congenital brain anomalies are among the most common birth defects, affecting 10 in 1000 live births. anencephaly is one example, the lack of growth of a brain due to a neural tube defect. its incidence has gone down in recent years because of the knowledge that folic acid supplementation pre-conception can significantly reduce the risk of developing anencephaly. microcephaly refers to abnormally small brain development, and can be due to fetal alcohol syndrome, trisomy 13, or HIV/rubella. polymicrogyri is a condition of excess gyri due to decreased white matter.
hydrocephalus is a condition of increased CSF, generally due to blocked drainage. this might be due to stenosis of the cerebral aqueduct or the foramen Monroe. it is associated with spina bifida and can be identified due to increased cerebral ventricals. normal pressure hydrocephalus is a variant that has intermittently elevated CSF pressure.
spina bifida is another congenital anomaly that results in failure of closure of the dorsal vertebral column, or its overlying skin. it is associated with elevated alpha fetal protein and might be linked to abdominal radiation and congenital rubella. sequelae might include paralysis and incontinence. there are several variants; spina bifida occulta refers to a missing vertebal segments without herniation, while a meningocele is an outpouching of the meninges, and a myelomeningocele is herniation of both the meninges and spinal cord.
cerebral palsy is a movement disorder due to damage to the motor centers of the brain, and most commonly develops in premature infants due to maternal infection during pregnancy. the most common type is spastic CP, which results in an "equinus deformity". patients with this variant are most likely to be able to walk, whereas patients with spastic quadriplegia are least likely to be able to walk. spastic quadriplegia affects all limbs equally and might be accompanied by hemiparetic tremors, which are uncontrollable shaking that affects one side of the body. morphological features of the brain affected by cerebral palsy might include paraventricular leukomalacia (necrosis and softening of paraventricular white matter) and gliosis (neuronal death and astrocyte proliferation).
meningitis is an infection of the meningeal layers which affects 17,000 people per year in the US. viral infections are the most common cause and are generally self limiting. on the other hand, bacterial meningitis is a medical emergency and is most commonly caused by strep pneumonia, e.coli, neisseria meningococci, h. influenza, and listeria monocytogenes. the main signs and symptoms include headache, fever, stiff neck, photophobia, and petechiae, among other things.
CSF analysis can serve to differentiate between the forms of meningitis. in bacterial meningitis, "opening pressure" will be increased, glucose will be decreased, and leukocytosis might be present. viral meningitis might have normal opening pressure, a lower degree of leukocytosis (100 WBC/mm^3 as opposed to 1000),
h. influenza is a meningitis that is caused by the haemophilus influenza bacteria type B, not to be confused with the virus that causes influenza. it is often caused by URI's which then travel through the bloodstream and infect the brain. the top demographic is 6-9 year olds who have recurrent URI's, are in day care, and Native Americans and Inuits have a particularly high incidence. potential complications are hearing loss, seizures, learning / speech / behavioral abnormalities, hydrocephalus.
cryptococcal meningitis is caused by cryptococcus neoformans, which is a yeast that is found in soil worldwide. those who have compromised immune systems are at greatest risk for contracting this disease. microscopy might reveal circular yeast bodies and CSF might grow cryptococcus cultures. fundoscopy might also reveal granulomas and papilledema.
viral meningitis generally follows a systemic viral infection, most commonly by arboviruses. other viruses also play roles, such as HSV-1. VM has a predilection for the temporal lobes, causing hemorrhage.
carcinomatous meningitis is a type of meningitis that is caused by tumors in and around the nervous system, commonly spread from lung, breast cancer, or melanoma. symptoms include headache, mental status changes, difficulty with vision/hearing/swallowing, and loss of sensation. fever is absent unless infection is present as well. CM is diagnosed definitively by tumor cells in the CSF.
brain abscesses are collections of pus, inflammatory / immune cells, and other material that accumulates in the brain due to infection, generally from multiple organisms. streptococcus is the most common cause in adults, and gram negative bacteria a common cause of abscess in infants. abscesses occur when infection causes inflammation, which then is walled off and increases in size, blocking blood flow to the area and causing necrosis of tissue and accumulation of immune cells.
questions
anatomy review...
1. how many pairs of nerves extend from the spinal cord?√√
2. what are the meningeal layers from outside to inside?√√
3. what is the space between the dura and arachnoid mater filled with?√√
congenital forebrain anomalies...
4. how common are birth defects related to the brain compared to other organs?√√
5. anencephaly is due to... √√
6. what is a supplement that might be helpful in reducing the risk for anencephaly and when should it be taken?√√
7. what are the potential etiologies for microcephaly?X†√
8. what is polymicrogyri? X†√
hydrocephalus...
9. what is hydrocephalus? what is commonly due to?XX†√
10. what condition is hydrocephalus associated with?XX√√
11. what is the imaging hallmark of hydrocephalus?X√√
12. describe how hydrocephalus might develop.X√
13. what is normal pressure hydrocephalus?X√√
spina bifida...
14. how common is brain hypoxia?x√
15. what is spina bifida?√√
16. what is a marker that is elevated in spina bifida?√√
17. what are two potential etiologies for spina bifida?XX
18. what are two major sequelae for spina bifida?X†
19. describe the various presentations of spina bifida. which is the most common?X†
cerebral palsy...
20. what is cerebral palsy?√√
21. when does most cerebral palsy develop?√√
22. which demographic is associated with cerebral palsy?√√
23. what is the most common type of CP?X√√
24. what is a characteristic PE finding for spastic hemiplegia?†√√
25. describe the hallmarks of spastic quadriplegia?X√√
26. some children with spastic quadriplegia have...X√√
cerebral palsy morphology, prognosis, sequelae...
27. what are two morphological signs in cerebral palsy?†X
28. what is PVL?X
29. what is gliosis?X√
meningitis introduction...
30. what are the most common causes of meningitis?√√
31. what is the difference in prognosis between viral and bacterial meningitis?√√
32. what are the most common bacterial strains that cause meningitis? X√√
33. how many cases of meningitis occur each year? X√√
34. what is the most common cause of bacterial meningitis for neonates?√√
35. what is the most common cause of bacterial meningitis for infants, adolescents, and young adults?√√
36. what is the most common cause of bacterial meningitis for the elderly?√√
37. what are the main signs and symptoms of meningitis?√
CSF diagnosis...
38. how can the "opening pressure" of CSF differentiate between causes of meningitis?√√
39. describe the white blood cell count in bacterial vs. viral meningitis?√√
40. what are the findings for a cell differential in the CSF of bacterial vs. viral meningitis?†√√
41. describe the CSF to glucose ratio for the different types of meningitis.√
42. describe the protein levels in the various types of meningitis. X√
43. the latex agglutination test is most sensitive for detecting which microorganism?√√
meningococcal meningitis...
44. how common is this form of meningitis?√√
45. what is a characteristic histomorphological feature of MM?X√√†
46. describe the exudate characteristics in MM. X√√√
47. describe the gross morphological changes in MM. X√√
48. what is a dermatological manifestation of MM? X√√
49. what are the potential complications of MM? XX†√
h. influenza meningitis...
50. what is the age of peak incidence for this disease?√√√
51. may follow...√√√
52. what are some risk factors for h. influenza meningitis?√√√
53. which demographic has a higher risk for h. flu meningitis?X√XX
54. what are the potential complications for h. flu meningitis?X√X
aseptic meningitis...
55. what is aseptic meningitis?√√√
56. which two viruses are the most common causes of aseptic meningitis?X√√†
57. what are the symptoms that characterize aseptic meningitis?†√√√
cryptococcal meningitis...
58. what is the etiological agent in CM?√√√√
59. what are the demographics at risk for CM?√√√X
60. which lab tests are used to diagnose CM?†√√√
61. what is another PE finding that can aid in the diagnosis of CM?††X†√
viral meningitis...
62. what are the different types of viral meningitis? √√√√
63. most cases arise as complications of...√√√√
64. what is the most common cause of VM?√XXX√√√√
65. which virus is responsible for 10-20% of cases of VM?√X√X√√√√
66. what is a distinct morphological feature of VM?√XXX√√√√
carcinomatous meningitis...
67. what are the most common non-hematologic causes of CM?√√
68. what are the symptoms of CM?X
69. how is CM diagnosed?†√
70. 1/3 of the patients have...√
71. what percentage of CM patients have fever?√√
brain abscess...
