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patho II > Neuro III (b) > Flashcards

Neuro III (b) Flashcards

1
Q

the 2 types of peripheral Nerve injury

A

1) Axonal injuries
2) Demyelinating Neuropathies

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2
Q

Morphological hallamrk in Axonal Neuropathies

A

Decrease in axons’ density –> Decrease in the strength of amplitude of nerve impulses

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3
Q

Morphological Hallmark in Demyelinating Neuropathies

A

Relative normal density of axons and signs of segmental demyelination and repair (remyelination) (axons with thin myelin sheaths and short internodes)

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4
Q

patho of Axonal Neuropathies

A

Direct injury to the axon –> Degeneration of the entire distal portion of the axon –> Secondary myelin loss (Wallerian degeneration)

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5
Q

Patho of Demyelinating Neuropathies

A

Damage to Schwann cells or myelin, but relative axonal sparing –> Occurrence of demyelination in individual myelin internodes (Segmental demyelination)

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6
Q

CM of Polyneuropathies

* peripheral nerve injury

A

Loss of sensation and paraesthesias (“stocking and glove” distribution -> Starts in the toes -> Spreads upward to the knees -> Lastly involves the hands)

* paraesthesias –> tingiling

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7
Q

3 types of Peripjeral nerve injury

A

1) Polyneuropathies (most common)
2) Poluneruritis Multiples
3) Mononeuropathy (involves a single nerver due to trauma or entrapment)

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8
Q

A mononeuropathy Syndrom

* peripheral nerve injury (single nerve)

A

Carpal Tunnel Syndrom
(compression of the median nerve)

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9
Q

cause of Gullain-Barre Syndrome

* Rapidly progressive acute demyelinating disorder

A

1) Infection (e.g. CMV, EBV, HIV, etc.) or vaccine –> Break down of self-tolerance –> Autoimmune response
2) Involvement of both humoral and cellular immune responses

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10
Q

Morphological featurs of Gullian-Barre Syndrome

A

Injury most extensive in the nerve roots and proximal nerve segments

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11
Q

CM of Gullian-Barre Syndrome

A

1) Parethesias (in the hands and feet)
2) Difficulty breathing (due to severe respiratory muscle weakness)
3) Absent or depressed deep tendon relfexes (paralysis)
4) Muscle weakness (begining in the legs and ascends)

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12
Q

CM of Chronic inflammatory Demyelinating polyneuropathy

A

1) Difficulty in walking
2) Weakness
3) Numbness
4) Pain or tingling sensations

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13
Q

Microscopic Findings:
* Peripheral nerves with segments of demyelination and remyelination

features of?

A

Chronic inflammatory demyelinating polyneuropathy

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14
Q

the most common peripheral neuropathy

A

Diabetic peripheral neuropathy
* px w/ long-standing DM

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15
Q

Risk factors of Diabetic Peripheral neuropathy

A

1) Microvascular changes (retinopathy, neuropathy, Nephropathy)
2) Hyperglycaemia
3) Accumulation of Glycosylated end products (HbA1c)
4) Changes in axonal metabolism
5) increased leveles of ROS

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16
Q

Type of Diabetic Neuropathies

A

1) Autonomic Neuropathy: Changes in bowel, cardiac or sexual function
2) Lumbosacral Radiculopathy: Lower extremity weakness and muscle atrophy
3) Distal Symmetric Sensorimotor Polyneuropathy: Paraesthesias and numbness

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17
Q

prognosis of Chronic inflammatory demylinating polyneuropathy

A

Complete recovery (some patients) but Recurrent bouts of symptomatic disease –> Permanent loss of nerve function (most common)

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18
Q

Toxic Form of Peripheral Neuropathy: Most susceptible <> —————–, Most pronounced <> ————–

A

Most susceptible –> Longest axons; Most pronounced –> Distal extremities

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19
Q

Examples of Systemic Vasculitides

A

Polyarteritis nodosa, Churg-Strauss Sy., Wegener granulomatosis

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20
Q

Most common clinical picture of Systemic Vasculitides

A

Mononeuritis multiplex (painful asymmetric mixed sensory and motor peripheral neuropathy)

