Pathology Flashcards

1
Q

what are the two types of inflammation within the kidney

A

infective- pyelonephritis

non- infective- glomerulonephritis

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2
Q

what is between the parietal and visceral epithelium in the glomerulus

A

the

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3
Q

what is glomerulonephritis

A

inflammation of the glomerulus

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4
Q

what are the two main groups of GMN

A

immune mediated (immune complexes within the glomerulus- either directed at it or circulating complexes getting stuck in the ‘sieve’)

or GMN relating to vasculitis

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5
Q

what causes immune complexes to be directed at the glomerulus

A

good pastures syndrome

IgG antibodies

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6
Q

what are the two main features of good pastures (why)

A

haemoptysis and renal failure

as IgG against alpha 3 subunit of collagen 4 which is in kidneys and lungs

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7
Q

what vasculitis’ are associated with GMN

A

GPA (cANCA)

MPA (pANCA)

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8
Q

how do immune complexes affect the glomerulus

A

disrupt membrane charge (also plasma proteins and RBCs to get through), block membranes

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9
Q

what are the features of nephritic syndrome

A

haematuria and hypertension

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10
Q

what are the features of nephrotic syndrome

A

heavy proteinuria: non dependent oedema, hyperlipideamia

also loose antibodies, complement and clotting cascade = immunosuppression and renal vein thrombosis

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11
Q

how do you classify GMN

A

light microscopy
electron microscopy
immunoflouresence

whether they cause nephritic/ nephrotic- are proliferative/ non proliferative

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12
Q

what are cresents

A

very bad prognostic signs= indicate rapidly progressive GMN

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13
Q

what causes granulomas in GMN

A

GPA, sarcoid

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14
Q

what is usually seen in light microscopy in all GMN types

A

hypercellularity (inflammatory cells and reactive proliferations) (= inflammation)

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15
Q

what is usually seen in electron microscopy in GMN

A

(allows you to see BM)

deposits of immune complexes whether they are subepithelial (in/ around podocytes)/ sub endothelial / mesangial

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16
Q

what does IMF show you

A

what kind of antibody and what distribution (IgG, IgM, IgA)

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17
Q

what does good pastures look like on IMF

A

linear IgG deposition

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18
Q

who gets minimal change GMN

A

children

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19
Q

what are the features of minimal change GMN

A

nephrotic syndrome

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20
Q

what is the Tx for minimal change GMN

A

usually resolves with steroids

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21
Q

what causes focal segmental glomerulosclerosis (FSGS)

A

obesity, HIV, sickle cell, IV drug users (esp heroin)

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22
Q

who gets FSGS GMN

A

adults with risk factors (can affect children)

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23
Q

what is the presentation of FSGS

A

nephritic syndrome (can cause nephrotic but less likely)

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24
Q

what is the appearance of FSGS

A

focal (just in glomeruli)
segmental (not whole glomeruli)
glomerulosclerosis

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25
Q

what is the prognosis for FSGS

A

v variable

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26
Q

what causes membranous GMN

A

infection (hepatitis, malaria, syphilis)
drugs (penicillamine, NSAID, captopril, gold)
malignancy (lung, colon, melanoma)
lupus (15% of all GMN in lupus)
autoimmune disease (thyroiditis)

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27
Q

who gets membranous GMN

A

adults with risk factors

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28
Q

what is the presentation of membranous GMN

A

nephrotic (can sometimes be nephritic)

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29
Q

what is the appearance of membranous GMN

A

thick membranes sub-epithelial immune deposits (makes BM look spikey)

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30
Q

what is the prognosis of membranous GMN

A

variable- slow indolent progression, less than 40% eventually develop renal failure

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31
Q

what is the cause of IgA GMN

A

genetic/ acquired defect (coeliac)

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32
Q

who gets IgA GMN

A

people get it after an infection (commonly strep)

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33
Q

how does IgA GMN present

A

follows an infection (strep throat)

nephritic syndrome

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34
Q

what is the appearance of IgA GMN

A

IgA deposition in mesangium

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35
Q

what is the test for coeliac disease

A

anti TTG

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36
Q

what is the prognosis of IgA GMN

A

variable depending on severity

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37
Q

what causes membranoproliferative GMN

A

idiopathic (type 2 - infection, lupus, malignancy (hodgkins lymphoma))

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38
Q

what is the presentation of membranoproliferative GMN

A

either nephritic/ nephrotic

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39
Q

who gets membranoproliferative GMN

A

adults and children

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40
Q

what is the appearance of membranoproliferative GMN

A

big lobulated hypercellular glomeruli with thick membranes (look like tram tracks due to the duplication of the BM)