72. what is a brain abscess?√√
73. which demographic has a higher incidence for brain abscesses?√√
74. what is the etiology of most brain abscesses?√√
75. what is the most common bug that causes brain abscesses?√√
76. which is found more commonly in infant brain abscesses, gram negative or positive bacteria?√√
77. describe the pathophysiology of brain abscesses.√√
78. what is the morphology of an aspergillus brain abscess?√
neurocysticercosis...
79. what is neurocysticercosis?√√√
80. what is the morphology of neurocysticercosis?√√√
neurosyphilis...
81. what is neurosyphilis caused by? √√√
82. which variant is associated with the middle cerebral artery or the branches of the basilar artery?√†√√
83. which variant is associated with widespread infection of parenchyma?√††
84. which variant is associated with demyelination and fibrosis of the posterior column of the spinal cord?àX
85. what are gummas?†√√
86. what is the jarisch-herxheimer reaction? what is the prognosis?√√√
progressive multifocal leukoencephalopathy...
87. what is PML caused by? XX√√√
88. what is PML? X√√√√
89. what are some symptoms of PML? X†√X
90. what is the gross morphological feature of PML? X††√XX√
subacute sclerosing panencephalitis...
91. what is SSPE caused by? X√√√
92. describe the course of SSPE. X√√√
93. what is a sign of poor prognosis for SSPE patients?√√√√
94. how is diagnosis of SSPE made? XX√
95. what is a morphological sign of SSPE? XX†X
poliomyelitis...
96. describe the infectious process in poliomyelitis.√√
97. what is post polio syndrome?√√
rabies...
98. what occurs in 1-3 months after rabies exposure? √√
99. what are some symptoms of rabies? √√
100. what is the diagnostic sign for rabies? †√√
AIDS dementia complex...
101. when during the course of AIDS does ADC emerge?√√
102. what are some nonspecific symptoms of ADC?√√
103. what are some late symptoms of ADC?√√
104. describe the pathophysiology of ADC.√√
105. what are the morphological changes of ADC?X√
reye's syndrome...
106. what is reye's syndrome characterized by?†√
107. what is reye's syndrome associated with?√√√
cerebrovascular disease...
108. how prevalent is cerebrovascular disease?√
109. what factors does the survival of ischemic tissue depend on?√
110. describe the histopathology of a stroke within the first 12-24 hours.√
111. describe the histopathology of a stroke at 24 hours.√
112. describe the histopathology of a stroke from 2-14 days.√
113. which heart condition is associated with ischemic stroke?
114. which artery is commonly affected by thrombosis leading to ischemic stroke?
115. what is the leading cause of hemorrhagic stroke?
answers
1. 31 pairs.
2. dura mater, arachnoid mater, pia mater.
3. CSF.
4. most common, 10 in 1000 live births.
5. neural tube defect.
6. folic acid pre-conception.
7. fetal alcohol syndrome, trisomy 18, congenital rubella, congenital HIV.
8. excess gyri due to decreased white matter.
9. excess CSF due to drainage problem.
10. spina bifida.
11. enlarged ventricles.
12. stenosis of the cerebral aqueduct or foramen of monroe.
13. a variant that has enlarged cerebral ventricles but only intermittent elevations of CSF pressure.
14. over 1/3 of the 30,000 children per year in the US that are born with congenital heart disease.
15. failure of closure of dorsal vertebral column or overlying skin.
16. AFP.
17. radiation to the abdomen and congenital rubella.
18. paralysis and incontinence.
19. spina bifida occulta: missing portion of dorsal vertebral body.
meningocele: herniation of the meninges but not the spinal cord.
myelomeningocele: herniation of meninges with spinal cord. most common.
20. a movement disorder related to damage to movement centers of the brain.
21. during pregnancy, due to a maternal infection.
22. premature infants, 8 months or less.
23. spastic.
24. equinus deformity, causing walking on the ball of one foot.
25. all four limbs equally affected, least likely to be able to walk.
26. hemiparetic tremors.
27. paraventricular leukomalacia and gliosis.
28. softening and necrosis of paraventricular white matter due to lack of blood supply.
29. neuronal cell death and phagocytosis, astrocyte proliferation.
30. viral infection, bacterial infection.
31. viral is generally self resolving, bacterial is generally emergency.
32. ecoli, strep pneumonia, h. influenza, neisseria meningitis, listeria monocytogenes. [ESHNL][HESNL][SHENL][SIENL][SENIL]
33. 17,000.
34. ecoli.
35. neisseria meningococci, strep pneumonia.
36. strep pneumonia.
37. fevers, headache, stiff neck, sensitivity to light and sound, petechiae.
38. increased in bacterial, normal in viral, variable in fungal and tubercular.
39. more than 1,000 / mm^3 in bacterial, more than 100/mm^3 in viral.
40. PMN's in bacterial, lymphocytes in other forms of meningitis.
41. decreased to normal in bacterial, normal in viral, decreased in fungal and tubercular.
42. increased in bacterial, fungal, tubercular, normal to increased in viral.
43. h. influenza.
44. most common form in children, second most common form in adults.
45. gram negative diplococci inside neutrophils
46. neutrophilic exudate that causes yellow/tan clouding of meninges.
47. prominent dilated vessels, edema and focal inflammation in the cortex.
48. rapidly spreading petechial rash.
49. mental retardation, permanent brain damage, hydrocephalus, myocarditis, waterhouse-friderichsen syndrome. [brain brain water water heart]
50. 6-9 months.
51. upper respiratory infection
52. recurrent URI's, daycare.
53. native americans and inuits.
54. hearing loss
seizures
learning / behavioral problems
hydrocephalus
[flu hear seize learn water] [hear the fluid water's seizing behavior]
55. signs and symptoms of meningitis are present but no bacteria is cultured in CSF.
56. coxsackie and echovirus.
57. headache, fever, inflammation of the meninges.
58. cryptoccal neoformans, a yeast that is found in soil around the world.
59. those with compromised immune systems.
60. india ink stain microscopy might reveal circular yeast bodies. CSF grows cryptococcus cultures.
61. fundoscopy: papilledema and granuloma.
62. focal, multifocal, diffuse.
63. systemic viral infections.
64. arboviruses transmitted by mosquitos and ticks.
65. HSV.
66. predilection for hemorrhage of the temporal lobe.
67. lung, breast cancer, melanoma.
68. headache
mental status changes
vision / hearing / swallowing difficulty
loss of sensation
69. presence of tumor cells in CSF.
70. headache.
71. only those with supervening infection.
72. mass of immune cells, pus, other material that accumulates in the brain due to infection.
73. immune compromised, first four decades of life.
74. generally more than one microorganism.
75. streptococcus.
76. negative.
77. infection causes inflammation and fibrosis, which leads to mass effect and blockage of blood flow to area, leading to necrosed tissue.
78. relatively slender hyphae with 45 degree angle branches.
79. infection of CNS by larvae of pork tapeworm, taenia solium.
80. multiple calcifications and viable cysts in brain parenchyma.
81. treponema pallidum infection.
82. meningovascular syphilis.
83. paretic syphilis.
84. tabes dorsalis.
85. meningeal granulomas which are well circumscribed masses of granulation tissue resulting from a cell mediated response to treponema.
86. a reaction from the treatment of treponema, resulting in headache, fever/chills, nausea. generally disappears in 24 hours.
87. members of the papovavirus family, usually JC virus.
88. rare demyelinating disease that results in the loss of oligodendrocytes.
89. memory, vision, mental function, coordination loss.
90. irregular areas of granularity in the white matter.
91. a rare complication of measles.
92. develops 1-20 years after measles.
93. deterioration of neurological function.
94. rubeola IgG antibody.
95. white matter hemorrhage and gliosis.
96. virus transmitted via oral/fecal route, replicates in nasopharynx and lymph tissues, leading to viremia, which then turns neurotropic and destroys neurons in the anterior horn and brainstem.
97. recurrent bouts of muscle weakness that occur 20-50 years after the initial polio episode. more of an "autoimmune reaction" than a reactivation of virus.
98. virus travels from peripheral nerves to the brain. time depends on depth and location of bite.
99. headache
irritability
salivation
water intolerance
muscle spasm
100. negri bodies within neurons.
101. late in the process, when CD4 count starts to drop.
102. difficulty concentration
poor coordination, muscle weakness
103.
104. uncertain, but: HIV infects CNS macrophages, which release substances that cause nerve dysfunction and death.
105. cortical atrophy and ventricular enlargement.
106. fever, vomiting
fatty infiltration
swelling of kidneys and brain
107. a previous infection and treatment using aspirin.
108. most prevalent neurologic disorder in terms of mortality and morbidity, third leading cause of death in US.
