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Histopathology 4

Alexander Wolff English 200 cards

list of clinical features of coeliac

Cards in this deck (200)

  1. 1list of clinical features of coeliaclist of clinical features of coeliac
  2. 2what are the long term complications of coeliac disease in adults- osteoporosis
    - intestinal T-lymphoma (EATL)
  3. 3what determines severity of coeliac disease?- correlates to your antibody
    look nearer the time    what determines severity of coeliac disease?
  4. 4more on histology of coeliacmore on histology of coeliac
  5. 5image of the MARSH classification for coeliac diseaseimage of the MARSH classification for coeliac disease
  6. 6what three broad causes are there for PCKD?- sporadic
    -genetic
    - acquired
  7. 7what mode of inheritance is PCKDautosomal recessive
  8. 8what is the result of many cases of autosomal recessive polycystic kidney disease ARPCKD?- stillbirth or early neonatal death (40%)
    - encountered in 1 in 20000 live births
    -enlarged cystic kidney at birth
  9. 9what gene is cited to be important in ARPCKD?- PKHD1 mapping onto chromosome 6 (6p21-p12)
    -encodes fibrocystin located in the cilium
    - >300 known mutations in PKHD1
  10. 10how often are PKHD1 mutations identified in cases of ARPCKD?- 80-85%
  11. 11histology of ARPCKDhistology of ARPCKD
  12. 12when do people present with adult polycystic kidney disease?in their 30-50's
  13. 13why is this the age, and not earlier?- cysts involve only a proportion of the nephron so there is redundancy
  14. 14how common is adult PCKD?- 1 in 400-500 live births
    -responsible for 5-10% of all CRF requiring dialysis
  15. 15what is the mode of inheritance for ADULT PCKD?-autosomal dominant
    - most common cystic renal disease
    -most common genetically transmitted disease
  16. 16diagnostic procedure after surgical species brought to a histology labdiagnostic procedure after surgical species brought to a histology lab
  17. 17why is knowing that most paediatric malignancies are genetic help us?- to prognose, diagnose, and for therapeutic information
    - malignancies associated with various genetic changes
  18. 18example of malignancy (childhood) multiple genetic changesexample of malignancy (childhood) multiple genetic changes
  19. 19who do pathologists get molecular investigations from ?- cytogenetic labs
  20. 20which two mainstay cytogenetic techniques are used in these labs?- FISH
    -PCR
    other techniques in some labs
  21. 21how are cytogenetic results used in diagnosis-used to substantiate a histological diagnosis
  22. 22example of Ewing sarcoma to show how histology and cytogenetic techniques are used to come to a diagnosisexample of Ewing sarcoma to show how histology and cytogenetic techniques are used to come to a diagnosis
  23. 23how is this cytogenetic/histological result dealt with?-taken to a clinician
    - liaised to MDT's
    - decisions for further treatment made
  24. 24list of limits to the current diagnostic methods discussed aboveroll for genomics in the futurelist of limits to the current diagnostic methods discussed above
  25. 25what is the prominent blood supply to the heart?- coronary arteries
    -remind yourself of the anatomy of the heart
  26. 26where do the coronary arteries arise from/- aorta
    -runs along the epicardial route before penetrating the myocardium as intramural arteries
  27. 27when does the coronary artery blood flow occur?- during ventricular diastole
    - microcirculation isn't compressed by cardiac contraction
    -therefore occurs within a fixed time span
  28. 28how thick are the walls of the left and right ventricle?- right ventricle 4mm
    left ventricle 10mm
  29. 29use this diagram of angiography to identify the various parts of the angiogram of he coronary arteriesuse this diagram of angiography to identify the various parts of the angiogram of he coronary arteries
  30. 30another angiogram of the heartanother angiogram of the heart
  31. 31the left heart is served by which coronary artery?- the left trunk
    -LAD and LCx
    -10% dominance
  32. 32what percentage are right CA dominant?- 90%
  33. 33what areas of myocardium does the LAD supply?- most of the apex of the heart
    - anterior wall of the left ventricle
    - anterior two thirds of the ventricular septum
