically lies quietly in bed, preferring
to avoid motion, in contrast to the patient with colic, who may be thrashing in discomfort
tonic reflex spasm of the abdominal musculature, localized to the involved body segment
The pain of peritoneal inflammation
Classically elicits intermittent or colicky abdominal pain that is not as well localized as the pain of parietal peritoneal irritation.
Intraluminal obstruction
often presents as poorly localized, intermittent
periumbilical or supraumbilical pain. As the intestine progressively dilates and loses muscular tone, the colicky nature of the pain may diminish. With superimposed strangulating obstruction, pain
may spread to the lower lumbar region if there is traction on the root of the mesentery.
Small-bowel obstruction
colicky pain of colonic obstruction is of lesser
intensity, is commonly located in the infraumbilical area, and may often radiate to the lumbar region
usually causes pain in the right upper quadrant with radiation to the right posterior region of the thorax or to the tip of the right scapula, but it is also not uncommonly found near
the midline.
Acute distention of the gallbladder
Often causes epigastric pain that may radiate to the upper lumbar region.
Distention of the common bile duct
Abdominal pain with radiation to the sacral region,
flank, or genitalia should always signal the possible presence of a
rupturing
abdominal aortic aneurysm.
Often accompanied by splinting
of the involved hemithorax with respiratory lag and decrease in excursion more marked than that seen in the presence of intraabdominaldisease.
Referred pain of thoracic origin
Hallmark of familial Mediterranean fever
Abdominal pain
associated with angioneurotic edema is often associated with episodes of severe abdominal pain.
C1 esterase deficiency
Should also be considered, especially when evaluating
patients with left upper quadrant or left flank pain.
Splenic abscesses due to Candida or
Salmonella infection
Clinically important weight loss is defined as the loss of
10 pounds (4.5 kg) or >5% of one’s body weight over a period of 6–12 months
IWL is encountered in up to
8% of all adult outpatients and
27% of frail persons age 65 years and older.
Significant weight loss is associated with increased mortality, which can range
from 9% to as high as 38% within 1 to 2.5 years in the absence of clinical awareness and attention
Among healthy aging people, total body weight peaks in the
sixth decade of life and generally remains
stable until the ninth decade, after which it gradually falls
lean body mass (fat-free mass) begins to decline at a rate of
0.3 kg per year in the third decade, and the rate of decline increases further beginning at age 60 in men and age 65 in women.
These changes in lean body mass largely reflect the age-dependent decline in growth hormone secretion and, consequently, circulating levels of
insulin-like growth factor type I (IGF-I) that occur with normal aging.
In the healthy elderly, an increase in fat tissue balances the loss in lean body mass until
very old age, when loss of both fat and skeletal muscle occurs
Between ages 20 and 80, mean energy intake is reduced by
up to 1200 kcal/d in men and 800 kcal/d in women
Half of all patients with cancer lose some body weight;
one-third lose more than 5% of their original body weight, and up to 20% of all cancer deaths are caused directly by cachexia (through immobility and/or cardiac/respiratory failure).
The greatest incidence of weight loss
is seen among patients with
solid tumors
Hyperthyroidism in the elderly may have less prominent sympathomimetic, features and may present as
“apathetic hyperthyroidism” or T3 toxicosis
may be one of the earliest manifestations
of Alzheimer’s dementia.
Involuntary weight loss
The four major manifestations of IWL are
(1) anorexia (loss of appetite),
(2) sarcopenia (loss of muscle mass)
(3) cachexia (a syndrome that combines weight loss, loss of muscle and adipose tissue, anorexia, and weakness), and
4) dehydration
Assessment and Testing for Involuntar y Weight Loss
5% weight loss in 30 d= Complete blood count
10% weight loss in 180 d =Comprehensive electrolyte andmetabolic panel, including liver and
renal function tests
Body mass index <21 =Thyroid function tests
25% of food left uneaten after 7 d =ESR
Change in fit of clothing= CRP
Change in appetite, smell, or taste =Ferritin
The first priority in managing weight loss
to identify and treat the underlying causes systematically. Treatment of underlying metabolic, psychiatric, infectious, or other systemic disorders may
be sufficient to restore weight and functional status gradually.
