1
Q
What sensations does the anterolateral system carry?
A
Pain and temperature.
2
Q
Anteriorlatedal What tract carries crude touch?
A
Anterior spinothalamic tract.
3
Q
What receptors detect pain and temperature?
A
Free nerve endings.
4
Q
Which fibers carry fast, sharp pain?
A
A‑δ fibers.
5
Q
Which fibers carry slow, dull pain?
A
C fibers.
6
Q
Where is the first‑order ALS neuron located?
A
Dorsal root ganglion.
7
Q
What tract does the first‑order ALS neuron ascend/descend in?
A
Lissauer’s tract.
8
Q
Where does the first‑order ALS neuron synapse?
A
Substantia gelatinosa or lamina I/V.
9
Q
Where does ALS decussation occur?
A
Anterior white commissure.
10
Q
Where do ALS second‑order neurons ascend?
A
Contralateral lateral funiculus.
11
Q
Where do ALS third‑order neurons project?
A
VPL → primary somatosensory cortex.
12
Q
What is the somatotopy of ALS?
A
Cervical medial, sacral lateral.
13
Q
What sensory loss occurs with a unilateral spinal cord lesion affecting ALS?
A
Contralateral pain/temp loss 2 levels below.
14
Q
What sensory pattern occurs in syringomyelia?
A
Bilateral cape‑like pain/temp loss.
15
Q
What sensory pattern occurs in Wallenberg syndrome?
A
Ipsilateral face + contralateral body pain/temp loss.
16
Q
Which spinal cord level has the most white matter?
A
Cervical.
17
Q
Which level has a lateral horn?
A
Thoracic (T1–L2).
18
Q
Which level contains Clarke’s nucleus?
A
T1–L2.
19
Q
Which level has large ventral horns for lower limb motor?
A
Lumbar.
20
Q
spinal cord
Which level is mostly gray matter?
A
Sacral.
21
Q
What does the anterior spinal artery supply?
A
Anterior 2/3 of the cord.
22
Q
anterior spinal a
What deficits occur with ASA infarct?
A
Motor paralysis + pain/temp loss with preserved dorsal columns.
23
Q
What do the posterior spinal arteries supply?
A
Dorsal columns and dorsal horns.
24
Q
What deficits occur with PSA infarct?
A
Loss of vibration and proprioception.
25
Where does the artery of Adamkiewicz arise?
Left T9–L2.
26
What region is most vulnerable to ischemia?
T4–T8.
27
What fibers run in the anterior limb of the internal capsule?
Frontopontine fibers and anterior thalamic radiations.
28
What fibers run in the genu?
Corticobulbar fibers.
29
What fibers run in the posterior limb?
Corticospinal and somatosensory fibers.
30
What arteries commonly infarct the internal capsule?
Lenticulostriate arteries.
31
What deficit occurs with posterior limb infarct?
Contralateral hemiparesis + hemisensory loss.
32
What produces CNS myelin?
Oligodendrocytes.
33
What produces PNS myelin?
Schwann cells.
34
What does myelin do to conduction?
Increases speed by saltatory conduction.
35
What channels are dense at nodes of Ranvier?
Voltage‑gated Na⁺ channels.
36
What immune cells mediate MS?
Th1 and Th17 T cells.
37
What CSF finding is characteristic of MS?
Oligoclonal IgG bands.
38
What is the mechanism of Guillain‑Barré syndrome?
Autoimmune attack on Schwann cells.
39
What is the hallmark of GBS?
Ascending paralysis with areflexia.
40
What is the target in AChR‑positive MG?
Nicotinic ACh receptors.
41
What is the mechanism of weakness in AChR MG?
Complement‑mediated receptor destruction.
42
What thymic abnormality is common in AChR MG?
Thymic hyperplasia or thymoma.
43
What is the target in MuSK‑positive MG?
Muscle‑specific kinase.
44
Does MuSK MG activate complement?
No.
45
What symptoms are prominent in MuSK MG?
Bulbar, facial, respiratory weakness.
46
What antibodies may be present in seronegative MG?
LRP4 antibodies.
47
Why does the deltoid have more motor units than ADM?
It is larger and generates more force.
48
Why does ADM allow fine control?
Each motor unit innervates few fibers.
49
What principle governs motor unit recruitment?
Henneman’s size principle.
50
What does lamina I do?
Responds to noxious/thermal stimuli.
51
What does lamina II do?
Modulates pain; substantia gelatinosa.
52
What does lamina III/IV do?
Light touch and mechanical sensation.
53
What does lamina V do?
Relays nociceptive info; receives descending CST.
54
What does lamina VI do?
Reflex interneurons; proprioceptive input.
55
What does lamina VII include?
Dorsal nucleus of Clarke; autonomic neurons.
56
What does lamina IX contain?
Motor neurons.
57
What occurs in lamina X?
Axon decussation.
58
Where is CSF produced?
Choroid plexus of lateral, third, and fourth ventricles.
59
How much CSF is produced per day?
~500 mL/day.
60
What is the total CSF volume?
~150 mL.
61
What drives CSF secretion?
Na⁺/K⁺ ATPase and carbonic anhydrase.
62
What is the CSF pH?
~7.33.
63
Why is CSF more acidic than plasma?
Lower protein → lower buffering capacity.
64
What chemoreceptors respond to CSF pH?
Central chemoreceptors.
65
What ventricle does CSF originate in?
Lateral ventricles.
66
What connects lateral ventricles to the third ventricle?
Foramen of Monro.
67
What connects the third ventricle to the fourth ventricle?
Cerebral aqueduct.
68
What openings allow CSF to exit the fourth ventricle?
Foramina of Magendie and Luschka.
69
Where does CSF go after exiting the fourth ventricle?
Cisterna magna and pontine cistern.
70
Where does CSF circulate after entering cisterns?