  34. 34what areas of myocardium does the LCx supply?- lateral wall of the left ventricle
  35. 35what areas of myocardium are served by the right coronary?- 80% of population it serves the right ventricle
    - the posterior third of the ventricular septum
    -posterior basal wall of the left ventricle (if right dominant)
  36. 36define ischaemic heart disease- generic name for a group of closely related syndromes that cause myocardial ischaemia
  37. 37what is the most common cause?- coronary artery blood flow reduction
    -90% of cases
  38. 38define properly ischaemic heart disease in terms of coronary artery obstruction- 90% cases -this is fixed coronary artery obstruction- wherein one or more lesions that cause a 75% reduction of the cross-sectional area of at least one of the major epicardial arteries
  39. 39image to demonstrate coronary atherosclerosis -fixedimage to demonstrate coronary atherosclerosis -fixed
  40. 40histology of coronary atherosclerosishistology of coronary atherosclerosis
  41. 41describe briefly the pathogenesis of a thrombus, starting from a fixed coronary obstruction- fixed coronary obstruction- 90% cases 75% cross sectional area occluded- angina
    - can either become severe fixed obstruction OR plaque can become disrupted by platelet aggregation
    - in the case of plaque disruption, mural thrombus OR occlusive thrombus is the result
  42. 42image to explain above -make sure you read carefully to define each pathologyimage to explain above -make sure you read carefully to define each pathology
  43. 43how might these pathologies manifest themselves clinically ?angina pectoralis
    - myocardial infarction
    - chronic ischaemic heart disease (as a result of previous MI leading to progressive heart failure)
    - sudden cardiac death
  44. 44information of the effect of ischaemia on myocytesinformation of the effect of ischaemia on myocytes
  45. 45what is transmural infarction?- ischaemic necrosis involving the full or nearly the full thickness of the ventricular wall in the distribution of a single coronary artery
  46. 46what is transmural infarction usually associated with?- chronic coronary atherosclerosis
    -acute plaque change
    - superimposed completely obstructive thromboses
  47. 47define a subendocardial infarctlimited to the inner one-third or at most one half of the ventricular wall
    -may extend laterally beyond the perfusion territory of a single coronary artery
  48. 48what do you see commonly in subendocardial infarcts?stenosing coronary atherosclerosis
  49. 49gross changes associated with MIgross changes associated with MI
  50. 50gross specimen of old and recent infarct -try to predict how long ago these occurredgross specimen of old and recent infarct -try to predict how long ago these occurred
  51. 51microscopic changes of MImicroscopic changes of MI
  52. 52how do we detect MI in the lab?- based on the measurement of intracellular macromolecules leaked from the damaged myocytes into the circulation
    -e,g creatine kinase- MB isoenzyme
    - lactate dehydrogenase
    - troponin 1 and troponin T
  53. 53what might be seen on ECG for MI?- Q waveswhat might be seen on ECG for MI?
  54. 54name three other diagnostic tools that could be useful for diagnosis of MI- echo
    - radio isotope studies
    - magnetic resonance imaging
  55. 55list the acute effects of MI- contractile dysfunction
    - arrhythmias
    -cardiac rupture
    -pericarditis
  56. 56how might sudden death occur in MI?- invariably due to lethal arrhythmia
    -asystole/ventricular fibrillation
  57. 57name three way in which the myocardium could rupture after MI- ventricular free wall
    - septum could rupture
    - papillary muscle could rupture
  58. 58name three other pathological complications of MI- infarct extension
    - mural thrombus
    - ventricular aneurysm
  59. 59image of a rupture in the myocardium due to infarctimage of a rupture in the myocardium due to infarct
  60. 60image of a ruptured papillary muscleimage of a ruptured papillary muscle
  61. 61another image of MI pathologyanother image of MI pathology
  62. 62what tends to happen to the unaffected ventricular wall if the other wall thins due to fibrous scarring?- hypertrophieswhat tends to happen to the unaffected ventricular wall if the other wall thins due to fibrous scarring?
