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Pathology Flashcards

1
Q

What name is given to an infective cause of nephritis?

A

Pyelonephritis

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2
Q

What name is given to a non-infective nephritis?

A

Glomerulonephritis

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3
Q

What structure is most important at holding the glomerulus together?

A

Mesangial Cells

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4
Q

What other name is given to the podocytes which surround the glomerulus?

A

Visceral epithelium

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5
Q

Why does immune related inflammation occur in the glomerulus?

A
  • immune response is directed at something in the glomerulus

- circulating complexes get stuck in the sieve

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6
Q

Immune reactions in what neighbouring structures can have glomerulonephritic effect?

A

Vasculitis in the afferent/efferent arteriole

NOTE - not in glomerulus itself

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7
Q

Give an example of an immune condition which attacks the glomerulus directly?

A

Good pasture’s syndrome

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8
Q

What is goodpastures syndrome?

A

IgG antibodies against a subunit of Collagen 4

This type of collagen is found in the glomerular basement membrane

=> attacks the glomerular basement membrane found in kidneys (and also lungs)

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9
Q

What can cause circulating immune complexes to deposit in the kidney?

A

Infection (Hepatitis, Group A Strep, HIV)
Drugs (Gold, Pencillamine)
Cancer (immune response mounted to “foreign” cancer cells)

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10
Q

What types of vasculitis are most likely to cause glomerulonephritis?

A

Granulomatosis with Polyangiitis (GPA) - cANCA

Microscopic polyangiitis – pANCA

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11
Q

What is the difference between c-ANCA and p-ANCA?

A

c-ANCA = cytoplasmic anti-neutrophil cytosplasmic antibody

p-ANCA = perinuclear anti-neutorphil cytoplasmic antibody

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12
Q

What are the main differences between Nephritic and Nephrotic syndrome?

A

Nephritic – haematuria, hypertension

Nephrotic – heavy proteinuria, oedema, hyperlipideamia

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13
Q

All causes of glomerulonephritis will cause wither a nephrotic or nephritic syndrome. TRUE/FALSE?

A

TRUE

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14
Q

What investigations can be used to classify glomerulonephritis?

A

Light microscopy
Electron microscopy (black and white)
Immunoflouresence

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15
Q

Crescents on light microscopy represent a good prognosis. TRUE/FALSE?

A

FALSE

Indicate rapidly progressive disease which could result in renal failure

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16
Q

What would be seen on Light microscopy in GPA causing glomerulonephritis?

A

Granulomas

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17
Q

Electron microscopy uses a high magnification to look for deposits in the basement membrane. Where are these usually found?

A

Subepithelial
Mesangial
Subendothelial

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18
Q

Why is immunofluorescence particularly useful in diagnosis goodpastures syndrome?

A

Can easily visualise the linear IgG deposition along the basement membrane

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19
Q

Who develops minimal change syndrome?

A

Kids

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20
Q

Does minimal change syndrome cause nephritic or nephrotic syndrome?

A

Nephrotic

children present with very puffy, oedematous faces

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21
Q

Is the prognosis for Minimal change good or bad?

A

Good (due to MINIMAL change)

Resolves after steriods

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22
Q

What is FSGS?

A

Focal Segmental GlomeruloSclerosis

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23
Q

Who gets FSGS?

A

Adults

Risks:

  • obesity
  • HIV
  • sickle cell
  • IVDUs
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24
Q

Describe what FSGS means?

A

Focal => not all glomeruli affected

Segmental => of the glomeruli affected, not ALL of one glomerulus is affected

Sclerosis => stiffening

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25
Q

What can cause membranous glomerulonephritis?

A 
– Infection (hepatitis, malaria, syphilis)
– Drugs  (NSAID, gold, penicillamine)
– Malignancy (lung, colon,melanoma)
– Lupus 
– Autoimmune thyroiditis
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26
Q

Lupus can cause any type of glomerulonephritis. TRUE/FALSE?

A

TRUE

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27
Q

What age group usually develop membranous glomerulonephritis?

A

Adults

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28
Q

Do patients with membranous glomerulonephritis eventually develop nephrotic or nephritic syndrome?

A

Nephrotic

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29
Q

How does membranous glomerulonephritis appear under the microscope?

A 
thick membranes (spiky)
Sub-epithelial immune deposits
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30
Q

What is the prognosis of membranous glomerulonephritis like?

A
  • variable
  • Disease has slow progression
  • <40% eventually develop renal failure
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31
Q

What type of stain is used to diagnose membranous glomerulonephritis?