Cranial and spinal subarachnoid space.
71
Where does CSF travel in the spine?
Down to lumbar cistern (L2–S2).
72
Where is a lumbar puncture performed?
L3–L4 or L4–L5.
73
Where is CSF reabsorbed?
Arachnoid granulations into superior sagittal sinus.
74
What drives CSF reabsorption?
Pressure gradient.
75
What is a minor route of CSF reabsorption?
Spinal nerve root sleeves and lymphatics.
76
What ventricles enlarge in aqueductal stenosis?
Lateral and third ventricles.
77
What ventricles enlarge in obstruction of Magendie/Luschka?
All ventricles.
78
What ventricles enlarge in communicating hydrocephalus?
All ventricles.
79
What causes communicating hydrocephalus?
Impaired reabsorption at arachnoid granulations.
80
What causes hydrocephalus after meningitis?
Fibrosis of arachnoid granulations.
81
What causes hydrocephalus after subarachnoid hemorrhage?
Blood obstructs arachnoid granulations.
82
What is the triad of normal pressure hydrocephalus?
Urinary incontinence, magnetic gait, cognitive decline.
83
What is hydrocephalus ex vacuo?
Ventricular enlargement due to brain atrophy.
84
What is a spinal CSF block?
Obstruction causing increased pressure above the lesion.
85
What is syringomyelia?
CSF‑filled cavity in spinal cord parenchyma.
86
What sensory loss occurs in syringomyelia?
Loss of pain/temp in a cape‑like distribution.
87
What causes low‑pressure headaches after LP?
CSF leak.
88
What is the effect of CSF leak on brain position?
Brain sagging.
89
What is the effect of adrenomedullary dysplasia on CSF?
None (but included for completeness).
90
what is the thyroid hormone production pwthway (hypothalamus to thyroid), what inhibits the pathway, what stimulates it?
91
what hormone does the hypothalamus release to stimulate cortisol production? what is the pathway?
92
what is the pathway pf the spinothalamic tract
93
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3
102
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107
9
108
10
109
11
110
what is the cushing's triad?
Increased systolic BP
decreased pulse
decreased respirations
111
What does the ventral trigeminothalamic tract carry?
Pain, temperature, and some touch/pressure from the spinal trigeminal nucleus.
112
Do ventral trigeminothalamic fibers cross?
Yes, most decussate to the contralateral side.
113
What does the dorsal trigeminothalamic tract carry?
Touch, pressure, and proprioception from the main sensory nucleus.
114
Do dorsal trigeminothalamic fibers ascend ipsilaterally?
Many ascend without crossing.
115
Where are first‑order trigeminal sensory neuron cell bodies?
Trigeminal (semilunar/Gasserian) ganglion.
116
Which nucleus processes facial pain and temperature?
Spinal trigeminal nucleus.
117
Which nucleus processes facial touch and pressure?
Main (principal) sensory nucleus.
118
Which nucleus processes facial proprioception?
Mesencephalic nucleus.
119
Where do trigeminal second‑order neurons synapse?
VPM of the thalamus.
120
Where do trigeminal third‑order neurons project?
Primary somatosensory cortex via internal capsule.
121
Where does the trigeminal lemniscus travel?
Brainstem, near the medial lemniscus.
122
What is the function of the trigeminal lemniscus?
Conscious, high‑fidelity facial sensation.
123
Which trigeminal modalities are contralateral?
Pain and temperature.
124
Which trigeminal modalities have mixed laterality?
Touch.
125
What fills Meckel’s cave?
CSF.
126
What structure sits inside Meckel’s cave?
Gasserian ganglion and proximal trigeminal roots.
127
Why is Meckel’s cave clinically important?
Trigeminal neuralgia and perineural tumor spread.
128
What supplies the medial homunculus?
ACA.
129
What supplies the lateral homunculus?
MCA.
130
Which MCA branch supplies the posterior limb of the internal capsule?
M1.
131
Where do vertebral arteries merge to form the basilar artery?
Pontomedullary junction.
132
What do vertebral arteries arise from?
Subclavian arteries.
133
What major branch do vertebral arteries give off?
Anterior spinal artery.
134
What does the anterior spinal artery supply?
Anterior two‑thirds of spinal cord and medulla.
135
What reinforces the ASA?
Artery of Adamkiewicz.
136
What does the basilar artery terminate as?
Posterior cerebral arteries.
137
What do thalamoperforating arteries supply?
Thalamus, subthalamus, midbrain.
138
What do thalamogeniculate arteries supply?
Posterior thalamus.
139
What do posterior choroidal arteries supply?
Thalamus, choroid plexus, midbrain.
140
What does the calcarine artery supply?
Visual cortex.
141
What does the parieto‑occipital artery supply?
Precuneus and occipital lobe.
142
What does the splenial (pericallosal) artery supply?
Supplies the splenium of the corpus callosum.
143
What does the artery of Davidoff & Schechter supply?
Tentorium and falx cerebri.
144
What is the most common spinal tumor at T9?
Spinal meningioma.
145
What is the behavior of spinal meningiomas?
Benign and slow‑growing.
146
Which tumor arises from nerve roots?
Schwannoma.
147
Which tumor is intramedullary and arises within spinal cord tissue?
Ependymoma.
148
Which tumor arises from spinal cord supporting cells?
Astrocytoma.
149
Which vascular lesion commonly occurs in thoracic spine?
Hemangioma.
150
What is the primary imaging modality for spinal tumors?
MRI.
151
What is the primary treatment for benign meningiomas?
Surgical removal.
152
1
extradural
153
2
intradural extramedullary
154
155
What defines a peptide hormone?
Chains of 3–191 amino acids that are water‑soluble and act on cell‑surface receptors.
156
What are examples of peptide hormones?
Insulin, oxytocin, growth hormone.
157
What defines an amine hormone?