  63. 63image of ventricular wall aneurysmimage of ventricular wall aneurysm
  64. 64describe the structure of the aortic valve- commonly tricuspid semi lunar valves
    -can be congenitally bicuspid
  65. 65describe the structure of the mitral valvebicuspid flaps supported by chordae tendinae attached to papillary muscles
  66. 66describe the structure of the pulmonary valvetricuspid semi lunar valves
  67. 67describe the structure of the tricuspid valve- tri-cuspid supported by chordae tendinae
  68. 68aortic valveaortic valve
  69. 69mitral valvemitral valve
  70. 70pulmonary valvepulmonary valve
  71. 71tricuspid valvetricuspid valve
  72. 72what does stenosis of a valve mean?- tightening of the valvular opening resulting in decreased flow of blood through the opening
  73. 73what does incompetence of a valve mean- incomplete closure of the valvular opening, allowing back flow of blood throughout the opening.
  74. 74what other effect of valvular disease can occur?- can have a mixture of signs resulting from incompetence and stenosis
    -therefore called mixed
  75. 75give a list of common degenerative valvular diseases-calcific aortic stenosis
    -mitral annular calcification
    - myxomatous degeneration of the mitral valves
  76. 76name a less common disease of the valves, that was common in the 60's-70's- thematic fever followed by rheumatic heart disease
  77. 77describe calcific aortic stenosis- most frequent of all valvular abnormalities
    - calcification induced by wear and tear
    -heaped up calcified masses
  78. 78at what age is the onset of calcific aortic stenosis most common?- 50's and 60's if congenital bicuspid individuals
    - 70's and 80's in those with previous normal valves
  79. 79quick look at normal aortic valves -note the distinctive commissures that demarcate each valvequick look at normal aortic valves -note the distinctive commissures that demarcate each valve
  80. 80an image to demonstrate calcification of the aortic valve, leading to aortic stenosis (failure to fully open and therefore failure to allow blood through)an image to demonstrate calcification of the aortic valve, leading to aortic stenosis (failure to fully open and therefore failure to all...
  81. 81image to show a bicuspid aorta calcified valve, wherein the aortic valve has fused together - shown by the arrowimage to show a bicuspid aorta calcified valve, wherein the aortic valve has fused together - shown by the arrow
  82. 82describe mitral annular calcification- degenerative calcific deposits in the ring of the mitral valve
    - generally not affecting the function, but can lead to mitral regurge.
  83. 83name some complications of mitral annular calcification- can be a source of thrombi and emboli
    -also prone to infective endocarditis
  84. 84in what population is mitral annular calcification most common?- women over the age of 60
  85. 85an image to demonstrate the calcification of the mitral valve ring in Mitra l annular calcificationan image to demonstrate the calcification of the mitral valve ring in Mitra l annular calcification
  86. 86mitral valve prolapse is caused by what?- myxomatous degeneration of the valve
  87. 87describe mitral valve prolapseballooning of the valvular cusps
    - leaflets thickened and rubbery
    - thought to be due to connective tissue abnormality
  88. 88what congenital syndrome is associated with mitral valve prolapse?-Marfan's syndrome
    - mutations in the gene encoding fibrillin
  89. 89image of mitral valve prolapse - note the ballooning and bicuspid valve leaflet looking notably thickenedimage of mitral valve prolapse - note the ballooning and bicuspid valve leaflet looking notably thickened
  90. 90tenting of the mitral valve characteristic of mitral valve prolapsetenting of the mitral valve characteristic of mitral valve prolapse
  91. 91what is rheumatic fever?- acute immunologically mediated
    -multi system inflammatory disease
    - occurs a few weeks after episode of group A (beta-haemolytic) strep pharyngitis
    -remember not so common now
  92. 92schematic of the processes involved in rheumatic heart diseaseschematic of the processes involved in rheumatic heart disease
  93. 93histologically, what could you see in rheumatic heart disease?- Aschoff bodieshistologically, what could you see in rheumatic heart disease?