Refers to an inherently subjective human experience of physical and mental weariness, sluggishness, and exhaustion.
In the context of clinical medicine, it is
most typically and practically defined as difficulty initiating or maintaining voluntary mental or physical activity
Fatigue
is a cardinal manifestation of some neuromuscular disorders such as myasthenia gravis and can be
distinguished from fatigue by finding clinically apparent diminution of the amount of force that a muscle generates upon repeated contraction
Fatigability of muscle power
On confrontational testing, they are able
to generate full power for only a brief period before suddenly giving way to the examiner. This type of weakness is often referred to as
breakaway weakness
is a reduction in the power that can be exerted by one or more muscles.
Weakness
It must be distinguished from increased fatigability (i.e., the inability to sustain the performance of an activity that should be normal for a person of the same age, sex, and size), limitation in function due to pain or articular stiffness, or impaired motor activity because severe proprioceptive sensory
loss prevents adequate feedback information about the direction and power of movements
also distinct from bradykinesia (in which increased time is required for full power to be exerted) and apraxia,
a disorder of planning and initiating a skilled or learned movement unrelated to a significant motor or sensory deficit
or the suffix “-plegia” indicates weakness so severe that a muscle cannot be contracted at all, whereas paresis refers to less severe weakness.
Paralysis
Weakness from involvement of
occurs particularly in the extensors and abductors of the upper limb and the flexors of the lower limb.
upper motor neurons
weakness depends on whether
involvement is at the level of the anterior horn cells, nerve root, limb plexus, or peripheral nerve—only muscles supplied by the affected structure are weak
Lower motor neuron
is generally most marked in
proximal muscles
Myopathic weakness
is the resistance of a muscle to passive stretch
Tone
is the increase in tone associated with
disease of upper motor neurons. It is velocity-dependent, has a sudden release after reaching a maximum (the “clasp-knife” phenomenon), and predominantly affects the antigravity muscles (i.e., upper-limb flexors and lower-limb extensors).
Spasticity
is hypertonia that is present throughout the range of motion (a “lead pipe” or “plastic” stiffness)
and affects flexors and extensors equally; it sometimes has a cogwheel quality that is enhanced by voluntary movement of the contralateral limb (reinforcement)
Rigidity
is increased tone that varies irregularly in a manner seemingly related to the degree of relaxation, is present throughout the range of motion, and affects flexors and extensors equally; it usually results from disease of the frontal lobes
Paratonia (or gegenhalten)
Weakness with decreased tone (flaccidity) or normal
tone occurs with disorders of motor units. A motor unit consists of
a single lower motor neuron and all the muscle fibers that it innervates
Generally is not affected by upper motor neuron lesions, although mild disuse atrophy eventually may occur.
Muscle bulk
By contrast, atrophy is often conspicuous when a lower motor neuron lesion is responsible for weakness and also may occur with advanced muscle disease
are usually increased with upper motor neuron lesions, but may be decreased or absent for a variable period immediately after onset of an acute lesion
Muscle stretch (tendon) reflexes
The muscle stretch reflexes are
depressed with
lower motor neuron lesions directly involving specific
reflex arcs. They generally are preserved in patients with myopathic weakness except in advanced stages, when they sometimes are attenuated.
In disorders of the neuromuscular junction, reflex responses may be affected by preceding voluntary activity of affected muscles; such activity may lead to enhancement of initially depressed reflexes in
Lambert-Eaton myasthenic syndrome
and, conversely, to depression of initially normal reflexes in myasthenia gravis
Lambert–Eaton myasthenic syndrome is caused by autoantibodies to the presynaptic membrane. Myasthenia gravis is caused by autoantibodies to the postsynaptic acetylcholine receptors
distal weakness is likely to be
neuropathic,
and symmetric proximal weakness
myopathic
distal muscle groups are affected more severely than proximal ones, and axial movements are spared unless the lesion is severe and bilateral.