109. duration of ischemia
rapidity of onset of ischemia
magnitude of ischemia
collateral circulation
110. red neurons: vacuolated, eosinophilic neuronal cytoplasm.
111. neutrophilic infiltrate at the edge of the lesion.
112. neutrophilic / macrophage infiltrate, gliosis.
113. atrial fibrillation.
114. middle cerebral artery.
115. HTN.
Showing posts with label pathology IV. Show all posts
Showing posts with label pathology IV. Show all posts
Monday, June 14, 2010
Thursday, June 10, 2010
pathology IV: skeletal muscle
muscular atrophy: can be generalized, as in prolonged bedrest, or localized, as in immobilization of a body part with a cast. neurogenic atrophy is muscle atrophy that is due to the lack of innervation of muscle fibers, which then necrose-- and can be mixed in next to healthy muscle fibers. neurogenic atrophy might result in contracture due to the reduced resistance of opposing muscle groups.
congenital myopathies are genetic disorders of muscle that present early on and have an insidious progression. they result in general muscle weakness and might have a connection with diet, as elucidated in "breaking the vicious cycle", which describes a possible connection between muscle weakness and intake of simple carbohydrates. duchenne's is one of many types of muscle dystrophy which develops early on and is generally fatal by the 20's. it results from an x linked genetic defect which leads to an absence of dystrophin, a component of the membrane of skeletal muscle. this leads to dysfunctional membrane permeability, which leads to excess calcium levels, cloudy swelling, and ultimately cell death.
myasthenia gravis is an autoimmune neuromuscular condition that results from antibodies to the acetylcholine receptors in neuromuscular junctions. the hallmark symptom is muscle weakness that is worse with activity and better with rest. there is also a strong association with thymic abnormalities, such as hyperplasia or thymomas. histomorphology includes large clusters of lymphocytes and pale / atrophic muscle fibers.
lambert-eaton syndrome is another autoimmune neuromuscular condition in which antibodies to the presynaptic calcium channels are produced, leading to decreased acetylcholine release. it is strongly associated with lung cancer-- in particular oat cell cancer of the lung, and generally appears first on the upper legs and upper arms. diagnosis is made by antibody tests, nerve stimulation tests, and chest xray to detect lung cancer. in contrast to MG, patients with LES might experience greater strength in the beginning of a mild exertion.
dermatositis is an idiopathic inflammatory connective tissue disorder which also has skin and muscle involvement. half of cases are associated with paraneoplastic syndrome. histomorphological signs include perivascular inflammatory infiltrate of mixed B and T cells, and perifascicular musclar atrophy. characteristic signs and symptoms include neck extensor weakness, periorbital heliotrope rash, grotton's sign (purple/red papular rash on the dorsal side of fingers).
questions
muscular atrophy...
1. what might cause generalized vs. localized atrophy?
2. what might atrophy be masked by?
3. what is neurogenic atrophy?
4. describe the morphology of neurogenic atrophy.
5. neurogenic atrophy might result in...
congenital myopathies...
6. describe the onset and course of most congenital myopathies.
7. what is a diet that might have a connection with muscle tone and what is the book in which these findings were presented?
8. what are the signs / symptoms of congenital myopathies?
muscle dystrophies...
9. how many forms of muscle dystrophies are there? which is most common?
10. muscular dystrophies are characterized by...
11. what is the etiology of duchenne's?
12. which gender is associated with duchenne's?
13. describe the pathophysiology of duchenne's.
14. what is the typical age of onset for duchenne's?
15. describe the distribution of duchenne's.
16. what is "pseudohypertrophy"?
17. describe the histomorphology of the early and late stages of duchenne's.
18. what is the prognosis of duchenne's?
myasthenia gravis...
19. what is the etiology of myasthenia gravis?
20. what is the hallmark symptom of MG?
21. there is an association between MG and...
22. what is the histomorphology of MG?
23. how is diagnosis of MG made?
lambert-eaton syndrome...
24. where is LES first noticed?
25. 60% associated with...
26. what is the etiology of LES?
27. describe the symptom picture of patients with LES.
28. how is LES diagnosed?
dermatositis...
29. what is dermatositis?
30. what is the etiology of dermatositis?
31. besides muscle weakness, how is dermatositis diagnosed?
32. what are the 2 characteristic histomorphological signs of dermatositis?
33. what are the characterizing signs/symptoms of dermatositis?
34. what is grotton's sign?
polymyositis...
35. what is the main difference between polymyositis and dermatositis?
36. which muscles are affected in polymyositis?
37. what is a sign that occurs in 1/3 of patients that indicates poor prognosis?
38. what is a common presentation of a patient with polymyositis?
39. what is the histomorphology of polymyositis?
40. describe the composition of the inflammatory infiltrate in polymyositis.
answers
1. generalized: lying in bed for a long time. localized: wearing a cast.
2. fat deposition in between muscle fibers.
3. muscle atrophy as a result of decreased nerve supply.
4. areas of atrophied tissue mixed with healthy tissue.
5. contractures due to reduced resistance in opposing muscle groups.
6. generally early onset and gradual progression.
7. specific carb diet, in "breaking the vicious cycle".
8. generalized or proximal muscle weakness, hypotonia.
9. hundred's, duchenne's.
10. progressive skeletal muscle weakness.
11. defective gene on X chromosome that leads to inability to produce dystrophin, a skeletal muscle membrane protein.
12. almost exclusively in boys.
13. absence of dystrophin leads to membrane permeability changes which leads excess calcium and ROS, cloudy swelling and ultimately to cell death.
14. 2-6yo.
15. proximal large muscles and spreads to all voluntary muscles.
16. muscle that is replaced by fat and thus appears to be hypertrophied.
17. early: scattered inflammatory cells. late: pseudohypertrophy.
18. wheelchair bound by age 12, generally fatal by 20's.
19. autoimmune condition in which antibodies are produced against the acetylcholine receptors at the neuromuscular junctions, resulting in an inhibition of acetyl choline's stimulatory activity.
20. muscular weakness that worsens with activity and improves with rest.
21. thymic abnormalities such as thymic hyperplasia.
22. large collections of lymphocytes, and pale/atrophic necrotic muscle fibers.
23. history, PE, and two positive diagnostic tests: serum antibodies, nerve stimulation studies, tensilon injection studies.
24. upper legs/upper arms.
25. oat cell cancer of the lung.
26. antibodies to the presynaptic calcium channels, resulting in inhibition of Ach release.
27. greater strength with initial exertion but weakness upon prolonged exertion.
28. chest x ray for lung involvement, antibody tests, nerve conduction studies.
29. connective tissue disease with muscle and skin involvement.
30. unknown, although 50% have an association with paraneoplastic syndrome.
31. skin involvement, elevated CPK, ESR, EMG, and muscle biopsy.
32. mixed B/T cell perivascular inflammatory infiltrate and perifascicular muscle atrophy.
33. neck extensor weakness
dysphagia / aspiration
periorbital heliotrope rash
grotton's sign
34. symmetrical purple/red papular rash over dorsal aspect of finger joints.
35. no skin involvement in polymyositis.
36. symmetric proximal muscles, especially neck flexors.
37. oropharyngeal and esophageal involvement.
38. inability to rise from a seated position.
39. pale and enlarged muscle fibers, surrounded by macrophages.
40. cytotoxic T8 lymphocytes.
congenital myopathies are genetic disorders of muscle that present early on and have an insidious progression. they result in general muscle weakness and might have a connection with diet, as elucidated in "breaking the vicious cycle", which describes a possible connection between muscle weakness and intake of simple carbohydrates. duchenne's is one of many types of muscle dystrophy which develops early on and is generally fatal by the 20's. it results from an x linked genetic defect which leads to an absence of dystrophin, a component of the membrane of skeletal muscle. this leads to dysfunctional membrane permeability, which leads to excess calcium levels, cloudy swelling, and ultimately cell death.
myasthenia gravis is an autoimmune neuromuscular condition that results from antibodies to the acetylcholine receptors in neuromuscular junctions. the hallmark symptom is muscle weakness that is worse with activity and better with rest. there is also a strong association with thymic abnormalities, such as hyperplasia or thymomas. histomorphology includes large clusters of lymphocytes and pale / atrophic muscle fibers.
lambert-eaton syndrome is another autoimmune neuromuscular condition in which antibodies to the presynaptic calcium channels are produced, leading to decreased acetylcholine release. it is strongly associated with lung cancer-- in particular oat cell cancer of the lung, and generally appears first on the upper legs and upper arms. diagnosis is made by antibody tests, nerve stimulation tests, and chest xray to detect lung cancer. in contrast to MG, patients with LES might experience greater strength in the beginning of a mild exertion.
dermatositis is an idiopathic inflammatory connective tissue disorder which also has skin and muscle involvement. half of cases are associated with paraneoplastic syndrome. histomorphological signs include perivascular inflammatory infiltrate of mixed B and T cells, and perifascicular musclar atrophy. characteristic signs and symptoms include neck extensor weakness, periorbital heliotrope rash, grotton's sign (purple/red papular rash on the dorsal side of fingers).
questions
muscular atrophy...
