Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

MS2 Unit 3 > Pathology > Flashcards

Pathology Flashcards

1
Q

Pseudotumor cerebri

A

No tumor or obstruction of CSF flow, CSF reabsorption is decreased in the arachnoid villi

No mental status changes
Do have increased intracranial pressure (papilledema), and decreased CF protein
Present with headache and diplopia

Causes: All-trans-retinoic acid to treat APL, Hypothyroidism, Cushings disease, OCPs

Treatment: Carbonic anhydrase inhibitor or systemic corticosteroids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Lewy Bodies

A

abnormal aggregates of protein that develop inside nerve cells in Parkinson’s disease and Lewy body dementia,

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Subfalcine herniation

A

cingulate gyrus herniates under the flax cerebri

compression of the anterior cerebral artery leads to infarction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Uncal herniation

A

temporal lobe uncus herniates under the tentorium cerebelli (btw the cerebellum and the brainstem)

  1. ) compresion of cranial nerve III leads to “down and out”
  2. ) Compression of poeterioir cerebral artery leads to infarction of the occipital lobe (contralateral homonymous hemianopsia)
  3. ) Rupture of the paramedian artery in the brainstem (Duret hemmorage)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Tonsillar herniation

A

cerebellar tonsils displace into the foramen magnum

compression of the brainstem leads to cardiopulmonary arrest.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

communicating hydrocephalous

A

causes:
1. ) increased CSF production from a choroid plexus papilloma
2. ) Obstruction of CSF reabsorption by the arachnoid villi from a tumor, postmeningitic scaring, or subarachnoid hemorrhage.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

MC cause of noncommunicating hydrocephalus in newborns

A

Stricture of aqueduct of sylvius

causes paralysis of upward gaze (parinaud syndrome)

ventricles dilate, head circumference increases (only in newborns)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Hydrocephalus ex vacuo

A

dilated appearance of ventricles when the brain mass is decreased from cerebral atrophy (ex in Alzheimer’s)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Normal pressure hydrocephalus

A

Wet, wachy, wobbly (due to stretching of fibers near the ventricle)
Dilated ventricles, but normal CSF pressure

causes: idiopathic, prior subarachnoid hemorrhage, prior trauma, prior intracranial surgery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Arnold-Chiari malformation

A

extension of the medulla and cerebellar vermis through the foramen magnum, usually results in hydrocephalus

associated with meningomyelocele (meninges and spimal cord) and syringomyelia

type 1 doesn’t go into the foramen magnum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Dandy-Walker malformation

A

partial or complete absence of the cerebellar vermis
cystic dilation of the forth ventricle
noncommunicating hydrocephalus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Syringomyleia

A

Cystic degeneration of the spinal cord, usually at C8-T1 (loss of pain and temp in the upper extremities, “cape-like distribution”)
damage to anterior white commissure- loss of pain and temperature sensation
If it expands to the anterior horns –> muscle atrophy and weakness

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Difference between syringomyleia and ALS

A

No sensory changes in ALS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Neurofibromatosis 1

A

mutation on chromosome 17 for neurofibromin (tumor suppressor)

associated with: Cafe au late spots,optic gliomas, astrocytomas, pheochromocytoma, wilm’s tumor, axillary and ingunial freckling, pigmented plexiform nuerofibromas

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

neurofibroma

A

benign nerve sheath tumor in the peripheral nervous system

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

pigmented plexiform nuerofibromas

A

(only in NF1) - involve large nerve, can appear in children, can become cancerous

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

pigmented cutaneous/subcutaneous neurofibromas

A

occur in NF1 and NF2
These Benign tumors grow from small nerves in the skin or just under the skin and appear as small bumps typically beginning around the time of puberty.
occur anywhere except for palms or soles

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Neurofibromatosis 2

A

mutation on chromosome 22 coding for merlin (tumor supressor gene)

associated with:
1.) Bilateral acoustic neuromas (SWANNOMA >90% of cases), benign CN VIII presenting with tumorsensorineural hearing loss

  1. ) Meningiomas
  2. ) Spinal schwannomas
  3. ) juvenile cataracts
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Tuberous sclerosis

A

2nd most common neurocutaneous syndrome (phakomatoses)

  1. ) mental retardation and seizures begining in infancy
  2. ) Angiofibromas (adenoma sebaceum) on the face
  3. ) shagreen patches or ash leaf spots (hypopigmented skin lesions, seen with wood lamp)
  4. ) Angiomyolipomas in the kidney’s
  5. ) Rhabdomyoma in the heart
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

cerebral contusion

A

permanent damage to small blood vessels on the surface of the brain
usually secondary to acceleration deceleration injury
usually seen at the tips of the frontal and temporal lobes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Epidural hematoma

A

fracture of temporalparietal bone causes severance of the middle meningeal artery
lucid interval may precede neurologic signs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Subdural hemotoma

