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pathology year 5 > Histopathology > Flashcards

Histopathology Flashcards

1
Q

Layers of the GI tract

A

1) Epithelium, lamina propria, muscularis mucosa
2) Submucosa
3) Muscularis propria (types include circular, longitudinal, oblique)
4) Serosa

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2
Q

Adenocarcinoma of oesophagus

A 
GORD
Barrett’s
Developed countries
Caucasian
Lower 1/3 of oesophagus
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3
Q

Squamous cell carcinoma of oesophagus

A

Smoking and alcohol
Middle 1/3 oesophagus
Developing countries

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4
Q

What is Barrett’s and what is a poor prognostic marker

A

Metaplasia from squamous to columnar

Goblet cells - intestinal metaplasia (more cancer risks)
No goblets cells - gastric metaplasia

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5
Q

Where in stomach does H.pylori occur?

A

Pyloric antrum and canal

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6
Q

Causes of acute gastritis

A

Chemicals, aspirin, NSAIDs, alcohol, corrosives, h.pylori

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7
Q

Causes of chronic gastritis

A

A - autoimmune (pernicious anaemia)
B - bacterial (h.pylori)
C - chemicals (NSAIDS, bile reflux)

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8
Q

Describe H.pylori

A
  • Spiral flagellated gram negative bacteria
  • 90% of chronic gastritis cases
  • can lead to development of lymphoid follicles + lymphoma (MALToma - Bcell)
  • can also lead to intestinal metaplasia (goblet cells) and cause adenocarcinoma
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9
Q

What is an ulcer?

A

Loss of tissue beyond the muscularis mucosa into the sub serosa

Chronic - scarring and fibrosis

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10
Q

Gastric vs duodenal ulcer

A

Gastric - worse when eating, older patients,

Duodenal- relieved by eating, worse on empty stomach, at night, younger patients

Biopsy all ulcers

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11
Q

Gastric cancer- adenocarcinoma and other types

A

M>F, Japan very high

Adenocarcinoma is >95%
Leather bottle stomach on endoscopy
Intestinal-> glands, well differentiated, mucin forming
Diffuse - no gland formation, signet ring cells, poor differentiation, poor prognosis

Others- MALToma, SCC, neuroendocrine, gastrointestinal stromal tumour

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12
Q

Menetriers disease

A

Hyperplasia of gastric pitts and increase in mucosal thickness

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13
Q

What is the histology of the duodenum?

A

Intestinal type epithelium, glandular columnar with goblet cells, has villi

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14
Q

What can H.pylori do in the duodenum?

A

It can cause gastric metaplasia and result in ulcers -> duodenitis

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15
Q

What is coeliacs disease?

Investigations and histology

A

IgA anti- tTG
Gold standard is duodenal biopsy and histology

Histology - villus atrophy, crypt hyperplasia, more infra epithelial lymphocytes

Enteropathy associated T cell lymphoma (EATL) risk increases

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16
Q

Liver histology, also describe the zones of the liver

A
  • Hepatic lobules, hexagonal shape
  • In each corner of lobule there is a portal triad of bile duct, portal venue and arteriole
  • Blood from portal triad to central vein (in centre of lobule from edges to centre) via sinusoids
  • Bile goes via caniculi away from, central vein to bile ducts

Zones:

  • Area between the triad and central vein is divided
  • 1 has most oxygen and highest ALP
  • 3 has most metabolically active cells so at risk of hypoxia
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17
Q

Acute hepatitis histology?

A

Spotty necrosis

Can be caused by viruses, drugs etc

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18
Q

Describe histology of chronic hepatitis

A

Piecemeal necrosis (Interface hepatitis)

Causes: viruses, drugs, PBC, PSC, Wilson’s, haemochromatosis

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19
Q

Features of obstructive jaundice

A
  • Itching
  • Pale stool
  • Dark urine (conjugated bilirubin in urine)
  • Lack of urinary urobiliogen (it’s is colourless)
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20
Q

What is urinary urobilinogen?

A

Bilirubin that has been converted by gut bacteria and reabsorbed by enterohepatic circulation for kidney excretion

Bilirubin must be conjugated by liver before excretion via bile or kidneys

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21
Q

What is transudate and some causes?

A

Protein <30g/L

Causes: cardiac failure, renal failure, cirrhosis, hypoalbuminaemia (like pressure is forcing it)

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22
Q

What is exudate and some of the causes?

A

Protein>30g/L

Inflammation, infection and malignancy, e.g. TB, malignant infiltration of peritoneum

This is to do with secretion

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23
Q

Histology of alcohol induced liver disease including the stages of steatosis, fibrosis and cirrhosis

A

Steatosis - fat, neutrophils (NASH looks like alcoholic fatty liver disease but is different based on Hx)

Alcoholic hepatitis - neutrophils, bile accumulation, bile flow blocked, balloon cells

Fibrosis - collagen blue stain chows collagen deposited, indicates scarring

Cirrhosis - regenerative nodules and cuff of fibrous connective tissue. Fibrous tissue between portal tracts too, distortion of vasculature architecture (disorganised regeneration that leads to portal HTN)

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24
Q

Features of CLD

A

Palmar erythema, gynaecomastia, spider naevi, dupytrens contracture

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25
Q

Features of portal HTN

A

Caput Medusae (swollen abdomen veins) splenomegaly, ascites

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26
Q

Feature of hepatic encephalopathy

A

Asterixis

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27
Q

Types of autoimmune hepatitis and the sequlae

A

Interface hepatitis
Inflammation, necrosis, fibrosis, cirrhosis and liver failure

1 - anti smooth muscle Abs and +- ANA, steroids Tx, from 10 years old onwards

2 - anti liver kidney microsomal Abs, poor steroid response, paeds

3 - anti soluble liver antigens Abs

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28
Q

PBC - antibodies, symptoms and associations

A
  • Antimithochondrial Abs
  • Intrahepatic bile ducts destroyed
  • Other AI disorders: scleroderma, RA
  • High ALP, bilirubin and cholesterol
  • Chronic granulomatous inflammation of bile duct
  • Itching, fatigue, abdo pain
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29
Q

Most common drug cause of hepatic adenoma

A

COCP

Hemangioma is most common benign lesion

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30
Q

What is portal inflammation vs interface vs lobular?