1. what might cause generalized vs. localized atrophy?
2. what might atrophy be masked by?
3. what is neurogenic atrophy?
4. describe the morphology of neurogenic atrophy.
5. neurogenic atrophy might result in...
congenital myopathies...
6. describe the onset and course of most congenital myopathies.
7. what is a diet that might have a connection with muscle tone and what is the book in which these findings were presented?
8. what are the signs / symptoms of congenital myopathies?
muscle dystrophies...
9. how many forms of muscle dystrophies are there? which is most common?
10. muscular dystrophies are characterized by...
11. what is the etiology of duchenne's?
12. which gender is associated with duchenne's?
13. describe the pathophysiology of duchenne's.
14. what is the typical age of onset for duchenne's?
15. describe the distribution of duchenne's.
16. what is "pseudohypertrophy"?
17. describe the histomorphology of the early and late stages of duchenne's.
18. what is the prognosis of duchenne's?
myasthenia gravis...
19. what is the etiology of myasthenia gravis?
20. what is the hallmark symptom of MG?
21. there is an association between MG and...
22. what is the histomorphology of MG?
23. how is diagnosis of MG made?
lambert-eaton syndrome...
24. where is LES first noticed?
25. 60% associated with...
26. what is the etiology of LES?
27. describe the symptom picture of patients with LES.
28. how is LES diagnosed?
dermatositis...
29. what is dermatositis?
30. what is the etiology of dermatositis?
31. besides muscle weakness, how is dermatositis diagnosed?
32. what are the 2 characteristic histomorphological signs of dermatositis?
33. what are the characterizing signs/symptoms of dermatositis?
34. what is grotton's sign?
polymyositis...
35. what is the main difference between polymyositis and dermatositis?
36. which muscles are affected in polymyositis?
37. what is a sign that occurs in 1/3 of patients that indicates poor prognosis?
38. what is a common presentation of a patient with polymyositis?
39. what is the histomorphology of polymyositis?
40. describe the composition of the inflammatory infiltrate in polymyositis.
answers
1. generalized: lying in bed for a long time. localized: wearing a cast.
2. fat deposition in between muscle fibers.
3. muscle atrophy as a result of decreased nerve supply.
4. areas of atrophied tissue mixed with healthy tissue.
5. contractures due to reduced resistance in opposing muscle groups.
6. generally early onset and gradual progression.
7. specific carb diet, in "breaking the vicious cycle".
8. generalized or proximal muscle weakness, hypotonia.
9. hundred's, duchenne's.
10. progressive skeletal muscle weakness.
11. defective gene on X chromosome that leads to inability to produce dystrophin, a skeletal muscle membrane protein.
12. almost exclusively in boys.
13. absence of dystrophin leads to membrane permeability changes which leads excess calcium and ROS, cloudy swelling and ultimately to cell death.
14. 2-6yo.
15. proximal large muscles and spreads to all voluntary muscles.
16. muscle that is replaced by fat and thus appears to be hypertrophied.
17. early: scattered inflammatory cells. late: pseudohypertrophy.
18. wheelchair bound by age 12, generally fatal by 20's.
19. autoimmune condition in which antibodies are produced against the acetylcholine receptors at the neuromuscular junctions, resulting in an inhibition of acetyl choline's stimulatory activity.
20. muscular weakness that worsens with activity and improves with rest.
21. thymic abnormalities such as thymic hyperplasia.
22. large collections of lymphocytes, and pale/atrophic necrotic muscle fibers.
23. history, PE, and two positive diagnostic tests: serum antibodies, nerve stimulation studies, tensilon injection studies.
24. upper legs/upper arms.
25. oat cell cancer of the lung.
26. antibodies to the presynaptic calcium channels, resulting in inhibition of Ach release.
27. greater strength with initial exertion but weakness upon prolonged exertion.
28. chest x ray for lung involvement, antibody tests, nerve conduction studies.
29. connective tissue disease with muscle and skin involvement.
30. unknown, although 50% have an association with paraneoplastic syndrome.
31. skin involvement, elevated CPK, ESR, EMG, and muscle biopsy.
32. mixed B/T cell perivascular inflammatory infiltrate and perifascicular muscle atrophy.
33. neck extensor weakness
dysphagia / aspiration
periorbital heliotrope rash
grotton's sign
34. symmetrical purple/red papular rash over dorsal aspect of finger joints.
35. no skin involvement in polymyositis.
36. symmetric proximal muscles, especially neck flexors.
37. oropharyngeal and esophageal involvement.
38. inability to rise from a seated position.
39. pale and enlarged muscle fibers, surrounded by macrophages.
40. cytotoxic T8 lymphocytes.
Friday, April 30, 2010
pathology IV- male genitalia quiz
a study guide for the pathology quiz on male genitalia. we started with a review of various conditions that can affect the male genitalia: phimosis refers to an inability to retract the foreskin of the penis, often due to adhesions formed from undifferentiated tissue in children less than 3 years old. paraphimosis is an inability of the foreskin to fold over the glans. condyloma acuminata are genital warts, caused by HPV strains 6 and 11, appearing as sessile or pedunculated, red papillary outgrowths on the coronal sulcus, inner prepuce, glans, or perianal area.
bowen's disease is commonly caused by HPV 16 and 18 and manifests as single, gray-white plaques with shallow ulcerations and crusting, either on the shaft of the penis or the scrotum. histologically, one might see dysplastic epithelium, scattered mitosis above the basal layer, and nuclear atypia.
bowen's might lead to squamous cell carcinoma, which might also be caused by HPV strains 16 / 18, or simply poor hygeine. SCC typically affects men 40-70 and manifests as painless lesions that may bleed. early lesions may just be epithelial thickening with some fraying / fissuring, while late or untreated lesions may develop into papules, ulcers with ragged and heaped up margins.
some assorted testicular disorders that we've already covered in CPD: cryptorchidism is an undescended testicle which can be associated with hormonal disorders of deficient LHRH and "trisomy 13". it might also be related to exposure to anti-androgenic compounds such as phthalates in plastics and tagamet, which is used to treat plantar warts and peptic ulcers. cryptorchidism increases the risk for infertility as well as testicular cancer of the fully descended side. hydroceles are serous fluid filled masses that can be caused by inflammation (sports) as well as structural / developmental abnormalities. varicoceles result from dilatation of the panpiniform plexus and is also associated with sports such as extreme mountain biking or soccer.
benign prostatic hypertrophy is nodular hyperplasia of the periurethral region of the prostate. it is associated with some dietary factors: deficiency of lycopene, nettles, zinc, EFA's, and amino acids- as well as dietary excess of alcohol, cadmium, cholesterol, and pesticides. the main growth factor for the prostate is DHT, which is converted from testosterone by 5-alpha reductase; cadmium and cholesterol both increase 5-alpha reductase activity, thus contributing to BPH. two other hormonal influences: estrogen increases stroma susceptibility to hyperplasia and prolactin increases androgen uptake.
prostate cancer is the most common type of cancer in men, generally of the type adenocarcinoma. it affects men over 50 with some racial demographic trends: asians tend to have a lower incidence and african americans have a higher incidence. genetic factors that have been identified are the p53 gene and hypermethylation of glutathione S-transferase. a diet high in arachidonic acid (found in meat products) can also be a risk factor. dietary protective factors might include lycopene, vitamin A and E, selenium, soy, and possibly fish oil. the lesions themselves are gritty and firm nodules on the posterior aspects of the lateral lobes, and if metastasis occurs, the bones are a high possibility-- osteoblastic lesions are a common finding in the lumbar / thoracic spine, femur, pelvis, ribs.
questions
various conditions...
1. what is phimosis?
2. how is phimosis related to age?
3. what is paraphimosis?
4. what is the etiology of condyloma acuminata?
5. what is the morphology of condyloma acuminata?
6. what locations are condyloma acuminata commonly found?
7. ∂escribe the histopathology of condyloma acuminata.
bowen's disease...
8. what age does bowen's disease usually affect?
9. what are the most common etiological agents for bowen's disease?
10. describe the morphology of the lesions in bowen's disease.