Derived from tyrosine or tryptophan; may be water‑soluble or lipid‑soluble.
158
What defines lipid‑based hormones?
Cholesterol‑derived, lipid‑soluble, bind intracellular receptors.
159
What is the only gaseous hormone?
Nitric oxide (NO).
160
How do acidophils stain?
Pink/orange‑red with H&E due to affinity for acidic dyes.
161
What do somatotrophs secrete?
Growth hormone (GH).
162
What do lactotrophs secrete?
Prolactin (PRL).
163
Where are acidophils located in the pituitary?
Primarily in the anterior wings.
164
How do basophils stain?
Dark blue or purple with H&E.
165
What do corticotrophs secrete?
ACTH.
166
What do thyrotrophs secrete?
TSH.
167
What do gonadotrophs secrete?
FSH and LH.
168
What are chromophobes?
Pale cells with few/no granules; resting or degranulated.
169
What cells produce GH?
Somatotrophs, the majority of pituitary cells.
170
What are two major functions of GH?
Mobilizes nutrients and stimulates muscle protein synthesis.
171
What does kisspeptin from adipose tissue regulate?
Fertility; requires adequate fat but excess fat impairs fertility via estradiol.
172
What is the main mediator of GH‑driven growth?
IGF‑1.
173
What protein stabilizes IGF‑1 in circulation?
IGFBP‑3.
174
Which test is better for adult GH deficiency?
IGF‑1.
175
Which test is better for pediatric GH deficiency?
IGFBP‑3.
176
What is a positive feedback loop?
A mechanism that amplifies output and disrupts homeostasis; less common.
177
What are examples of positive feedback?
Childbirth, blood clotting, fruit ripening.
178
What is a negative feedback loop?
A mechanism that inhibits/slows a process and maintains homeostasis.
179
What are examples of negative feedback?
Body temperature, blood pressure, fluid balance.
180
What causes gigantism vs acromegaly?
Excess GH before epiphyseal closure → gigantism; after closure → acromegaly. (Implied from “in adults…acromegaly; in children…gigantism.”)
181
What is the most common cause of GH excess?
Pituitary tumors.
182
What are skeletal effects of GH excess?
Thickened bones of face, jaw, hands, feet; enlarged features.
183
What are organ effects of GH excess?
Enlargement of heart, liver, spleen → heart failure, hypertension.
184
What metabolic effect does GH excess cause?
Insulin resistance and increased risk of type 2 diabetes.
185
What neurologic/musculoskeletal issues occur in GH excess?
Joint pain, stiffness, carpal tunnel, nerve compression.
186
Which pituitary hormone is secreted without stimulation?
Prolactin.
187
What normally inhibits prolactin release?
Dopamine (PIH) from the hypothalamus.
188
What receptor does dopamine act on to inhibit prolactin?
D2 receptors on lactotrophs.
189
What does the zona glomerulosa secrete?
Aldosterone (mineralocorticoids).
190
What does the zona fasciculata secrete?
Cortisol (glucocorticoids).
191
What does the zona reticularis secrete?
Androgens (e.g., DHEA).
192
What does the adrenal medulla secrete?
Epinephrine and norepinephrine.
193
What is homonymous hemianopia?
Loss of the same half of the visual field in both eyes.
194
What causes homonymous hemianopia?
Stroke, tumors, trauma along visual pathways.
195
What are common symptoms of hemianopia?
Bumping into objects, reading difficulty, visual neglect, reduced scanning.
196
How does ACTH affect sodium?
Increases sodium retention via aldosterone and cortisol pathways.
197
What blood pressure effect does excess ACTH cause?
Salt‑sensitive hypertension.
198
How does ACTH affect potassium?
Increases potassium loss (kaliuresis).
199
What renal channel does ACTH stimulate?
ENaC via glucocorticoid and mineralocorticoid receptors.
200
What drug class is octreotide?
Somatostatin analog (octapeptide).
201
What are major uses of octreotide?
Acromegaly, carcinoid syndrome, VIPomas, bleeding esophageal varices.
202
How is octreotide administered?
Subcutaneous, IV, or IM depot.
203
What are common side effects of octreotide?
Gallstones/sludge, diarrhea, abdominal pain, nausea, dizziness, glucose changes.
204
What serious side effects can octreotide cause?
Pancreatitis, arrhythmias, severe biliary issues, allergic reactions.
205
What monitoring is recommended with octreotide?
Gallbladder ultrasound, blood sugar, thyroid function.
206
How does octreotide affect fertility?
May increase fertility in women.
207
What long‑term effect may octreotide have in children?
May slow growth if used over a year.
208
What hormone is produced by the zona glomerulosa?
Aldosterone.
209
What hormone is produced by the zona fasciculata?
Cortisol.
210
What hormones are produced by the zona reticularis?
Androgens.
211
What does the adrenal medulla produce?
Catecholamines (epinephrine, norepinephrine).
212
How does light project onto the retina?
Reversed left–right and inverted top–bottom.
213
Which retinal sides receive the left visual field?
Right side of each retina (left eye nasal retina, right eye temporal retina).
214
Which retinal sides receive the right visual field?
Left side of each retina (right eye nasal retina, left eye temporal retina).
215
Which retinal area receives the superior visual field?
Inferior retina.
216
Which retinal area receives the inferior visual field?
Superior retina.
217
Which retinal region sees the temporal visual field?
Nasal retina.
218
Which retinal region sees the nasal visual field?
Temporal retina.
219
Which fibers cross at the optic chiasm?
Nasal retinal fibers.
220
Which fibers stay ipsilateral at the optic chiasm?
Temporal retinal fibers.
221
What does the optic nerve contain?
All fibers from one eye (nasal + temporal retina).
222
What does each optic tract carry?
Ipsilateral temporal retina fibers + contralateral nasal retina fibers.
223
Which visual field is carried by the right optic tract?