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41
Q

what is the prognosis of membranoproliferative GMN

A

depends on severity

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42
Q

how does diabetes affect the kidney

A

diffuse/ nodular glomerulosclerosis
nodules- kimmel stiel wilson lesion
microvascular disease (arterial sclerosis)
infection- pyelonephritis, papillary necrosis

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43
Q

what are the types of cysts in the liver

A

congenital
inherited (polycystic
acquired

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44
Q

what are a lot of early renal cancers

A

cystic/ partly cystic

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45
Q

what score predicts renal cancer

A

bosniak score (5= malignant)

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46
Q

what are the features of an acquired cyst

A

very common
associated with long term dialysis

simple cysts- attenuated lining
degenrate type of change
(benign)

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47
Q

what are the subtypes of polycystic kidneys

A

autosomal dominant and recessive PCKD

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48
Q

what are the features of ADPCKD

A

uncommon
mutation in nephrin
lots of cysts- kidney can be enlarged
secondary changes= haemorrhage, infarction, rupture,

can be bi or uni lateral

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49
Q

what are the cysts like in ADPCKD

A

lined by a simple epithelium

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50
Q

how does ADPCPKD present

A

presents as an adult as cysts take while to develop)
mass effect= feel it in flanks- pain, mass like lesion, haematuria (infraction/ rupture)

systemic disease:

  • liver cysts
  • cerebral aneurysms
  • sub arachnoid haemorrhage
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51
Q

what are the features of ARPCKD

A

several subtypes
all present before 20s
rarer than ADPCKD
kidney is normal size and has a smooth surface

systemic issues= liver cysts

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52
Q

what is the prognosis for ARPCKD

A

the younger you present the worse your prognosis

neonate subtype fatal

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53
Q

what is xanthogranulomatous pyelonephritis

A

infection that creates a mass (in kidneys)

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54
Q

what are the benign tumours of the kidney

A

oncocytoma

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55
Q

what are the malignant tumours of the kidney

A

chromophobe
clear cell
papillary
collecting duct

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56
Q

what is the paediatric renal tumour

A

wilms tumour

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57
Q

what are the features of oncocytoma

A

small, oval and well circumscribed
mahogany brown with a crentral stellate scar
very pink and granular cytoplasma

(benign)

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58
Q

what are the features of chromophobe tumours

A

v similar to oncocytomas- hard to differentiate

main difference is raisonoid nuclei and perinuclear haloes

(malignant)

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59
Q

what are the features of a papillary tumour

A

2nd most common renal malignancy
generally low grade
finger like projections
malignant

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60
Q

what are the features of a collecting duct carcinoma

A
least common 
c high grade
desmoplastic stroma 
poor survival 
(malignant)
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61
Q

what are the features of clear cell carcinomas

A

a.k.a renal cell carcinomas
common

macro- partly cystic, heterogenous surface, bright yellow

micro- clear cells

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62
Q

what are the RF for clear cell carcinomas

A

obesity +++

genetic influence

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63
Q

what are the presenting complaints of a clear cell carcinoma

A

haematuria, mass, hypertension (rarely)

64
Q

how do you stage clear cell cancer

A

size and invasion of other structures

65
Q

where does clear cell carcinoma commonly invade

A

renal vein, extend into vena cava (risk of thromboembolic disease), grow upwards towards the heart

66
Q

what gene is associates with most sporadic renal cancers

A

VHL (encodes for HIF- hypoxia inducible factor)

67
Q

what is the role of VHL anf HIF

A

Normally VHL ubiquitinates (adds ubiquin) HIF

In low O2 they dissociate and HIF acts as a transcription factor for VEGF, PDGFRB and EPO (erythropoietin)

68
Q

what cells line the bladder

A

transitional epithelium (stratified)

this covers all the way from the collecting system of the kidneys to parts of the urethra

69
Q

what cells are on the surface of the epithelium

A

umbrella cells

70
Q

what are common causes of cystitis

A

infection, aseptic, reactive to catheters

71
Q

what parasite commonly causes cystitis

A

schistosomaisis (haematobium)

swims up the urethra

72
Q

why is schistosomiasis infection so bad

A

bug not toxic but body cant get rid of it- leaves eggs
causes persistent inflammation
- squamous metaplasia- SCC

73
Q

how can catheters cause bladder cancer

A

persistent injury- scarring- squamous metaplasia- SCC

74
Q

what is aseptic cystitis

A

persistent symptoms of dysuria (and infection) with consistently negative cultures and urinalysis

75
Q

what causes aseptic cystitis

A

unknown- inflammation, congestion, mast cells so maybe hypersensitivity

76
Q

what is seen pathologically in aseptic cystitis

A

inflammation, congestion, mast cells

77
Q

what is cystitis cystica

A

infolding of the bladder mucosa into cysts (reactive phenomenon- shows inflammation)