11. what locations are affected in bowen's disease?
12. what are some histopathological features of bowen's disease?
SCC...
13. what are the most common etiologies for SCC?
14. where are SCC lesions located?
15. describe the morphology of early SCC lesions.
16. describe the morphology of late SCC lesions.
17. what age does SCC generally occur in?
18. what is the relationship to regional lymph nodes and metastasis of SCC?
19. what is the clinical presentation of SCC?
various testicular disorders...
20. what are some intrinsic risk factors for cryptorchidism?
21. what are some extrinsic risk factors for cryptorchidism?
22. what are the sequelae for cryptorchidism?
23. what is a hydrocele and what is it commonly due to?
24. how common in a varicocele?
25. what are examples of types of hobbies that are associated with varicoceles?
26. which side is more commonly affected by varicoceles?
benign prostatic hypertrophy...
27. what are some etiological factors for BPH related to dietary deficiency?
28. what are some etiological factors for BPH related to dietary excess?
29. what is the mechanism by which cadmium and cholesterol are related to BPH?
30. what are DHT and 5-alpha reductase and how are they involved in BPH pathophysiology?
31. what is the effect of estrogen and prolactin in the prostate?
prostate cancer...
32. how common is prostate cancer?
33. what age group does prostate cancer affect?
34. what are the demographic groups that have high and low risks for developing prostate cancer?
35. what are two genetic factors that have been identified as etiological agents in prostate cancer?
36. what is a dietary risk factor for prostate cancer?
37. what are some protective factors for prostate cancer?
38. what is the most common location for prostate cancer?
39. what is the morphology of the lesions in prostate cancer?
40. what is a common area for metastasis and what are the type of lesions found?
testicular cancer...
41. testicular cancer cells are most commonly derived from which cell line?
42. germ cell vs. non germ cell derived testicular cancer: which is more likely malignant?
43. what is the racial trend for incidence of testicular cancer?
44. what is the serum marker for a seminoma?
45. which condition is a seminoma associated with?
46. what is the prognosis for a seminoma?
47. what is the prognosis for an embryonal carcinoma?
48. what are the serum markers for an embryonal carcinoma?
49. which age group does the yolk sac tumor affect?
50. what are the serum markers for a yolk sac tumor?
51. are teratomas considered benign or malignant?
52. what are the serum markers for a teratoma?
53. what is the prognosis for a choriocarcinoma?
54. which age group is lymphoma most common?
answers
1. abnormal tightness of the prepuce that prevents retraction over the glans.
2. may be related to adhesions from lack of tissue differentiation that occurs before ~3 years.
3. tissue gets stuck behind the glans.
4. HPV 6 and 11
5. sessile or pedunculated, red papillary outgrowths that may be verrucous or flat.
6. coronal sulcus, inner prepuce, glans, perianal.
7. acanthosis, koilocytosis, intact basement membrane.
8. over 35yo.
9. HPV 16 and 18.
10. solitary thickened gray/white plaque with shallow ulcerations and crustin.
11. the shaft or scrotum.
12. dysplastic epithelium
scattered mitosis above basal layer
nuclear abnormalities: large, odd shaped, or multiple.
13. bowen's disease, HPV 16 + 18
14. most on the glans or the inner surface of the prepuce.
15. epithelial thickening with fraying and fissuring.
16. papules and large, infected ulcers with ragged, heaped up margins.
17. 40-70yo.
18. regional nodes may be swollen without spread of SCC.
19. painless lesions that bleed.
20. hormonal disorders of deficient LHRH
trisomy 13
21. phthalates (in plastic)
tagamet (used to treat plantar warts and peptic ulcers)
22. increased risk for testicular cancer
increased risk for infertility
23. build up of serous fluid in the scrotum, from trauma or due to structural abnormalities.
24. 10% of men have them.
25. extreme mountain biking and soccer players.
26. mostly left side.
27. lycopene
nettles
zinc
EFA's
amino acids
28. alcohol
pesticides
cadmium
cholesterol
29. increase in 5-alpha reductase activity.
30. testosterone is converted by 5-alpha reductase to DHT, which is the main prostatic growth factor.
31. estrogen increases stroma susceptibility and prolactin increases androgen uptake.
32. the most common cancer in males.
33. after 50 years old.
34. low risk in asians, high risk in african americans.
35. loss of p53 gene, hypermethylation of glutathione S-transferase.
36. high arachidonic acid content.
37. lycopene
vitamin A, E
fish oil
soy, selenium
38. posterior aspect of lateral lobes.
39. gritty, firm nodules.
40. osteoblastic bone lesions characteristic of boney metastasis to lumbar/thoracic, femur, pelvis, ribs.
41. germ cells.
42. germ cells.
43. whites: blacks 5:1
44. HCG.
45. cryptorchidism.
46. good with removal of affected testes. >95%.
47. worse than seminoma; tends to grow rapidly and spread outside the testicle.
48. HCG or AFP.
49. children under 3yo.
50. AFP.
51. benign until puberty, malignant afterwards.
52. no increase in HCG or AFP levels.
53. poor; fast growing.
54. over 65yo.
bowen's disease is commonly caused by HPV 16 and 18 and manifests as single, gray-white plaques with shallow ulcerations and crusting, either on the shaft of the penis or the scrotum. histologically, one might see dysplastic epithelium, scattered mitosis above the basal layer, and nuclear atypia.
bowen's might lead to squamous cell carcinoma, which might also be caused by HPV strains 16 / 18, or simply poor hygeine. SCC typically affects men 40-70 and manifests as painless lesions that may bleed. early lesions may just be epithelial thickening with some fraying / fissuring, while late or untreated lesions may develop into papules, ulcers with ragged and heaped up margins.
some assorted testicular disorders that we've already covered in CPD: cryptorchidism is an undescended testicle which can be associated with hormonal disorders of deficient LHRH and "trisomy 13". it might also be related to exposure to anti-androgenic compounds such as phthalates in plastics and tagamet, which is used to treat plantar warts and peptic ulcers. cryptorchidism increases the risk for infertility as well as testicular cancer of the fully descended side. hydroceles are serous fluid filled masses that can be caused by inflammation (sports) as well as structural / developmental abnormalities. varicoceles result from dilatation of the panpiniform plexus and is also associated with sports such as extreme mountain biking or soccer.
benign prostatic hypertrophy is nodular hyperplasia of the periurethral region of the prostate. it is associated with some dietary factors: deficiency of lycopene, nettles, zinc, EFA's, and amino acids- as well as dietary excess of alcohol, cadmium, cholesterol, and pesticides. the main growth factor for the prostate is DHT, which is converted from testosterone by 5-alpha reductase; cadmium and cholesterol both increase 5-alpha reductase activity, thus contributing to BPH. two other hormonal influences: estrogen increases stroma susceptibility to hyperplasia and prolactin increases androgen uptake.
prostate cancer is the most common type of cancer in men, generally of the type adenocarcinoma. it affects men over 50 with some racial demographic trends: asians tend to have a lower incidence and african americans have a higher incidence. genetic factors that have been identified are the p53 gene and hypermethylation of glutathione S-transferase. a diet high in arachidonic acid (found in meat products) can also be a risk factor. dietary protective factors might include lycopene, vitamin A and E, selenium, soy, and possibly fish oil. the lesions themselves are gritty and firm nodules on the posterior aspects of the lateral lobes, and if metastasis occurs, the bones are a high possibility-- osteoblastic lesions are a common finding in the lumbar / thoracic spine, femur, pelvis, ribs.
questions
various conditions...
1. what is phimosis?
2. how is phimosis related to age?
3. what is paraphimosis?
4. what is the etiology of condyloma acuminata?
5. what is the morphology of condyloma acuminata?
6. what locations are condyloma acuminata commonly found?
7. ∂escribe the histopathology of condyloma acuminata.
bowen's disease...
8. what age does bowen's disease usually affect?
9. what are the most common etiological agents for bowen's disease?
10. describe the morphology of the lesions in bowen's disease.
11. what locations are affected in bowen's disease?
12. what are some histopathological features of bowen's disease?
SCC...
13. what are the most common etiologies for SCC?
14. where are SCC lesions located?
15. describe the morphology of early SCC lesions.
16. describe the morphology of late SCC lesions.
17. what age does SCC generally occur in?
18. what is the relationship to regional lymph nodes and metastasis of SCC?
19. what is the clinical presentation of SCC?
various testicular disorders...
20. what are some intrinsic risk factors for cryptorchidism?
21. what are some extrinsic risk factors for cryptorchidism?
22. what are the sequelae for cryptorchidism?