Left visual field.
224
Which visual field is carried by the left optic tract?
Right visual field.
225
What do LGN layers 1–2 process?
Motion (magnocellular).
226
What do LGN layers 3–6 process?
Detail and color (parvocellular).
227
What mapping is preserved in the LGN?
Retinotopic mapping.
228
What fibers does Meyer’s loop carry?
Inferior retinal fibers (superior visual field).
229
What deficit results from a Meyer’s loop lesion?
Contralateral superior quadrantanopia.
230
What fibers do parietal radiations carry?
Superior retinal fibers (inferior visual field).
231
What deficit results from a parietal radiation lesion?
Contralateral inferior quadrantanopia.
232
Which part of V1 represents the inferior visual field?
Upper bank (cuneus).
233
Which part of V1 represents the superior visual field?
Lower bank (lingual gyrus).
234
Which part of V1 represents the macula?
Posterior V1.
235
Which part of V1 represents peripheral vision?
Anterior V1.
236
Where does the left visual field ultimately project?
Right V1.
237
What deficit results from an optic nerve lesion?
Monocular vision loss.
238
What deficit results from an optic chiasm lesion?
Bitemporal hemianopia.
239
What deficit results from an optic tract lesion?
Contralateral homonymous hemianopia.
240
What deficit results from a V1 lesion?
Contralateral homonymous hemianopia with macular sparing.
241
What deficit results from a right optic nerve lesion (diagram)?
Blindness in the right eye.
242
What deficit results from a chiasm lesion (diagram)?
Bitemporal hemianopia.
243
What deficit results from an optic tract lesion (diagram)?
Contralateral homonymous hemianopia.
244
What deficit results from an LGN lesion (diagram)?
Contralateral superior quadrantanopia.
245
What deficit results from an optic radiation lesion (diagram)?
Contralateral inferior quadrantanopia.
246
What deficit results from combined radiation lesions?
Contralateral homonymous hemianopia.
247
What deficit results from left optic nerve compression?
Unilateral left-eye field loss.
248
What deficit results from chiasmal compression by a pituitary tumor?
Bitemporal hemianopia.
249
What deficit results from a left cerebrovascular event?
Right homonymous hemianopia.
250
What fibers run in the anterior limb of the internal capsule?
Thalamocortical and frontopontine fibers.
251
What fibers run in the genu of the internal capsule?
Corticobulbar fibers.
252
What fibers run in the posterior limb of the internal capsule?
Corticospinal, corticobulbar, thalamocortical fibers.
253
What fibers run in the retrolenticular part of the internal capsule?
Geniculocalcarine fibers.
254
What fibers run in the sublenticular part of the internal capsule?
Geniculo-temporal fibers.
255
What is the visual field?
The external world the patient sees; used to describe deficits.
256
What is the retinal field?
The internal retinal map where light lands.
257
Why are visual and retinal fields inverted?
The eye optically reverses and inverts images.
258
Which retinal hemifields receive the left visual field?
Left eye nasal retina + right eye temporal retina.
259
Which retinal hemifields receive the right visual field?
Right eye nasal retina + left eye temporal retina.
260
What receptor does strychnine block?
Glycine receptors.
261
What is the effect of glycine blockade?
Loss of inhibition → tonic convulsions.
262
How does hyperventilation cause alkalosis?
CO₂ loss → ↓H⁺ → ↑pH.
263
How does alkalosis increase neuronal excitability?
More Ca²⁺ binds albumin → ↓ionized Ca²⁺ → unstable Na⁺ channels → lower threshold.
264
Why does hyperventilation provoke seizures?
It increases cortical excitability.
265
What is decremental conduction?
Graded potentials weaken as they spread.
266
What is the labeled-line principle?
Stimulating a sensory pathway produces its modality regardless of stimulus type.
267
What happens when the optic nerve is electrically stimulated?
Flashes of light.
268
What is dying-back neuropathy?
Distal axon degeneration progressing proximally.
269
What part of the neuron is intact early in dying-back neuropathy?
The soma.
270
What degenerates first in dying-back neuropathy?
Axon terminals and distal axon segments.
271
How does dying-back neuropathy differ from Wallerian degeneration?
Wallerian is distal to focal injury; dying-back is length-dependent.
272
What are early sensory symptoms of dying-back neuropathy?
Distal numbness, tingling, burning.
273
What motor symptom appears later in dying-back neuropathy?
Foot drop.
274
Which reflex is lost first in dying-back neuropathy?
Ankle reflex.
275
What is the distribution pattern of dying-back neuropathy?
Stocking-glove.
276
Is dying-back neuropathy symmetric or asymmetric?
Symmetric.
277
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278
2
279
3
280
4
281
5
282
5 and 6
283
1
284
2
285
3
286
4
287
What does double vision that resolves when one eye is covered indicate?
Binocular diplopia due to misalignment of the eyes.
288
What does binocular diplopia imply about eye alignment?
The eyes are not aligned properly because coordination of extraocular muscles is disrupted.
289
What major categories of pathology commonly cause binocular diplopia?
Tumor, aneurysm, or nerve damage affecting ocular motor control.
290
Which cranial nerves, when affected by a tumor, most commonly cause binocular diplopia?
CN III, IV, and VI.
291
Why do CN III, IV, and VI lesions cause diplopia?
They innervate extraocular muscles; dysfunction prevents coordinated gaze.
292
What tumor location can affect CN III, IV, and VI simultaneously as they travel to the orbit?
The cavernous sinus.
293
Why do cavernous sinus tumors cause multiple ocular motor palsies?
All three ocular motor nerves pass through the cavernous sinus.
294
What skull‑base tumors commonly compress ocular motor nerves?
Meningiomas and chordomas.
295
How can pituitary adenomas cause diplopia?
By compressing nearby ocular motor nerves, especially during pituitary apoplexy.