A
  • bleeding btw the dura and the arachnoid membranes. -Bridging veins are torn ( conditions causing decreased brain mass increase the traction on the brides increasing the likelihood of a subdural hemotoma, e.x. elderly persons or alcoholics)
  • Usually due to blunt trauma or coagulation deficiency
  • consciousness level fluctuates, presents with progressive neurologic signs
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Global hypoxic injury

A

causes: cardiac arrest, hypovolemic shock, septic shock, chronic CO poisoning, (hypoglycemia can also present similarly)

Signs: cerebral atrophy is caused by apoptosis in layers 3,5&6 (neurons are most susceptible to hypoxic damage), produces laminar necrosis
Red neurons
Watershed infarcts

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Lacunar strokes

A

occur secondary to hyaline arteriolosclerosis (occurs with benign HTN or Diabeties). usually involves the lenticulostriate vessels.

  • involvement of the internal capsule leads to a pure motor stroke
  • involvement of the thalamus leads to a pure sensory stroke
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

intracerebral hemorrhage

A

Classically due to rupture of Charcot-Bouchard microaneurysms of the lenticulostriate vessels (complication of HTN)

Basal ganglia is the most common site

symptoms: severe headache, nausea, vomiting, and eventual coma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Subarachnoid Hemorrhage

A

Worst headache of my life, and nuchal rigidity
lumbar puncture shows xanthochromia ( yellow hue due to bilirubin)
usually due to berry aneurysm

27
Q

Berry aneurysm

A

thin walled saccular outpouchings that lacka media layer

usually located at the anterior circle of Willis at branch point of anterior communicating artery

associated with: Marfan syndrome and autosomal dominant polycytic kidney disease

28
Q

Thrombotic stroke locations

A

MC is middle cerebral artery

also internal carotid artery near the bifurcation

29
Q

Gliosis

A

reaction to injury to infarct
astrocytes proliferate at the margins of the infarct
microglial cells remove lipid debris

cystic area area develops after 10 days to 3 weeks due to liquefactive necrosis

30
Q

Retinal TIA

A

amaurosis fugax, caused by microembolism of atherosclerotic material (Hollenhorst plaque) to a bifurcation of retinal arteries

31
Q

Strokes involving the Middle Cerebral Artery (MCA)

A

contralateral hemiparesis and sensory loss in the face and upper extremity
expressive aphasia
head and eyes deviate twds the side of the lesion

32
Q

Strokes involving the Anterior Cerebral Artery (ACA)

A

contralateral hemiparesis and sensory loss in the lower extremity

33
Q

Strokes involving the vertebrobasilar arterial system

A

Ataxia, vertigo
Ipsilateral sensory loss in the face
Contralateral hemiparesis and sensory loss in the trunk and limbs

34
Q

MC cause of viral meningitis

A

enterovirus, ex. coxsackievirus, poliovirus and echoviruses

35
Q

MC cause of neonatal meningitis

A

Group B strep

36
Q

MC cause of meningitis in adults

A

Streptococcus pneumoniae

37
Q

MC fungal CNS infection in AIDS

A

Cryptococcus neoformans

causes both meningitis and encephalitis

38
Q

MC space-occupying lesion in AIDS

A

Toxoplasma gondii
Ring enhancing lesion on CT
causes Encephalitis

39
Q

Multiple Sclerosis

A

MC demyelinating disease

Episodic course punctuated by acute relapses and remissions (80%-90% of cases)

  1. ) Sensory dysfn
  2. ) UMN dysfn
  3. ) Autonomic dysfn ( urge incontinence[hyperactive detrusor muscle], bowel dysfn, sexual dysfn)
  4. ) optic neuritis (blurry vision)
  5. ) Cerebellar ataxia
  6. ) Scanning speech
  7. ) Intention tremor
  8. ) Bilateral internuclear ophthalmoplegia (demyelination of MLF (slow progressive inability to move the eyes and eyebrows)
  9. ) Flexion of the neck produces an electrical sensation down the spine
40
Q

Multiple Sclerosis Pathogenesis

A

1.) CD4 TH1 cells secrete interferon gamma, which activates macrophages–> produce TNF alpha

TH17 cells release cytokines that recruit neutrophils and monocytes (type IV HSR)

2.) Antibodies produced against the myelin sheath & the oligodendrocytes (type II HSR)

41
Q

Multiple sclerosis microscopic findings

A

associated with: HLA-DR2

demyelinating plaques occur in white matter of brain/spinal cord

Inflammatory infiltrate in plaques is composed predominantly of CD4 T cells, monocytes and microglial cells with phagocytosed lipid.