  94. 94image of rheumatic vavulitisimage of rheumatic vavulitis
  95. 95what is the most important consequence of rheumatic fever?- chronic rheumatic valvular heart disease
  96. 96what does chronic rheumatic valvular heart disease cause?- almost ALWAYS involvement of the mitral valve
    - commonly involves aortic and other valves
  97. 97most commonly affected valve in - chronic rheumatic valvular heart disease- mitral valve
    almost always affected
    -make sure you look at images to familiarise yourself
  98. 98give the characteristics of rheumatic valvular disease in the chronic form- leaflet thickening
    - commissure fusion
    - shortening, thickening and fusion of chordae tendinae
  99. 99example of chronic rheumatic disease o th mitral valveexample of chronic rheumatic disease o th mitral valve
  100. 100give some information regarding the site of infection for endocarditis- most commonly the left heart valves
    - tricuspid typically in intravenous drug users
    - preventable by antibiotics for surgical or dental procedure
  101. 101look at images of bacterial endocarditiscome back when done
  102. 102gross anatomy of the thyroidgross anatomy of the thyroid
  103. 103describe the normal thyroid- colloid filled acini lined by follicular epithelial cells
    -vascular organ
    - thyroxine produced and secreted into blood
    -regulates the basal metabolic rate
  104. 104normal thyroid histologyadd
  105. 105what is the most common cause of hypothyroidism?- Hashimoto's thyroiditis
  106. 106how is Hashimoto's caused?- anti-thyroid antibodies
    leads to lymphocytic destruction of the thyroid
    much more common in females (10:1)
  107. 107name two other reasons that might cause Hashimoto's- removal of the thyroid
    - radio iodine treatment
  108. 108what is the common name for severe hypothyroidism?- Myxoedema
  109. 109list symptoms of hypothyroidism- weight gain
    - cold intolerance
    - tiredness, depression
    - big tongue, deep voice *deposition of matrix substances in viscera and skin
    - thin hair
    - weak heartbeat
    - slow reflexes
  110. 110gross change demonstrating Hashimoto's -remember can also be called lymphocytic thyroiditisgross change demonstrating Hashimoto's -remember can also be called lymphocytic thyroiditis
  111. 111histology of hashimoto's lack of follicular structure -lymphocytic infiltratehistology of hashimoto's lack of follicular structure -lymphocytic infiltrate
  112. 112name a common cause of hyperthyroidism- Graves - 85% of cases
    F10:M1
  113. 113describe other causes of hyperthyroidism- hyperfunctional multinodular goitre - usually euthyroid
    - hyperfunctional adenoma (benign follicular tumour)- rarely
  114. 114describe symptoms/signs of hyperthyroidism- sweating, heart intolerance
    -weight loss
    - diarrhoea
    - tachycardia, arrhythmias
    - tremor, anxiety, hyperactivity, brief reflexes
    - staring gaze, lid lag
    EXOPTHALMOS
  115. 115what is graves disease also known as?- diffuse toxic goitre
  116. 116describe the cause of Graves'- autoimmune
    -TSH receptor autoantibodies that up regulate hormone production
    - SYMMETRICAL enlargement of thyroid
  117. 117why do we see exophthalmos in Graves?- due to deposition of connective tissue behind the eyeball
  118. 118image of exophthalmosimage of exophthalmos
  119. 119image of mutlinidular goitre/nodular hyperplasiaremember to add
  120. 120describe mutlinodular goitreusually euthyroid
    - large goitre may cause tracheal compression and dysphagia
    - cosmetic effect
  121. 121slide on follicular adenomaslide on follicular adenoma
  122. 122how do we treat follicular adenoma ?- thyroid lobectomy
  123. 123which sex has predominance in thyroid carcinoma ?-females in most types
  124. 124what proportion of carcinoma of the thyroid are 1)papillary 2) follicular -3)anaplastic 4) medullary1)80%
    2)15%
    3)2%
    4)3%
  125. 125image of a papillary carcinoma of the thyroid -notice the usual cystic structureimage of a papillary carcinoma of the thyroid -notice the usual cystic structure
  126. 126name a common histological feature of papillary carcinoma-psammoma bodies
    Orphan Annie eye inclusion bodies
  127. 127papillary carcinoma histology showing a psammoma bodypapillary carcinoma histology showing a psammoma body
  128. 128how can papillary carcinoma be commonly caused?- via lymphatics from cervical lymph nodes
  129. 129what other exposure is highly associated with papillary carcinoma?- radiation
  130. 130what feature of follicular carcinoma gives it away?- the fact it is widely invasivewhat feature of follicular carcinoma gives it away?
  131. 131histological picture of follicular carcinoma -note the invasion of thyroid and blood vesselshistological picture of follicular carcinoma -note the invasion of thyroid and blood vessels
  132. 132how might follicular carcinoma present?- shows up on x rays after bone pain (spread via blood)how might follicular carcinoma present?