296
How can brainstem tumors cause diplopia?
They disrupt central coordination of eye movements.
297
What type of tumor is a medulloblastoma?
A malignant embryonic neuroepithelial tumor.
298
Where do medulloblastomas originate?
The cerebellum.
299
What is the cerebellum’s primary function?
Coordination of muscle movements and balance.
300
How do medulloblastomas typically spread?
Through CSF to other brain and spinal cord areas.
301
Do medulloblastomas commonly metastasize outside the CNS?
No, they rarely spread beyond the CNS.
302
What is the lateral ventricle?
A paired CSF‑filled cavity in each cerebral hemisphere.
303
What connects the third and fourth ventricles?
The cerebral aqueduct (aqueduct of Sylvius).
304
What is the third ventricle?
A midline CSF cavity between the thalami.
305
What is the fourth ventricle?
A CSF cavity between the pons/medulla and cerebellum.
306
What is the normal function of p53?
A tumor suppressor transcription factor that induces p21.
307
What is the role of p21?
A CDK inhibitor that blocks CDK2/cyclin E, preventing G2→M progression.
308
What happens when p53 is mutated?
p21 is not expressed, CDK2/cyclin E becomes uncontrolled, and mitosis proceeds unchecked.
309
Why does loss of p21 lead to uncontrolled cell division?
CDK2/cyclin E remains active without inhibition.
310
What lesion causes left hemianopia?
Left optic nerve lesion.
311
What lesion causes bitemporal hemianopia?
Optic chiasm lesion, commonly pituitary tumor.
312
What lesion causes right nasal hemianopia?
Outer optic tract lesion, often from internal carotid artery thrombus.
313
What lesion causes right homonymous hemianopia?
Optic tract lesion.
314
What lesion causes right superior quadrantanopia?
Meyer's loop lesion (left temporal lobe).
315
What lesion causes right inferior quadrantanopia?
Dorsal optic radiation lesion (left parietal lobe).
316
What lesion causes right hemianopia with macular sparing?
PCA infarct.
317
What hormone does the hypothalamus release to stimulate the pituitary?
TRH.
318
What hormone does the pituitary release to stimulate the thyroid?
TSH.
319
What are the daily production amounts of T3 and T4?
~6 mcg/day T3; ~100 mcg/day T4.
320
Where is T4 converted to T3?
Liver, kidney, brain, skeletal muscle.
321
What enzyme converts T4 to T3?
Iodothyronine deiodinase.
322
What is rT3?
Inactive byproduct of T4 deiodination.
323
How do thyroid hormones affect RBC production?
They stimulate bone marrow erythropoiesis.
324
Why does hypothyroidism cause anemia?
Lack of thyroid hormone reduces marrow stimulation.
325
How does hyperthyroidism affect bone?
Accelerates bone turnover → osteoporosis.
326
How does hypothyroidism affect bone?
Slows bone turnover → increased fracture risk.
327
Why does hypothyroidism increase LDL?
Liver produces fewer LDL receptors → reduced clearance.
328
What does the water bottle sign indicate on CXR?
Large pericardial effusion (>250 mL).
329
Why does the cardiac silhouette appear flask‑shaped?
Sagging pericardium from slow fluid accumulation.
330
Why does hypothyroidism cause pleural/pericardial/ascitic effusions?
Increased capillary permeability → leakage of protein‑rich fluid.
331
What role does myxedema play in effusions?
Tissue swelling impairs lymphatic drainage.
332
What are classic signs of uncal herniation?
Blown pupil + contralateral hemiparesis.
333
Why does uncal herniation cause a blown pupil?
Compression of CN III parasympathetic fibers.
334
What G‑protein does α1 couple to?
Gq → ↑IP3/DAG.
335
What G‑protein does α2 couple to?
Gi → ↓cAMP.
336
What G‑protein does β1 couple to?
Gs → ↑cAMP → ↑HR and ↑renin/angiotensin.
337
What G‑protein does β2 couple to?
Gs → ↑cAMP → vasodilation.
338
What are Q‑type calcium channels?
Voltage‑gated Ca²⁺ channels involved in neurotransmitter release.
339
Where are Q‑type channels primarily located?
Presynaptic terminals.
340
What activates Q‑type channels?
High‑voltage depolarization.
341
What are L‑type calcium channels?
High‑voltage channels in cardiac/smooth muscle; target of dihydropyridines.
342
What are N‑type calcium channels?
Neuronal channels mediating neurotransmitter release.
343
What are P/Q‑type calcium channels?
Channels in cerebellar Purkinje cells and presynaptic terminals.
344
What are T‑type calcium channels?
Low‑voltage channels involved in pacemaker activity and absence seizures.
345
What are R‑type calcium channels?
Resistant channels contributing to dendritic Ca²⁺ entry.
346
What molecule is the starting point for adrenal steroidogenesis?
Cholesterol.
347
What protein transports cholesterol into mitochondria to begin steroid synthesis?
StAR protein.
348
What enzyme converts cholesterol into pregnenolone?
P450scc.
349
What is the first product formed from cholesterol in adrenal steroidogenesis?
Pregnenolone.
350
What enzyme converts pregnenolone to 17‑OH pregnenolone?
17α‑hydroxylase.
351
What enzyme converts 17‑OH pregnenolone to DHEA?
17,20 lyase.
352
What enzyme converts DHEA to androstenediol?
17β‑HSD.
353
What enzyme converts pregnenolone to progesterone?
3β‑HSD.
354
What enzyme converts progesterone to 17‑OH progesterone?
17α‑hydroxylase.
355
What enzyme converts 17‑OH progesterone to androstenedione?
17,20 lyase.
356
What enzyme converts androstenedione to testosterone?
17β‑HSD.
357
What enzyme converts testosterone to estradiol?
Aromatase.