(can get it in urethera and ureter aswell)

78
Q

what is a bladder diverticulae and what can it cause

A

pouch or sac protruding outwith the bladder wall (can be congenital or acquired)

causes stangant urine- infection, stones and cancer

79
Q

what happens to the bladder when there is chronic obstruction

A
become trabeculated (due to working hard) 
- hypertrophy and hyperplasia
80
Q

what does a urinary tract obstruction (stone, tumour ect) cause

A

back pressure:

  • collecting system dilates
  • renal parenchyma becomes atrophic
  • hydronephreisis
81
Q

when will a urinary tract obstruction affect both kidneys

A

when blockage is in the bladder or urethera

82
Q

who gets bladder cancer

A
relatively common 
middle age/ elderly 
no sex predilection 
smokers +++++++
beta napthyline (dye industry- regulated now)
83
Q

what cancer do you get in the bladder

A

transitional cell carcinoma (also adenocarcinoma and squamous)

84
Q

what are transitional cell carcinomas like

A

papillary (finger like projections)

can be carcinoma in situ (flat)

85
Q

what else is at risk in bladder cancer

A

common to get cancer in whole urinary system as all exposed to the same RF

86
Q

when do you get adenocarcinomas in the bladder

A

when there is a background of metaplasia

hard to differentiate from bowel cancer that has invaded through

87
Q

what is urachal adenocarcinoma

A

urachus= the remnant of alantosis (what bladders forms from) = from dome of bladder to the umbilicus
adenomas can arise here- confined to dome of bladder
need to resect to umbilicus

88
Q

why do you get squamous cell cancer in the bladder

A

persistent inflammation
squamous metaplasia
SCC

89
Q

what is the role of the prostate

A

prostatic fluid combines with fluid from seminal vesicles

some contractile function during ejaculation

90
Q

what is the histology of the prostate

A

bi layered acinar cells

91
Q

what is BPH

A

prostate enlarges due to hormonal effect from androgens, obstructs the flow of urine
(hyperplasia= more cells)

92
Q

what zone is affected in BPH

A

central and transitional (why you get transurethral resection as a treatment option)

93
Q

how common is prostate cancer

A

@ 50 30% of men
70 70%
90 90%

94
Q

is prostate cancer aggressive

A

no
most slow growing and low grade
even when diagnosed only followed up until gets worse

95
Q

is there a hormonal cause in prostate cancer

A

less of a link than BPH (so no probably)

96
Q

where do you get prostate cancer

A

in the peripheral zones

97
Q

what biopsy for prostate cancer

A

transrectal/ rectal core (as most in peripheral gland)

take 10/12 samples - 5/6 from each lobe

98
Q

what is PSA

A
glycoprotein enzyme (kallikrein 3) 
liquidifies semen in ejaculate, allows sperm to swim
99
Q

why is PSA not an effective marker of prostate cancer

A

as high grade prostate cancers dont produce PSA

can be increased by prostatits, PR exam, riding a bike, spironolactone or if you have a large prostate

100
Q

what is PSA useful for

A

monitoring treatment (decreases as prostate decreases in size)

101
Q

what score is used to grade prostate cancers

A

gleason grading system

lowest grade is 6, highest score is ten) (combination of score from both lobes/ beyond the prostate

102
Q

what is the corpus cavernosum

A

the erectile tissue of the penis - network of blood vessels

103
Q

what is the corpus spongiosum

A

part of penis that contains the urethra (doesnt expand as much during an erection)

104
Q

why are penile tumours highly associated with mets

A

as have access to lots of blood vessels

105
Q

what cells line the foreskin and glans

A

squamous cells (why can get skin diseases on penis)

106
Q

what is balanitis xerotic obliterans (BXO)

A

aka lichen sclerosis

inflammation of the glans penis

107
Q

who gets BXO

A

young (neonates, toddlers, primary school children) or elderly

108
Q

what are the common presentations of BXO

A

phimosis (unretractable foreskin), paraphimosis (can retract but not replace foreskin)
sore, inflamed and swollen glans/ foreskin
penile ulceration/ plaques
dysuria

109
Q

what is the histology of BXO

A

get lichen planus on skin
chronic inflammatory infiltrate
hyalinised scar tissue beneath infiltrate

110
Q

what virus causes penile papillomas

A

HPV infection

111
Q

which HPV causes genital warts

A

types 6 and 11

112
Q

what HPV is high risk

A

types 16 and 18

113
Q

what neoplasms do you get in the penis

A

PEin- penile intraspethial neoplasia (same is CIN)

can be differentiate or dedifferentiated

114
Q

what are the types of penile intraspethial neoplasia associated with

A
differentiated= non HPV, background of inflammation 
dedifferentiated= HPV related
115
Q

what is penile cancer associated with

A

chronic inflammation

HPV

116
Q

what is the functional unit of the testes

A

seminiferous tubules (site of sperm production)