23. what is a hydrocele and what is it commonly due to?
24. how common in a varicocele?
25. what are examples of types of hobbies that are associated with varicoceles?
26. which side is more commonly affected by varicoceles?
benign prostatic hypertrophy...
27. what are some etiological factors for BPH related to dietary deficiency?
28. what are some etiological factors for BPH related to dietary excess?
29. what is the mechanism by which cadmium and cholesterol are related to BPH?
30. what are DHT and 5-alpha reductase and how are they involved in BPH pathophysiology?
31. what is the effect of estrogen and prolactin in the prostate?
prostate cancer...
32. how common is prostate cancer?
33. what age group does prostate cancer affect?
34. what are the demographic groups that have high and low risks for developing prostate cancer?
35. what are two genetic factors that have been identified as etiological agents in prostate cancer?
36. what is a dietary risk factor for prostate cancer?
37. what are some protective factors for prostate cancer?
38. what is the most common location for prostate cancer?
39. what is the morphology of the lesions in prostate cancer?
40. what is a common area for metastasis and what are the type of lesions found?
testicular cancer...
41. testicular cancer cells are most commonly derived from which cell line?
42. germ cell vs. non germ cell derived testicular cancer: which is more likely malignant?
43. what is the racial trend for incidence of testicular cancer?
44. what is the serum marker for a seminoma?
45. which condition is a seminoma associated with?
46. what is the prognosis for a seminoma?
47. what is the prognosis for an embryonal carcinoma?
48. what are the serum markers for an embryonal carcinoma?
49. which age group does the yolk sac tumor affect?
50. what are the serum markers for a yolk sac tumor?
51. are teratomas considered benign or malignant?
52. what are the serum markers for a teratoma?
53. what is the prognosis for a choriocarcinoma?
54. which age group is lymphoma most common?
answers
1. abnormal tightness of the prepuce that prevents retraction over the glans.
2. may be related to adhesions from lack of tissue differentiation that occurs before ~3 years.
3. tissue gets stuck behind the glans.
4. HPV 6 and 11
5. sessile or pedunculated, red papillary outgrowths that may be verrucous or flat.
6. coronal sulcus, inner prepuce, glans, perianal.
7. acanthosis, koilocytosis, intact basement membrane.
8. over 35yo.
9. HPV 16 and 18.
10. solitary thickened gray/white plaque with shallow ulcerations and crustin.
11. the shaft or scrotum.
12. dysplastic epithelium
scattered mitosis above basal layer
nuclear abnormalities: large, odd shaped, or multiple.
13. bowen's disease, HPV 16 + 18
14. most on the glans or the inner surface of the prepuce.
15. epithelial thickening with fraying and fissuring.
16. papules and large, infected ulcers with ragged, heaped up margins.
17. 40-70yo.
18. regional nodes may be swollen without spread of SCC.
19. painless lesions that bleed.
20. hormonal disorders of deficient LHRH
trisomy 13
21. phthalates (in plastic)
tagamet (used to treat plantar warts and peptic ulcers)
22. increased risk for testicular cancer
increased risk for infertility
23. build up of serous fluid in the scrotum, from trauma or due to structural abnormalities.
24. 10% of men have them.
25. extreme mountain biking and soccer players.
26. mostly left side.
27. lycopene
nettles
zinc
EFA's
amino acids
28. alcohol
pesticides
cadmium
cholesterol
29. increase in 5-alpha reductase activity.
30. testosterone is converted by 5-alpha reductase to DHT, which is the main prostatic growth factor.
31. estrogen increases stroma susceptibility and prolactin increases androgen uptake.
32. the most common cancer in males.
33. after 50 years old.
34. low risk in asians, high risk in african americans.
35. loss of p53 gene, hypermethylation of glutathione S-transferase.
36. high arachidonic acid content.
37. lycopene
vitamin A, E
fish oil
soy, selenium
38. posterior aspect of lateral lobes.
39. gritty, firm nodules.
40. osteoblastic bone lesions characteristic of boney metastasis to lumbar/thoracic, femur, pelvis, ribs.
41. germ cells.
42. germ cells.
43. whites: blacks 5:1
44. HCG.
45. cryptorchidism.
46. good with removal of affected testes. >95%.
47. worse than seminoma; tends to grow rapidly and spread outside the testicle.
48. HCG or AFP.
49. children under 3yo.
50. AFP.
51. benign until puberty, malignant afterwards.
52. no increase in HCG or AFP levels.
53. poor; fast growing.
54. over 65yo.
Friday, April 16, 2010
pathology IV: female genitalia
some notes for the pathology test on the female reproductive system.
ovarian cysts-- made up of unruptured graffian follicles or ruptured graffian follicles that immediately reseal. they can be follicular (first 2 weeks of cycle, estrogen related), or luteal (second 2 weeks of cycle, progesterone related). within follicular cysts there is also a subcategory of "cystic follicles" which refers to small, common, physiological cysts less than 2cm, generally filled with serous fluid. luteal cysts are the product of failure of degeneration of the corpus luteum, and rupture of these may lead to peritoneal irritation.
PCOS is a condition we learned about in CPD II and is basically the combination of anovulation and androgenism. theca lutein cells of the ovaries, along with the adrenals, overproduce androstenedione which is then converted to testosterone and estrogen in the periphery. anovulation produces low levels of progesterone and a LH:FSH ratio of 3:1 instead of the normal 1:3. one possible mechanism for the hyperandrogenism is via dysfunction of cytochrome P450c17, which is the enzyme involved in the rate limiting steps for synthesis of androgens. a common allopathic treatment, metformin, seems to work via this pathway, related to reduction of insulin levels.
ovarian tumors are relatively common neoplasms that are more likely to be malignant in 40-60 year olds. risk factors that can increase incidence include nulliparity, family history, BRCA1 and 2 mutations, gonadal dysgenesis. there is also a connection between ovarian adenocarcinoma and abnormal expression of the her2/neu oncogene. the WHO classification of ovarian tumors is based upon the tissue of origin: epithelial, germ cell, or sex cord.
mullerian epithelial tumors are derived from the coelemic mesothelial layer and come in three main flavors: serous, endometroid, and mucinous-- cells that are related to uterine tubes, endometrium, and the cervix, respectively. the more developed the epithelial growth is, the greater likelihood for malignancy. symptoms for tumors may include abdominal pain and GI distress, urinary symptoms, and may progress to ascites and peritoneal implants for carcinoma. the benign mullerian tumors are generally unilateral with no epithelial thickening and abundant cilia / papillae, while the malignant tumors are bilateral with large amounts of tissue mass, increased complexity and stratification of the epithelium, which may also show nuclear atypia.
questions
ovarian cysts...
1. ovarian cysts are generally made up of...
2. what age and demographic is most likely to have ovarian cysts? what percentage has regular vs. irregular menstrual cycles?
3. what is the relationship between hypothyroidism and ovarian cysts?
4. what are some risk factors for ovarian cysts?
5. what is "mittelschmerz"?
6. what are the two different types of ovarian cysts and what distinguishes them?
7. what are the two different types of follicular cysts and what distinguishes them?
8. what is hyperthecosis?
9. what are luteal cysts due to?
10. what is the histological apperance of luteal cysts?
11. rupture of luteal cysts may lead to...
PCOS...
12. what is the pathophysiological connection between PCOS and theca lutein cells?
13. what is a typical hormone imbalance seen in PCOS and why?
14. what is cytochrome P450c17 and how is it related to PCOS?
15. full expression of PCOS may require...
16. what is the morphology of PCOS?
ovarian tumors...
17. in what age group are malignant ovarian tumors more common?
18. what are some risk factors for developing ovarian tumors?
19. what is a genetic marker for ovarian adenocarcinomas that can indicate poor prognosis?
20. epithelial tumors are usually...
21. what is the WHO classification of ovarian tumors based upon?
mullerian epithelial tumors...
22. what germ layer are mullerian epithelial tumors derived from?
23. what are the three major types of mullerian epithelial tumors? what cell types are they from?
24. risk of malignancy increases as...
25. what are the symptoms of a mullerian epithelial tumor?
26. what are the symptoms of a mullerian epithelial carcinoma?
27. what is the morphology of benign mullerian epithelial tumors?
28. what is the morphology of a malignant mullerian epithelial tumor?
serous tumors...
29. describe the morphology of serous tumors.
30. what percentage of serous tumors are benign or borderline malignant?
31. what are "psammoma" bodies?
32. what is the most common type of malignant ovarian tumor?
mucinous tumors...
33. what portion of ovarian neoplasms do mucinous tumors account for?