358
What enzyme converts androstenedione to estrone?
Aromatase.
359
What enzyme converts deoxycorticosterone to corticosterone?
11β‑hydroxylase.
360
What enzyme converts 11‑deoxycortisol to cortisol?
11β‑hydroxylase.
361
What enzyme converts corticosterone to 18‑OH corticosterone?
18‑hydroxylase.
362
What enzyme converts 18‑OH corticosterone to aldosterone?
18‑oxidase.
363
What is the primary epithelial cell type in the late distal tubule and collecting duct?
Principal cells.
364
What channel mediates sodium reabsorption in principal cells?
ENaC.
365
What channel mediates potassium secretion in principal cells?
ROMK.
366
What hormone regulates water reabsorption in principal cells?
Vasopressin (ADH).
367
What water channel is inserted into the apical membrane in response to vasopressin?
Aquaporin‑2.
368
What hormone increases ENaC activity and Na⁺/K⁺‑ATPase expression?
Aldosterone.
369
What cardiac symptoms occur in hyperkalemia?
Palpitations, arrhythmias, chest pain, slow/weak pulse.
370
What neuromuscular symptoms occur in hyperkalemia?
Weakness, fatigue, paralysis, tingling, numbness.
371
What systemic symptoms occur in hyperkalemia?
Nausea, vomiting, diarrhea.
372
What severe complication can hyperkalemia cause?
Ventricular fibrillation or cardiac arrest.
373
What neurological symptoms occur in hyponatremia?
Headache, confusion, fatigue, irritability.
374
What muscular symptoms occur in hyponatremia?
Muscle spasms, cramps, weakness.
375
What severe complications occur in hyponatremia?
Seizures, coma, brainstem herniation.
376
How is total cholesterol affected in untreated adrenal insufficiency?
Often elevated.
377
How is LDL affected in untreated adrenal insufficiency?
Often elevated.
378
How is HDL affected in untreated adrenal insufficiency?
Low.
379
How are triglycerides affected in untreated adrenal insufficiency?
Often elevated.
380
Which CAH enzyme deficiency is most common?
21‑hydroxylase deficiency.
381
Which CAH enzyme deficiency is rare?
17α‑hydroxylase deficiency.
382
What happens to androgens in 21‑hydroxylase deficiency?
High.
383
What happens to androgens in 17α‑hydroxylase deficiency?
Low.
384
What happens to aldosterone in 21‑hydroxylase deficiency?
Low.
385
What happens to aldosterone in 17α‑hydroxylase deficiency?
High.
386
What blood pressure pattern occurs in 21‑hydroxylase deficiency?
Low or normal.
387
What blood pressure pattern occurs in 17α‑hydroxylase deficiency?
High.
388
What genital phenotype occurs in 46,XX with 21‑hydroxylase deficiency?
Ambiguous genitalia.
389
What genital phenotype occurs in 46,XX with 17α‑hydroxylase deficiency?
Normal genitalia, no puberty.
390
What genital phenotype occurs in 46,XY with 21‑hydroxylase deficiency?
Normal genitalia.
391
What genital phenotype occurs in 46,XY with 17α‑hydroxylase deficiency?
Ambiguous or female genitalia.
392
What is the goal of the Ortolani maneuver?
Detect a dislocated but reducible hip.
393
What motion is used in the Ortolani maneuver?
Abduction with anterior pressure.
394
What indicates a positive Ortolani test?
A palpable or audible clunk.
395
What is the goal of the Barlow maneuver?
Detect an unstable, dislocatable hip.
396
What motion is used in the Barlow maneuver?
Adduction with posterior pressure.
397
What indicates a positive Barlow test?
A clunk as the hip dislocates.
398
What is the mechanism of fludrocortisone?
Potent mineralocorticoid agonist.
399
How does fludrocortisone affect sodium?
Increases sodium reabsorption.
400
How does fludrocortisone affect potassium?
Increases potassium excretion.
401
How does fludrocortisone affect water balance?
Increases water retention.
402
How does fludrocortisone affect blood pressure?
Raises blood pressure.
403
What is the primary clinical use of fludrocortisone?
Mineralocorticoid replacement in adrenal insufficiency.
404
Why is fludrocortisone used in CAH?
Replaces deficient mineralocorticoid activity.
405
Why is fludrocortisone used cautiously in hypertension?
It increases fluid retention.
406
Why is fludrocortisone used cautiously in heart failure?
It can worsen volume overload.
407
Why is fludrocortisone used cautiously in hypokalemia?
It increases potassium loss.
408
What is the mechanism of sodium chloride administration?
Restores extracellular sodium and osmolality.
409
How does sodium chloride affect intravascular volume?
Expands extracellular fluid volume.
410
What is sodium chloride used for in adrenal insufficiency?
Sodium replacement.
411
Why is sodium chloride used in salt‑wasting CAH?
Replaces sodium lost from low aldosterone.
412
Why is sodium chloride used cautiously in heart failure?
It can worsen fluid overload.
413
Why is sodium chloride used cautiously in kidney disease?
Risk of edema and hypertension.
414
What is the mechanism of hydrocortisone cypionate?
Glucocorticoid agonist mimicking cortisol.
415
How does hydrocortisone affect inflammation?
Suppresses inflammatory cytokines.
416
How does hydrocortisone affect metabolism?
Increases gluconeogenesis.
417
How does hydrocortisone affect immune function?
Decreases lymphocyte activity.
418
What is the primary use of hydrocortisone in adrenal insufficiency?
Cortisol replacement.
419
Why is hydrocortisone used in CAH?
Suppresses ACTH to reduce androgen excess.
420
Why is hydrocortisone used cautiously in infections?
It suppresses immune responses.
421
Why is hydrocortisone used cautiously in diabetes?
It raises blood glucose.
422
Why is hydrocortisone used cautiously in osteoporosis?