A

Portal - within the portal
Interface - between portal tract and parenchyma
Lobular - across whole lobe

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31
Q

Stages of fibrosis

A

0: no fibrosis

F1: portal fibrosis without septa

F2: portal fibrosis with few septa

F3: numerous septa without cirrhosis

F4: cirrhosis

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32
Q

What is Wilson’s disease and the signs?

A

Recessive, copper transport gene mutation, copper accumulated causing Parkinsonism features, liver disease, Kayser Fleisher rings, psychiatric problems

Rhodanine stain

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33
Q

Hereditary haemochromatosis - symptoms, management and pathophysiology

A

Recessive, excess iron absorption and deposition, haemosiderin deposited in organs causing rusty brown appearance

Brown bronze skin colour, steatorrhoea, diabetes, therapeutic phlebotomy

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34
Q

What is Gilbert’s?

A

Recessive, reduces UDP glucoronyl transferase and reduced bilirubin conjugation

Normal LFTs, raised unconjugated bilrubin

Fasting is trigger

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35
Q

What is Budd chiari syndrome?

A

Hepatic vein thrombosis, outflow obstruction, associated with polycythaemia rubra vera, hepatosplenomegaly, ascites

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36
Q

Pemphigus vulgaris

A 
Superficial
Easily ruptures
Nikolsky sign
Antibodies to desmoglein 1/3
Acantholytic cells - separation of keratinocytes due to loss of cadherin
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37
Q

Bullpus pemphigoid

A

Elderly
Flexor surfaces
Anti-hemidesmosome Abs
Tense bullae do not repute easily, sub epidermal

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38
Q

Pemphigous foliaceus

A

So superficial rarely see intact bullae, stratum corneum separates from epidermis

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39
Q

Dermatitis herptiformis

A

Coeliac disease, itchy bullous rash on extensor surfaces

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40
Q

Epidermolysis bullosa

A

Collagen autoantibodies, induced by trauma

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41
Q

Vitiligo

A

Anti melanocytes antibodies

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42
Q

Psoriasis

A

Parakeratosis - thick keratin layer, silvery scales

Munro microabscess

Loss of stratum granulosum - auspitz sign

Clubbing of rete ridges - test tube rack on histology

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43
Q

Lichen planus

A

Purple, pruritic, papules and plaques

White lacy appearance of mouth

Inner surface of wrists

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44
Q

Pyoderma gangrenosum

A

Form of vasculitis not gangrene

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45
Q

Seborrheic keratosis

A

Elderly, benign

Pigmented, stuck on appearance, cauliflower

Over proliferation of epidermis

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46
Q

Actinic keratosis

A

Pre malignant -> SCC

Sun exposed areas, sandpaper like, warty

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47
Q

Sebaceous cyst

A

Smooth, non mobile, punctum, smelly

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48
Q

Pityriasis rosea

A

Salmon pink lesion, multiple oval machines in fir tree distribution, follow an URTI

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49
Q

BCC

A

Smooth, pearly, central ulcer and fine telangiectasia, sun exposed area, elderly, locally invasive

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50
Q

SCC

A

Invasion through BM, can metastasise, sun exposed areas,

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51
Q

Bowen’s disease

A

SCC in situ, full thickness, no BM invasion

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52
Q

Erythema multiforme

A

Macules, papules, urticaria

Stevens Johnson’s syndrome - affects mucosa too

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53
Q

What are two key functioning parts of the pancreas

A

Islet of langeehans

Acini- glandular functional units

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54
Q

Acute pancreatitis sequale

What is the most sensitive marker of pancreatitis?

Causes

Histology

A

Insult, necrosis, enzyme release, acute inflammation

Lipase

I GET SMASHED- idiopathic, gallstones, ethanol, trauma, steroids, mumps, autoimmune, scorpion venom, hyperlipiadaemia, hypercalcaemia, hypothermia, ERCP, drugs (thiazides)

Acute inflammation and necrosis

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55
Q

What is a pseudocyst and what causes it?

A

Collection of fluid after acute pancreatitis. Lined by fibrous tissue containing enzymes and necrotic material. Can get infected and form abscess,

Causes abdominal discomfort

Spontaneous resolution

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56
Q

Chronic pancreatitis causes, histology, symptoms and investigations

A

Alcohol, haemochromatosis, gallstones, CF, tumours

Parenchyma fibrosis, atrophic acini, dilation of ducts, duct strictures, intrapancreatic caliculi

Severe epigastric pain radiating to back, steatorrhoea, malabsorption

Pancreatic calcifications on AXR/CT

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57
Q

Pancreatic cancer, presentation, epidemiology, investigations

A

Ductal adenocarcinoma is most common

> 60, M>F
5 year survival 5%
At head >body>tail
Due to location causes jaundice

Weight loss, abdo and back pain, painless jaundice, pruritis, steatorrhoea, DM, ascites, VTE

Tumour marker CA19-9

Whipples for head of cancer, palliative chemo

Acinar cell adenocarcinoma, pancreatoblastoma (childhood, rare)

No SCC

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58
Q

Neuroendocrine tumours

A

Tail>body>head

Men1 associated

Chromoganin levels in blood

Can be functioning or non - e.g. insulinoma, gastrinoma

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59
Q

Gallstones - RF, types

A

Female, Native American, OCP, rapid weight loss e.g. surgery

Cholesterol (won’t show on x ray), pigmented (calcium salts, unc bilirubin)

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60
Q

Acute vs chronic cholecystitis

A

Acute- lots of neutrophils, due to stones

Chronic - fibrosis, rokitansky aschoff sinuses (diverticula)

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61
Q

Gallbladder cancer

A

Mostly due to gallstones, uncommon though

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62
Q

Diverticulitis

A

Old
Rectal bleeding
Fever
LIF

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63
Q

UC

A

Continuous from rectum proximally, no granulomas, mucosal inflammation

Blood and mucus, associated with PSC, can have pseudo polyps in bowel, can get ulcers

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64
Q

Crohns

A

Patchy inflammation, full thickness, non caseating granulomas, anywhere in GI tract, common at terminal ileum, thickness wall (rubber hose)

Cobblestone mucosa

Tend to get fistula and fissures

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65
Q

Colorectal cancer

A

Older age, western populations, mostly adenocarcinoma, CFA tumour marker

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66
Q

Adenomas (polyps)

Sequence to adenocarcinoma and types of polyps

A

Precursor to colorectal ca

Types: tubular, tubolovillous, villus

First mutation in APC, then second puts at risk of adenoma. Kras or p53 then turns into adenocarcinoma

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67
Q

Peutz jegher syndrome

A

dominant, multiple polyps, bleeding, freckles around mouth, palm and soles, increased risk of intususception, mucocutanenous pigmentation

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68
Q

Juvenile polypsosis

A

Dominant inheritance, lots of polyps, may need colectomy

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69
Q

FAP

A

APC gene mutation most common, lots of adenomatous polyps, high risk of adenocarcinoma, prophylactic colectomy.