117
Q

what stimulates sertoli cells

A

FSH

118
Q

what does FSH stimulation of sertoli cells cause

A

produce proteins which bond to testosterone and stimulate spermatogenesis (control the environment within the tubules)

119
Q

what are germ cells

A

primitive sperm

120
Q

what stimulates leydig cells

A

LH

121
Q

what do leydig cells do

A

convert DHEA to testosterone

122
Q

what is found in the seminferous tubules

A

germ cells, maturing spematozoa and sertoli cells

123
Q

what are the common causes of lumps in the testes

A

hernia
cystocoele
hydrocoele
spermatocoele

adenomatoid tumour
mesothelioma
liposarcoma

124
Q

what is a hydrocoele

A

accumulation of fluid around the testes between the tunica vaginalis and the mesothelial lining

125
Q

what does a hydrocoele look like

A

unicystic, smooth, fluid filled, well circumscribes, lucent- transilluminable

adjacent to the testes proper

126
Q

what is a spermatocoele

A

cystic change within the vas of the epididymis
unknown causes
usually asymptomatic

127
Q

what is seen in biopsy of spermatocoele

A

sperm

128
Q

what is a varicocoele

A

varicosities of venous plexus that drain the testes
usually asymptomatic
can feel like bag of worms

129
Q

what should you feel for in a testes exam

A

if the lump is in the testes or separate
whether in epididymis or separate
can you get above it- if not then likely to be hernia
solid/ unicystic
thin walled, hard, painful etc

130
Q

what is testicular torsion

A

emergency
testes and chord rotate around arterial blood supply
causes ischaemia and then cell death

131
Q

what is the presentation of torsion

A

extreme pain
no particular precipitant
common in neonates and adolescents
occurring as much in sleep as it does in sport

132
Q

what is a bell clapper deformity

A

when the insertion of the tunica vaginalis is high
the testes can rotate and even sit laterally (as not as well encased by TV)
more likely to get torsion

133
Q

who gets testicular neoplasms

A

20-50s

134
Q

what is the prognosis for testicular cancer

A

generally good
often found in early stages
even when advanced is responsive to chemo/ radio therapy

135
Q

what are the two main groups of testicular cancer

A

seminomatous and non semimatous (can get mixed of these in tumours)

136
Q

what do seminomas look like

A

potato

white consistent colour

137
Q

what is the most common type of testicular cancer

A

seminoma

138
Q

who gets seminoma

A

40 y/os

139
Q

what are the RFs for a seminoma

A

undescended testes - contralateral testes will also share risk

140
Q

what is the histology of a seminoma

A

inflammatory infilrates

arises from germ cells

141
Q

what is the prognosis for a seminoma

A

95% cure rate
v responsive to radiotherapy even when advances
usually localised

142
Q

what is a non seminomatous tumour like

A

less common than semi
affects younger age group 30s
far more aggressive than semi, can metastasise

143
Q

what is the histology of a non seminoamtous testicular neoplasm

A

cystic change and haemorrhage

144
Q

what is the prognosis for a non seminomatous testicular cancer

A

reasonable- very chemo sensitive

have to treat v early, can spread in days

145
Q

what are the four types of non seminomatous testicular tumours

A

mature teratoma (3 germ layer: endo, meso and ecto) (all classified as malignant)

yolk sac tumour

embryonal (aggressive, high grade, associated with mets)

trophoblastic (choriocarcinoma)

146
Q

what are the tumour markers for most non seminomatous tumours

A

LDH

147
Q

what is the tumour marker for a yolk sac tumour

A

alpha feto protein

148
Q

what is the tumour marker for a trophoblastic tumour (choriocarcinoma)

A

beta HCG (men with positive pregnancy tests)

149
Q

what is pyelonephritis

A

infection (bacterial) of the kidneys

150
Q

what predisposes to pyelonephritis

A
catheters
urinary retention
developmental abnormalities (e.g. horseshoe kidney)
women (short urethera)
renal parenchyma
151
Q

what organisms usually cause UTIs

A

gut organisms- coliforms (e. coli)

152
Q

what vasculitis can cause glomerulonephritis

A

GPA

HSP

153
Q

what is the most common renal tumour in children

A

nephroblastoma

154
Q

what does clear cell carcinoma arise from

A

nephron

155
Q

what staging score system for prostate cancer

A

gleeson

156
Q

where does prostate cancer metastasise to

A

bones

157
Q

what is a germ cell tumour

A

the other name for non seminoma testicular cancers