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21
Q

Inherited Form of Peripheral Neuropathy: Most common cause –> Mutations in the ——— gene

A

PMP22 gene

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22
Q

Epi of Myasthenia Gravis

A
  • More common in females
  • Thymic hyperplasia (reactive hyperplasia of intra-thymic B cells) –> About 60% of patients
  • Thymoma –> 20% of patients
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23
Q

cause/ patho of Myasthenia Gravis

A

Auto-Antibodies blocking the function of Acetylocholine receptors at motor end-plates –> Degradation and depletion of the receptors

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24
Q

CM of Myasthenia Gravis

A

Ptosis (droping eyelids) or Diplopia (double vision), due to weakness in the extra-ocular muscles

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25
Q

causes of Lambert-Eaton Syndrome

A

Auto-Antibodies inhibiting the function of pre-synaptic Calcium channels -> Reduction of Acetylocholine release into the synaptic cleft

26
Q

CM of Lambert-Eaton Syndrome

A

Paraneoplastic Syndrome in patients with Small Cell Lung Carcinoma (SCLC)

27
Q

Epi of Schwannomas (Neurilemmomas)

A
  • bening
  • Sporadic (most common); 10% associated with familial NF2
28
Q

loc of Schwannomas

A
  • Soft tissues
  • Internal organs
  • Spinal nerve roots
  • Cranial nerves (Vestibular portion of the 8th nerve
29
Q

Macroscopic Features:
* Circumscribed masses next to a nerve
* Globualr enlargment of a fascicle
* Yellow colouration of the cut surface, due to lipid accumulation

Microscopic Findings:
* Alternating areas of dense (“Antoni A”) and loose (“Antoni B”) texture
* **“Antoni A” **areas: Bland spindle cells arranged into intersecting fascicles
* “Verocay bodies”: Structures composed of alternating bands of nuclear palisading and anuclear strands between them
* Thick-walled hyalinised vessels
* Possible, presence of haemorrhage or cystic changes

features of?

A

Shwannomas (Neurilemmomas)

30
Q

caues of Neurofibromatois Type 2

A

Loss of function mutation of the NF2 gene affecting Merlin (Schwannomin) protein

31
Q

CF of NF2

A

Bilateral vestibular Schwannomas -> Hallmark of Neurofibromatosis Type 2

32
Q

Hallmark of Neurofibromatosis Type 2?

A

Bilateral vestibular Schwannomas

33
Q

———— : Familial condition associated with multiple Schwannomas, Ass. w/ the Absence of vestibular Schwannomas

A

Schwannomatosis

34
Q

Microscopic Findings:
* Non-encapsulated tumours
* Haphazard cellular growth pattern
* Admixture of Schwann cells w wavy nuclei, mast cells, fibroblast-like cells and perineurial-like cells
* Background stroma: Loose wavy or dense collagen bundles or even myxoid consistency

features of?

A

Neurofibromatosis Type 2

35
Q

localized Cutaneous Neurofibromas can exist as?

A
  • solitary lesions or multiple in the context of NF1
  • Superficial nodular or polypoid masses
36
Q

Pathogonomic (symptom/sign) of NF1

A

Plexiform Neurofibromas

37
Q

Microscopic Findings:
* Presence of residual axons found among the neoplastic cells
* Proliferation of schwann cells and fibroblasts
* Enlargement of the nerve
* Intact perineurium
* Classic “bag of worms appearance”

features of?

A

Plexifrom Neurofibromas

38
Q

Diffuse Neurofibromas are ass w/?

A

NF1

39
Q

Microscopic findings:
* Extensive infiltration of the dermis and subcutis
* Subcuataneous masses
* Marked expansion of dermal tissue

features of?

A

Diffuse Neurofibromas

40
Q

Neurofibromatosis Type 1 is AKA?