At birth have hypertrophy of retinal pigment epithelium

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70
Q

Lynch syndrome (HNPCC)

A

Dominant inheritance, carcinomas before 30, few polyps, associated with endometrial/ovarian/small bowel/stomach ca

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71
Q

Acute mastitis

A

Red, painful, tender, hot, neutrophils

Lactational - cracked skin, stasis of milk, staph aureus, must continue expressing milk, surgically drain if abscess

Non-lactational - peri ductal inflammation

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72
Q

Duct ectasia

A

40-60, multiparous, smoker

Inflammation and dilation of breast ducts, nipple greeny brown discharge, breast pain, nipple retraction, periareolar mass

Mammography may mimic cancer, no risk of malignancy

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73
Q

Fat necrosis of breast

A

After trauma, in middle aged women, obese, after surgery or radiotherapy too, painless for, breast mass, can cause nipple retraction

Empty fat spaces, histocytes, multinucleated giant cells

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74
Q

Fibroadenoma

A

20-30, freely mobile breast lump

Changes in size with hormones

Stromal and glandular tissue

Has stromal, glandular cells

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75
Q

Fibrocystic disease

A

Hormone responsive, lumpy, common in premenopausal women, may be related to menstruation, dilated large calcified ducts

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76
Q

Intraductal papilloma

A

Bloody nipple discharge
Middle aged
Not seen on mammogram
Papillary mass within dilated duct

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77
Q

Flat epithelial atypia and in situ lobar neoplasia

A

FEA - earliest presentation of DCIS potentially, 4x increased cancer risk, cribriform areas (punched out holes)

ISLN - solid proliferation of cells, 7-12x times increased risk of cancer

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78
Q

Breast cancer

  • carcinoma in situ, invasive breast carcinoma and basal like carcinoma
A

Most common ca in women, gold standard for diagnosis is histopathology

Carcinoma in situ:
- not invaded BM
Complete excision with clear margin in curative
- lobular(no necrosis, pre menopausal) and ductal (necrosis, pre or post, ducts with atypical cells)

Invasive breast carcinoma:
Ductal, lobular, tubular, mucinous
Indications: peau d’orange, tethering, pagers disease (eczema), nipple retraction, lymphadenopathy, bloody discharge, ulceration

Basal-like carcinoma: sheets of atypical cells, lymphocytic infiltrate and central necrosis

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79
Q

Grading of invasive breast cancer and immunotyping

A

Grading: core biopsy & histological analysis of 3 things = mitotic figures, nuclear pleomorphism, tubule
formation

Higher grade = poorly differentiated

Once diagnosed all are assessed for ER/PR/HER2 receptors

ER/PR +ve = good prognosis - will respond to Tamoxifen

HER2 +ve = worse prognosis - treat with Herceptin

Most important prognostic factor for BC = status of the axillary LNs

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80
Q

PSC

A

Inflammation causes scars within the bile ducts - makes the ducts hard and narrow and gradually causes liver damage.
Associated with UC

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81
Q

Pathogenesis of atherosclerosis

A

Pathogenesis: endothelial injury → LDL adhesion → oxidised LDL → monocyte
adhesion to the endothelium → macrophages take up LDL & form foam cells → platelet adhesion & smooth muscle recruitment → smooth muscle cells form fibrous cap

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82
Q

Histology following an MI

A
  • Under 6 hours – normal by histology
  • 6–24 hrs - loss of nuclei, homogenous cytoplasm, necrotic cell death, contraction band necrosis (dark
    red/pink wavy lines extending across the myocardial fibres)
  • 1-4 days – infiltration of polymorphs (neutrophils) then macrophages (clear up debris), cytoplasm is
    homogenous so it is difficult to see outlines between myocardial fibres
  • 5-10: days removal of debris
  • 1-2 weeks: granulation tissue, new capillaries, myofibroblasts & macrophages present in large numbers,
    collagen synthesis, young scar
  • Weeks-months: strengthening, decellularising scar - a pale white collagenous area within the interstitium
    between myocardial fibres
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83
Q

Dilated, hypertrophic, restrictive cardiomyopathy

A

Dilated - progressive loss of myocyte
Idiopathic, infective, alcohol, chemo, diabetes, thyroid issues, haemochromatosis

Hypertrophic - LVH,, familial, cause of sudden death in young person

Restrictive -too stiff, idiopathic, amyloidosis, sarcoidosis, IBD

84
Q

Rheumatic heart disease

A

Follows from rheumatic fever, mostly affects mitral valves

Antigenic mimicry and cross reactivity -> mitral stenosis or prolapse

Beady/warty fibrous vegetation, granulomas, regenerating myocytes

85
Q

Mitral valve disease causes of each

A

AS: Elderly, Calcification, ejection-systolic murmur

AR: Causes = rheumatic HD, microbial endocarditis, Marfan’s, dissecting aneurysm, AS

MR: Left ventricular dilation, IE, CTD, post-MI, Rheumatic fever

Mitral valve prolapse (aka myxomatous mitral valve): middle-aged women, mid systolic click + late systolic
murmur

86
Q

Non bacterial thrombotic endocarditis

A

> 40, no inflammation or bacteria, mitral

Associated with malignancy, Dic, hyperccoagulable state

RECURRENT EMBOLI

87
Q

Infective endocarditis - acute

A

Staph aureus, strep pyogenes, IVDU, tricuspid valve, larger thrombi, flucoxacillin IV