  133. 133describe anaplastic thyroid carcinoma-elderly patients
    - aggressive- local invasion, metastases
    - no response to treatment
    - fatal in a few months
  134. 134histological appearance of anaplastic thyroid carcinoma obvious cells incorporating each otherhistological appearance of anaplastic thyroid carcinoma obvious cells incorporating each other
  135. 135what do the c cells of the thyroid do?- secrete calcitonin (calcium metabolism)
  136. 136how is medullary carcinoma caused?- arises from c cells
    - neuroendocrine tumour
    - amyloid stroma
  137. 137what is found histologically in medullary carcinoma?-amyloid stroma
    -also brown stain positive cells- calcitonin
  138. 138what proportion of medullary carcinoma's are sporadic?- 70%
  139. 139which genes are associated with medullary carcinoma?-MEN 2A
    -MEN 2B
    -FMTC
    -in 30% of cases
  140. 140histology of medullary carcinoma showing amyloid stroma- pink -also shows a positive brown stain for calcitonin - present in tumour§§histology of medullary carcinoma showing amyloid stroma- pink -also shows a positive brown stain for calcitonin - present in tumour§§
  141. 141name some techniques used to diagnose hypo/hyperthyroidismthyroid function tests
    autoantibodies (graves/hashimotos)
  142. 142what test is commonly used for thyroid enlargement-ultrascan
  143. 143how do we manage and diagnose thyroid nodulesFNA cytology
    -excision if indicated
    -lobectomy OR total
  144. 144image to display normal parathyroid morphologyimage to display normal parathyroid morphology
  145. 145describe a situation in which PTH is produced more- low serum calcium
    - bones mobilise calcium into blood, less resorption into gut/ more absorption of calcium FROM gut and more kidney retainment of calcium
  146. 146schematic to explain aboveschematic to explain above
  147. 147therefore, what will primary hyperparathyroidism cause?- hypercalcemia
  148. 148list of causes of primary hyperparathyroidismlist of causes of primary hyperparathyroidism
  149. 149give a list of symptoms associated with hyperparathyroidism- painful bones- osteoporosis, osteitis, fibrosa cystica
    - renal stones pain
    - abdominal groans
    -psychic moans- depression, seizures
  150. 150what is the most common cause of secondary hyperparathyroidism?- chronic renal failure
    - hypocalcemia- loss through kidneys
    - leads to hyperplasia of all 4 glands
  151. 151give some less common causes of secondary hyperparathyroidismgive some less common causes of secondary hyperparathyroidism
  152. 152what does stones, moans and groans refer to in hyperparathyroidism- renal stones
    -psychic moans- depression
    - abdominal groans
  153. 153what radiological technique can be used to localise a parathyroid tumour?- sestamibi scan
  154. 154what radioactive element is used in sestambi scanning?- technetium-99
    -highlights hyperactive parathyroid glands
    -results are variable in hyperplasia
  155. 155image of sestambi scanimage of sestambi scan
  156. 156what pattern of size is seen in a parathyroid adenoma?-three normal sized glands
    -one large adenoma    what pattern of size is seen in a parathyroid adenoma?
  157. 157what is the difference in terms of sizing between P/T hyperplasia and adenomain hyperplasia, all 4 will be biggerwhat is the difference in terms of sizing between P/T hyperplasia and adenoma
  158. 158describe parathyroid carcinoma- rare
    -very high calcium of >3.5mmol/l
    -bone disease, renal stones
    -metastases
    -adherent to surgery
  159. 159what calcium level is indicative of p/t carcinoma?->3.5mmolL-1
  160. 160where does a parathyroid carcinoma invade commonly?- the thyroidwhere does a parathyroid carcinoma invade commonly?