A

Von Recklinghausen disease

41
Q

Genetic predisposition of NF1

A

AD ; Mutations in the tumour suppressor gene Neurofibromin

42
Q

CM of NF1

A

1) Learning disabilities
2) Seizures
3) Skeletal abnormalities (e.g. scoliosis)
4) Vascular abnormalities with arterial stenoses
5) Pigmented nodules of the iris (Lisch nodules)
6) Pigmented skin lesions (axillary freckling and café au lait spots)
7) Optic Glioma
8) Neurofibromas
9) Bone defects

43
Q

who is likely to develop Malignant Peripheral Nerve Sheath tumours?

A

NF1 px

44
Q

patho of Malignant Peripjeral nerve Sheat tumours

A

May originate from transformation of a Neurofibroma, usually of the plexiform type

45
Q

cause of Traumatic Neuroma

A

Previous injury of a peripheral nerve

46
Q

patho of Traumatic Neuroma

A
  • Transection (divides) of axon –> Activation of regeneration mechanism –> Sprouting and elongation of processes (from the proximal axonal stump)
  • Severe injury –> Disruption of the peri-neurial sheath –> Failure of proximal end to “meet” the distal end of the transected nerve –> Induction of a Schwann cell proliferation –> Development of a haphazard mixture of axons, Schwan cells and connective tissues
47
Q

Occular Disroders

A

1) Conjunctivitis
2) Retinopathy of prematurity
3) Retinitis Pigmentosa
4) Diabetic Retinopathy
5) Senile Macular Degeneration
6) Glaucoma
7) Retinoblastoma

48
Q

Cause of Conjuctivitis

A

Adenovirus (most common), bacteria

49
Q

Prgnosis of Retinopathy of Prematurity

A

Blindness

50
Q

casue of Retionopathy of prematurity

A

Toxicity of oxygen, administered because of NRDS (Newborn respiratory distress syndrome)

51
Q

CM of Retinitis Pigmentosa

A

1) Retinal pigmentation
2) Peripheral vision loss (“Tunnel vision”) and progressive loss of Central Vision

52
Q

cause of Diabetic Retinopathy

A

1) Non-proliferative:
- Micro-aneurysms, haemorrhages, soft (cotton-wool) exudates (micro-infarcts) and hard exudates (protein from damaged capillaries)
2) Proliferative:
- Neo-vascularisation and fibrosis
- Possible progression to haemorrhage and retinal detachment

53
Q

patho of Senile Macular Degenration

A

Loss of central vision and pigmentary changes or haemorrhage in the macula

54
Q

patho/CM of Open Angle Galucoma

A

1) Open Angle Glaucoma: Gradually increasing intraocular pressure –> Visual impairment –> Blindness

55
Q

patho/CM of Angle-Closure Galucoma

A

Angle-Closure Glaucoma:
* Narrow anterior chamber angle
* Increase in intraocular pressure on dilatation of pupil

56
Q

symptoms of open angle Glaucoma

A

1) Gradual loss of peripheral (side to side & up/down) visions, usually in both eyes
2) Tunnel vission

57
Q

Smptoms of Closed angle Glaucoma

A

1) sudden,sever blurred vision
2) Severe pain- often affecting one eye at a time

58
Q

Risk factors of Glaucoma

A

1) increased eye pressure
2) High bp
3) Family history of Glaucoma
4) >60 yrs

59
Q

Gentic predispostion of Retinoblastoma

A

Homozygous deletion of Rb gene

60
Q

Explain the “two hit” hypothesis of tumour development in Retinoblastoma

A

1) First “hit”: Inherited deletion in germ cells (familial cases) or somatic mutation (sporadic cases)
2) Second “hit”: Somatic mutation (both familial and sporadic cases)

61
Q

Signs of Retinoblastoma

A

1) swollen eyes
2) shrunken eyes
3) A red, sore or swollen eye w/o infection
4) A white refelction in the pupil

62
Q

Microscopic features:
- Multiple foci of necrosis
- Numerous apoptotic cells
- True rosette
- scant cytoplasm
- Flexner-Wintersteiner rosette
- Round to oval nuceli and finely granualr chromattin

features of?

A

Retinoblastoma

patho II (29 decks)

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