FOR MRSA: rifampicin, vancomycin, gentamicin

88
Q

Subacute infective endocarditis- more common

A

PUO for months, strepviridans, aortic and mitral valves, post dental treatment soft thrombi

Microscopic haematuria, splenomegaly, heart murmurs

Benzypenicilln and gentamicin IV

89
Q

Histology of thyroid gland

A

Follicles containing colloid, stroma between follicles, parafollicular cells secrete calcitonin

90
Q

Histology of Hashimoto’s thyroiditis

A

Lymphoid cells, germinal centres

Epithelial cells enlarge and develop eosinophilic cytoplasm - hurthle cells

91
Q

Histology of adrenal gland

A

Zona glomerulosa - aldosterone

Zone fasciculata - glucocorticoids

Zona reticularis - androgens and glucocorticoids

Medulla - noradrenaline and adrenaline

92
Q

Thyroid carcinoma

A

Papillary - most common, IR, psammoma bodies, non functional, any age, good prognosis, may have cervical nodes mets

Follicular - middle aged,looks like normal thyroid, metastasise v blood

Medullary - parafollicular cell origin, produce calcitonin, staining positive with Congo red and apple green, CEA and calcitonin tumour marker

Anaplastic - aggressive, early mets, elderly, poor prognosis

93
Q

Men syndrome

A

MEN 1: pituitary tumours, parathyroid tumours, pancreatic neuroendocrine tumours, facial angiofibromas &
collagenomas

MEN 2A: pheochromocytoma, hyperparathyroidism, medullary thyroid cancer

MEN2B: phaeochromocytoma, medullary thyroid cancer, marfanoid phenotype, neuromas of the GI tract

94
Q

Fibrous dysplasia

A
  • Females, age<30
  • Proximal femur/tibia/skull/ribs
  • Bone pain from early adulthood
  • Soap bubble osteolytis
  • Shepherds crook deformity
  • Marrow replaced by fibrous stroma, rounded trabecular bone
95
Q

Osteochondroma

A

10-20, males
End of long bones, common benign tumour
Bony protuberance with cartilage cap

96
Q

Osteitis osteoma

A

Bone forming, adolescent, dull pain at night, relieved by aspirin, bulls eye x ray, normal bone

97
Q

Enchondroma

A

Fingers and hands
Middle aged
Risk of malignant transformation
Popcorn/cotton wool calcification

98
Q

Osteoma

A

Middle aged
Head and neck
Bony outgrowths
Associated with Gardner syndrome

99
Q

Bone cyst

A

Fluid filled cyst, asymptomatic

Lytic well defined lesion

100
Q

Osteoblastoma

A

Speckled mineralisation

101
Q

Osteosarcoma

A 
Forms bone
10-30
End of long bones, most common is knee
Pain and mass
Elevated periosteum - codmans triangle
Sun-burst appearance
ALP positive
Poor prognosis
102
Q

Chondrosarcoma

A 
Cartilage producing
>40
Axial skeleton, proximal femur/tibia/pelvis 
Lytic lesions with fluffy calcification
Surgery
103
Q

Ewings sarcoma

A

<20
Diaphysis and metaphysics of long bones or pelvis
Onion skinning or periosteum,
Sheets of small round cells, ALP negative
Translocation of 11:22

104
Q

Giant cell tumour

A 
Knee
20-40
Lytic lesions, soap bubble appearance
Giant multinucleate osteoblasts
Tumour cells are the stromal cells
105
Q

What is a green stick fracture?

A

Paediatric fracture, transverse but partial, remains attached

106
Q

What is a comminuted fracture?

A

Segmental fracture, bone is splintered

107
Q

What is a compound fracture?

A

Penetration of skin surface, open fracture

108
Q

What is an impacted fracture?

A

Fracture site is crushed inwards

109
Q

What is cancellous and cortical bone?

A

Cortical - calcified, long bones, mechanical and protective

Cancellous - axial Skelton, vertebrae, pelvis etc

110
Q

What is osteoarthritis?

A

Loss of joint space, subchondral cysts and subchondral sclerosis

111
Q

What is RA? Signs, diagnosis and characteristic deformities

Histology

A

Symmetrical, small joints of hands and feet and ankles, elbows and knees.

Serology – RF +ve in 60-70%, anti-CCP is more sensitive & specific than RF

Characteristic deformities:

  • Radial deviation of wrist and ulnar deviation of fingers.
  • swan neck” and “Boutonniere” deformity of fingers
  • Z shaped thumb
  • Synovial swelling

Swan neck = hyperextension of PIPJ & flexion of DIPJ

Boutonniere = flexion of PIPJ & hyperextension of DIPJ

Extra-articular features: Pulmonary fibrosis, vasculitis, amyloidosis, pericarditis, subcutaneous nodules, DVT

Histopathology – thickening of synovial membrane, hyperplasia of surface synoviocytes, intense inflammatory cell infiltrate & fibrin deposition & necrosis

112
Q

What is ankylosing spondylitis?

A

An inflammatory disease

Can cause some of the bones in the spine (vertebrae) to fuse - bamboo spine

113
Q

What is psoriatic arthritis?

A

New fluffy bone. Associated nail changes like pitting

114
Q

Osteoporosis

A

Reduction in bone density
Normal biochemistry
Increased translucency

115
Q

What is reactive arthritis?

A

HLA B27
Sacroiliac and knee joints, feet, ankles

Joint pain and swelling triggered by an infection in another part of the body — most often the intestines, genitals or urinary tract.

116
Q

Small cell carcinoma

A 
20%
Smoking, poor prognosis
Paraneoplastic syndromes (SIADH, hyponatraemia, ectopic ACTH)
Oat shaped cells
P53, RB1 mutation 
Central
117
Q

Squamous cell lung cancer

A

Smoking, most common subtype, central from bronchial epithelium, males, keratin and intracellular bridges, spread locally and metastasise late, kras - poor prognosis

118
Q

Adenocarcinoma lung cancer

A

Non smokers, females, Asians, peripherally located, glandular differentiation, cells with mucin vacuoles, EGFR mutation, early mets, kras is poor prognosis

119
Q

Large cell lung carcinoma

A

Poor differentiated large cells and large nuclei, no squamous or glandular differentiation, diagnosis of exclusion, poor

120
Q

Asbestos lung conditions

A

Plumber and ship workers
Plaques are benign

Mesothelioma - thickened
pleura, malignant, latency or 25-45 years

Pneumoconiosis - fibrosis, benign, affects lower lobe

121
Q

Extrinsic allergic alveolitis

A

Persistent productive cough, SOB, clubbing, weight loss

Mouldy hay, farmers lung

122
Q

Heart failure - right and left sequence

A

LHF → pulmonary oedema → intra-alveolar fluid & iron-laden macrophages

RHF → systemic oedema → venous congestion in organs → nutmeg liver

123
Q

Pulmonary oedema

A

Presentation of PO = SOB, coughing up pink frothy sputum

Main cause = LHF

Nom-cardiac causes = fluid overload, RF, alveolar injury, neurogenic, high altitude

Cardiac causes on CXR → Kerley B-lines, bats wing appearance, cardiomegaly, upper lobe diversion of blood vessels, effusion

124
Q

Pattern or acute lung injury - causes in adults and neonates

3 phases and histology

A

Rapid respiratory failure due to damage to alveolar epithelium & endothelium

Adults - ARDS
- 24-48 hrs post-trauma, burns or sepsis

Neonates - RDS (hyaline membrane disease)

Histology → diffuse alveolar damage, lungs are plum coloured, heavy & airless

3 phases of the acute lung injury pattern:

  • Exudative phase: lungs become leaky
  • Hyaline membrane phase: hyaline membranes line the alveolar spaces
  • Organising phase: organisation of exudates to form granulation tissue
125
Q

Asthma

A

Eosinophils and mast cells.muscular hypertrophy, airway narrowing, mucus plugging

Charcot Leyden crystals - eosinophils inflammation

Goblet cell hyperplasia

126
Q

COPD - emphysema and chronic bronchitis

Complications, sequence and symptoms

A

Chronic bronchitis and emphysema

Chronic Bronchitis:
Chronic productive cough present on most days for 3 months over 2 consecutive years

Airway damage → dilated airways, goblet cell hyperplasia, inflammation, hypertrophy of mucous
glands

Complications: lung cancer (independent of smoking), recurrent infections, chronic respiratory failure,
pulmonary hypertension → cor pulmonale (RHF)

Emphysema:
Smoking → activation of macrophages & neutrophils → release of proteases → permanent loss of alveolar
parenchyma

Main 2 causes = smoking, alpha-1 antitrypsin deficiency

Smoking → loss centred around a bronchiole (centrilobular)

Doesn’t cause a productive cough / recurrent infections - just causes SOB

Complications: bullae → pneumothorax, respiratory failure, PH → cor pulmonale

127
Q

Bronchiectasis

A

Permanent abnormal bronchial dilation with inflammation and fibrosis

Causes: infection, CF, immunodeficiency,obstruction, asthma, sarcoidosis, obstruction

Complications: haemoptysis, infections, amyloidosis, RHF

Signer ring sign, tram track opacities

128
Q

Lobar and bronchopulmomary pneumonia

A

Bronchopulmonary: infection is centred around an airway
Elderly, H.influenzae, Staph, Strep, Pneumococcus, patchy bronchial and peribronchial distribution

Lobar: infection within a specific lobe
Strep.pneumoniae

Histology: congestion (intra-alveolar fluid) → red hepatisation (intra-alveolar neutrophils) → grey
hepatisation (dry and firm as cells disintegrate & formation of intra-alveolar connective tissue) →
resolution (back to normal architecture)

129
Q

Seminoma

A

Radiosensitive, germinal tumour, most common

130
Q

SLE

A

Malar rash histology: lymphocytic infiltration of dermis, vacuolation of the basal epidermis, extravasation of RBCs in the upper dermis, immune complex deposition at dermal-epidermal junction

Kidney histology: Immune complex deposition in capillaries → ‘wire loop capillaries’, deposition of immune
complexes & complement in GBM in a lumpy-bumpy granular fashion

Libman-Sacks Endocarditis: non-infective endocarditis associated with SLE, vegetations are made of immune cells & fibrin strands → murmur

131
Q

Alzheimer’s disease

A

Beta amyloid, NFTS made of tau

Generalised brain atrophy, widened sucks, narrowed gyri, enlarged ventricles

132
Q

Parkinson’s disease

What is it, signs and symptoms?

A

Loss of DA neurones from substantia migraine which project to basal ganglia. ↓ stimulation of the motor cortex

‘TRAP’ Tremor, Rigidity, Akinesia, Postural instability

Some develop psychiatric features later in disease e.g. Parkinsons Disease Dementia, hallucinations, anxiety

Lewy bodies present in affected neurons (alpha synuclein protein is main component; mutations reported in familial PD)

Familial Parkinson’s - worse

133
Q

Huntingtons disease

A

Cerebral atrophy in caudate nucleus and putamen

Number of repeats increases, earlier onset, dominant

134
Q

Multiple sclerosis

A

Autoimmune demyelinating disease Usually presents with focal sx: optic neuritis, poor coordination.

Myelin basic protein & proteolipid protein = what is targeted

MRI: Demyelinating plaques - number of plaques is indicative of the severity of the disease

Females, 20-40 yrs of age

135
Q

Oligodendroma

A

Soft gelatinous, calcified

136
Q

Medulloblastoma

A

Always Grade 4, from embryonal cells - neuroepithelial precursors of brainstem / cerebellum, in the cerebellum! 2nd most common primary CNS tumour in children

Histology → high grade, small blue round cells with hyperchromatic cytoplasm, stains +ve for synaptophysin

137
Q

Ependymoma

A

From ependymal cells lining the ventricles, hydrocephalus and ventricular tumour

138
Q

Meningioma

A

Most benign, >40, mass under dura, mostly frontal lobe, focal symptoms, doesn’t really invade brain

Neurofibromatosis type 2

139
Q

Schwannoma

A

Acoustic neuroma

140
Q

Glioma types

A

Oligodendrogliomas

Diffuse astrocytoma

Pilocytic astrocytoma

Glioblastoma multiformw

Can be diffuse or circumscribed

141
Q

Pilocytic astrocytoma

A

Most common type of primary CNS tumour in children

Slowly growing benign tumour

MRI → well-circumscribed, cystic enhancing lesion

Histology → piloid (hairy) cells, Rosenthal fibres, low mitotic activity,
well-differentiated astroglial cells

142
Q

Diffuse Astrocytoma

A

20-40
Cerebral hemispheres
Ill defined non enhancing lesion
Can become gliobastoma

143
Q

Glioblastoma multiforme

A

Can arise from astrocytomas

Most common primary CNS tumors in adults

> 50 yrs

MRI → heterogeneous enhancement, neoangiogenesis

Histology → large cells, highly polymorphic, high mitotic activity, microvascular proliferation and necrosis, pathological blood vessels

144
Q

Oligodendroglioma

A

Diffuse, 20-40, slow growing, less aggressive, long hx of neurological signs, fried egg cells on histology

145
Q

Subfalcine, subtentorial, tonsillar herniation

A

Subfalcine: cortex pushed under rigid falx cerebri of the dura, usually due to a SOL

Subtentorial (Uncal): herniation of medial temporal lobe through the tentorial notch, most common type

Tonsillar: cerebellar tonsils herniate through the foramen magnum - death due to pressure on medulla

146
Q

Grading of CNS tumours

A

Classified according to tumour type & grade (level of
differentiation)

NO staging - primary CNS tumours don’t spread

WHO Grading system:
- LOW Grades: 
Grade 1: benign, long-term survival
Grade 2: survival > 5 years
  • HIGH Grades:
    Grade 3: survival <5 years
    Grade 4: survival <1 year
147
Q

Symptoms of Stroke :
ACA
MCA
PCA

A

ACA: contralateral hemiplegia & sensory loss leg>arm/face, personality
changes

MCA: contralateral hemiplegia & sensory loss arm/face>leg, if on the left - Broca’s aphasia & Wernicke’s
aphasia, if on the right - neglect

PCA: contralateral hemianopia or quadrantopia, CN palsies

148
Q

common cause of SAH

A

SAH: due to congenital berry aneurysm (most common at bifurcation of internal carotid), sudden onset thunderclap
headache

149
Q

HIV tuberculoma

A

Ring enhancing lesion

150
Q

Tuberous sclerosis

A

Epileptic with patch on back and lumps in brain

151
Q

Neurofibromatosis 1

A

Characterized by changes in skin coloring (pigmentation) and the growth of tumors along nerves in the skin, brain, and other parts of the body

152
Q

Ovarian tumours

A

Epithelial most common

  • serous cystadenoma
  • mucinous cystadenoma
  • endometriod carcinoma
  • clear cell carcinoma

Germ cell tumours

  • dysgerminoma
  • cystic teratoma
  • choriocarcinoma

Sex chord /stromal

  • granulosa/thecal cell
  • sertoli leydig cell tumour
  • fibroma

Metastases
- krukenberg tumour

153
Q

Serous cystadenoma - ovary

A

Most common, usually unilocular, can be benign, borderline or malignant

Histology: columnar epithelium, psammoma bodies (concentric laminated calcifications)

154
Q

Mucinous cystadenoma- ovary

A

Mucin secreting cells, epithelium may resemble GI or endocervix, benign borderline or malignant, Kras mutation

155
Q

Endometriod carcinoma

A

Malignant, mimics endometrium, better than mucinous or serous for prognosis, tubular glands on histology, endometriosis risk factor

156
Q

Clear cell carcinoma

A

Clear cells with lots of glycogen, hobnail appearance- bulbous nucleus and nuclear projections into cytoplasm,malignant, poor prognosis, endometriosis association

157
Q

Dysgerminoma

A

Most commmon ovarian ca in young women, no differentiation, can give raise to any cancer if malignant

158
Q

Cystic teratoma or dermoid cyst

A 
Mature:
Aka dermoid cyst
Benign usually
Differentiation into mature tissues e.g. skin, teeth, hair, bone, cartilage
Usually bilateral & asymptomatic
Most common type of germ cell tumour

Immature:
Tend to be malignant
Solid
Contain immature embryonal tissue - tends to be neural tissue
Secrete AFP

159
Q

Choriocarcinoma

A

Mimics pregnancy secretes hcG

160
Q

Sertoli Leydig cell tumour

A

Secrete androgens -> virilisation, breast atrophy, hirsutism, enlarged clitoris

161
Q

Granulosa/thecal cell tumour

A

Secrete oestrogen → PMB, IMB, endometrial cancer, breast cancer, breast enlargement

162
Q

Krukenberg tumour

A

Malignancy of the ovary due to metastasis from usually gastric/colonic/breast cancer

Signet ring cells - mucin producing

163
Q

Endometrial cancer

A

Endometrioid (85%):

Subtypes - mucinous adenocarcinoma, secretory adenocarcinoma
Younger patients
Related to excess oestrogen

Non-Endometrioid (15%):
Subtypes - papillary, clear cell, serous
Older patients
Less oestrogen dependent
Tend to have a higher grade, deeper invasion & higher stage
164
Q

Naming malignancies

A

Histology of cells: large nuclei, lots of mitoses, large nucleo-cytoplasmic ratio

Carcinoma: derived from epithelial cells

Squamous cell carcinoma: keratin (swirly appearance), intercellular bridges

Adenocarcinoma: from glandular epithelium, glands, mucin producing

Sarcoma: derived from connective tissue

165
Q

Granulomas

A

An organised collection of activated epithelioid macrophages

Epithelioid - look like epithelial cells; can also be called histiocytes

Lymphocytes around the outside

Giant Cells of Langhans (multinucleate) may be present - these are just
multiple epithelioid macrophages fused together, nuclei may have a
horseshoe appearance around outside of cell

Caseating granuloma (cheesy area) = TB

Non-caseating granuloma = sarcoidosis, leprosy, cat scratch fever, fungal infections