A

Silver stain
Spiky membrane
White/negative space indicates immune deposits in the basement membrane

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32
Q

What can predispose to IgA glomerulonephritis ?

A

genetic

acquired defect – coeliac

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33
Q

What group of patients develop an IgA glomerulonephritis?

A

Post infection

- usually Group A strep. throat

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34
Q

Does IgA glomerulonephritis usually cause a nephrotic or nephritic syndrome?

A

Nephritic

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35
Q

How does IgA glomerulonephritis look under the microscope?

A

IgA deposition in mesangium

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36
Q

Prognosis of IgA glomerulonephritis varies. TRUE/FALSE?

A

TRUE

varies depending on severity

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37
Q

What usually causes Membranoproliferative glomerulonephritis?

A

idiopathic

OR if Type 2 => infection, lupus, malignancy

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38
Q

Usually only adults develop membranoproliferative glomerulonephritis. TRUE/FALSE?

A

FALSE

both adults AND kids develop this

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39
Q

In membranoproliferative glomerulonephritis, do you develop nephrotic or nephritic syndrome?

A

can develop EITHER!

one or the other

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40
Q

How does membranoprliferative glomerulonephritis look under the microscope?

A

Large lobulated glomeruli

thick DUPLICATED membranes => tram tracks

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41
Q

Diabetes can predispose to what disease processes in the kidney?

A

Diffuse and Nodular Glomerulosclerosis
Nodules – Kimmel Stiel Wilson Lesion

Microvascular disease – arterial sclerosis

Infection – pyelonephritis, papillary necrosis

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42
Q

Why are the differentials for cystic kidney diseases difficult?

A

early cancers are cystic or partly cystic

=> more difficult to identify cancer EARLY

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43
Q

What score can be used by radiology to predict the probability of a cyst being cancerous?

A

Bosniak score

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44
Q

Acquired cysts are so common that they are often seen on autopsy. TRUE/FALSE?

A

TRUE

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45
Q

What long term treatment can predispose to acquired renal cysts?

A

Long term dialysis

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46
Q

What are the two main subtypes of Polycystic Kidney Disease?

A

Autosomal Dominant

Autosomal Recessive

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47
Q

When does Autosomal Dominant Polycystic Kidney Disease usually present?

A

Adulthood as cysts take a while to develop

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48
Q

What complications can occur in Autosomal dominant polycystic kidney disease?

A

Kidneys can become HUGE
Cysts can rupture (due to simple epithelium lining)
Cyst can infarct or haemorrhage also

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49
Q

What is the normal presenting complaint in Autosomal dominant polycystic kidney disease?

A

Mass like lesion (due to growth of kidney)

Pain/haematuria - due to rupture, infarction of cyst

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50
Q

What other parts of the body can become affected in autosomal dominant polycystic kidney disease?

A

liver cysts and cerebral aneursyms

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51
Q

Who usually presents with Autosomal Recessive Polycystic Kidney Disease?

A

Children

younger presentation = worse prognosis

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52
Q

What is difference about the appearance of the kindey in Autosomal Recessive Polycystic Kidney Disease?

A

Kidney is of normal size and has a smooth surface

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53
Q

What disease process is known to create a mass specifically associated with infection?

A

Xanthogranulomatous pyelonephritis

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54
Q

Name a benign renal tumour

A

Oncocytoma

55
Q

Name 4 types of malignant renal tumour.

A

Chromophobe
Papillary
Collecting duct Carcinoma
Clear cell carcinoma

56
Q

Name a type of renal tumour which specifically presents in children

A

Paediatric tumour – Wilm’s tumour

57
Q

Describe the macroscopic appearance of an oncocytoma

A

Small, oval and well circumscribed

Mahogany brown with a central scar

58
Q

Deescribe the microscopic appearance of an oncocytoma

A

Full of Oncocytes – big pink cells

Fluffy cytoplasm - full of mitochondria

59
Q

What malignant renal tumour looks similar to oncocytoma on histology?

A

CHromophobe

60
Q

Describe the histological appearance of a chromophobe which causes it to differ from a Oncocytoma?

A

Oncocytic

  • raisonoid nuclei
  • perinuclear haloes (white around the nuclei)
61
Q

Papillary renal tumours are typically high grade. TRUE/FALSE?

A

FALSE
Low grade (1/2)
Low potential for metastases

62
Q

Describe the microscopic appearance of a Collecting Duct carcinoma and state whether it is High or Low grade.

A

desmoplastic stroma (new growth of dense CT and unstable blood vessels)

High grade

63
Q

What cancer do people usually mean when they refer to a “Renal Cell Cancer”?

A

Clear cell carcinoma

64
Q

What risk factors can predispose someone to clear cell carcinoma?

A

obesity

genetics

65
Q

What is the most common presenting complaint in clear cell carcinoma?

A

haematuria
noticeable mass
hypertension (RARE)

66
Q

Describe the macroscopic appearance of a clear cell carcinoma?

A
  • partly cystic

- bright yellow tumour surface

67
Q

How does a clear cell carcinoma appear microscopically and why is this?

A

Cells look “clear”

Due to hypoxia in the process of visualisation under the microscope

68
Q

Where can clear cell carcinoma invade into?

A

Renal vein

Can track up IVC to heart

69
Q

What gene is important for many sporadic renal cancers?

A

VHL - Von Hippel Lindau

70
Q

How is VHL involved in the development of renal cancers?

A
  • VHL codes for HIF - hypoxia inducible factor
  • Usually VHL modifies the proteins on HIF

However, in low O2, they dissociate and HIF acts as a transcription factor for VEGF, EPO etc
=> causing cancers to grow

71
Q

What links the citric acid cycle to renal cancers?

A

A mutation in any part of the citric acid cycle can predispose to the development of a renal cancer

72
Q

What features can be seen in Von Hippel Lindau SYNDROME?

A
  • Renal Cell Carcinoma (KIDNEY)
  • Cerebellar haemangioblastoma (BRAIN)
  • Pancreatic serous cystadenoma (PANCREAS)
  • Tumours of endolymphatic sac (EAR)
  • Epididymal serous cystadenomas (TESTES)
73
Q

What structures are covered by urothelium?

A

bladder
ureters
collecting system in the kidney
urethra

74
Q

Cystitis is rarely biopsied. TRUE/FALSE?

A

TRUE

75
Q

What parasite is known to cause cystitis?

A

Schistosomiasis

most likely schistosomiasis haematobium

76
Q

What causes the inflammation in schistosomiasis cystitis?

A

the body’s immune response to the parasite

NOT the parasite itself (it does not release any toxins)

77
Q

What can be left behind after chistosomiasis is cleared?

A

Eggs (which calcify)

these can then cause a persistent immune response

78
Q

What can the inflammation in schistosomiasis cause?

A 
Squamous metaplasia
(changes from transitional to squamous epithelium to help deal with the inflammation)
79
Q

Squamous metaplasia can eventually develop into what?

A

Squamous cell carcinomas

80
Q

What is the main iatrogenic cause of persistant inflammation, leading to squamous metaplasia?

A

Indwelling catheters

81
Q

Why is it a problem if patients with inflammation in their bladder are paraplegic?

A

They cant feel the symptoms of inflammation
=> wont present to their doctor
=> more likely to present with SCC

82
Q

What is aseptic/interstitial cystitis?

A
  • Persistent dysuria symptoms
  • Persistently negative cultures and urinalysis
  • thought to maybe be a hypersensitivity reaction
83
Q

What can be seen on aseptic/interstitial cystitis pathology?

A

Variable pathology

sometimes mast cells = visible

84
Q

What is meant by cystitis cystica?

A

Infolding of bladder mucosa into cysts

85
Q

What is the risk with Diverticulae in the bladder?

A

stagnant urine sits in the out-pouching:
infection
stones
cancer

86
Q

What changes can occur in the bladder post-obstruction?

A

Bladder muscle works hard and becomes trabeculated
hyperplasia and hypertrophy occurs
Eventual persistent back pressure

87
Q

What is the last point affected by back pressure of urine?

A

Collecting system dilates
Renal parenchyma becomes atrophic

=> This is Hydronephrosis

88
Q

What is the main cause of transitional cell cancer?

A

smoking

due to carcinogens/ waste sitting in the bladder

89
Q

What previous industry predisposed to transitional cell cancer?

A

Beta-naphthyline – dye industry

90
Q

What are the main types of transitional cell cancer which are seen in the urinary tract

A

Papillary – finger like projections

Carcinoma In Situ – flat

91
Q

When can adenocarcinoma occur in the bladder?

A
  • After glandular metaplasia
  • colon cancer that has invaded through
  • Urachal Adenocarcinoma (from embryonic remnant)
92
Q

What are the main functions of the prostate?

A
  • prostatic fluid
  • add fluid from seminal vesicles
  • contractile function during ejaculation
93
Q

What is hyperplasia and what is the stimulus for this in the prostate?

A

Increase in cell number in response to a stimulus

Stimulus = androgens

94
Q

How is BPH treated and why?

A

transurethral resection (shaving away part of the prostate from the centre of the prostatic urethra)

  • have to get to the centre of the prostate to reach the transitional zone which enlarges in BPH
95
Q

Some prostatic cancers grow so slowly that they are not given any treatment. TRUE/FALSE?

A

TRUE

only follow up

96
Q

What is PSA?

A

Prostate Specific Antigen

- Glycoprotein enzyme

97
Q

Some very nasty cancers dont produce PSA. TRUE/FALSE?

A

TRUE

98
Q

Give an example of a drug which can increase PSA level?

A

spironolactone

99
Q

Why is the urethra located in the corpus spongiosum and not the corpus cavernosum?

A

So that it is not constricted in the erectile tissue and is patent for sperm to pass through at ejaculation

100
Q

What parts of penile tissue are covered by squamous epithelium?

A

Glans
Foreskin
Distal urethra

101
Q

Who usually gets Balanitis Xerotic Obliterans?

A

Young males

even neonates, toddlers

102
Q

What is the difference between Phimosis and paraphimosis?

A

phimosis - cant retract foreskin

paraphimosis - can retract foreskin but cant restore it to normal position

103
Q

What is often the cause of penile papillomas?

A

HPV infection

104
Q

What strains of HPV can cause genital warts?

A

HPV 6 and 11

105
Q

What strains of HPV are particularly high risk?

A

HPV 16 and 18

106
Q

What is penile intra-epthelial neoplasia?

A

dysplastic process related to cervical intra-ep. neoplasia

Can eventually form cancer

107
Q

What are the two types of penile intra-epithelial neoplasia?

A

Differentiated – non HPV

Dedifferentiated – HPV related

108
Q

Penile cancer is relatively uncommon. TRUE/FALSE?

A

TRUE

Mainly HPV related

109
Q

Describe the appearance of seminiferous tubules on histology?

A

Primitive sperm generation from germ cells at edge
sertoli cells maturing sperm
Mature sperm in middle
Pink fluffy cells round outside = leydig cells

110
Q

What hormones influence sertoli and leydig cells?

A

Sertoli FSH

Leydig LH

111
Q

What is the role of leydig cells?

A

convert testosterone to DHEA (more active)

112
Q

What is a hydrocoele?

A

fluid around the testes

Between the two layers of the tunica vaginalis

113
Q

How do hydrocoeles appear?

A 
Unicystic, smooth and fluid filled
can transilluminate (shine light through them)
114
Q

What is a spermatocoele and when is it ususally found?

A

Cystic change within the vas of the epididymis

Pts feel a fullness on self-examination

115
Q

What can be seen on histology of a spermatocoele?

A

Sperm and some macrophages

116
Q

What is a varicocoele?

A

Varicosities of venous plexus that drains the testis

117
Q

How do patients describe a varicoele as feeling on self-examination?

A

like a “bag of worms”

118
Q

If you feel a testicular lump but you cannot palpate above it, it has likely descended from the abdomen. What is it likely to be?

A

Hernia

119
Q

What is testicular torsion?

A

Testis and cord rotate around arterial supply

=> ischaemia

120
Q

After what point in testicular torsion is the testis thought to no longer be viable?

A

> 6hrs

121
Q

What is the prognosis like for testicular cancer?

A

good prognosis – even at advanced stage

Very responsive to chemo

122
Q

How does a seminoma appear macroscopically?

A

looks like a potato

123
Q

At what age do patients normally develop a seminoma?

A

40 (older than others)

124
Q

What it the main risk factor for seminoma?

A

undescended testes

/ orchidopexy

125
Q

Seminomas respond to radiotherapy even if they are advanced. TRUE/FALSE?

A

TRUE

126
Q

Non seminomatous tumours rarely exist as “pure” tumours, they are often mixed with seminomas or other types. TRUE/FALSE?

A

TRUE

127
Q

Who is at risk of developing non-seminomatous tumours?

A

<30

128
Q

Are non-seminomatous tumours usually more advanced than seminomas?

A

Yes = more aggressive and can metastasize

BUT outcome is reasonable – very chemosensitive

129
Q

What is needed for a diagnosis of Mature teratoma?

A

three germ layers present on histology

Ecto, endo and mesoderm

130
Q

Where else can teratomas occur?

A

OVARIES (except they are usually benign there)

131
Q

What tumour marker is produced by yolk sac tumours?

A

alpha feto protein

132
Q

What tumour marker is secreted by trophoblasts/choriocarcinomas?

A 
beta HCG (human chorionic gonadotrophin)
positive pregnancy test
133
Q

What is the most aggresive form of non-seminomatous tumour?

A

Embryonal – high grade with freq mets

RENAL (24 decks)

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