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Year 3 > Pathology 2 > Flashcards

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
Q

Causes of ischaemia

A

Intrinsic disease of vessel e.g. atherosclerosis
Occlusion by thrombus/embolus
External compression of artery

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26
Q

Stages of infarction

A
  1. Necrosis 6-12h
  2. Acute inflammation 24h-7d
  3. Organisation 3d-2wks
  4. Scar formation 2wks-3m
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27
Q

Consequences of a pulmonary embolism

A
  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
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28
Q

Clinical manifestations of a pulmonary infarct

A

Haemoptysis - cough up to get rid

Pleuritic chest pain - pain as pleurae laying over it will become inflammed

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29
Q

The peak time at which V wall rupture occurs following MI is:

A

4-10 days

Dead muscle starts to break down + very weak as no collagen yet so susceptible to rupture

30
Q

What is gangrene?

A

Necrosis + superadded bacterial infection

31
Q

Commonest type of skin cancer

A

Basal cell carcinoma (75%)

32
Q

What % of lung cancers are central (carina, main + lobar bronchi)

A

70%

33
Q

How do you describe a basal cell carcinoma?

A

Enlarging annular plaque with focal ulceration and rolled out margin on nose

34
Q

Where does basal cell carcinoma arise from?

A

The epidermis

35
Q

Histological subtypes of BCC

A

Nodular
Superficial
Infiltrative (aggressive)
Micronodular (aggressive)

36
Q

What do you see in histology of squamous cell carcinoma?

A

Keratin pearls + infiltrative nests of malignant squamous cells

37
Q

Which biopsies are used for which skin cancer?

A

Skin punch biopsy - basal and squamous cell carcinoma

Excision biopsy - melanoma

38
Q

Subtypes of melanoma

A

Superficial spreading (most common - significant epidermal component)

Nodular

39
Q

What is used to assess the stage of melanoma?

A 
Breslows thickness
Clark's scale
Microsatellites
Mitotic figures
Ulceration
Vascular invasion

Not size or diameter

40
Q

Which skin cancer is not associated with metastasis

A

Basal cell carcinoma

41
Q

What determines the stage in basal and squamous cell carcinoma?

A

Size and diameter

42
Q

What determines the stage in melanoma?

A

Thickness

43
Q

How many lung cancers are treated by surgery?

A

15%

44
Q

Where does paracetemol cause damage in the liver?

A

Perivenular/centrilobular - furthest away from portal blood supply where P450 enzymes greatest

45
Q

Pattern of damage in liver disease

A

Fatty change - steatohepatitis/fibrosis - cirrhosis

46
Q

Fatty liver disease histology

A

Macrovesicular staeatosis - stored as triglycerides that take over the cytoplasm

47
Q

Steatohepatitis histological features

A

Hepatocellular injury - fatty change, ballooning, mallory-denk bodies, apoptosis/necrosis

Inflammation

Fibrosis - perisinusoidal, pericellular

48
Q

what increases the risk of cholangiocarcinoma?

A

PSC - get premalignant changes due to periods of ucleration + regeneration

49
Q

Features of liver cirrhosis

A

Loss of normal lobular architecture
Nodular regeneration
Fibrosis

50
Q

How does skin heal?

A

Primary or secondary intention

51
Q

Primary intention

A

1 linear incision - can bring 2 ends together

52
Q

Secondary intention

A

e.g. leg ulcer - can’t bring together 2 ends so leave open, epidermis grows up + takes longer to heal

53
Q

Strength of a wound

A

10% at week 1
50-60% at 1m
70-80% plateau at 3m

54
Q

What are the 2 ways the liver heals?

A

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
Q

What regulates liver repair?

A

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
Q

what factors influence healing of the liver?

A

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
Q

what is hypoplasia?

A

NOT THE OPPOSITE OF HYPERPLASIA

failure of tissue/organ to reach normal size during development e.g. genetic defects

58
Q

What is atrophy?

A

decrease in size of tissue/organ at a stage after initial dvelopment. may be decrease in cell size or number

59
Q

what is metaplasia?

A

replacement (potentially reversible) of 1 differentiated cell type by another differentiated cell type

60
Q

What is dysplasia?

A

Disordered development

Changes resemble those seen in neoplastic cells - not yet invasive but can progress to invasive carcinoma if not treated

61
Q

Oncocytomas

A

Benign

Unformally large cells with eosinophils

62
Q

Chromophobes

A

Perinuclear halos

63
Q

Clear cell carincoma

A

Large cells with clear cytoplasm

64
Q

Transitional cell carcinoma

A

Papillary architecture with layers of urothelium

65
Q

Papillary

A

Papillae and eosinophilic cells. Foci of calcification

66
Q

Which zone of the prostate is BPH in?

A

Transitional

67
Q

Which zone of the prostate is cancer in?

A

Peripheral

68
Q

Eosinophilic oesophagitis

A

Hx of allergy + eosinophilia
Dysphagia
Mid oesophagus
Endoscopy: concentric rings ‘trachealisation’ of oesophagus

69
Q

Coeliac

A

Villous atrophy
Intra epithelial lymphocytosis
Chronic inflammation in lamina propria
Crypt hyperplasia

70
Q

UC

A 
Uniform diffuse lesions 
Superficial - mucosa 
Associated with PSC 
Absence of granulomas
Cryptitis and crypt abscess formation 
Crypt mucin depletion
71
Q

Crohns

A

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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