Week 2 (Test 1) Flashcards
(202 cards)
1
Q
What is pseudocyesis?
A
The false belief that you are pregnant
2
Q
Atypical signs and symptoms that did not conform to established diseases
A
hysteria
3
Q
What symptoms are necessary to make a diagnosis of Somatic Symptom Disorder?
A
A. Somatic sx: 1 or more, distressing, & disrupting of daily life B. Excessive thoughts, feelings, behaviors with >1 – Disproportionate & persistent thoughts of seriousness – Persistent high related anxiety – Excessive time & energy devoted to sxs or healthcare C. Chronicity > 6 months
4
Q
What symptoms are necessary to make a diagnosis of Illness Anxiety Disorder?
A
A. Somatic sx are absent or mild B. Preoccupation with having or acquiring a serious illness C. >6 months
5
Q
What do patients have in Conversion Disorder?
A
Nonintentionally produced symptoms or deficits affecting voluntary motor or sensory function —Commons presentation include pseudoseizures, blindness, deafness, sensory loss, paralysis or gait issues
6
Q
How would you best manage Conversion Disorder?
A
–Direct confrontation is not recommended –Conservative approach of reassurance and relaxation is often effective ===“Suggestion” of recovery w/o intervention (Prognosis surprisingly good with >1/2 completely resolved by time of discharge) –Identifying underlying conflict and finding resolution can “cure” the symptoms
7
Q
Physical or psychological symptoms are intentionally produced to assume sick role –Conscious/voluntary symptom production
A
Factitious disorder
8
Q
Often in Factitious Disorder cases, the patients will inject themselves with insulin to become hypoglycemic. What can you do to help determine whether this symptom is legitimate?
A
check for increased serum insulin/C-peptide ratio during a hypoglycemic episode
9
Q
How would you best manage Somatic Symptom Disorder?
A
–Frequent visits (15 min/month) –Short physical exam, nothing invasive –Aim: Prevent new symptoms Decrease admissions and ER visits –Discuss emotions/fears, use open ended questions
10
Q
Intentional production of false or grossly exaggerated physical or psychological symptoms – motivated by external incentives
A
malingering
11
Q
List the ectoderm germ layer derivatives.
A
CNS, PNS, sensory epithelium of nose, eye and ear, epidermis including hair and nails, pituitary gland, sweat glands, mammary glands and enamel of teeth, some eye mm neural crest cell derivatives
12
Q
List the mesoderm germ layer derivatives.
A
muscle, cartilage and bone/connective tissues, subcutaneous tissue of skin, spleen and cortex of suprarenal glands vascular system (heart and vessels), urogenital system (kidneys, gonads, ducts) dura mater and connective tissue envestments of peripheral nerves
13
Q
List the endoderm germ layer derivatives.
A
epithelial lining of the GI tract, respiratory tract and urinary bladder; the parenchyma of the tonsils, thyroid, parathyroid, thymus, liver and pancreas
14
Q
the separation of the neural tube from the surface ectoderm
A
dysjunction
15
Q
What marks the end of primary neurulation?
A
the completion of ectoderm fusion
16
Q
When does the anterior neuropore (cranial end) close?
A
day 25
17
Q
When does the posterior neuropore (caudal end) close?
A
day 27
18
Q
Failure of the anterior neuropore to close will result in what?
A
anencephaly
19
Q
Failure of the posterior neuropore to close will result in what?
A
spina bifida occulta
20
Q
defect vertebral arches, covered by skin, patch of hair?, does not involve neural tissue, no clinical signs, ~10% population has this anomaly.
A
spina bifida occulta
21
Q
neural tissue is included in the fluid-filled sac protruding through the defect. neurological symptoms present
A
myelomeningocele
22
Q
a fluid-filled sac of meninges protrudes through the defect. neurological symptoms present
A
meningocele
23
Q
total failure of neurulation; No dysjunction- incompatible with life, hemorragic fibrotic, degenerated mass
A
craniorachischisis totalis
24
Q
What are the defects related to secondary neuralation?
