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Pathology 2 Flashcards

1
Q

Glomerular lesion terminology

A

Focal - less than 50% all gloms involved

Diffuse - more than 50%

Segmental - less than 50% of individual glom involved

Global - more than 50% of individual glom

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2
Q

Causes of glomerular diseases

A

Primary

Secondary to systemic disorder - DM, SLE, vasculitis, amyloidosis, HTN

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3
Q

What happens in primary glomerular disease?

A

Usually immune mediated
AB against a constituent of the glom e.g. bm

AB against somethign that has been deposited in the glom

Deposition of a circulating Ag-Ab immune complex

This produces an inflammatory response –> tissue damage –> decreased GFR (tubular injury) and production of ECM (sclerosis + obliteration of glom)

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4
Q

Histological alterations in glomeruli

A

Hypercellularity

BM thickening

Hyalinisation + sclerosis

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5
Q

Acute glomerulonephritis

A

Haematuria, increased Cr and Ur, oliguria +/- proteinuria

Inflammatory alteration in glomeruli

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6
Q

Causes of acute glomerulonephritis

A

Postinfectious e.g. children following a streptococcal infection (skin, pharynx) - anti-streptococcal ABs

Necrotising/crescentic - anti-GBM, immune complex mediated, ANCA associated - these are poor prognosis + most need dialysis

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7
Q

Nephrotic syndrome

A 
Massive proteinuria (Causing oedema)
Hyperlipidaemia

Hypoalbumin, proteinuria, hyperlipidaemia, oedema

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8
Q

Causes of nephrotic syndrome

A

Membranous nephropathy
Minimal change disease
FSGS

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9
Q

Membranous nephropathy

A

Most common cause in adults
Diffuse thickening of GBMs
Subepithelial immune complex deposition
Anti-PLA2R ABs

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10
Q

Minimal change disease

A 
Most common in children 2-6yrs 
Normal glomeruli on microscopy 
EM fusion of epithelial foot processes 
Follows respiratory tract infection 
Responds to steroids
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11
Q

Causes of haematuria with normal renal function

A

IgA nephropathy (deposits of IgA in mesangium)
Alports syndrome
Thin glomerular BM disease

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12
Q

Chronic glomerulonephritis

A

End stage of acute
Chronic renal failure
Small symmetrical kidneys
Diffusely granular surface

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13
Q

Diabetic nephropathy

A

Leading cause of chronic renal failure
Thickening of GBMs
Mesangial increase +/- nodules

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14
Q

Amyloidosis

A

Abnormal proteinaceous material deposited in tissues
Congo red +ve + birefringence under polarised light

Primary - light chains - multiple myeloma
Secondary - chronic disease e.g. TB, Crohns

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15
Q

Hypertension in the kidneys

A

Affects arteries + arterioles
Intimal thickening with narrowing of lumen
Hyalinosis
Leads to ischaemic changes in the kidney - glomerular sclerosis, tubular atrophy, IS fibrosis

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16
Q

Chronic pyelonephritis

A

Chronic tubulointerstitial inflammation
2 forms: obstructive + reflux nephropathy

Assymetrical irregular kidneys, coarse discrete corticomedullary scar overlying a dilated, blunted or deformed calyx

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17
Q

What are lines of Zahn?

A

Feature of thrombi that occur particularly when formed in the heart or aorta

Alternating layers of plts + fibrin (pale) and RBCs (darker)

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18
Q

Virchow’s triad

A

Changes in vessel wall (endothelial damage)
Changes in BF (stasis, turbulence)
Changes in blood composition (many e.g. COCP, Ca, polycythaemia, myeloproliferative disorders)

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19
Q

What are arterial thrombi made up of?

A

Rapid flow - mainly plts (pale)
Mural or occlusive depending on SIZE of vessel
Predisposing factors usually endo damage

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20
Q

What are venous thrombi made up of?

A

Slow flow - mainly blood clot (red)
Usually occlusive
Predisposing factors cause abnormalities of BF

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21
Q

What happens when a thrombus is formed?

A

Resolution (dissolution of clot by fibrinolysis)

Organisation - ingrowth of fibroblasts, capillaries, phagocytes (granulation tissue)

Recanalisation - restore original lumen
OR
Fibrosis - formation of webs, cords

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22
Q

What is an embolus?

A

Passage of insoluble mass within the blood steam and impaction at a site distant from its point of origin

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23
Q

What are emboli made of?