166
Q

Congo red and apple green birefringence stain

A

Positive for amyloidosis

167
Q

Fontana stain

A

Positive for melanin and melanoma

168
Q

Rhodanine

A

Golden brown, positive for copper in Wilson’s disease

169
Q

Prussian blue stain

A

Positive for iron, haemochromatosis

170
Q

Cytokerarin stain

A

Epithelial marker, immunohistochemical stain = Carcinoma

171
Q

Zeihl neeson stain

A

Red against blue background, acid-fast bacilli = TB

172
Q

Fite stain

A

Mycobacterium leprae

173
Q

India ink stain

A

Cryptococcosus neoformams

174
Q

Auramine stain

A

Bright yellow fluorescence for TB

175
Q

Different cell types and what it means histology

A

Neutrophils - Acute inflammation (sterile or non-sterile)

Lymphocytes - Chronic inflammation, lymphoma

Macrophages - Late acute inflammation, chronic inflammation (including granulomas e.g. Sarcoidosis)

Plasma Cells - Chronic inflammation, myeloma

Eosinophils - Allergic reactions, parasitic infections
Tumours e.g. Hodgkin’s disease

176
Q

What three categories can renal pathologies be divided into? Give examples of each

A

Those affecting the glomerulus, tubes and insterstitium, and blood vessels

Glomerulus - nephrotic syndrome, nephritic syndrome

Tubules and interstitium - acute tubular necrosis, tubulointerstitial nephritis

Blood vessels - HUS, TTP

177
Q

What is nephrotic syndrome?

A

Can be primary or secondary (diabetes, SLE)

Characterised by triad of proteinuria (pcr>300), hypoalbuminaemia (<30) and oodema

Swelling classically periorbital in children and frothy urine

Loss of podocyte foot processes, may have immune deposits, may have glomerulae BM thickening, scarring

Management with steroids generally and ACEi/ARN for BP control

178
Q

Nephrotic syndrome diagnosis

A
  • Urine dip – proteinuria, NO haematuria
  • Urine PCR - >300mg/mmol
  • Serum albumin – low
  • Total cholesterol – high
  • Immunoglobulins – low
  • Renal biopsy – diagnostic investigation of choice in adults (avoided in children)
179
Q

What is nephritic syndrome?

A

Glomerular inflammation characterised by

PHAROH
proteinuria, haematuria, azootemia (high urea and creatinine), red cell blasts, oliguria and hypertension

180
Q

Causes of nephritic syndrome

A

1) Post strep throat infection or impetigo (1-3 week), granular deposits of IgG in GBM
2) Berger disease - IgA deposits in glomeruli, 1-2 days after URTI with frank haematuria, can progress to ESRF, South Asians
3) Rapidly progressive GN - most aggressive, can go to ESRF, more pronounced oliguria and renal failure, crescents in glomeruli (from macrophages and parietal cells I’m Bowman’s space). Can get vascularised as rashes.
4) Hereditary - alports syndrome, x linked, sensorineural deafness, eye disorders e.g. cataracts, 5-20 yo
5) Thin basement membrane disease- dominant, microscopic haematuria usually asymptomatic

181
Q

Describe the types of rapidly progressive GN

A

Type 1 - goodpastures disease with anti GBM antibodies
Type 2 - immune complex mediated and associated with SLE, post infection and IgA
Type 3 - lack of immune complex c-ANCA associated (Webber’s granulomatosis) or pANCA (microscopic polyangilitis)

182
Q

Causes of asymptomatic haematuria

A

Thin basement membrane disease aka benign familial haematuria (renal functional normal and excellent prognosis)

IgA nephropathy - Berger disease, more likely than TBMD to cause haematuria and is more common in Asians

Alports syndrome

183
Q

Acute tubular necrosis/injury, causes and sequence

A

Most common cause of ARF

Damage to tubular epithelial cells -> reduced flow and increased haemodynamic pressure in nephron -> reduced pressure gradient across BM -> acute renal failure -> tubular glomerular feedback reduces blood supply to kidneys further

Causes include:

  • hypovaelamia
  • drugs (amino glycosides, NSAIDs), radiographic contrast agents, myoglobin (e.g. secondary to rhabdomyolysis), heavy metals

Histopathology: necrosis of short segments of tubules

184
Q

What is tubulointerstitial nephritis? Give types too

A

Renal inflammatory disorders affecting tubules and interstitium

Acute pyelonephritis - e.coli, fever chills sweats flank pain renal angle tenderness and leukocytosis with maybe urinary symptoms and even haematuria

Chronic pyelonephritis - caused by recurrent infections, scarring and inflammation, can be from urine reflux, chronic obstruction from calculi

Acute interstitial nephritis - hypersensitivity reaction to drug e.g. NSAIDs, begins a day after with fever skin rash haematuria proteinuria and esosinophilia

Chronic interstitial nephritis - in elderly on long term analgesics, late in disease get symptoms like HTN, proteinuria and haematuria

185
Q

HUS

A

Children,
MAHA, thrombocytopenia, renal failure
Associated with diarrhoea from e.coli
Thrombi confined to kidneys

186
Q

TTP

A

Affects adults
MAHA, thrombocytopenia, fever, renal failure, neurological signs

Generic ADAMTS13 mutation, thrombi throughout circulation

187
Q

Diagnosis of TTP or HUS

A

Low hb, platelets,

Signs of haemolytic: high bilirubin, reticulocytes, ldh

fragmented red cells

Coombs negative

Differentiate on symptoms

188
Q

Acute renal failure

Pre renal, renal and post renal causes

A

A rapid loss of renal function manifesting as increased serum creatinine and urea.

  1. PRE-RENAL
    Caused by renal hypo-perfusion e.g. hypovolaemia, sepsis, burns, acute pancreatitis, and renal
    artery stenosis.
  2. RENAL
    Acute tubular necrosis, acute glomerulonephritis and thrombotic microangiopathy.
  3. POST-RENAL
    Obstruction to urine flow as a result of stones, tumours (primary & secondary), prostatic hypertrophy and retroperitoneal fibrosis
189
Q

Chronic renal failure - what is it and list it’s causes

A

Progressive, irreversible loss of renal function characterized by prolonged symptoms and signs of uraemia (fatigue, itching, anorexia and if severe eventually confusion).