A
diastematomyelia and tethered spinal cord
25
persistence of neurenteric canal causes split spinal cord
diastematomyelia
26
fixed caudal end (filum terminale) of spinal cord
tethered spinal cord
27
What is the most common environmental cause of neural tube defects?
mom has a folic acid deficiency
28
What secretes Sonic hedgehog (Shh) protein and what does this protein do?
secreted by the notochord and it induces overlying ectoderm to differentiate into neuroectoderm
29
What are the 3 primary vesicles of the rostral part of the neural tube?
prosencephalon, mesencephalon, rhombencephalon
30
hindbrain
rhombencephalon
31
forebrain
prosencephalon
32
midbrain
mesencephalon
33
What does the prosencephalon differentiate into?
Diencephalon and Telencephalon
34
What does the mesencephalon differentiate into?
midbrain
35
What does the rhombencephalon differentiate into?
metencephalon and and myelencephalon
36
becomes the thalamus/hypothalamus
diencephalon
37
becomes the pons and cerebellum
metencephalon
38
becomes the medulla
myelencephalon
39
becomes the cerebral hemispheres
telencephalon
40
Failure to Form the Two Cerebral Hemispheres (fails to cleave and remains fused as single midline entity)
holoprosencephaly
41
What do you see in holoprosencephaly cases?
malformation of the brain and face; facial defects (cleft lips, single nostril, single eye)
42
cleft brain
schizencephaly
43
smooth brain (few gyri)
Lissencephaly
44
broad gyri, too few gyri
Pachygyri
45
small gyri
polygyri
46
At what vertebral level will you see conus medullaris?
L1
47
Which part of the spinal cord did this section come from?
sacral; 'ugly butterfly', lots of gray matter and little white matter
48
Which part of the spinal cord did this cross section come from?
lumbar; 'perfect butterfly'
49
Which part of the spinal cord is this cross section from?
thoracic; skinny butterfly and you can see Clark's columns really well; the Thin white part of the gray matter (making it a skinny butterfly) is the substantia gelatinosa
50
Which part of the spinal cord did this cross section come from?
cervical; typically oval shaped and the white matter is very large
51
Which part of the spinal cord did this cross section come from?
cervical (C1 level); bunny ears
52
occurring on the same side of the body
ipsilateral
53
relating to or denoting the side of the body opposite to that on which a particular structure or condition occurs
contralateral
54
At what level does the spinal cord end?
L1-2
55
specializations of the pia matter that connect the dura mater to the spinal cord
denticulate ligaments
56
At what level does the dural sac end?
S2
57
During week 10 within the developing spinal cord, the alar plate forms _____ and provides \_\_\_\_\_\_\_\_\_.
forms dorsally and provides sensory function
58
During week 10 within the developing spinal cord, the basal plate forms ______ and provides \_\_\_\_\_\_\_.
forms ventrally and provides motor function
59
is a tough, pia derived extension from the conus medullaris that attaches to the coccyx
filum terminale
60
a clinical sign in which forced flexion of the neck elicits a reflex flexion of the hips.
Brudzinski’s sign
61
Can't straighten the hamstring to 90 degrees without pain
Kernig's sign
62
Which two physical signs are seen in meningitis patients?
Brudzinski’s sign and Kerning's sign
63
What are the symptoms you see in patients with meningitis?
- -Sudden onset of fever, nausea, vomiting, headache, decreased ability to concentrate, and myalgias in an otherwise healthy patient
- -also commonly see petechiae rash
64
What causes Disseminated intravascular coagulation (DIC) ?
- -Cause is activation of extrinsic and intrinsic clotting cascade by macrophage production of procoagulant tissue factor.
- -Widespread ischemic changes and bleeding due to using up of clotting factors
65
Describe the structure of Neisseria meningitidis
--Gram-negative
- -Kidney bean-shaped diplococci
- -Cell wall - typical gram negative cell wall; thicker peptidoglycan layer [makes them susceptible to beta lactams and glycopeptides]
66
What is the major cause of meningitis pathology?
Lipooligosaccharide (LOS)
67
How does Lipooligosaccharide (LOS) bring about the symptoms of meningitis ?
- Activates macrophages through Toll pathway
- Production of proinflammatory cytokines, especially TNF-a; may result in septic shock, increased vascular permeability
- Induces macrophage production of procoagulant tissue factor which may lead to clotting and subsequent bleeding.
- Petechial hemorrhages result from TNF-a and bleeding.
68
What is the gold standard for diagnosing meningitis?
Culture of CSF on blood and chocolate agars
--problem is, this takes 24 hours so you need to do something with the patient before then
69
life cycle in cat gut
Toxoplasma gondii
70
In what patients are we really concerned with toxoplasmosis?
immunocompromised patients; disease is more severe and may be fatal
71
How would you diagnose toxoplasmosis from serum samples?
--Determination of 4-fold increase in titer essential to diagnosis of acute infection
72
- Free-living amebo-flagellate in soil and water
- Found in 50% of fresh water bodies; seems to prefer warm water
- Opportunistic infection
- Acquired by human by getting water in nose and penetration of cribiform plate by amoeba
Naegleria fowleri
73
Function: fine touch, proprioception, two-point discrimination
Dorsal column system
74
Function: sharp pain, temperature, crude touch
spinothalamic tracts
75
Function: movement and position mechanisms
Dorsal spinocerebellar tract
76
Function: movement and position mechanisms
ventral spinocerebellar tract
77
Function: fine motor function (controls distal musculatrue) modulation of sensory functions
--descending pathway
Lateral corticospinal (pyramidal) tract
78
Function: gross and postural motor function (proximal and axial musculature)
--descending pathway
Anterior Corticospinal tract
79
Spinal cord is a derivative of the \_\_\_\_\_
nerual tube
80
Where do we see CSF in (or rather around) the spinal cord?
We see CSF between arachnoid and pia, i.e., in the subarachnoid space.
81
dermatome for upper arm (lateral surface)
C5
82
Dermatome for middle finger
C7
83
Dermatome for thumb and lateral forearm
C6
84
Dermatome of little finger
C8
85
Dermatome of nipple
T4
86
Dermatome of umbilicus
T10
87
Dermatome of calf
L4,L5
88
Dermatome of big toe
L5
89
Dermatome of heel
S1
90
Dermatome of back of thigh
S2
91
Where does the spinal cord get its blood supply?
The anterior spinal artery irrigates the anterior 2/3 of the cord.
92
In a spinal cord specimen, the anterior spinal artery is commonly hidden in a fissure called \_\_\_\_\_\_\_\_
ventral median fissure
93
Where does the cell body of a pre-ganglionic sympathetic neuron reside?
intermediolateral cell column (stretches from T1-L2)
94
In the dorsal column medial lemniscus pathway, if the sensation comes below T6, it enters the ____ part of the dorsal column, and the info travels in a fiber band collectively called \_\_\_\_\_\_.
medial
Gracile Fasciculus
95
In the dorsal column medial leminscus pathway, if sensation comes above T6, it enters the ____ part of the dorsal column, and the info travels in a fiber band collectively called the \_\_\_\_\_\_.
lateral; Cuneate Fasciulus
96
The "pain/temp" pathway
spinothalamic tract
97
a drastic measure of pain relief; remember, the cut should be about ____ segments above the sensory fiber entry zone.
cordotomy
2-3 segments
98
upper motor neuronal cell bodies reside in the \_\_\_\_
brain
99
lower motor neuronal cell bodies reside in the \_\_\_\_
spinal cord
100
What is the treatment for toxoplasmosis?
The treatment of toxoplasmosis is pyrimethamine (most effective) and sulfadiazine.
101
What happens in Myasthenia Gravis?
•Autoantibodies against acetylcholine receptors on the
## Footnote
post-synaptic membrane.
* Immunological destruction of neuromuscular junction
* Rapidly fading strength (‘myasthenia’)
due to depletion of synaptic acetylcholine
102
What is this and what causes it?
Ragged red fibers. Ragged red fibers occur as a result of compensatory proliferation of mitochondria in mitochondrial disorders
103
Polymyositis is associated with sarcolemmal expression of \_\_\_\_\_\_\_\_.
polymyositis is associated with sarcolemmal expression of **major histocompatibility antigen 1 (MHC-I)**
104
Dermatomyositis is associated with \_\_\_\_\_\_.
dermatomyositis is associated with **vascular expression of complement component C5b9, also known as membrane attack complex (MAC). **
105
What is the pathology, pathogensis, and clinical presentation of polymyositis?