A

> 95% are dislodged thrombi

Other: fat, air, tumour, amniotic fluid, infective material

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24
Q

Emboli sites of impaction

A

Pulmonary arteries - thrombi from veins, R side of heart

Systemic arteries - thrombi from L side of heart + aorta

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25
Causes of ischaemia
Intrinsic disease of vessel e.g. atherosclerosis Occlusion by thrombus/embolus External compression of artery
26
Stages of infarction
1. Necrosis 6-12h 2. Acute inflammation 24h-7d 3. Organisation 3d-2wks 4. Scar formation 2wks-3m
27
Consequences of a pulmonary embolism
1. Sudden death - massive embolism 2. Pulmonary infarction - pulmonary venous congestion, haemorrhagic, peripheral, wedge shaped (due to venous back pressure) 3. Pulmonary HTN 4. Asymptomatic
28
Clinical manifestations of a pulmonary infarct
Haemoptysis - cough up to get rid | Pleuritic chest pain - pain as pleurae laying over it will become inflammed
29
The peak time at which V wall rupture occurs following MI is:
4-10 days | Dead muscle starts to break down + very weak as no collagen yet so susceptible to rupture
30
What is gangrene?
Necrosis + superadded bacterial infection
31
Commonest type of skin cancer
Basal cell carcinoma (75%)
32
What % of lung cancers are central (carina, main + lobar bronchi)
70%
33
How do you describe a basal cell carcinoma?
Enlarging annular plaque with focal ulceration and rolled out margin on nose
34
Where does basal cell carcinoma arise from?
The epidermis
35
Histological subtypes of BCC
Nodular Superficial Infiltrative (aggressive) Micronodular (aggressive)
36
What do you see in histology of squamous cell carcinoma?
Keratin pearls + infiltrative nests of malignant squamous cells
37
Which biopsies are used for which skin cancer?
Skin punch biopsy - basal and squamous cell carcinoma Excision biopsy - melanoma
38
Subtypes of melanoma
Superficial spreading (most common - significant epidermal component) Nodular
39
What is used to assess the stage of melanoma?
``` Breslows thickness Clark's scale Microsatellites Mitotic figures Ulceration Vascular invasion ``` Not size or diameter
40
Which skin cancer is not associated with metastasis
Basal cell carcinoma
41
What determines the stage in basal and squamous cell carcinoma?
Size and diameter
42
What determines the stage in melanoma?
Thickness
43
How many lung cancers are treated by surgery?
15%
44
Where does paracetemol cause damage in the liver?
Perivenular/centrilobular - furthest away from portal blood supply where P450 enzymes greatest
45
Pattern of damage in liver disease
Fatty change - steatohepatitis/fibrosis - cirrhosis
46
Fatty liver disease histology
Macrovesicular staeatosis - stored as triglycerides that take over the cytoplasm
47
Steatohepatitis histological features
Hepatocellular injury - fatty change, ballooning, mallory-denk bodies, apoptosis/necrosis Inflammation Fibrosis - perisinusoidal, pericellular
48
what increases the risk of cholangiocarcinoma?
PSC - get premalignant changes due to periods of ucleration + regeneration
49
Features of liver cirrhosis
Loss of normal lobular architecture Nodular regeneration Fibrosis
50
How does skin heal?
Primary or secondary intention
51
Primary intention
1 linear incision - can bring 2 ends together
52
Secondary intention
e.g. leg ulcer - can't bring together 2 ends so leave open, epidermis grows up + takes longer to heal
53
Strength of a wound
10% at week 1 50-60% at 1m 70-80% plateau at 3m
54
What are the 2 ways the liver heals?
Resolution - normal liver Repair - cirrhosis - failure of resolution --> nodules surrounded by fibrous tissue + lose structural integrity of sinusoids so can't go back to normal
55
What regulates liver repair?
Stellate + kupffer cells produce GFs + cytos which stimulate healing HGF plays key role in stimulating hepatocytes to enter cell cycle TGF-B one of key regulators of fibrosis Deposited collagen remodelled by MMPs and TIMPs
56
what factors influence healing of the liver?
Time course of injury e.g. paracetamol cause liver injury at 1 time point so no cirrhosis v alcohol which is less severe injury over long period so cirrhosis Anatomic site of injury - damage to parenchyma e.g. alcohol causes cirrhosis with fibrosis mediated by stellate cells in sinusoids
57
what is hypoplasia?
NOT THE OPPOSITE OF HYPERPLASIA failure of tissue/organ to reach normal size during development e.g. genetic defects
58
What is atrophy?
decrease in size of tissue/organ at a stage after initial dvelopment. may be decrease in cell size or number
59
what is metaplasia?
replacement (potentially reversible) of 1 differentiated cell type by another differentiated cell type
60
What is dysplasia?
Disordered development | Changes resemble those seen in neoplastic cells - not yet invasive but can progress to invasive carcinoma if not treated
61
Oncocytomas
Benign | Unformally large cells with eosinophils
62
Chromophobes
Perinuclear halos
63
Clear cell carincoma
Large cells with clear cytoplasm
64
Transitional cell carcinoma
Papillary architecture with layers of urothelium
65
Papillary
Papillae and eosinophilic cells. Foci of calcification
66
Which zone of the prostate is BPH in?
Transitional
67
Which zone of the prostate is cancer in?
Peripheral
68
Eosinophilic oesophagitis
Hx of allergy + eosinophilia Dysphagia Mid oesophagus Endoscopy: concentric rings 'trachealisation' of oesophagus
69
Coeliac
Villous atrophy Intra epithelial lymphocytosis Chronic inflammation in lamina propria Crypt hyperplasia
70
UC
``` Uniform diffuse lesions Superficial - mucosa Associated with PSC Absence of granulomas Cryptitis and crypt abscess formation Crypt mucin depletion ```
71
Crohns
Typically ileocaecal junction Segmental lesions Deep lesions up to serosa - patchy ulceration, abscesses, fissures, lymphoid hyperplasia, epithelioid granulomas

Year 3 (14 decks)

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