Causes: diabetes, glomerulonephritis, hypertension, vascular disease, chronic pyelonephritis, polycystic kidney disease

190
Q

5 stags old chronic renal failure

A

Classified into 5 stages by GFR:

1 - normal renal function, proteinuria maybe, GFR>90
2 - 60-89
3 - 30-59
4 - severely impaired function, 15-29
5 - renal failure, <15
191
Q

Polycystic kidney disease

A

Group of disorders characterised by renal cysts and numerous systemic extra-renal manifestation

Clinical features: MISHAPES
o Abdominal Mass
o Infected cysts & increased BP
o Stones
o Haematuria
o Aneurysms (Berry)
o Polyuria & nocturia
o Extra-renal cysts e.g. liver, ovaries, pancreas, seminal vesicles 
o Systolic murmur – due to mitral valve prolapse
192
Q

Renal cell carcinoma

A

Types:

  1. Clear cell carcinoma – well differentiated
  2. Papillary carcinoma – commonest in dialysis-associated cystic disease
  3. Chromophobe renal carcinoma – pale, eosinophilic cells

Risk factors: smoking, obesity, HTN, unopposed oestrogen, heavy metals, CKD

Clinical features: costovertebral pain, palpable mass, haematuria

Paraneoplastic syndrome: polycythaemia, hypercalcaemia, HTN, Cushing’s syndrome, amyloidosis

193
Q

Temporal arteritis

A

Elderly, scalp tenderness, temporal headache, jaw claudication, blurred vision, high ESR, biopsy needed, granulomatous and giant cells

Prednisolone

194
Q

Takayasu arteritis

A

Pulseless disease, low Bp in arms, cold hands, high in Japanese women

195
Q

Kawasaki disease

A

Children under 5, fever, red rash on palms and soles with desquamation, conjunctivitis, strawberry tongue, aneurysm formation

196
Q

Polyarteritis nodosa

A

Renal involvement, micro aneurysm, string of pearls

197
Q

Wegners granulomatosis

A

Triad of:

(1) Upper resp tract: sinusitis, epistaxis, saddle nose
(2) Lower resp tract: cavitation, pulmonary haemorrhage
3) Kidneys: crescentic glomerulonephritis-> haematuria & proteinuria

cANCA (anti-PR3) +ve

198
Q

Churg strauss or eosinophilic granulomatosis with polyangiitis

A

Asthma, allergic rhinitis, eosinophilia

pANCA positive

199
Q

Henoch Schlonein Purpura

A 
IgA mediated vasculitis
In children < 10 years
Preceding URTI
Palpable purpuric rash (lower libs extensors + buttocks)
Colicky abdo pain
Glomerulonephritis 
Arthritis
Orchitis
200
Q

Microscopic polyangitis

A

Pulmonary renal syndrome:

(a) Pulmonary haemorrhage
(b) Glomerulonephritis

pANCA (anti-MPO) +ve

201
Q

Amyloidosis

A

Multisystem disorder caused by abnormal folding of proteins that are deposited as amyloid fibrils in tissues, disrupting their normal function.

Clinical features:
KIDNEY: nephrotic syndrome = most common presentation

HEART: conduction defects, heart failure, cardiomegaly

LIVER/SPLEEN: hepatosplenomegaly

TONGUE: macroglossia in 10%

NEUROPATHIES: incl carpal tunnel

202
Q

Sarcoidosis - what is it and the signs and diagnosis

A

A multisystem disease of unknown cause, commonly affecting young adults, characterized by non-caseating granulomas in many tissues

Bilateral hilar lymphadenopathy, worse in Afro Caribbean, females, fine modular mid zone shadowing, SOB, cough, chest pain, night sweats

SKIN: erythema nodosum, lupus pernio (red/purple
lesions around nose), skin nodules

LNs: lymphadenopathy, painless and rubbery

JOINTS: arthritis, bone cysts

EYES: anterior uveitis, keratoconjunctivitis, lacrimal gland enlargement

LIVER/SPLEEN: Hepatosplenomegaly

BLOOD: Leukopaenia/ anaemia

Hypercalcaemia/hypercalciuria → renal calculi + nephrocalcinosis

HEART→ dysrhythmias, cardiomyopathy, conduction defects, pericarditis, valvular
lesions

CONSTITUTIONAL SX: malaise, fever, wt loss, night sweats

DIAGNOSIS OF EXCLUSION
Investigations: ↑Ca2+, ↑ESR, ↑ACE

203
Q

Perl stain

A

Positive for haemachromatosis

204
Q

Lewy body dementia

A

Psychological disturbances occur early. Day-to-day fluctuations in cognitive performance, visual hallucinations, spontaneous motor signs of Parkinsonism, recurrent falls and syncope, pathologically indistinguishable from PD

205
Q

What is dementia?

What are the different types of cognitive disturbances?

A

A global impairment of cognitive function and personality without impairment of consciousness.

Includes memory impairment and at least one of the following cognitive disturbances: aphasia, apraxia, agnosia or a disturbance in executive functioning”.

  • Aphasia= language disorder (may be expressive or receptive)
  • Apraxia= loss of ability to carry out learned purposeful tasks
  • Agnosia= loss of ability to recognise object, people etc.
206
Q

Acute rheumatic fever - what is it ask what systems does it affects

A

Occurs at a peak age of 5-15years. It is a multisystem illness affecting:

Heart: pancarditis i.e. endocarditis, myocarditis, pericarditis;

Joints: arthritis and synovitis;

Skin: Erythema marginatum, subcutaneous nodules

CNS: Encephalopathy, Sydenham’s chorea

Clinical features:

  • develop 2-4 weeks after strep throat infection.
  • diagnosis: group A strep infection + 2 major criteria or 1 major + 2 minor criteria
207
Q

Diagnostic criteria for rheumatic fever

A

Need two major or one major and two minor

Jones’ Major Criteria (CASES):

  • Carditis
  • Arthritis
  • Sydenham’s chorea
  • Erythema marginatum
  • Subcutaneous nodules

Minor criteria:

  • fever
  • raised ESR or CRP
  • migratory arthralgia
  • prolonged PR interval
  • previous rheumatic fever
  • malaise
  • tachycardia

Commonly affects mitral valve only

pathology year 5 (2 decks)

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