Pathology: intrafascicular inflammation
Pathogenesis: cytotoxic t cells
Clinical expression: pain
106
What is the pathology, pathogenesis, and clinical presentation of dermatomyositis?
Pathology: extrafascicular inflammation; perifascicular atrophy
Pathogenesis: humoral
Clinical presentation: pain and rash
107
What is the pathology, pathogenesis, and clinical presentation of Inclusion Body Myositis?
Pathology: inclusions; rimmed vacuoles
Pathogenesis: degenerative
Clinical presentation: steroid resistance
108
what is this a picture of?
**Dermatomyositis**
The inflammation is predominantly in the perimysium, the connective tissue around (rather than within, which is endomysium) the fascicle. Also note that the fibers at the very periphery of the fascicle are smaller; hence, perifascicular atrophy.
109
What is this a picture of?
**Polymyositis**
110
What is this a picture of?
**Inclusion Body Myositis**
In spite of its name, this is not a viral disease and the inclusion refers to the eosinophilic material within the vacuole (as seen in this picture).
111
What is this a picture of?
Duchenne MD: endomysial fibrosis with fiber ‘rounding,’ variation in fiber size, and myofiber regeneration (small blue fibers)
112
What is this a picture of?
Central core myopathy: note central pale areas
113
What is this a picture of?
**rod body, or nemaline myopathy**
## Footnote
Material similar to Z-bands accumulates into rod-shaped structures (nemaline rods).
114
What is this an image of?
**centronuclear myopathies**
There is one central nucleus uniformly in essentially every fiber. Some appear like they don’t have a central nucleus, because the section did not pass through the nucleus.
115
What causes Devic Disease
(neuromyelitis optica)?
•Autoantibodies to aquaporin-4 receptors (a water channel protein)
--causes Synchronous blindness and paraplegia
116
* Autoimmune myelin destruction
* Mainly CD 4+ and some CD 8+ T-cells, and macrophages
multiple sclerosis
117
•line ventricles can differentiate into choroid plexus cells (make CSF)
ependymal cell
118
axonal swelling
spheroids
119
single nerve, usually traumatic or entrapment (carpal tunnel)
mononeuropathy
120
–random damage to individual nerves (wrist drop, radial neuropathy)
polyneuritis multiplex
121
–symmetric, length dependent (worse in distal long nerves). “Stocking glove” pattern
polyneuropathy
122
Describe Guillain- Barre Syndrome.
•Rapid demyelination of motor axons that can lead to weakness / respiratory failure
–Weakness starts distally (feet/hands) moves proximally
•Caused by infection or vaccine
123
How do you treat Guillain- Barre Syndrome?
plasmapharesis
124
Chronic Inflammatory Demyelinating Polyneuropathy (CIDP) is similar to GBS, but less severe. What is the major difference between the two?
CIDP Follows a chronic, relapsing and remitting course
125
What gene is mutated in duchennes muscular dystrophy?
Dystrophin gene (Xp21) [x linked]
126
sustained muscle contraction
myotonia
127
What causes Myotonic Dystrophy?
•Autosomal Dominant mutation in DMPK leading to increased CTG repeats (\>30, usually 1000’s)
–Undergoes anticipation like Huntington Dz
128
* Myelin is not formed properly or is degraded faster than it is made
* Usually due to a genetic defect associated with myelin production
dysmyelinating disease
129
* Normal myelin is lost
* Typically (auto)immune mediated
demyelination
130
* Usually seen in the central pons
* Often associated with rapid correction of hyponatremia (low sodium)
Central Pontine Myelinolysis
131
What causes Progressive multifocal leukoencephalopathy (PML)?
polyoma virus (JC virus), which infects and kills oligodendrocytes
132
•Posterior fossa abnormality
•Part of cerebellum missing
Presents with hydrocephalus
Dandy-Walker Malformation
133
What are the 3 causes of hydrocephalus?