42
Q

Multiple sclerosis lab findings

A

Increased CSF leukocyte count (primarily C lymphocytes/monocytes)

Increased CSF protein (from the gamma globulin)

43
Q

Central pontine myelinolysis

A

most often occurs in alcoholics who have hyponatremia

Rapid IV correction causes demyelination in the basis pontis

44
Q

Adrenoleukodystrophy

A

Enzyme deficiency in beta oxidation of fatty acids, cause accumulation of long chain fatty acids and subsequent loss of myelin in the brain and adrenal insufficiency
X-linked recessive disorder

45
Q

Krabbe Disease

A

Galactocerebroside Beta-galactocerebrosidase defiency
Brain shows large mutlinucleated, histiocytic cells (globoid cells)
Autosomal recessive

46
Q

Sporadic early onset Alzheimer disease

A

related to apolipoprotein gene E allele e4

47
Q

Familial early-onset Alzheimer disease

A

mutation of amyloid precursor protein (APP) on chromosome 21
mutations in presenilin 1 on chromosome 14
mutations in presenilin 2 on chromosome 1

48
Q

Beta-amyloid (ABeta) and Alzheimers

A

Wnt activates GSK
Activation of glycogen synthase kinase-3Beta (GSK) causes phosphorylation of ABeta–> neuronal and synaptic dysfn as well as positive feedback to GSK

ABeta also deposits on the walls of cerebral vessels (amyloid angiopathy)

Abeta stains positive with Congo Red

Abeta is a metabolic product of APP. Alpha secretases cleave APP into fragments that cannot produce Abeta. Beta-secretases followed by gamma-secretases cleave APP into fragments that are converted to ABeta

Insulin degrading enzyme is involved in the clearance of ABeta so those with DM2 have increased risk for Alzheimers disease.

49
Q

tau protein

A

normal function is to maintain microtubules in neurons.

Activation of GSK causes hyperpolarization of tau, which results in nuerofibrillary tangles–> neuronal dysfn and death

50
Q

Gross and microscopic findings of Alzheimer Disease

A

Hydrocephalus ex vacuo
Neurofibrillary tangles
Senile (neuritic) plaques (core of ABeta surrounded by cell processes containing tau protein, microglial cells, and astrocytes
amyloid angiopathy (increased risk for cerebral hemorrhage)

51
Q

Parkinsonism causes

A
  1. ) idiopathic
  2. ) Encephalitis, ischemia
  3. ) CO poisoning (necrosis of globus pallidus)
  4. ) Wilson Disease (copper not properly eliminated)
  5. ) Addition to MPTP
  6. ) Antipsycholtic drugs
52
Q

Parkinson disease

A
  • degeneration/ depigmentation of neurons in the substainia nigra
  • neurons contain intracytoplasmic, eosinophilic bodies called lewy bodies (ubiquinated damaged neurofilaments)
53
Q

Clinical findings in parkinsons

A 
cogwheel rigidity
bradykinesia (slowness of voluntary movement) 
Resting tremor (ex pill rolling)
Expressionless face
Seborrheic dermatitis
dementia (in some)
54
Q

Huntington’s disease

A

CAG repeat on chromosome 4
Autosomal dominant
Atrophy of striatal neurons ( caudate, putamen)

55
Q

Clinical findings in Huntington’s disease

A

Chorea (irregular rapid nonstereotyped movements)
Oculomotor abnormalities
Parkinsonism in later stages
Depression

56
Q

Friedreich ataxia

A

GAA repeat leads to frataxin deficiency –> impaired mitochondrial iron hemostasis makes cell more prone to apoptosis

Sites of degeneration: dorsal root column posterior columns, spinocerebellar tract, lateral corticospinal tracts, large sensory peripheral neurons

57
Q

Clinical Findings in Friedreich ataxia

A

progressive gait ataxia
loss of deep tendon reflexes
loss of vibratory sensation and proprioception
muscle weakness in the legs

58
Q

Amyotrophic lateral sclerosis

A

Degenerative disease of upper and lower motor nuerons due to a misfolded Superoxide dismutase (SOD) 1 leading to apoptosis

59
Q

Clinical findings in ALS

A

spasticity (UMN)
weakness and eventual paralysis of respiratory muscles (LMN)
NO sensory changes
Preserved bowel and bladder function

60
Q

Wilson disease

A

defect in copper excretion in bile
defect in the incorportation of copper into ceruloplasmin
leads to liver cirrhosis (through the fenton reaction) and excess free copper in the blood

CNS findings: Atrophy and cavitation of the basal ganglia
sings of parkinsonism, chorea and dementia

61
Q

Acute Intermittent porphyria

A

Deficiency of uroporphyrinogen synthase
proximal increase in PBG and ALA
exposure to light oxidizes PBG to porphobilin producing port-wine color

clinical presentation: recurrent sever abdominal pain, psychosis, peripheral neuropathy, dementia

62
Q

Vitamin B12 deficiency

A

posterior column and lateral corticospinal tract demylination

clinical presentation: dementia, peripheral neuropathy

63
Q

Wernicke-Korsakoff syndrome

A

usually due to a thiamine deficiency (B1)
hemorrhages of small vessels with hemosiderin deposits in the mammillary bodies and walls of the third and the forth ventricles
neuronal loss gliosis and hemorrhages

clinical presentation:confusion, ataxia, nystagmus, opthalmoplegia

MS2 Unit 3 (1 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions