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Julija's Path > Histopathology ✔ > Flashcards

Histopathology ✔ Flashcards

1
Q

what is the blood supply of the liver?

A

portal vein & hepatic artery (dual)

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2
Q

what are the 6 types of cells in the liver?

A 
hepatocytes
bile ducts
Kupffer cells (immune) 
stellate cells
blood vessels/cells
endothelial cells
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3
Q

what is the maturity process of liver cells?

A

born in ‘zone 1’ and die in ‘zone 3’ so most metabolic enzymes near zone 3. Most active metabolites in zone 3 (think acetaldehyde from alcohol, paracetamol-induced disease). Zone 3 is nearest to vein. Zone 1 - arteries.

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4
Q

what is the ‘limiting plate’ in the liver?

A

site of much pathology, a line on the slides between the portal triad & the hepatocytes outside it

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5
Q

what is unique about the endothelial cells on the hepatic sinusoid?

A

not attached to any BM, not attached to each other meaning that blood can easily pass between endothelial cells and the hepatocytes

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6
Q

what is the space of Disse in the liver?

A

the site of the stellate cells in the liver. lie between the hepatic sinusoid endothelial cells and the hepatocytes

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7
Q

what is the cellular difference between normal and diseased liver with regards to Stellate cells?

A

stellate cells in Space of Disse activate - flatten out. the endothelial cells join up - losing the gaps that allow blood to travel between. the stellate cells also begin to deposit collagen which leads to formation of a scar matrix. the fenestrae are lost and the microvilli of hepatocytes are lost so diffusion cannot occur as normally.

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8
Q

what is the cellular definition of liver cirrhosis ? (4 parts)

A

1) whole liver involved
2) fibrosis
3) nodules of regenerating hepatocytes
4) distortion of liver vascular architecture (intra/extra hepatic shunting of blood)

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9
Q

what are 2 main causes of fatty liver disease?

A

alcohol, insulin resistance

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10
Q

what type of cirrhosis does alcohol cause?

A

fatty liver disease, micronodular

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11
Q

what are the 3 main complications of cirrhosis?

A

1) portal hypertension (loss of blood flow shunts)
2) hepatic encephalopathy (blood not cleared)
3) HCC

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12
Q

T or F: cirrhosis is reversible

A

T. It may be reversible (as of a decade ago) with aggressive treatment of the underlying cause

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13
Q

What are the two main causes of acute hepatitis?

A

1) viruses (Hep A-E)

2) drugs (antibotics esp)

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14
Q

what is the presence of acute hepatitis on histopathology?

A

spotty necrosis

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15
Q

what are 3 main causes of chronic hepatitis?

A

1) viruses (Hep B,C,D)
2) drugs (eg isoniazide)
3) autoimmune

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16
Q

how do we classify chronic liver disease?

A

severity of inflammation - grade

severity of fibrosis - stage

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17
Q

describe histopath of portal inflammation:

A

no inflammation crosses the limiting plate

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18
Q

describe histopath of interface hepatitis: (inflammation induced apoptosis)

A

‘piecemeal necrosis’

inflammation across the interface (portal triad and hepatocytes)

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19
Q

how does intrahepatic shunting look on a cirrhotic liver?

A

‘bridging fibrosis’

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20
Q

what are the 3 types of alcoholic liver disease?

A

1) fatty liver
2) alcoholic hepatitis
3) cirrhosis

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21
Q

what does fatty liver look like re: histopath?

A

1) pale, enlarged

2) microscopically - each cell is full of fatty changes (large droplet fatty change)

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22
Q

in viral hepatitis what is the key inflamed cell?

A

the lymphocytes

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23
Q

in fatty liver, what is the key inflamed cell?

A

neutrophil polymorph

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24
Q

what is seen in alcoholic hepatitis histologically?

A

Mallory Denk bodies/Mallory hyaline (pink colored)
inflammation
fibrosis around individual hepatocytes (esp in zone 3)

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25
Q

what is the histological view of alcoholic cirrhosis?

A

fatty, pale, nodules small (micronodular)

microscopically - nodular hepatocytes, fibrosis, some fat

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26
Q

what is the cause of NAFLD (non-alcoholic fatty liver) including NASH?

A

histologically - alcoholic liver disease

cause - raised BMI, insulin resistance, diabetes

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27
Q

what is histologically PBC (primary biliary cirrhosis)?

A

bile duct loss associated with chonic inflammation (with granulomas) due to anti-mitochondrial antibodies

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28
Q

what is the cellular cause of PSC (primary sclerosing cholangitis)?

A

periductal bile duct fibrosis leading to loss. Strongly associated with ulcerative colitis, increased risk of cholangiocarcinoma. Diagnosis via ERCP

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29
Q

what is the cellular cause of hemochromatosis:

A

gene on chromosome 6 (HFE gene) leading to increased gut iron absorption leading to secondary iron deposition parenchymal damage to organs.

(‘bronzed diabetes’)
histo - parenchymal iron; ‘full of iron’
Prussian blue = iron stain
chocolate brown liver (macro)

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30
Q

cellular cause of hemosiderosis

A

iron deposition in macrophages - hemosiderosis from blood transfusions. Does not produce scarring or cirrhosis.

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31
Q

cellular cause of Wilson’s disease

A

genes on chromosome 13 leading to excess of copper in the body from failure of excretion by hepatocytes so it accumulates in the liver & CNS (hepato-lenticular degeneration)

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32
Q

cellular cause of autoimmune hepatitis:

A

interface hepatitis with plasma cells due to anti-smooth muscle actin antibodies. Responds to steroids.

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33
Q

cellular cause of alpha one antitrypsin deficiency:

A

blood deficiency, not liver. Liver has excess of alpha one antitrypsin - cannot be secreted from hepatocytes so it stays there and damages them in the RER of cells. Leads to intra-cytoplasmic inclusion bodies and then further to hepatitis/cirrhosis

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34
Q

paracetamol -liver damaged, histologically

A

it is the cells in zone 3 that are heavily damaged. those right by the arteries tend to survive well. Worse with alcohol because alcohol is liver enzyme-inducer

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35
Q

causes of liver granulomas: (4)

A

PBC, drugs, TB, sarcoidosis

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36
Q

3 types of liver tumors that are benign:

A

liver cell (hepatocytes) adenoma, bile duct (cholangi cells) adenoma, hemangioma (endothelial cells)

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37
Q

malignant liver tumors can be primary or secondary. what are the 4 types of malignant primary liver tumors?

A

hepatocellular carcinoma/HCC
hepatoblastoma
cholangiocarcinoma
hemangiosarcoma

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38
Q

which is the commonest carcinoma in the liver?

A

metastatic adenocarcinoma

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39
Q

which of these is not associated with fatty changes in the liver?

a) diabetes
b) hep B
c) hep C
d) alcohol

A

Hep B

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40
Q

which of these is not associated with genetic hemochromatosis?

a) cirrhosis
b) diabetes
c) Kaiser-Fleischer rings
d) myocardial damage

A

c) Kaiser-Fleischer rings

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41
Q

what are the 6 skin reaction patterns?

A 
vesiculobullous
spongiotic
psoriasiform
lichenoid
vasculitic
granulomatous
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42
Q

histological view of pemphogoid bullae reaction skin

A

IgG and C3 are destroying the ‘bottom layer of foundation of the house’ so basement membrane destroyed, elastase produced, epidermis is raised. This present as sub-epidermal bullae. Agitation of IgG and C3 along basement membrane in a linear fashion of band on immunofluorescence

sub-epidermal split

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43
Q

histological view of pemphigus vulgaris

A

IgG reacting against the keratinocytes so that the split occurs mid-epidermal

‘cement has been destroyed, foundation is secure, but the bricks of the house are free-floating’

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44
Q

histological view of pemphigus folicaeous

A

the ‘roof’ has fallen off so that the keratinocytes are intact but the rest have fallen off
–> epidermis split

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45
Q

Discoid eczema or contact dermatitis are examples of spongiotic skin reaction. What is the histological facts of it?

A

-atopy
- epidermis falling apart
(‘cement of house is soggy)
-whiteness around keratinocytes because fluid has stretched them apart but not pulled them apart
-eosinophils within infiltrate in underlying dermis

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46
Q

Psoriasis on the extensor surfaces, is an example of a t-cell mediated reaction process, a psoriasiform

A
  • perikeratosis on the top layer of the dermis
  • very rapid turnover leading to loss of granular cell layer at the top
  • epidermis looks thicker
  • neutrophils in the super-epidermal layer instead of eiosinphils
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47
Q

histological parts of a lichenoid reaction pattern (think of lichen planus)

A
  • white striae within buccal areas (wickham’s striae)
  • destroying bottom layer/basement membrane
  • can’t see the difference between dermis and epidermis
  • lymphocytes spread throughout because attacking the skin
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48
Q

licen planus is an example of which type of inflammatory reaction pattern?

A

lichenoid

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49
Q

where in the epidermis does the bullae in pemphigus vulgaris occur?

A

mid-epidermal

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50
Q

histological view of seborrheic keratosis

A

proliferation of basal keratinocytes

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51
Q

histological view of sebaceous cyst

A

occlusion cyst
cyst lined with epithelium same as epidermis
hair or sebaceous material going through cyst

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52
Q

histological view of BCC

A

Histologically, BCC is characterized by clusters of darkly staining basaloid cells with a palisade arrangement of nuclei at the periphery of the clusters. The stroma adjacent to the tumor epithelium has a characteristic blue “myxoid” appearance, and clefts often separate the nests of basaloid cells from the surrounding dermal stroma. Don’t kill people because they don’t metastasize.

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53
Q

histological view of Bowen’s disease

A

atypical mitotic figures, atypical keratinocytes

dysplasia

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54
Q

histological view of SCC

A

will progress to LNs and metastasize.

islands invaded into the dermis from the squamous epithelium

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55
Q

histological view of naevus (moles)

A

classified based on where the melanocytes nests in the dermis -
junctional naevus: within epidermis
compound naevus: within epidermis & dermis
intradermal naevus: within dermis

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56
Q

histological view of malignant melanoma:

A

Histologically, melanomas are asymmetrical and poorly circumscribed lesions with architectural disturbance and usually marked cytological atypia. Specific features include consumption of the epidermis, pagetoid spread of melanocytes, nests of melanocytes with variable size and shape (which may be confluent and lack maturation), melanocytes within lymphovascular spaces, deep and atypical mitoses and increased apoptosis. Mitotic figures are common.

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57
Q

which common skin cancer does not metastasize?

A

BCC

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58
Q

how do mesangial cells work in the kidneys?

A

stop bits of capillary wall to stop any leakage - connects the cells to the meansgium (like mesentery of the kidney)

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59
Q

Cywhat are the components of the kidney filtration barrier?

A

1) endothelial cells - fenestrated
2) BM - primarily type 4 collagen
3) podocyte - with foot processes on the outside of BM

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60
Q

what is the podocyte responsible for in the kidney?

A

selective filtration at the kidney filtration barrier

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61
Q

which 2 cellular processes can cause glomerular disease?

A

failure to filter an adequate amount of blood or leaky barriers that fail to maintain adequate barrier function

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62
Q

what cellular process causes immune-mediated glomerulonephritis?

A

immune complexes forming and causing damage to the glomeruli, or even cause leakages in the glomerular barriers. May be auto-antigens (eg SLE) or derived from infectious organisms. They may also be slow or quick onset.

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63
Q

what is the cellular process of PCKD?

A

AD inheritance of PKD1 or PKD2 genes. CKD usually onsets by 40 -50 years. Cysts arise from all portions of the kidneys & can also be seen in liver and cause aneurysms

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64
Q

what is the cellular process leading to AKI?

A

a rapid loss of glomerular filtration and tubular function leading to rapid imbalance of electrolytes and reduced GFR. acidosis, hyperkalemia, fluid overload w/hypertension, increased creatinine & urea

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65
Q

how do we classify renal failure?

A

pre-renal, renal, post-renal

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66
Q

what is the cellular process of ATN (acute tubular necrosis)?

A

commonest cause of acute renal failure from damage to tubular epithelial cells by toxins or ischemia.

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67
Q

histologically what is seen in acute tubular injury?

A
  • flattened epithelium

- granular casts throughout

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68
Q

why does acute tubular injury cause failure of glomerular filtration?

A

blockage of tubules by cast
leakage of fluid from tubules to interstitium (reduced flow)
secondary hemodynamic changes

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69
Q

what is the cellular process of acute glomerulonephritis?

A

acute inflammation of glomeruli leading to reduction in GFR; see red/white blood cell casts in the urine with oliguria. Almost always associated with glomerular crescent - accumulation of inflammatory cells within Bowman’s space from breaks in the glomerular BM. Silver stain will stain BM

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70
Q

what are 3 causes of crescentic glomerulonephritis?

A

1) pauci -immune (ANCA antibodies)
2) anti-GBM disease
3) immune complex (SLE, IgA nephropathy)

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71
Q

what is the cellular process of anti-GBM disease?

A

antibodies against glomerular BM, esp the type 4 collagen. Characterized by IHC showing linear deposition of IgG on GBM. Antibodies may also bind to alveolar basement membrane and may cause a lung hemorrhage.

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72
Q

what is Goodpasture’s syndrome?

A

lung hemorrhage & crescentic glomerulonephritis

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73
Q

histopath of anti-GBM disease?

A

Characterized by IHC showing linear deposition of IgG on GBM

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74
Q

cellular process of pauci immune glomerulonephritis?

A

inflammation of blood vessels elsewhere often too - vasculitic rash or lung hemorrhages

ANCA antibodies. most common crescentic glomerulonephritis.

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75
Q

histopath of pauci immune?

A

large destructive crescentic damage that spreads beyond Bowman’s capsule into the interstitium

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76
Q

what is thrombotic microangiopathy?

A

platelet thrombi within glomeruli, arterioles, or arteries leading to thrombi. Usually develop MAHA/HUS. RBC have been damaged by fibrin.

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77
Q

blood film in thrombotic microangiopathy?

A

RBC shows shistocytes (those damaged by the fibrin) , anemia

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78
Q

histopath of amyloidosis?

A

pink in an H&E stain; depositions of extracellular proteinaceous material. Stains Congo-Red, looks green under polarized light.

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79
Q

Stains Congo-Red, looks green under polarized light. What’s the diagnosis?

A

amyloidosis

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80
Q

two main proteins in amyloidosis in the kidney?

A

SAA (serum amyloid associated protein) and AL (amyloid light chain protein)

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81
Q

what is the main cell involved in primary kidney glomerular disease?

A

podocytes -

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82
Q

in what kidney disease do glomeruli look normal other than effacement of the foot processes in the podocytes?

A

minimal change kidney disease; most common children’s nephrotic syndrome

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83
Q

what is the cellular change in minimal change kidney disease?

A

glomeruli look normal other than effacement of the foot processes in the podocytes

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84
Q

what is the cellular change in focal/segemental glomerulosclerosis?

A

similar to minimal change kidney disease BUT glomeruli develop segmental scars

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85
Q

cellular changes of membranous glomerulonephritis?

A

immune deposits on outside of BM; no inflammatory changes. many associated with phospholipid A2 receptor antibodies if primary.

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86
Q

what are the causes of membranous glomerulonephritis?

A

autoantibody to phospholipid A2 receptor (primary)

SLE, infection, drugs, malignancy (secondary)

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87
Q

what is the cause of isolated microscopic hematuria?

A

thin basement membranes hereditary defect in type 4 collagen, IgA nephropathy.

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88
Q

histopath difference in microscopic hematuria:

A

IgA nephropathy or hereditary defect in type 4 collagen leading to thin basement membranes

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89
Q

commonest cause of glomerular nephritis worldwide?

A

igA nephropathy

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90
Q

what is the cellular difference in igA nephropathy?

A

igA deposits in glomeruli

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91
Q

what cell forms the outer layer of the glomerular filtration barrier?

A

podocytes

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92
Q

what percentage of end stage renal disease is due to autosomal dominant PCKD?

A

10%

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93
Q

what type of amyloid is formed in patients with multiple myeloma?

A

AL

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94
Q

what’s the commonest cause of nephrotic syndrome in children?

A

minimal change disease

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95
Q

antibodies to phospholipid A2 receptor are associated with what form of glomerulonephritis?

A

primary membranous

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96
Q

what are the 3 layers of the gut?

A

muscularis propria, submucosa, epithelium (squamous in esophagus, columnar elsewhere)

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97
Q

what is the main inflammatory cell involved in acute oesophagitis?

A

the neutrophil polymorph

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98
Q

what histopath changes are seen in GORD/GERD?

A

commonest cause of acute oesophagitis.
see necrotic slough, inflammatory exudate, granulation tissue and later on, fibrosis. This is the commonest cause of oesophagitis.

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99
Q

the difference between an acute & chronic ulcer?

A

the presence of fibrosis & scarring at the base of the chronic ulcer

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100
Q

what are the cellular changes in Barett’s esophagus?

A

re-epithelization by metaplastic columnar epithelium usually with goblet cells (intestinal type epithelium)

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101
Q

what are the histological changes in esophageal cancer?

A

squamous epithelium, underneath is glandular neoplasm. Glands full of mucus. Adenocarcinoma is the commonest cause of esophageal cancer in england

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102
Q

where do adeno & SCC of the esophagus tend to be?

A

SCC- tends to be higher up in esophagus; assoc with alcohol and smoking
adenocarcinoma - tends to be lower down in the esophagus. related to GERD.

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103
Q

histopath differences in SCC esophageal cancer?

A

have fibrin bridges & make keratin

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104
Q

cellular insult causes of chronic gastritis:

A

A - autoimmune (MALT)
B - bacteria (H Pylori)
C - chemicals (NSAIDs, bile)

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105
Q

when do you find lymphoid follicles in the stomach?

A

only if patient has had H Pylori infection

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106
Q

what does H Pylori infection cause?

A

chronic gastritis/ulcer
CLO - intestinal dysplasia
adenocarcinoma
lymphoma in stomach (MALT tissues)

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107
Q

how does one get H Pylori infection and what is the process in the body?

A

8x increased risk of gastric cancers once infected. Infection is via cag-A + H Pylori to inject toxins into intercellular junctions for bacteria to attach more easily. This leads to chronic inflammation. Treat with antibiotics and get rid of increased cancer risk

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108
Q

when do you see goblet cells in the stomach?

A

only with chronic inflammation or dysplasia.

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109
Q

what is the most common type of malignant tumor in stomach?

A

> 95% are adenocarcinomas

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110
Q

what are the two types of stomach adenocarcinomas and describe them:

A

intestinal adenocarcinoma - well differentiated glands; better prognosis

diffuse adenocarcinoma - poorly differentiated (Linitis plastica), includes signet ring cell carcinoma

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111
Q

what are the 5 types of potential stomach carcinomas

A 
lymphoma (MALToma)
squamous cell 
GIST (gastrointestinal stromal tumors- soft tissue; Cahal cells)
neuroendocrine tumors
adenocarcinoma (95%)
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112
Q

what types of cancer are MALTomas?

A

lymphomas; marginal zone

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113
Q

what are the 2 most important intestinal infections related to gastritis or duodenitis?

A

giardia, CMV

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114
Q

MALToma in the duodenum is associated with…

A

celiac’s disease (enteropathy associated T-cell lymphoma)

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115
Q

MALToma in the stomach is associated with…

A

H Pylori infections (MALT activation)

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116
Q

T or F: most esophageal and gastric cancer arise from pre-existing adenomas

A

false

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117
Q

in a patient with celiac’s disease who is currently on a gluten diet, what is the histopath most likely to show?

A

atrophy & intra-epihtelial lymphocytes

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118
Q

which of the following is not a cause of chronic gastritis?

a) autoimmune
b) infection
c) drugs
d) metabolic disease

A

metabolic disease

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119
Q

what are the diaphysis, epiphysis, metaphysis in bone?

A

diaphysis - long part of bone
metaphysis - connecting plate between dia & epi
epiphysis- knuckle shaped end (think, epithelium)

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120
Q

what are the two types of bone?

A

cortical & cancellous

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121
Q

describe cortical bone:

A

long bones that make up 80% of the skeleton; they are appendicular and 80-90% calcified. They are mainly mechanical and protective.

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122
Q

describe cancellous bone:

A

the vertebrae & pelvis. They make up 20% of the skeleton in an axial fashion. They are only 15-25% calcified and serve mainly a metabolic purpose.

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123
Q

describe cortical bone microanatomy:

A

from inside –> out

trabecular lamellae –> interstitial and concentric lamellae layered –> circumferential lamellae

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124
Q

T or F: calcified cortical or cancellous bone stains pink on H&E

A

True

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125
Q

what are the 3 types of bone cells and what do they do?

A

osteoblasts - build bone by laying down osteoid
osteoclasts- multinucleate cells of macrophage family that absorb/chew up bones
osteocytes - osteoblast-like cells which sit in bony lacunae

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126
Q

what cells show up on silver staining of cancellous bones?

A

osteocytes

canaliculae

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127
Q

what is the etiology of primary & secondary osteoporosis?1

A

primary - age, post menopausal

secondary - drugs, systemic disease

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128
Q

what are risk factors for osteoporosis?

A

low BMI, poor diet/dec. vit D intake, female, older age, smoking/etoh, early menopause, low testosterone, CKD, steroids

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129
Q

there is ‘high turnover’ osteoporosis and ‘low turnover’ osteoporosis. what is the difference?

A

high turnover - increased osteoclast (resorption)

low turnover - decreased osteoblast (making less)

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130
Q

what are the two types of osteomalacia?

A

lack of vitamin D or lack of PO4

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131
Q

when do we see issues with ‘Looser’s zone’?

A

win osteomalacia - horizontal fractures in looser’s zones

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132
Q

what are the two causes of primary hyperparathyroidism?

A

parathyroid adenoma (85-90% of the time) or chief cell hyperplasia

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133
Q

what are the two causes of secondary hyperparathyroidism?

A

malabsorption/vit D deficiency

renal deficiency

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134
Q

Renal osteodystrophy describes all of the skeletal changes in CKD, what are they?

A
  1. osteitis fibrosa cystica (increased bone resorption)
  2. osteomalacia
  3. osteosclerosis
  4. growth retardation
  5. osteoporosis
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135
Q

what are the biochemical changes in renal osteodystrophy?

A 
hyperphosphatemia - PO4 retention
hypocalcemia - decreased Vit D
secondary hyperparathyroidism
metabolic acidosis
aluminum deposition
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136
Q

what would be some clinical indications for a bone biopsy?

A

suspected osteomalacia
dx classification of renal osteodystophy
osteopenia in patients < 50 years
osteopenia assoc. with abnormal Ca metabolism

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137
Q

what is the cellular process behind Hirschsprung’s disease?

A

absence of ganglion cells in gut myenteric plexus so that distal colon fails to dilate. Presents with constipation, abdo distension, ‘overflow’ diarrhea

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138
Q

what chromosomal abnormality is Hischsprung’s disease associated with?

A

Down’s syndrome

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139
Q

what age group is most associated with small bowel volvulus?

A

infants

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140
Q

what age group is most associated with large bowel volvulus? (sigmoid colon/caecal)

A

elderly

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141
Q

where & why do diverticular disease occur?

A

90% in L colon

weak points of the bowel wall has high intraluminal pressure on it so it ‘pops’ out

142
Q

what are complications of diverticular disease?

A 
pain
diverticulitis 
perforation
obstruction
fistulae
143
Q

what do toxins cause

A

secretory

144
Q

what type of diarrhea does inflammation and mucosal damage in the colon cause?

A

exudative

145
Q

what acute colitis is associated with antibiotic use?

A 
pseudomembranous colitis (C. difficile toxin)
Treat with metronidazole or vancomycin
146
Q

what is ischemic colitis?

A

acute or chronic vascular disorder of intestinal tract. Tends to be in ‘watershed’ areas ( splenic flexure, rectosigmoid).

What dies is epithelium –> mucosal –> mural –> transmural (perforates)

147
Q

aetiology of ischemic colitis:

A

arterial/venous occlusions
small vessel disease (eg cholesterol, DM)
low flow states (eg hemorrhage, shock)
obstruction (eg hernia, intussception)

148
Q

risk factors/associations for Crohn’s disease:

A

late teens-early 20s onset
white 2-5x> non-white
particularly seen in Celtic and Jewish populations
smoking

149
Q

what sort of histological keys are seen in Crohn’s disease:

A 
'skip lesions' (mouth-anus)
transmural inflammation
non-caseating non-necrotizing granulomas
sinus/fistula formation
'fat wrapping' around thick 'rubber hose' wall
narrow lumen
'cobblestone mucosa'
linear ulcers;fissures; abscesses
150
Q

what are the extra-intestinal manifestations of crohn’s disease?

A

arthritis
uveitis
stomatitis
skin: pyoderma gangrenosum; erythema multiforme; erythema nodosum

151
Q

what sort of histological keys are seen in UC:

A 
involves large bowel ONLY 
backwash ileitis (some inflammation in terminal ileum if severe)
bowel wall is over normal thickness
ulcers are shallow
ulcers only go as far as mucosal 
BIGGER risk of toxic megacolon
152
Q

what are the extra-intestinal manifestations of UC?

A 
arthritis
myositis
uveitis
erythema nodosum, pyoderma gangrenosum
PSC
153
Q

we can have non-neoplastic or neoplastic polyps. what re examples of each?

A

non-neoplastic: hyperplastic, pseudo-polyps (inflammatory), haratamomous ( Peutz-Jehger’s, juvenile)

neoplastic polyps: lead to carcinomas if you don’t remove them. Tubular, tubulovillous, villous

154
Q

what do adenomas look like histologically?

A 
increased mitotic activity
disordered proliferation
dyskaryotic
hyperchromatic
increased nucleocyte:intraplasmic ratio (purple is bad, pink is good)
NOT CANCER
155
Q

what are the risk factors/facts about FAP?

A 
AD inheritance
average age of onset is 25 years old
adenomatous polyps (100- 1000)
chromosome 5q21
APC tumor suppressor gene
will develop cancer within 10-15 years
156
Q

what are the risk factors/facts about HNPCC?

A
  • 1 of 4 DNA mismatch repair genes involved (mutation)
  • numerous RER DNA replication errors
  • high frequency of carcinomas proximal to splenic flexure
  • poorly differentiated; mucinous carcinomas more frequent
  • higher presence of extracolonic cancers
157
Q

what type of carcinoma is CRC?

A

98% is adenocarcinomas

158
Q

what do we use to grade/stage CRC?

A 
Duke's Staging: 
A - confirmed to wall of bowel
B- through wall of bowel
C- lymph node mets
D- distant mets
Grade =  level of differentiation
159
Q

what sort of polyp most commonly predisposes to adenocarcinoma of the colon?

A

adenoma

160
Q

how do we classify causes of acute pancreatitis?

A

duct obstruction (gallstones, trauma, tumor)
metabolic/toxic (alcohol, drugs, hypercalcemia, hyperlipidemia)
poor blood supply (shock, hypothermia)
infection/inflammation (viruses)
autoimmune
idiopathic (15%)

161
Q

what percentage of acute pancreatitis is caused by gallstones?

A

up to 50%

162
Q

what percentage of acute pancreatitis is caused by alcohol?

A

up to 33%

163
Q

how do gallstones cause acute pancreatitis?

A

gallstones get stuck distal to where the common bile ducts and the pancreatic ducts join to reflux the bile up to the pancreatic duct followed by damage to acini which releases proenzymes that then become activated

164
Q

how does alcohol cause acute pancreatitis?

A

leads to spasms/edema of the sphincter of oddi where the pancreas meets the duodenum and thus causes a formation of protein rich pancreatic fluid that obstructs the pancreatic ducts

165
Q

how does drugs, shock, infection, inflammation, etc cause acute pancreatitis?

A

direct acinar cell injuries

166
Q

the pattern of injury tells you what the likely cause was of the acute pancreatitis. There is (1) periductal, (2) perilobular, and (3) panlobular. What does this tell you?

A

1 - periductal - necrosis of acinar cells near ducts (think obstruction)
2- perilobular - necrosis at the edges of lobules (think direct acinar cell injury; poor blood supply)
3- panlobular - from combination of 1 or 2

167
Q

how does acute pancreatitis damage tissue outside the pancreas?

A

Via the enzymes. Most importantly, lipases from pancreas cause hydrolyzed triglycerides of the fats which combine with calcium to form yellow-white foci of calcium salts. These bits of fat are seen all over the abdominal cavity –> fat necrosis

Proteases –> proteins tissue
elastases –> blood vessels –> hemorrhage

168
Q

complications (not death) of acute pancreatitis:

A

pseudocyst formation (lack epithelial lining that true cysts have), abscess, shock, hypoglycemia, hypocalcemia

169
Q

causes of chronic pancreatitis:

A 
alcohol (80%) 
hemochromatosis
gallstones
CF
tumors
autoimmune
170
Q

pathogenesis of chronic pancreatitis?

A

acute pancreatitis which is repeating until fibrosis is seen. Once you have scarring - loss of acinar cells, loss of parenchyma, and later on loss of neuro-endocrine cells. this leads to ductal obstructions and the cycle repeats. Calcified gallstones is often seen and calcification in the body of the pancreas itself.

171
Q

what are complications of chronic pancreatitis?

A

malabsorption (loss of enzymes)
DM (if lose islet cells - later on)
pseudocysts
?carcinoma of pancreas

172
Q

what is the process of a pancreatic pseudocyst developing?

A

associated with acute/chronic pancreatitis.
Lined by fibrous tissue or necrotic material (no epithelial lining) and contains fluid rich in pancreatic enzymes. Communicate with pancreatic duct system. If you leave them - they may resolve, but they may rupture or become infected

173
Q

what is the characterizing factor of autoimmune pancreatitis?

A

IgG4 + cells (IgG4 disease)

may involve pancreas, bile ducts, or any other part of the body

174
Q

what types of tumors of the pancreas exist?

A

epithelial carcinomas - ductal or acinar
glandular cystic neoplasms - serous or mucinous cystic
islet cell tumors (pancreatic neuroendocrine)

175
Q

what is the percentage of pancreas tumors that are ductal?

A

85%

176
Q

what are the characteristics of ductal pancreatic carcinoma?

A

dysplastic ductal lesions - Pancreatic Intraductal Neoplasia (PanIn)
k-ras mutations in 95% of cases

177
Q

what is the histological characteristic of ductal pancreatic carcinoma?

A

adenocarcinomas - mucin secreting glands set in desmoplastic stroma

178
Q

b. duwhat percentage of ductal pancreatic carcinomas are in which part of the pancreas?

A

head (60%)
body
tail

179
Q

what are the complications of pancreatic ductal carcinomas?

A

depends on spread…

but always chronic pancreatitis, venous thrombosis (‘migratory thrombophlebitis’)

180
Q

what are the characteristics of pancreatic endocrine neoplasms?

A

associated with MEN1
contain neuroendocrine markers (eg chromogranin)
usually non-secretory

181
Q

what is the difference between acute and chronic cholcystitis

A

fibrosis in chronic cholecystitis. 90% contain gallstones.

also chronic contains Rokitansky -Aschoff sinuses punched into mucosa (diverticulae)

182
Q

what is the commonest type of pancreatic neoplasm?

a. neuroendocrine
b. ductal
c. serous
d. pseudocysts

A

b. ductal

183
Q

all of the following are causes of chronic pancreatitis except..

a. alcohol
b. gallstones
c. CF
d. drugs

A

d. drugs

184
Q

the following are all complications of gallstones except….

a. acute cholecystitis
b. gall bladder cancer
c. hemolytic anemia
d. obstructive jaundice

A

c. hemolytic anemia

185
Q

what are non-neoplastic bone disorders?

A

benign. They can be congenital or acquired. Acquired causes include trauma, infection, degeneration, inflammation.

186
Q

what are the 4 types of broken bones?

A

Fractures can be complete or Incomplete

Closed (Simple)- clean break with intact soft tissue
Comminuted - splintered bone with intact soft tissue
Compound - fracture site communicates with skin surface (bone sticks out of surface)

187
Q

what are the 4 stages of fracture repair?

A

1) organization of hematoma at fracture site (‘pro-callus’)
2) formation of fibrocartilagenous cells
3) mineralization of fibrocartilagenous callus
4) remodeling of bone along weightbearing lines

periosteal perforation turns into hyaline cartilage. the hyaline cartilage hardens into newly formed bone. then the fracture heals with secondary bone.

188
Q

what is the source of osteomyelitis?

A

almost always bacterial, infection from trauma, direct extension, or hematogenous sources

189
Q

what are the causative organisms of osteomyelitis in adults?

A

Staph aureus 90% of the time in adults.

Can also be: E. Coli, klebsiella, salmonella (esp with sickle cell), pseudomonas (IVDU)

190
Q

what are the causative organisms of osteomyelitis in kids?

A

H. Influenzae

Group B strep

191
Q

what are the x-ray changes seen in osteomyelitis?

A

1) mottled rarefaction and lifting of periosteum
2) after 1week - irregular sub-periosteal new bone formation (“involucrum”)
3) irregular lytic destruction (takes 10-14days)
4) after 3-6 weeks: some areas of necrotic cortex may become detached (“sequestra”)

192
Q

how do we stage osteomyelitis?

A

Cierny-Mader staging system

193
Q

what chronic infections can cause osteomyelitis?

A

TB
Syphilis (congenital or acquired)
Lyme Disease

194
Q

name 3 congenital skeletal lesions from syphilis:

A

Osteochondritis
Osteoperiostitis
Diaphyseal osteomyelitis

195
Q

name 3 skeletal lesions acquired from syphilis infections:

A

Non-gummatous periostitis
gummatous inflammation of bone and joints
Neuropathic joints (Tabes Dorsalis)
Neuropathic shaft fractures

196
Q

what happens in lyme disease?

A

inflammatory arthropathy as part of a complex multisystem illness resulting from tick bite (from organism borrelia burgdorferri). Associated with rash ‘erythema chronicum migrans’

197
Q

what are the 3 stages of lyme disease?

A

stage 1 - early localized (rash in 90% within 7-10days, between 1&50cm diameter)
stage 2 - early disseminated (affects many organs, musc system, heart, nervous system)
stage 3- late, persistent, arthritis

198
Q

what are the main sites osteoarthritis is seen?

A

Main sites: vertebrae, hips, and knees
DIPJ/PIPJ of the hand
carpometacarpal and metatarsophalangeal joints

199
Q

what are the characteristic deformities of RA?

A

Radial deviation of wrist
Ulnar deviation of fingers
‘Swan neck’ & ‘Boutonniere’ deformity of fingers
‘Z’ shaped thumb

200
Q

what are the usual sites of OA?

A

Small joints
hands and feet, sparing DIPJ
Wrists and elbows
ankles and knees

201
Q

what are the 4 histological steps to development of Rheumatoid Arthritis?

A
  1. Thickening of synovial membranes (villous)
  2. Hyperplasia of surface synoviocytes
  3. Intense inflammatory cell infiltrate
  4. Fibrin deposition and necrosis

fundamentally, based on proliferative synovitis

202
Q

what is pannus with regards to Rheumatoid Arthritis?

A

the exuberant inflamed synovium on the articular surface

203
Q

when are Grimley -Sokoloff cells seen?

A

histology of rheumatoid arthritis

204
Q

what inflammatory processes are invoked in rheumatoid arthritis?

A

Intense inflammatory cell infiltrate
Production of IL6, TNFα and CRP by liver

(IL1 & IL6 induce MMPs – joint destruction )

205
Q

describe the 5 developmental steps of rheumatoid arthritis:

A
  1. Unknown antigen in synovial membrane
  2. T – cell proliferation associated with increased B - cells and angiogenesis
  3. Chronic inflammation with inflammatory cytokines
  4. Pannus formation (inflamed synovium on articular surface)
  5. Cartilage and bone destruction
206
Q

what pathologically defines gout?

A

urate (birefringence strongly negative) crystals (of MSU)

These form hard, painless deposits of uric acid crystals known as tophi.

207
Q

what pathologically defines pseudogout?

A

Calcium pyrophosphate (in knees) or Calcium phosphates (hydroxyapatite) (in knees and shoulders). These are POSITIVELY birefringent.

208
Q

name some benign conditions that mini malignant bone tumors?

A

bone cyst
fibrous dysplasia
ossifying or non-ossifying fibroma

209
Q

what are the x-ray changes seen on fibrous dysplasia?

A

any bone, but proximal femur is most common.

Appears ‘soap bubble’ oteolysis.

210
Q

what is McCune Albright syndrome?

A

fibrous dysplasia in many bones associated with endocrine problems and rough border café au lait spots on the skin

211
Q

what genetic mutation causes fibrous dysplasia?

A

GNAS mutation of G-protein on chr20 q13

212
Q

what are the types of benign bone tumors?

A

cartilaginous: osteochondroma; chondroblastoma

bone producing: osteoid osteoma, osteoblastoma

213
Q

what is the most common malignant tumor in the bone?

A

metastases
Adults - breast, prostate, lung, kidney, thyroid
Children - Wilm’s tumor, primary bone osteosarcoma, neuroblastomas

214
Q

3 types of malignant bone tumors:

A

osteosarcoma - bone producing
chondrosarcoma - cartilage producing
Ewing’s tumors - undifferentiated mesenchymal tumor

215
Q

where do osteosarcomas occur?

A

60% occur around the knee

216
Q

what are the x-ray changes seen in osteosarcomas?

A

metaphyseal, lytic, permeative and elevated periosteum (Codman’s triangle)

217
Q

where do chondrosarcomas occur?

A

pelvis/axial skeleton
proximal femur
proximal tibia

218
Q

what are the x-ray changes seen in chondrosarcomas?

A

lytic with fluffy calcification

219
Q

what does the histology show in chondrosarcomas?

A

conventional (myxoid/hyaline)
clear cell (‘low grade’)
undifferentiated (‘high grade’)

220
Q

what is Ewing’s sarcoma and where does it usually occur?

A

highly malignant small round cell tumor usually in diaphysis/metaphysis of long bones and pelvis

221
Q

what x-ray changes are seen in Ewing’s sarcoma?

A

onion skinning of the periosteum (lytic +/- sclerosis)

222
Q

what genetic mutation is associated with Ewing’s sarcoma?

A

11:22 chromosomal translocation

EWSR1 - FLI1 fusion protein

223
Q

what histology is associated with Ewing’s sarcoma?

A

sheets of small blue round cells

224
Q

what 3 cell types in the CNS system interface with CSF?

A

epndyma, meninges, choroid plexus epithelium

225
Q

what 2 cell types in CNS system interface with blood?

A

endothelium
pericytes
(blood brain barrier)

226
Q

what 3 cell types in CNS system act as the ‘glue’ or glia?

A

astrocytes
oligodendrocytes
microglia

227
Q

what are 2 of the most common genetic pre-disposers to CNS tumors?

A 
neurofibromatosis 2 (22q12)
von hippel lindau (3q25)
228
Q

what do neurofibromatosis 2 and von hippel lindau syndromes predispose you to?

A

CNS tumors

229
Q

what are the presenting symptoms of supratentorial tumors?

A

focal neurological deficits
headaches
changes in mental status
seizures

230
Q

what are presenting symptoms of subtentorial tumors?

A

cerebellar ataxia
cranial nerve palsy
long tract signs

231
Q

what is the most common primary intrinsic CNS tumor in adults?

A

glial cell tumors

over half of these are glioblastomas

232
Q

what is the most common type of glioma?

A

infiltrative glioma

233
Q

what is the most aggressive glioma?

A

de novo glioblastoma (GB - multiforme = GBM)

234
Q

what gene mutation is associated with diffuse astrocytomas and with oligodendeogliomas?

A

IDH1 gene

235
Q

where do oligodendrogliomas tend to present?

A

50-60% present in frontal lobe with long history of neurological signs (often seizures)

236
Q

what is the hallmark feature of pilocytic astrocytomas?

A

piloid ‘hairy’ cells; granular bodies; Rosenthal fibres

never diffuse infiltration because of compressive margins

237
Q

how do medulloblastomas present?

A

cerebellar signs, cranial hypertension

tend to be in vermis in children and hemispheric in adults

238
Q

how do meningiomas present?

A

encapsulated and not infiltrative

tend to cause focal symptoms - seizure, compression

239
Q

what cancers tend to metastasize to brain?

A

lung, melanoma, colon, breast, renal

240
Q

where do mets in brain tend to occur?

A

watershed areas or grey-white matter interfaces

241
Q

what is the morphology of piloid cells?

A

hairy

242
Q

according to WHO criteria, a grade III CNS tumor causes death within…

A

5 years

243
Q

define cerebral edema:

A

xs accumulation of fluid within the brain parenchyma; either vasogenic (disrupted BBB) or cytotoxic (secondary to cellular injury). Presents with inc. ICP

244
Q

define hydrocephalus:

A

disruption of CSF flow within the brain. Either…

1) non-communicating/obstructive: physical obstruction of flow (commonly - blockage of cerebral aqueduct by choroid plexus bits)
2) communicating: no obstruction, but problem with resorption of CSF (meningitis, etc)

245
Q

Normal ICP is 7-15mmHg. What is the biggest potential complication of increased ICP?

A

herniation of brain

  • tonsillar (brain stem)
  • transtentorial (uncal, below hemsipheres to pons)
  • subfalcine (between hemispheres)
246
Q

what are the two types of potential stroke?

A

hemorrhagic

infarction (ischemic)

247
Q

define a non-traumatic intra-parenchymal hemorrhage:

A

rupture of a small parenchymal vessel leading to a bleed into the substance of the brain, most common in basal ganglia

248
Q

how does a non-traumatic intra-parenchymal hemorrhage present?

A

severe headache, vomiting, rapid LoC, focal neuro signs

249
Q

what is the risk of CNS A-V malformations?

A

these are arterio-venous malformations that usually become symptomatic in middle age. they are worrisome because they are under high pressure - thus causing a massive hemorrhage if they burst!

250
Q

what is a cavernous angioma and why do we care about them?

A

a well-defined malformative lesion of closely packed vessels with no parenchyma in between. (just a bundle of vessels)
low pressure environment - may be recurrent bleeds.

251
Q

what is a sub-arachnoid hemorrhage and why do we care?

A

often a berry aneurysm rupture (congenital weakness in vessel walls of circle of Willis) - massive headache, vomiting
80% at the internal carotid artery bifurcation

252
Q

what is the commonest form of cerebrovascular disease?

A

infarction - 80% of strokes often from cerebral atherosclerosis but leading to death of tissue from lack of blood supply

focal - local blood supply; global - systemic circulation failing

253
Q

when the integrity of the BBB is disrupted the resultant edema is described as….?

A

vasogenic

254
Q

which of the following types of herniation does not involve cerebral cortex?

a. subfalcine
b. transtentorial
c. tonsillar
d. uncal

A

c. tonsillar

255
Q

what percentage of patients who experience a TIA will get a significant infarct within 5 years?

A

33%

256
Q

what is the most common cause of non-traumatic intraparenchymal hemorrhage?

A

hypertension

257
Q

T or F: prion disease occurs without exchange of any DNA or RNA material.

A

true - completely infectious proeinaceous disease

258
Q

name 4 types of prion disease:

A

CJD
Gertzmann- Straussler-Sheinker (GSS) syndrome
Kuru
Fatal familial insomnia

259
Q

what happens in prion disease?

A

PrP converts host protein into pathological form, and can’t be then digested in the body. at some point this is not reversible, and deposits into the brain

260
Q

what is ‘new variant CJD’ (vCJD)?

A

sporadic neuropsychiatric disorder that onsets in patients <45 years old. Leads to cerebellar ataxia, dementia

261
Q

what is the pathology of Alzheimer’s dementia?

A

formation of oligomers of amyloid-beta plaques, causing protein buildups. interfere with production of reactive oxygen species, calcium homeostasis, etc. the protein build up of both a-beta and tau proteins (microtubules associated) causes all the problems

262
Q

what staging system is used in Alzheimer’s dementia pathology?

A

Braak’s staging looking at the primary visual cortex histopathology (6 stages)

263
Q

what defines Parkinson’s disease?

A

Lewy bodies throughout the brain; but specifically in the substantia nigra mid-brain. normally black from dopaminergic metabolism - in Parkinson’s there is no substantia nigra left because no dopamine. That is the main determinant of motor dysfunction. (‘nigrastriatal projections’)

264
Q

list several Parkinsonisms…

A

drug-induced parkinsonism
PSP - progressive supranuclear palsy (tau protein)
CBD - corticobasal degeneration (tau protein)
MSA -multiple system atrophy

265
Q

what are the characteristics of Pick’s disease?

A

loss of neuronal bodies
fronto-temporal atrophy
tau positive pick bodies
marked gliosis

266
Q

what are tauopathies?

A

on chromosome 17 mutation (single gene 17q21)
PSP, CBD examples
16 exons with alternative splicing –> 6 isoforms (with different numbers of binding domains giving different propensity to aggregate) dependent on exon 10

267
Q

which of the following is not a prion disease?

a. CJD
b. Huntingtons
c. Familial fatal insomnia
d. Kuru

A

B. huntington’s

268
Q

excluding Parkinson’s disease, which other parkinsonism is associated with alpha-synuclein body?

A

MSA - multiple system atrophy

269
Q 
which of the following proteins is not associated with forms of frontotemporal dementia?
a. APP
b. Tau
c TDP
d. FUS
A

APP (Alzheimer’s)

270
Q

what are

a) neutrophils associated with in the body?
b) Lymphocytes?
c) eosinophils?
d) macrophages?

A

Neutrophils - acute inflammation
Lymphocytes - chronic inflammation
Eosinophils - Allergic reactions; Parasitic infections
Macrophages - Late acute inflammation; Chronic inflammation

271
Q

what is the stain we use to detect Haemochromatosis?

A

Prussian Blue Iron desposits

272
Q

when is prussian blue stain used?

A

Haemochromatosis

273
Q

when do we use congo red staining?

A

detect amyloidosis

274
Q

when do we use apple green birefringence?

A

detect amyloidosis

275
Q

what stains/histochemical tests are used for amyloidosis?

A

congo red stain

apple green birefringence

276
Q

what happens in an MI to the tissue of the heart:

a) after 1-6 hours vs 6-24 hours
b) 24 hours later
c) 3-4 days later
d) 1-3 weeks later
e) 3-6 weeks later

A

a) no visible changes at 6 hours. Then some cytoplasm loss and cell death 6-24 hours
b) edema, inflammation; infilatration of polymorphs & macrophages
c) necrosis, granulation; removal of debris
d) granulation tissue; new tissues forming, myofibroblasts
e) dense fibrosis; strengthening/decellularising scar

277
Q

what are some further complications of MI?

A
  • Dressler syndrome: pericarditis 2-3 days later
  • RV infarction
  • Infarct extension – new necrosis adjacent to old
  • Infarct expansion – necrotic muscle stretches ->mural thrombus
  • Ventricular aneurysm, late -> thrombus, heart failure, arrhythmia, do not rupture
  • Papillary muscle rupture
  • Chronic IHD = progressive late heart failure
278
Q

what are the causes & pathological presentation of dilated cardiomyopathy?

A
  • Progressive loss of myocytes
  • Dilated heart
    Causes:
    *Idiopathic
    *Infective – viral myocarditis
    *Toxic: alcohol, chemotherapy (adriamycin, daunorubicin), cobalt, iron
    *Genetic – haemochromatosis, Fabry’s, McArdle’s
    *Immunological – myocarditis incl. Viral (hypersensitivity component)
279
Q

what is the main cause and presentation of hypertrophic cardiomyopathy?

A
  • LVH (Thickening of septum narrows left ventricular outflow tract)
  • Familial in 50% (autosomal dominant, variable penetrance) - HOCM
  • Beta-myosin heavy chain
280
Q

what happens in restrictive cardiomyopathy?

A
  • Impaired ventricular compliance
  • Idiopathic or secondary to myocardial disease (eg amyloid, sarcoidosis)
  • Normal size heart but big atria
281
Q

what happens in chronic rheumatic valvular disease?

A

*Sequelae of earlier rheumatic fever
* Predominantly in left-sided valves; thickened valve leaflet
(( Mitral > Aortic > Tricuspid > Pulmonic ))
*Thickening, shortening and fusion of chordae tendineae

282
Q

what happens in calcific aortic stenosis?

A

Commonest cause of aortic stenosis, presents in 70s or 80s. Due to Calcium deposits on the outflow side cusp impairing opening and compromising outflow tract

283
Q

what are the potential causes and the pathogenesis that happens in aortic regurgitation?

A

Causes: rheumatic, degenerative (rigidity); microbial endocarditis (destruction), Marfan’s, syphilitic aortitis, ank. spondylitis

Disease of aortic valve ring –> dilatation –> valve insufficient to cover increased area

284
Q

what is duct ectasia and what would cytology of it show?

A

Benign condition with no increased risk of
malignancy. Inflammation and dilation of large breast ducts.

Usually presents with nipple discharge.Can cause breast pain, breast mass and nipple retraction.

Cytology of nipple discharge: proteinaceous
material and inflammatory cells

285
Q

what causes acute mastitis?

A

Usually Staphylococci - painful, red breast; acute inflammation

286
Q

what is fat necrosis of the breast?

A

a benign condition where trauma or surgery or RT cause an inflammatory condition to damage adipose tissue

287
Q

what are Phyllodes tumors of the breast?

A

A group of potentially aggressive fibroepithelial
neoplasms of the breast. Present as enlarging masses in women aged over 50.

Vast majority behave in a benign fashion but a small
proportion can behave more aggressively.

288
Q

what is an intraductal papilloma of the breast?

A

A benign papillary tumour arising within the duct
system of the breast - within small terminal ductules (peripheral) or larger lactiferous ducts (central, sometimes nipple discharge). Common condition usually seen in 40-60 year olds.

289
Q

what is a ‘radial scar’ breast lesion?

A

A benign sclerosing lesion characterised by a central
zone of scarring surrounded by a radiating zone of
proliferating glandular tissue. Reasonably common and due to exuberant reparative works in response to areas of tissue damage of the breast.

Usually present as stellate masses on screening
mammograms which may closely a carcinoma.

Excision is curative.

290
Q

what cellular growth changes are a morphological precursor to low grade DCIS of the breast:

A

Flat epithelial atypia/Atypical ductal carcinoma

291
Q

Define DCIS of the breast:

A

A common neoplastic intraductal epithelial proliferation in the breast with an inherent, but not inevitable, risk of
progression to invasive breast carcinoma.
‘DCIS’ - Ductal Carcinoma in Situ
Most are seen as microcalcification.on mammography. However some may show skin changes, lumps, or even Paget’s disease of the nipple.

292
Q

what are some risk factors for breast cancer?

A
  • BRCA genes 1 & 2
  • Early menarche, late menopause,
  • increased weight,
  • high alcohol consumption,
  • oral contraceptive use
  • family history
293
Q

describe basal-like carcinoma of the breast:

A
  • Histologically characterised by sheets of markedly atypical cells with a prominent lymphocytic infiltrate.
  • Central necrosis is common.

    Immunohistochemically: positive for ‘basal’ cytokeratins CK 5/6 and CK14.

Seem to have particular propensity to vascular invasion and distant mets

294
Q

what 3 receptors are all breast cancers screened for?

A

ER
Progesterone Receptor
Her2

295
Q

how do ER, PR, and Her2 receptors affect the grading of breast tumors?

A 
Low grade tumors:  ER/PR + and Her2 -

High grade tumors:  ER/PR - and Her2 + .

Basal-like carcinomas: ER/PR/Her2 negative 
(“triple negative”).
296
Q

what histological changes occur in gynecomastia?

A

breast ducts show epithelial hyperplasia with

typical finger like projections extending into the duct lumen.

297
Q

what element are most renal calculi made of and why?

A

75% are calcium oxalate. Most related to absorptive hypercalciuria = too much calcium absorbed from gut.
Some have renal hypercalciuria = calcium absorption from proximal tubule impaired.

298
Q

what type of stones (i.e. made of what) are most common in staghorn calculi?

A

magnesium ammonium phosphate aka “triple stones”

Formed largely as a result of infections with
urease producing organisms e.g

299
Q

what are common points of impaction for renal calculi on their way out?

A

Common points of impaction = PUJ, pelvic brim,

VUJ.

300
Q

what are renal papillary adenomas and how do they look on histology?

A

Benign renal epithelial tumor with a papillary
or tubular architecture and a size of 5 mm or
less. (well circumscribed cortical nodules)
Histologically: bland epithelial cells growing in a papillary or tubulopapillary pattern.

301
Q

what is an angiomyolipoma of the kidney?

A

Benign mesenchymal tumor of the kidney composed of variable amounts of fat, smooth muscle and thick walled blood vessels.
Most picked up incidentally but may present with
flank pain due to haemorrhage into the tumor.

302
Q

what is the most common type of renal cell carcinoma? How does it appear on histology?

A

Clear cell.
Grossly appear as golden yellow tumours with haemorrhagic areas.

Histologically: nests of epithelial cells with clear cytoplasm set in a delicate capillary vascular network

303
Q

How common are papillary renal cell carcinomas? How do they appear on histology?

A

15% of all renal carcinomas.
Grossly appear as friable brown tumours.

Histologically: epithelial tumours with a papillary growth pattern and measuring >5 mm in size.

304
Q

what is the least common renal cell carcinoma (5% of all of them)?
How does it appear on histology?

A

Chromophobe RCC.
Macroscopically appear as solid brown tumours.

Histologically: sheets of large cells with distinct cell borders and a thick walled vasculature.

305
Q

what system is used to grade renal cell carcinomas?

A

Fuhrman system

306
Q

what is the histological appearance of a nephroblastoma, or Wilm’s tumor?

A

Histologically composed of undifferentiated
“small round blue cells” with areas of more
differentiated epithelial and stromal components.

307
Q

what are ‘transitional cell carcinomas’?

A

-carcinoma of the urothelial tract; often bladder
-noninvasive (papillary) or invasive
-present with haematuria.
Noninvasive usually appear as frond like growths projecting from the surface of the bladder mucosa.

308
Q

what is prostatic carcinoma?

A

Arises from a precursor lesion known as prostatic intraepithelial neoplasia (PIN).Malignant epithelial neoplasm arising in the prostate. The most common malignant tumour in men.

Usually presents incidentally on needle biopsy for raised PSA (which is often just BPH). LUTS may be present.

Gleason score prognosis for staging.

309
Q

what are testicular germ cell tumors?

A

A group of malignant tumors of the testis
arising from germ cells. Account for >90% of all testicular tumours.
Most arise in young men aged 20-45; present with painless testicular lump.
Most arise from a precursor lesion known as intratubular germ cell neoplasia (ITGCN).
may be… seminoma, embryonal carcinoma, immature or mature teratoma, choriocarinoma, or yolk sac tumor.

310
Q

what are non-germ cell testicular tumors?

A
  • Testicular lymphoma (in older men.)
  • Leydig cell tumors (usually benign)
  • sertoli cell tumors (usually benign)
311
Q

what are the two types of cervical cell cancers?

A

-squamous
-adeno
FIGO staging

312
Q

how does HPV transform cervical cells?

A

E6 and E7 bind to and inactivate two tumour
suppressor genes: Retinoblastoma gene (Rb) via (E7)
and P53 via (E6)
•Both effects interfere with apoptosis and increase unscheduled cellular proliferation both of which contribute to oncogenesis

313
Q

what is a uterine leiomyoma?

A

commonest uterine tumor; smooth muscle of myometrium …. aka fibroid (intramural, subserosal, or submucosal)

314
Q

what is the malignant counterpart of a leiomyoma in the uterus (aka fibroid)?

A

Leiomyosarcoma - usually a solitary one and in post menopausal women

315
Q

there is type I and type II endometrial cancer. Which is most common and what distinguishes it?

A

Type 1 - 80-85% 
Endometrioid, mucinous or secretory adenocarcinomas
Younger age
Estrogen dependent
Low grade tumours, superficially invasive
At least 4 different genes involved (p53, k-ras, PTEN,…)

316
Q

describe what differentiates type II endometrial cancer?

A 
Serous or clear cell carcinomas
Older, postmenopausal women
Less estrogen dependent
Arise in atrophic endometrium

High grade, deeper invasion, higher stage
317
Q

what 3 conditions fall under the umbrella of gestation trophoblastic diseases?

A

– Complete and partial mole
– Invasive mole
– Choriocarcinoma

318
Q

what are the two key differences between partial & complete hydatidiform moles?

A

partial - triploid; none progress to cancer

complete - diploid; some can progress to cancer

319
Q

what is the cellular origin & progression of endometriosis?

A

– Metaplasia of pelvic peritoneum
– Implantation of endometrium, retrograde menstruation

Ectopic endometrial tissue is functional and bleeds at time of menstruation -> pain, scarring and infertility

320
Q

what is the cellular change that happens in adenomyosis?

A

Ectopic endometrial tissue deep within the

myometrium

321
Q

what are the most common type of ovarian tumors?

A

Epithelial tumors make up 65% of all ovarian tumors

& 95% of malignant ovarian tumors

322
Q

what gene is mutated in >75% of all type II ovarian cancers?

A

p53

323
Q

List the 5 types of epithelial ovarian tumors:

A 
Serous
Mucinous
Endometrioid 
Clear cell (strongly assoc. with endometriosis)
Transitional
324
Q

what is a Krukenberg tumor in the ovaries?

A

bilateral metastases composed of mucin producing signet ring cells – most often of gastric origin or breast

325
Q

which ovarian cancer is BRCA associated?

A

serous tumors (30%)

326
Q

which ovarian cancers are HNPCC mutation associated with?

A

mucinous (10%) , endometroid (20%)

327
Q

which vaginal adenocarcinoma is Diethyl stilbosterol in threatened miscarriage treatment associated with?

A

clear cell adenocarcinoma

328
Q

what happens to cells in pulmonary oedema and what presents on histology?

A

Accumulation of fluid in alveolar spaces as consequence of “leaky capillaries” or “backpressure” from failing left ventricle. (due to LHF or high altitude…)

Pathology:
Heavy watery lungs, intra-alveolar fluid on histology
“Heart failure cells” – iron laden macrophages

329
Q

what is Hyaline membrane disease of newborn?

A

insufficient surfactant production in premature babies leading to rapid respiratory failure due to diffuse alveolar damage, including to epithelium (same as ARDS in adults). Lungs will be expanded, firm, ‘plum colored’ , heavy and airless.

330
Q

what are some complications of hyaline membrane disease?

A 
Respiratory failure and death (within 48 hours)
Pneumonia
Interstitial emphysema
Bronchopulmonary dysplasia
fibrous scarring
331
Q

what sorts of gross and micro-histology is seen in asthma patients?

A

Gross: mucus plugs, overinflated lungs
Histology: Curschmann’s spiral, Charcot Leyden crystals

332
Q

define COPD:

A

Damage to airways (CHRONIC BRONCHITIS) and alveolar parenchyma (EMPHYSEMA), often both in same patient.
Caused by pollution, dusts, severe chronic asthma, smoking.

333
Q

define chronic bronchitis and complications of it:

A

Definition- Chronic productive cough most days for >3 months over 2 consecutive years
Complications: Repeated infections, chronic hypoxia, cor pulmonale (RHF), pulmonary HTN, inc. risk of lung cancer

334
Q

what histological features are seen in COPD?

A

goblet cell hyperplasia, dilatation of airways, Hypertrophy mucous glands (Reid Index)

335
Q

define emphysema and its potential complications:

A

definition- Emphysema is a permanent loss of the alveolar parenchyma distal to the terminal bronchiole
Due to smoking, alpha-1 antitrypsin deficiency, or more rarely can be IVDU
complications: bullae which rupture and cause a pneumothorax, Respiratory failure, Pulmonary hypertension and cor pulmonale.

336
Q

Emphysema histological features vary depending if the cause is

a) smoking
b) alpha-1-antitrypsin deficiency , describe:

A

a) alveolar Loss centred on bronchiole - CENTRILOBULAR

b) alveolar diffusely lost
PANACINAR

337
Q

define bronchiectasis and list some potential complications:

A

Defined as: Permanent abnormal dilatation of bronchi from congenital or inflammatory causes
Complications:
Recurrent infections, Haemoptysis, Pulmonary Hypertension and right sided heart failure (cor pulmonale), Amyloidosis

338
Q

define cystic fibrosis:

A

-autosomal recessive inherited gene with mutation on CFTR gene leading to abnormal chloride channels
Leads to: Lung -> airway obstruction, respiratory failure, recurrent infection (Staph aureus, H. influenza…), Allergic bronchopulmonary aspergillosis , bronchiectasis
GI tract -> meconium ileus, malabsorption
Pancreas -> pancreatitis, malabsorption
Liver -> cirrhosis
Male reproductive system -> infertility

-treatment is MDT, supportive, chest physio, antibiotics, supplements. Lung transplants can help prolong survival.

339
Q

what are the 4 stages of lobar pneumonia in histopathlogical development?

A
  1. Congestion: Intra-alveolar fluid
  2. Red hepatization: Intra-alveolar neutrophils
  3. Grey hepatization: Intra-alveolar connective tissue
  4. Resolution: Restoration normal architecture.
340
Q

what is the histological difference of atypical pneumonias?

A

Interstitial inflammation (pneumonitis) WIHTOUT accumulation of intra-alveolar inflammatory cells

Chronic inflammatory cells within alveolar septa and edema +/- viral inclusions

341
Q

what histological changes are seen in influenza?

A
  • diffuse alveolar damage

- small airway inflammation & necrosis

342
Q

what is the histology definition of granulomas?

A

Collection of histiocytes/macrophages +/- multinucleate giant cells; Necrotising or non necrotising

343
Q

what lung involvement pathology exists in sarcoidosis?

A

Discrete epithelioid and giant cell granulomas, in upper zones with tendency to be perilymphatic/peribronchial

+increased ACE levels

344
Q

what are some causes of pulmonary hypertension?

A
  • chronic hypoxia (eccentric intimal fibrosis, cell wall thickened)
  • chronic liver disease
  • HIV
  • widespread pulmonary fibrosis
  • thromboembolic disease
  • LHF
345
Q

what is ‘nutmeg liver’ associated with?

A

right HF

346
Q

what happens in asbestosis?

A

Fine subpleural basal fibrosis with asbestos bodies in tissue. Increased risk of lung cancer.

347
Q

what happens in coal workers pneumoconiosis?

A

Carbon in upper lobes leads to macrophages containing pigment accumulating around airways with mild fibrosis. If severe, we see large fibrotic nodules in the lungs.

348
Q

what happens in pneumoconiosis?

A

We also call this ‘dusty lung’ because ‘permanent alteration of lung structure by inhaled inorganic dust and the tissue reaction of the lung leads to its presence, excluding bronchitis and emphysema

349
Q

what happens in extrinsic allergic alveolitis?

A

“farmers lung”

Reaction to inhaled antigen, acute and in presence of antigen (i.e. better when home from work)
Respond well to avoiding antigen and steroids. Some develop fibrosis

350
Q

what happens in idiopathic pulmonary fibrosis?

A

Also known as cryptogenic fibrosing alveolitis. Usually a male >50 years of age.

Macro histology – Basal and peripheral fibrosis and cyst formation
Micro histology - interstitial fibrosis at varying stages

Julija's Path (6 decks)

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