Long‑term use decreases bone density.
423
Why is hydrocortisone used cautiously in hypertension?
It can cause sodium retention.
424
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425
2
426
3
427
4
428
5
6
429
6
430
7
431
8
432
9
433
10
434
What two functional components does CN III carry?
GSE somatic motor fibers to extraocular muscles + GVE parasympathetic fibers to pupil and lens.
435
Into what two divisions does CN III split in the orbit?
Superior division and inferior division.
436
What type of fibers are carried in the superior division of CN III?
Pure GSE motor fibers.
437
What muscle elevates the eye and is innervated by the superior division of CN III?
Superior rectus.
438
What actions does the superior rectus contribute to besides elevation?
Intorsion and adduction.
439
What eyelid muscle is innervated by the superior division of CN III?
Levator palpebrae superioris.
440
What happens with a superior division CN III lesion?
Ptosis + impaired upgaze; pupil normal.
441
What types of fibers run in the inferior division of CN III?
GSE motor fibers + GVE parasympathetic fibers.
442
What muscle adducts the eye and is innervated by the inferior division?
Medial rectus.
443
What muscle depresses the eye (especially in adduction)?
Inferior rectus.
444
What muscle elevates the eye in adduction and causes extorsion?
Inferior oblique.
445
Where do preganglionic parasympathetic fibers of CN III synapse?
Ciliary ganglion.
446
Through what nerves do postganglionic parasympathetic fibers travel?
Short ciliary nerves.
447
What muscle constricts the pupil?
Sphincter pupillae.
448
What muscle thickens the lens for accommodation?
Ciliary muscle.
449
What happens to the pupil in an inferior division CN III lesion?
Dilated pupil (mydriasis).
450
What accommodation deficit occurs in inferior division lesions?
Loss of accommodation.
451
Why does the eye become “down and out” in CN III palsy?
Unopposed LR6 + SO4.
452
Why are parasympathetics affected early in uncal herniation?
They run superficially on CN III.
453
What functions are isolated in the superior division of CN III?
Vertical gaze + eyelid elevation.
454
What functions are isolated in the inferior division of CN III?
Adduction, depression, elevation in adduction, parasympathetics.
455
What deficits define a superior division palsy?
Ptosis + impaired elevation.
456
What deficits define an inferior division palsy?
Pupil involvement + impaired adduction/depression/elevation in adduction.
457
What is macular sparing?
Homonymous hemianopia with preserved central vision.
458
Why does macular sparing occur?
Dual blood supply from PCA + MCA.
459
What lesion classically causes macular sparing?
Occipital lobe lesion, especially PCA infarct.
460
Is macular sparing seen in optic nerve, chiasm, or optic tract lesions?
No.
461
Why is the macula resistant to ischemia?
Large cortical representation + redundant supply + high‑acuity priority.
462
What visual field defect occurs in left PCA stroke?
Right homonymous hemianopia with macular sparing.
463
What lesion most commonly causes hemineglect?
Right parietal lobe lesion (inferior parietal lobule).
464
Why does right parietal damage cause left neglect?
Right parietal attends to both sides; left attends mostly to right.
465
What visual information does each optic tract carry?
Contralateral visual field from both eyes.
466
What type of defect results from any post‑chiasmal lesion?
Homonymous visual field defect.
467
What is the function of the Edinger–Westphal nucleus?
Parasympathetic control of pupil constriction and lens accommodation.
468
Where is the EWN located?
Midbrain at superior colliculus, medial to CN III motor nucleus.
469
What retinal cells initiate the light reflex?
Retinal ganglion cells.
470
Where do light reflex fibers branch off before reaching the LGN?
Pretectal nuclei.
471
Why does shining light in one eye constrict both pupils?
Pretectal nuclei project bilaterally to both EWNs.
472
In which division of CN III do preganglionic parasympathetic fibers travel?
Inferior division.
473
Where do these fibers synapse?
Ciliary ganglion.
474
What nerves carry postganglionic fibers to the eye?
Short ciliary nerves.
475
What three components define the accommodation reflex?
Convergence, lens thickening, pupil constriction.
476
What cortical area recognizes a near target?
Visual association cortex.
477
What frontal area sends signals to EWN and CN III motor nucleus?
Frontal eye fields.
478
What happens in an EWN lesion?
Dilated pupil; no light or accommodation response.
479
What lesion causes light‑near dissociation?
Pretectal lesion (Parinaud syndrome).
480
Why does uncal herniation cause early pupillary dilation?
Compression of superficial parasympathetic fibers of CN III.
481
What is a cerebral watershed zone?
Cortex supplied by distal branches of two arterial territories.
482
Why are watershed zones vulnerable?
Lowest perfusion pressure; first to infarct in hypotension.
483
What syndrome is classic for ACA–MCA watershed infarct?
Man‑in‑the‑barrel syndrome.
484
What is the deficit pattern in man‑in‑the‑barrel syndrome?
Proximal arm/leg weakness with distal strength preserved.
485
What deficits occur in MCA–PCA watershed infarcts?
Higher‑order visual deficits, visual agnosias, possible language issues.
486
What are the four midline “M” structures in the Rule of 4s?
Motor pathway, Medial lemniscus, Medial longitudinal fasciculus, Motor nuclei.
487
What deficit results from damage to the motor pathway (corticospinal tract)?
Contralateral arm and leg weakness.
488
What deficit results from damage to the medial lemniscus?
Contralateral loss of vibration and proprioception.
489
What deficit results from damage to the medial longitudinal fasciculus (MLF)?
Ipsilateral internuclear ophthalmoplegia.
490
What cranial nerve nuclei are midline according to the Rule of 4s?
CN III, IV, VI, XII.
491
What is the rule for determining which motor nuclei are midline?
Motor nuclei that divide evenly into 12 (except I & II) are midline.