–3 causes (all dealing with CSF)
•Impaired flow
•Impaired reabsorption
•Increased production (rare, tumors)
134
Describe Type I muscle fibers.
Slow twitch fibers (I)- fatigue resistant
Smaller soma & smaller axon
\*Many mitochrondria (oxidative metabolism)
\*Extensive capillary blood supply
\*Myoglobin for O2 storage
135
Describe Type IIa muscle fibers
Intermediate fibers (IIA)- fast twitch, fatigue resistant
Intermediate in properties
136
Describe Type IIb muscle fibers.
Fast twitch fibers (IIB)- fatigue rapidly
Larger soma & larger axon
\*Fewer mitochondria
\*Less extensive blood supply
\*Glycogen store & glycolytic enzymes
Extensive sarcoplasmic reticulum (Ca++)
137
What determines muscle fiber type?
the particular innervation of the muscle
138
In regards to reflexes what do you see with upper motor neuron lesions?
hyperactive reflexes
139
In regards to reflexes what do you see in regards to lower motor neuron lesions?
hypoactive reflexes
140
a muscle twitch; a small, local, involuntary muscle contraction and relaxation which may be visible under the skin
fasciculation
141
In regards to muscle tone, what do you see in upper motor neuron syndromes?
Increased muscle tone - Spasticity
142
In regards to muscle tone, what do you see in lower motor neuron syndromes?
Decreased muscle tone – Flaccidity
143
What's the dermatome level for the little toe?
S1
144
What's the dermatome level for the perineum?
S3-S5
145
What do you suspect when you see cape like distribution of pain and temperature loss?
Syringomyelia
146
What distinguishes B12 deficiency from copper deficiency?
The types of anemia they cause. B12 deficiency causes megaloblastic anemia while copper deficiency causes microcytic anemia
147
What are the presynaptic neuromuscular junction disorders?
* Lambert Eaton myasthenic syndrome
* Botulism
148
What causes Lambert Eaton Myasthenic Syndrome (LEMS)?
•Voltage gated calcium channel antibodies impede release of acetylcholine
149
Lambert Eaton Myasthenic Syndrome (LEMS) is Associated with a cancer in 40-60% of patients (paraneoplastic). Which cancer is the most common?
small cell lung cancer
150
* Most common of the adult dystrophies
* Autosomal dominant
myotonic dystrophy
151
How do you treat Polymyositis?
§Treatment with immunosuppression
- Prednisone
- Methotrexate
- Azathioprine
152
What are the ectoderm derivatives in the head and neck?
- neural tube (CNS-motor neurons, preganglionic ANS)
- neural crest (PNS-postganglionic ANS)
- epithelial component of the skin (glands, invaginations, other structures)
stomodeum (lining of the future oral cavity)
nasal pit, external auditory meatus
-thickens to form placodes (olfactory, lens and otic)
153
what are the endoderm derivatives in the head and neck?
-epithelial lining (pharynx, larynx, trachea, esophagus, pharyngotympanic tube,
middle ear)
- glands develop as evaginations of endodermal tube - “pharyngeal pouches”
(thymus, parathyroid, tonsil, thyroid, mucosal)
154
What are the mesodermal derivatives in the head and neck?
- notochord (nucleus pulposus)
- somites that form bones, muscles, connective tissue
155
What are the Pharyngeal (Branchial) Arches composed of?
migrating neural crest cells in the head
156
Which cranial nerve grows into the 1st pharyngeal arch?
Trigeminal nerve (V)
157
Which cranial nerve grows into the 2nd pharyngeal arch?
facial nerve (VII)
158
Which cranial nerve grows into the 3rd pharyngeal arch?
glossopharyngeal nerve (IX)
159
Which cranial nerve grows into the 4th pharyngeal arch?
vagus nerve (X)
160
Which cranial nerve grows into the 6th glossopharyngeal arch?
vagus nerve (X)
161
What is the muscle derivative of the 1st pharyngeal arch?
muscles of mastication
162
What is the muscle derivative of the 2nd pharyngeal arch?
muscles of facial expression
163
What is the muscle derivative of the 3rd pharyngeal arch?
stylopharyngeus muscle
164
What is the muscle derivative of the 4th pharyngeal arch?
laryngeal muscle
165
What is the muscle derivative of the 6th pharyngeal arch?