  161. 161what techniques are useful in the diagnosis of parathyroid pathology?-ultrasound +- sestambi scan
    - excision of one or more parathyroid for histology
    -can use intra-operative frozen section to confirm that it is parathyroid tissue
  162. 162which 3 steroid types are produced In the cortex?- glucocorticoids- mainly cortisol
    - mineralocorticoids- aldosterone
    -sex steroids- oestrogen and androgens
  163. 163what does the medulla of the adrenals produce?- catecholamines
    mainly adrenaline
  164. 164image of internal adrenal surfaceimage of internal adrenal surface
  165. 165what is the other name for Addison's disease?- primary adrenocortical insufficiency
  166. 166a list of reasons for Addisons basically a lack of cortisol/aldosteronea list of reasons for Addisons basically a lack of cortisol/aldosterone
  167. 167how might secondary adrenocorticol insufficiency be caused?-hypothalamic/pituitary dysfunction leading to reduced output of ACTH
  168. 168how is secondary adrenocortical insufficiency treated?- treatment with steroids
    need to be long term
  169. 169image to demonstrate the adrenal atrophy commonly found in Addison'simage to demonstrate the adrenal atrophy commonly found in Addison's
  170. 170list the symptoms of Addison'slist the symptoms of Addison's
  171. 171what is the reason for hyper pigmentation in Addison's?- pro-opiomelanocortin from pituitary
    is a precursor ACTH and melanocyte stimulating hormone
  172. 172how can Addison's be fatal ?- in the case of an acute adrenal crisis
  173. 173outline the signs of an acute adrenal crisis- precipitated by infection, trauma /surgical procedures
    -shows signs of : vomitting, abdominal pain, hypotension and can lead to coma
  174. 174how do you treat acute adrenal crisis- rapid corticosteroid treatment
  175. 175what is an overactive adrenal cortex usually called?-Cushing's syndrome
  176. 176what are the clinical signs of Cushin's?- central obesity
    - abdo striae
    - moon faces
    -thin skin
    - easy bruising
    -hypertenison
    - can get glucose intolerance
  177. 177typical appearance of a Cushing's patienttypical appearance of a Cushing's patient
  178. 178what is the most common cause of Cushing's?- iatrogenic
    -through administration of glucocorticoid
  179. 179Cushing's DISEASE is caused by what ?- pituitary adenoma
  180. 180name the two ACTH endogenous causes of Cushing's- pituitary adenoma
    - ectopic ACTH production- small cell carcinoma
  181. 181name some ACTH independent cause of Cushing'sname some ACTH independent cause of Cushing's
  182. 182hyperaldosteronism can cause what and how is it caused?- causes hypertension
    - caused by an increase in aldosterone
  183. 183what can occur with adrenal cortical carcinoma ?-most are functional and cause virilism
    - often large and invasive
    - venous spread+ lymphatic
  184. 184image of a adrenal cortical carcinomaimage of a adrenal cortical carcinoma
  185. 185information on Pheochromocytomainformation on Pheochromocytoma
  186. 186image of Pheochromocytomaimage of Pheochromocytoma
  187. 187what does 'rule of 10's' mean in relation to Pheochromocytoma?- 10% extra adrenal
    10% bilateral
    10% malignant
    10% not associated with hypertension
  188. 188name three techniques used to diagnose adrenal pathology-biochemical
    - radiological
    -tumour excision - histology
  189. 189what does MEN stand for?- multiple endocrine neoplasia syndromes
  190. 190describe MEN- inherited- autosomal dominant
    - proliferative lesions
    - involve multiple endocrine organs
    - types 1 and 2. 2A, 2B and FTMC
    -symptoms due to hormones produced/ effect of a mass
  191. 191read through the last few slides of MEN on this lectureMAKE SURE YOU DO THIS
  192. 192name the structures of the female genital tract- vulva/vagina
    - cervix
    - uterus
    - fallopian tubes
    - ovaries
  193. 193anatomical image of the female genital tractanatomical image of the female genital tract
  194. 194have a brief understanding of the embryological differentiation between males and femaleshave a brief understanding of the embryological differentiation between males and females
  195. 195what two types of epithelium exist in the cervix?- columnar and squamous
    - differentiated at the squamocolumnar junction
  196. 196cervical histology- squamo columnar junctioncervical histology- squamo columnar junction
  197. 197what virus are we most concerned about in the cervix?human papilloma virus
  198. 198images of HPVimages of HPV
  199. 199people infected episomally with HPV (low risk 6,11) are at risk of what?- condyloma
  200. 200those exposed to higher risk HPV (16,18) amongst others, are at risk of what?-cervical intraepithelial neoplasia (CIN) (million per year)
    - remember that this is the result of viral integration

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Flashcards on Histopathology 4, created by Alexander Wolff on 05/11/2017.
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