34. what percentage of mucinous tumors are malignant?
35. what is the histomorphology of mucinous tumors?
36. what are pseudomyoma peritonei?
endometroid tumors...
37. what percentage of ovarian neoplasms do endometroid tumors account for?
38. most endometroid tumors are...
39. describe the morphology of endometroid tumors.
40. what is "seeding" in the context of ovarian neoplasms?
cancer markers...
41. what is CA-125?
42. what is the relationship between tubal ligation, oral contraceptives and the risk of cancer?
teratomas...
43. what are mature/benign dermoid cysts derived from?
44. about 1% of dermoids undergo...
45. what is the morphology of an immature/malignant dermoid?
46. what are the most common monodermal teratomas?
47. what is the average ages that are affected by immature and mature teratomas?
48. what is the cell of origin of a struma ovarii?
49. what is the cell of origin of an ovarian carcinoid?
50. what is carcinoid syndrome?
yolk sac...
51. what is the cell of origin for yolk sac tumors?
52. what is a schiller-duval structure?
53. what markers are present in yolk sac tumors?
granulosa cell tumors...
54. does granulosa theca cell secretion indicate malignancy?
55. what are some other conditions that might result from granulosa cell tumors?
meig's syndrome...
56. meig's syndrome is associated with...
57. what cell type is overproduced in meig's syndrome?
58. what is meig's syndrome called when malignant?
59. what is the clinical presentation of meig's syndrome?
abnormal pregnancy, placental issues...
60. what are the most common sites of implantation for ectopic pregnancies?
61. what are the major risk factors for ectopic pregnancy?
62. what is the clinical presentation of an ectopic pregnancy?
63. what is a hydatidiform mole?
64. what is the difference between a complete and partial molar pregnancy?
65. what is the morphology of a molar pregnancy?
66. what are the risk factors for choriocarcinoma?
67. describe the course of a choriocarcinoma.
answers
1. unruptured graffian follicles or ruptured follicles that immediately reseal.
2. women of childbearing age: 50% with irregular cycles, 30% with regular cycles.
3. TSH is similar to HCG and stimulates the growth of cysts.
4. smoking
ovarian cancer
hormonal imbalance
early menarche
nulliparity
tamoxifen
[s o h e n t] [hes not]
5. unilateral sharp pain that occurs during ovulation in 25% of women that can be related to rupture of a follicular cyst.
6. ovarian and luteal, during the first 2 weeks and second 2 weeks of the menstrual cycle, respectively.
7. cystic follicles: small, common, physiological, less than 2cm, filled with serous fluid.
follicular cysts: larger than 2cm and may cause pain.
8. outer theca cells with increased cytoplasm and pale appearance which may cause increased estrogen production and an abnormal endometrium.
9. failure of corpus luteum to degenerate.
10. rim of bright yellow luteal tissue with luteinizing granulosa cells.
11. peritonitis.
12. theca lutein cells produce androstenedione (also produced in the adrenals) which is then converted into testosterone and estrone.
13. LH:FSH ratio is 3:1 instead of 1:3 due to deficient progesterone due to anovulation.
14. cytochrome p450c17 is a rate limiting enzyme involved in androgen synthesis that can be functionally abnormal in PCOS.
15. insulin resistance and a defect in androgen synthesis.
16. gray-white ovaries that are twice the normal size with thickened superficial cortex and numerous subcortical cysts 0.5-1.5cm.
17. 40-60yo.
18. nulliparity
family history
BRCA1, BRCA2 mutations
"gonadal dysgenesis" in children
[tumors parity family broca gonads] [risk for tumors in the broca family assessed by gonad parties]
19. high levels of expression from her2/neu gene.
20. bilateral.
21. tissue of origin: epithelial, germ cell, sex cord.
22. coelomic mesotheium.
23. serous (tubal), endometriod (endometrium), and mucinous (cervix).
24. discernable epithelial cell growth increases.
25. abdominal pain and enlargement
urinary frequency and dysuria
GI complaints
26. weight loss / cachexia
ascites with peritoneal implants of exfoliated tumor cells
27. unilateral, no epithelial thickening, abundant cilia and papillae
28. bilateral, large amounts of tumor mass, increased complexity and stratification of epithelium, nuclear atypia.
29. lined with tall, columnar ciliated epithelium, filled with clear serous fluid.
30. 75%.
31. concentric calcifications
32. serous cystadenocarcinoma.
33. 25%.
34. 15% malignant.
35. columnar epithelial cells with apical mucin and no cilia.
36. cancer of the peritoneum.
37. 20%.
38. carcinomas.
39. tubular glands that look like endometrium.
40. the spread of a ovarian neoplasm to the peritoneal cavity by bits of malignant tissue that resemble salt or spots.
41. high molecular weight glycoprotein that is present in greater than 80% of serous and endometrial carcinomas.
42. both decrease the risk for cancer by 50%.
43. ectodermal differentiation of totipotent cells.
44. malignant transformation of any one of the component elements.
45. more primordial / embryonic tissue, bulky tumors with smooth external surface.
46. struma ovarii, carcinoid.
47. immature- 18yo. mature- young women during reproductive years.
48. germ cell tumor, mature thyroid tissue.
49. germ cell tumor, intestinal epithelial cell.
50. cutaneous flushing and cramps
diarrhea, cramping, nausea, vomiting
cough, weeding, dyspnea
hepatomegaly
51. malignant germ cells differentiated towards extraembryonic yolk sac structure.
52. glomerular-like structure that involves central blood vessels surrounded by germ cells in a space surrounded by germ cells.
53. AFP, alpha 1 antitrypsin
54. potentially, in 5-25% of cases.
55. precocious puberty
endometrial hyperplasia, carcinoma
cystic breast disease
56. sex cord stromal tumors, such as fibroma thecomas.
57. basal cell.
58. fibrosarcoma.
59. pain, pelvic mass, ascites, hydrothorax.
60. uterine tubes (90%)
ovary
abdominal cavity
corona of tubes
61. PID with chronic salpingitis.
peritubal adhesions
leiomyoma
IUD
62. acute onset of severe abdominal pain ~6 weeks after normal menstrual flow.
63. cystic swelling of chorionic villi with variable trophoblastic growth.
64. complete is diploid, from sperm, no viable embryo. partial is triploid or more, viable embryo for several weeks.
65. may see fetal parts in partial mole
uterus filled with delicate, grape like edematous villi.
66. hydatidiform mole (complete)
previous pregnancy / abortion
67. invades myometrium
penetrates adjacent vasculature
metastasizes to lungs, vagina, brain, bone marrow, liver, kidney
ovarian cysts-- made up of unruptured graffian follicles or ruptured graffian follicles that immediately reseal. they can be follicular (first 2 weeks of cycle, estrogen related), or luteal (second 2 weeks of cycle, progesterone related). within follicular cysts there is also a subcategory of "cystic follicles" which refers to small, common, physiological cysts less than 2cm, generally filled with serous fluid. luteal cysts are the product of failure of degeneration of the corpus luteum, and rupture of these may lead to peritoneal irritation.
PCOS is a condition we learned about in CPD II and is basically the combination of anovulation and androgenism. theca lutein cells of the ovaries, along with the adrenals, overproduce androstenedione which is then converted to testosterone and estrogen in the periphery. anovulation produces low levels of progesterone and a LH:FSH ratio of 3:1 instead of the normal 1:3. one possible mechanism for the hyperandrogenism is via dysfunction of cytochrome P450c17, which is the enzyme involved in the rate limiting steps for synthesis of androgens. a common allopathic treatment, metformin, seems to work via this pathway, related to reduction of insulin levels.
ovarian tumors are relatively common neoplasms that are more likely to be malignant in 40-60 year olds. risk factors that can increase incidence include nulliparity, family history, BRCA1 and 2 mutations, gonadal dysgenesis. there is also a connection between ovarian adenocarcinoma and abnormal expression of the her2/neu oncogene. the WHO classification of ovarian tumors is based upon the tissue of origin: epithelial, germ cell, or sex cord.
mullerian epithelial tumors are derived from the coelemic mesothelial layer and come in three main flavors: serous, endometroid, and mucinous-- cells that are related to uterine tubes, endometrium, and the cervix, respectively. the more developed the epithelial growth is, the greater likelihood for malignancy. symptoms for tumors may include abdominal pain and GI distress, urinary symptoms, and may progress to ascites and peritoneal implants for carcinoma. the benign mullerian tumors are generally unilateral with no epithelial thickening and abundant cilia / papillae, while the malignant tumors are bilateral with large amounts of tissue mass, increased complexity and stratification of the epithelium, which may also show nuclear atypia.
questions
ovarian cysts...