Pharyngeal muscles
166
What are the derivatives of the 1st pharyngeal arch cartilage?
Malleus, Incus, (sphenomandibular lig.), rest of Meckel’s cartilage disappears
"M arch"
167
What are the derivatives of the 2nd pharyngeal arch cartilage?
Stapes, Styloid process, Superior half of body of hyoid, (Stylohyoid lig.)
"S arch)
168
What are the derivatives of the 3rd pharyngeal arch cartilage?
inferior half of body and greater horn of hyoid
169
What are the derivatives of the 4th pharyngeal arch cartilage?
thyroid and epiglottic cartilages of larynx
170
What are the derivatives of the 6th pharyngeal arch cartilage?
Laryngeal cartilages (cricoid, arytenoid, corniculate)
171
Which nerves are tested in the biceps reflex?
C5, C6
172
Which nerves are tested in the brachioradialis reflex?
C5, C6, C7
173
Which nerves are tested in the patellar reflex?
L2, L3, L4
174
Which nerves are tested in the achilles reflex?
S1, S2
175
Which nerves are tested in the pupillary light reflex?
CN II, CN III
176
Which nerves are tested in the jaw jerk reflex?
CN V
177
Which nerves are tested in the corneal (blink) reflex?
CN V, CN VII
178
which nerves are tested in the gag reflex?
CN IX, CN X
179
CAPE-LIKE BILATERAL loss of pain and temperature sensation of the shoulders and upper extremities due to damage of the ANTERIOR WHITE COMMISSURE
Syringomyelia
180
Where is the lumbosacral enlargement?
Around L1-S3
181
Where is the cervical enlargement?
Around C3-T1
182
Where is the intermediolateral cell column?
T1-L2
183
In what part of the spinal cord are sympathetics located?
lateral/intermediate horn
184
What can you see in lesions of the dorsal column medial lemniscus tract?
multiple sclerosis, Tabes Dorsalis (from syphilis), and vitamin B 12 deficiency
185
What can you see with lesions of the spinothalamic tract?
Syringomyelia and Brown-Sequard syndrome
186
What can you see with lesions of the corticospinal tract?
ALS and vitamin B 12 deficiency
187
What are the functions of free nerve endings?
Free nerve endings function as thermoreceptor. Some of them also function as norciceptors that detect noxious stimuli.
188
senses vibration of the skin
Pacinian corpuscle
189
senses stretching of the skin
ruffini ending
190
this occurs at the sensory receptor level; the receptor decreases its firing frequency
adaptation
191
receptors that completely adapt to a stimulus, i.e., stop firing after some time
phasic receptor
192
receptors that continue to fire as long as the stimulus is present
tonic receptor
193
this occurs at the CNS level. The brain pays less attention to a constant stimulus
habituation
194
The area of the body from which a stimulation influences the discharge rate of that neuron.
receptor field
195
Pain is transmitted by which two fiber types?
A-delta and C
196
What is involved in the triple vascular response of T Lewis?
redness (local vasodilation), flare (vasodilation in a wider area caused by axon reflex), weal (edema)
197
Extrafusal fibers are activated by \_\_\_\_\_.
Extrafusal muscle fibers are activated by α-motor neuron
198
Intrafusal muscle fibers are activated by \_\_\_\_\_.
gamma motor neurons
199
* Arranged in “parallel” with the regular muscle fibers, i.e., extrafusal fibers
* It detects “stretch” when the muscle is stretched
muscle spindle
200
* Arranged in “series” with the muscle mass
* It detects “tension” either when the muscle contracts by itself or is stretched passively
golgi tendon organ
201
•What is the mechanism of action for local anesthetics?
Application of local anesthetics, such as lidocaine, can block Na+ channel on C fibers quickly, thus the transmission of action potentials signaling pain.
202
•What is hyperalgesia?
an increased sensitivity to pain, which may be caused by damage to nociceptors or peripheral nerves.