492
What are the four lateral “S” structures in the Rule of 4s?
Spinocerebellar tract, Spinothalamic tract, Sensory nucleus of CN V, Sympathetic pathway.
493
What deficit results from damage to the spinocerebellar tract?
Ipsilateral limb ataxia.
494
What deficit results from damage to the spinothalamic tract?
Contralateral pain and temperature loss in the body.
495
What deficit results from damage to the sensory nucleus of CN V?
Ipsilateral facial pain and temperature loss.
496
What deficit results from damage to the sympathetic pathway?
Ipsilateral Horner syndrome.
497
Which cranial nerves originate in the medulla?
CN IX, X, XI, XII.
498
Which cranial nerves originate in the pons?
CN V, VI, VII, VIII.
499
Which cranial nerves originate above the pons (midbrain)?
CN III, IV.
500
What supplies the medial medulla?
Paramedian branches of the vertebral artery.
501
What supplies the lateral medulla?
Posterior inferior cerebellar artery (PICA).
502
What supplies the medial pons?
Paramedian branches of the basilar artery.
503
What supplies the lateral pons?
AICA and long circumferential branches of the basilar artery.
504
What supplies the medial midbrain?
Paramedian branches of the posterior cerebral artery (PCA).
505
What supplies the lateral upper pons / lower midbrain region?
Superior cerebellar artery (SCA).
506
A lesion causes contralateral weakness + contralateral loss of vibration/proprioception + ipsilateral tongue deviation. Where is it?
Medial medulla (vertebral artery paramedian branches).
507
A lesion causes ipsilateral facial pain/temp loss + contralateral body pain/temp loss + ipsilateral Horner + dysphagia/hoarseness. Where is it?
Lateral medulla (PICA).
508
A lesion causes ipsilateral facial paralysis + decreased lacrimation/salivation + contralateral body pain/temp loss. Where is it?
Lateral pons (AICA).
509
A lesion causes vertical gaze palsy + CN III palsy + contralateral weakness. Where is it?
Medial midbrain (PCA paramedian branches).
510
What are the major terminal branches of the internal carotid artery?
Anterior cerebral artery (ACA) and middle cerebral artery (MCA).
511
What cortical region does the ACA supply?
Medial frontal and parietal lobes.
512
What motor deficit results from ACA infarct?
Contralateral leg > arm weakness.
513
What sensory deficit results from ACA infarct?
Contralateral leg > arm sensory loss.
514
What behavioral deficit can ACA infarct cause?
Abulia or personality changes.
515
What deep structure does the recurrent artery of Heubner supply?
Head of caudate and anterior limb of internal capsule.
516
What cortical regions does the MCA supply?
Lateral frontal, parietal, and temporal lobes.
517
What motor deficit results from MCA infarct?
Contralateral arm/face > leg weakness.
518
What sensory deficit results from MCA infarct?
Contralateral arm/face > leg sensory loss.
519
What deficit occurs with left MCA superior division infarct?
Broca aphasia.
520
What deficit occurs with left MCA inferior division infarct?
Wernicke aphasia.
521
What visual deficit occurs with MCA inferior division infarct?
Contralateral superior quadrantanopia.
522
What deep structures do MCA lenticulostriate arteries supply?
Putamen, globus pallidus, posterior limb of internal capsule.
523
What classic stroke syndrome results from lenticulostriate infarct?
Pure motor stroke.
524
What does the anterior communicating artery connect?
The two ACAs.
525
What visual deficit can an anterior communicating artery aneurysm cause?
Bitemporal hemianopia.
526
What major branches arise from the vertebral arteries?
PICA and anterior spinal artery.
527
What brainstem region does PICA supply?
Lateral medulla.
528
What cerebellar region does PICA supply?
Inferior cerebellar hemisphere.
529
What syndrome results from PICA infarct?
Lateral medullary (Wallenberg) syndrome.
530
What medullary region does the anterior spinal artery supply?
Medial medulla.
531
What spinal region does the anterior spinal artery supply?
Anterior two‑thirds of the spinal cord.
532
What syndrome results from anterior spinal artery medullary infarct?
Medial medullary syndrome.
533
What major branches arise from the basilar artery?
AICA, pontine paramedian branches, SCA, PCA.
534
What brainstem region do basilar paramedian branches supply?
Medial pons.
535
What syndrome results from basilar paramedian infarct?
Medial pontine syndrome.
536
What brainstem region does AICA supply?
Lateral pons.
537
What cerebellar region does AICA supply?
Anterior inferior cerebellum.
538
What syndrome results from AICA infarct?
Lateral pontine syndrome.
539
What cranial nerve is commonly affected in AICA infarct?
CN VII.
540
What cerebellar region does SCA supply?
Superior cerebellum.
541
What brainstem region does SCA supply?
Upper pons and lower midbrain dorsolateral region.
542
What deficits occur in SCA infarct?
Ipsilateral ataxia and contralateral pain/temperature loss.
543
What cortical region does the PCA supply?
Occipital lobe and inferior temporal lobe.
544
What visual deficit results from PCA infarct?
Contralateral homonymous hemianopia with macular sparing.
545
What deep structures do PCA thalamogeniculate branches supply?
Thalamus (VPL/VPM).
546
What syndrome results from thalamic PCA infarct?
Dejerine–Roussy syndrome.
547
What midbrain region does PCA paramedian supply?
Medial midbrain.
548
What syndrome results from PCA paramedian infarct?
Weber syndrome.
549
What arteries form the Circle of Willis?
ACA, ACom, ICA, PCA, PCom.
550
What artery commonly causes CN III palsy when aneurysmal?
Posterior communicating artery.
551
What are the major cerebral watershed zones?
ACA–MCA and MCA–PCA border zones.
552
What deficits occur in watershed infarcts?
Proximal arm and leg weakness (man‑in‑the‑barrel).