1. ovarian cysts are generally made up of...
2. what age and demographic is most likely to have ovarian cysts? what percentage has regular vs. irregular menstrual cycles?
3. what is the relationship between hypothyroidism and ovarian cysts?
4. what are some risk factors for ovarian cysts?
5. what is "mittelschmerz"?
6. what are the two different types of ovarian cysts and what distinguishes them?
7. what are the two different types of follicular cysts and what distinguishes them?
8. what is hyperthecosis?
9. what are luteal cysts due to?
10. what is the histological apperance of luteal cysts?
11. rupture of luteal cysts may lead to...
PCOS...
12. what is the pathophysiological connection between PCOS and theca lutein cells?
13. what is a typical hormone imbalance seen in PCOS and why?
14. what is cytochrome P450c17 and how is it related to PCOS?
15. full expression of PCOS may require...
16. what is the morphology of PCOS?
ovarian tumors...
17. in what age group are malignant ovarian tumors more common?
18. what are some risk factors for developing ovarian tumors?
19. what is a genetic marker for ovarian adenocarcinomas that can indicate poor prognosis?
20. epithelial tumors are usually...
21. what is the WHO classification of ovarian tumors based upon?
mullerian epithelial tumors...
22. what germ layer are mullerian epithelial tumors derived from?
23. what are the three major types of mullerian epithelial tumors? what cell types are they from?
24. risk of malignancy increases as...
25. what are the symptoms of a mullerian epithelial tumor?
26. what are the symptoms of a mullerian epithelial carcinoma?
27. what is the morphology of benign mullerian epithelial tumors?
28. what is the morphology of a malignant mullerian epithelial tumor?
serous tumors...
29. describe the morphology of serous tumors.
30. what percentage of serous tumors are benign or borderline malignant?
31. what are "psammoma" bodies?
32. what is the most common type of malignant ovarian tumor?
mucinous tumors...
33. what portion of ovarian neoplasms do mucinous tumors account for?
34. what percentage of mucinous tumors are malignant?
35. what is the histomorphology of mucinous tumors?
36. what are pseudomyoma peritonei?
endometroid tumors...
37. what percentage of ovarian neoplasms do endometroid tumors account for?
38. most endometroid tumors are...
39. describe the morphology of endometroid tumors.
40. what is "seeding" in the context of ovarian neoplasms?
cancer markers...
41. what is CA-125?
42. what is the relationship between tubal ligation, oral contraceptives and the risk of cancer?
teratomas...
43. what are mature/benign dermoid cysts derived from?
44. about 1% of dermoids undergo...
45. what is the morphology of an immature/malignant dermoid?
46. what are the most common monodermal teratomas?
47. what is the average ages that are affected by immature and mature teratomas?
48. what is the cell of origin of a struma ovarii?
49. what is the cell of origin of an ovarian carcinoid?
50. what is carcinoid syndrome?
yolk sac...
51. what is the cell of origin for yolk sac tumors?
52. what is a schiller-duval structure?
53. what markers are present in yolk sac tumors?
granulosa cell tumors...
54. does granulosa theca cell secretion indicate malignancy?
55. what are some other conditions that might result from granulosa cell tumors?
meig's syndrome...
56. meig's syndrome is associated with...
57. what cell type is overproduced in meig's syndrome?
58. what is meig's syndrome called when malignant?
59. what is the clinical presentation of meig's syndrome?
abnormal pregnancy, placental issues...
60. what are the most common sites of implantation for ectopic pregnancies?
61. what are the major risk factors for ectopic pregnancy?
62. what is the clinical presentation of an ectopic pregnancy?
63. what is a hydatidiform mole?
64. what is the difference between a complete and partial molar pregnancy?
65. what is the morphology of a molar pregnancy?
66. what are the risk factors for choriocarcinoma?
67. describe the course of a choriocarcinoma.
answers
1. unruptured graffian follicles or ruptured follicles that immediately reseal.
2. women of childbearing age: 50% with irregular cycles, 30% with regular cycles.
3. TSH is similar to HCG and stimulates the growth of cysts.
4. smoking
ovarian cancer
hormonal imbalance
early menarche
nulliparity
tamoxifen
[s o h e n t] [hes not]
5. unilateral sharp pain that occurs during ovulation in 25% of women that can be related to rupture of a follicular cyst.
6. ovarian and luteal, during the first 2 weeks and second 2 weeks of the menstrual cycle, respectively.
7. cystic follicles: small, common, physiological, less than 2cm, filled with serous fluid.
follicular cysts: larger than 2cm and may cause pain.
8. outer theca cells with increased cytoplasm and pale appearance which may cause increased estrogen production and an abnormal endometrium.
9. failure of corpus luteum to degenerate.
10. rim of bright yellow luteal tissue with luteinizing granulosa cells.
11. peritonitis.
12. theca lutein cells produce androstenedione (also produced in the adrenals) which is then converted into testosterone and estrone.
13. LH:FSH ratio is 3:1 instead of 1:3 due to deficient progesterone due to anovulation.
14. cytochrome p450c17 is a rate limiting enzyme involved in androgen synthesis that can be functionally abnormal in PCOS.
15. insulin resistance and a defect in androgen synthesis.
16. gray-white ovaries that are twice the normal size with thickened superficial cortex and numerous subcortical cysts 0.5-1.5cm.
17. 40-60yo.
18. nulliparity
family history
BRCA1, BRCA2 mutations
"gonadal dysgenesis" in children
[tumors parity family broca gonads] [risk for tumors in the broca family assessed by gonad parties]
19. high levels of expression from her2/neu gene.
20. bilateral.
21. tissue of origin: epithelial, germ cell, sex cord.
22. coelomic mesotheium.
23. serous (tubal), endometriod (endometrium), and mucinous (cervix).
24. discernable epithelial cell growth increases.
25. abdominal pain and enlargement
urinary frequency and dysuria
GI complaints
26. weight loss / cachexia
ascites with peritoneal implants of exfoliated tumor cells
27. unilateral, no epithelial thickening, abundant cilia and papillae
28. bilateral, large amounts of tumor mass, increased complexity and stratification of epithelium, nuclear atypia.
29. lined with tall, columnar ciliated epithelium, filled with clear serous fluid.
30. 75%.
31. concentric calcifications
32. serous cystadenocarcinoma.
33. 25%.
34. 15% malignant.
35. columnar epithelial cells with apical mucin and no cilia.
36. cancer of the peritoneum.
37. 20%.
38. carcinomas.
39. tubular glands that look like endometrium.
40. the spread of a ovarian neoplasm to the peritoneal cavity by bits of malignant tissue that resemble salt or spots.
41. high molecular weight glycoprotein that is present in greater than 80% of serous and endometrial carcinomas.
42. both decrease the risk for cancer by 50%.
43. ectodermal differentiation of totipotent cells.
44. malignant transformation of any one of the component elements.
45. more primordial / embryonic tissue, bulky tumors with smooth external surface.
46. struma ovarii, carcinoid.
47. immature- 18yo. mature- young women during reproductive years.
48. germ cell tumor, mature thyroid tissue.
49. germ cell tumor, intestinal epithelial cell.
50. cutaneous flushing and cramps
diarrhea, cramping, nausea, vomiting
cough, weeding, dyspnea
hepatomegaly
51. malignant germ cells differentiated towards extraembryonic yolk sac structure.
52. glomerular-like structure that involves central blood vessels surrounded by germ cells in a space surrounded by germ cells.
53. AFP, alpha 1 antitrypsin
54. potentially, in 5-25% of cases.
55. precocious puberty
endometrial hyperplasia, carcinoma
cystic breast disease
56. sex cord stromal tumors, such as fibroma thecomas.
57. basal cell.
58. fibrosarcoma.
59. pain, pelvic mass, ascites, hydrothorax.
60. uterine tubes (90%)
ovary
abdominal cavity
corona of tubes
61. PID with chronic salpingitis.
peritubal adhesions
leiomyoma
IUD
62. acute onset of severe abdominal pain ~6 weeks after normal menstrual flow.
63. cystic swelling of chorionic villi with variable trophoblastic growth.
64. complete is diploid, from sperm, no viable embryo. partial is triploid or more, viable embryo for several weeks.
65. may see fetal parts in partial mole
uterus filled with delicate, grape like edematous villi.
66. hydatidiform mole (complete)
previous pregnancy / abortion
67. invades myometrium
penetrates adjacent vasculature
metastasizes to lungs, vagina, brain, bone marrow, liver, kidney
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