Spasticity is typical but may not be present acutely. Rapid repetitive movements are slowed and coarse, but normal rhythmicity is maintained.
Upper motor neuron lesion
(EMG) shows that with weakness of the upper motor neuron type, motor units have a diminished maximal
discharge frequency.
Bilateral corticobulbar lesions produce a
pseudobulbar palsy: dysarthria, dysphagia, dysphonia, and emotional lability accompany bilateral facial weakness and a brisk jaw jerk
disorders brainstem motor nuclei and the anterior
horn of the spinal cord or from dysfunction of the axons of these neurons as they pass to skeletal muscle
Weakness is due to a
decrease in the number of muscle fibers that can be activated through a loss of α motor neurons or disruption of their connections to muscle. Loss of γ motor neurons does not cause weakness but decreases tension on the muscle spindles, which decreases muscle tone and attenuates
the stretch reflexes
Lower Motor Neuron lesion
When a motor unit becomes diseased, especially in anterior horn cell diseases, it may discharge spontaneously, producing
fasciculations
Atrophy
Fasciculations
Tone Decreased
Distal/segmental Distribution of weakness
Hypoactive/absent Muscle stretch reflexes
Absent Babinski
Lower Motor Neuron
Tone Spastic Atrophy Absent Fasciculations Absent Hyperactive Babinski sign Present
Upper Motor Neuronn
The bulbospinal system sometimes is referred to as the
extrapyramidal upper motor neuron system
The larger α motor neurons are more numerous and innervate the extrafusal muscle fibers of the motor unit.
Loss of α motor neurons or disruption of their axons produces
Lower motor neuron weakness
The smaller, less numerous γ motor neurons innervate the _
and contribute to normal tone and stretch reflexes
intrafusal muscle fibers of the muscle spindle
is produced by a decrease
in the number or contractile force of muscle fibers activated within motor units
Myopathic weakness
On EMG, the size of each motor
unit action potential is decreased, and motor units must be recruited more rapidly than normal to produce the desired power.
Some myopathies produce weakness through loss of contractile force of muscle fibers or through relatively selective involvement of type II (fast)
Weakness may occur without a recognizable
organic basis. It tends to be variable, inconsistent, and with a pattern
of distribution that cannot be explained on a neuroanatomic basis
Psychogenic Weakness
Causes of Episodic Generalized Weakness
- Electrolyte disturbances, e.g., hypokalemia, hyperkalemia, hypercalcemia,
hypernatremia, hyponatremia, hypophosphatemia, hypermagnesemia - Muscle disorders
a. Channelopathies (periodic paralyses)
b. Metabolic defects of muscle (impaired carbohydrate or fatty acid utilization;
abnormal mitochondrial function) - Neuromuscular junction disorders
a. Myasthenia gravis
b. Lambert-Eaton myasthenic syndrome - Central nervous system disorders
a. Transient ischemic attacks of the brainstem
b. Transient global cerebral ischemia
c. Multiple sclerosis - Lack of voluntary effort
a. Anxiety
b. Pain or discomfort
c. Somatization disorder
results from an upper motor neuron lesion
above the midcervical spinal cord; most such lesions are above the foramen magnum.
Hemiparesis
reflect either a cortical or a subcortical hemispheric lesion.
Homonymous visual field defects
produce “crossed paralyses,” consisting of ipsilateral cranial nerve signs and contralateral hemiparesis
brainstem lesions
The absence of cranial nerve signs or facial weakness suggests that a hemiparesis is due to a lesion in the high cervical spinal cord, especially if associated with the
Brown-Séquard syndrome