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Dylan's flashcards > histo path > Flashcards

histo path Flashcards

1
Q

Neutrophils

A

Acute inflammation (sterile or non-sterile)
Raised due to corticosteroid use

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2
Q

Macrophages

A

Late acute inflammation
Chronic inflammation (including granulomas e.g. Sarcoidosis)

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3
Q

Lymphocytes

A

Chronic inflammation
Lymphoma (sheets of clonal cells ie. Identical)

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4
Q

Plasma Cells

A

Chronic inflammation
Myeloma

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5
Q

Eosinophils

A

Allergic reactions
Parasitic infections
Tumours e.g. Hodgkin’s disease

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6
Q

Mast Cells

A

Allergic reactions
Parasitic infections

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7
Q

Fontana stain :

A

+ve for melanin

identifying Capsule-Deficient Cryptococcus Neoformans and typical Cryptococcus Neoformans.

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8
Q

Congo Red stain :

A

+ve for Amyloid (Apple green birefringence)

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9
Q

Prussian Blue:

A

+ve for iron (haemochromatosis)

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10
Q

Go-to stain for most histological samples is?

A

Hemotoxylin and Eosin (H&E).

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11
Q

what happens to serum transferrin in iron def anaemia and why ?

A

Serum Transferrin increases in IDA, as the liver increases transferrin production to
bind to as much available iron it can to compensate for low iron levels

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12
Q

Evolution of MI – Histological findings**:

A

Under 6 hours - normal by histology (CK-MB also normal)

6–24 hrs - loss of nuclei, homogenous cytoplasm, necrotic cell death

1-4 days - infiltration of polymorphs then macrophages (clear up debris)

5-10 days - removal of debris

1-2 weeks - granulation tissue, new blood vessels, myofibroblasts, collagen synthesis

Weeks-months - strengthening, decellularising scar tissue.

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13
Q

most common cause of RV failure

A

Most common cause is secondary to LVF but can be primarily caused by chronic severe pulmonary hypertension

most common cause of LVF is CAD

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14
Q

what is dilated cardiomyopathy and is its mechanism of heart failure ?

A

dilated = too thin

systolic dysfunction

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15
Q

restrictive cardiomyopathy what is it ?

A

too stiff
diastolic dysfunction

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16
Q

Hypertrophic obstructive cardiomyopathy (HOCM) - what is it ?

A

– septal hypertrophy resulting in an outflow tract obstruction

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17
Q

pathogensis of rheumatic fever ?

A

you get a strep throat infection usually 2-4 weeks before

cell-mediated immunity and antibodies to streptococcal antigen cross-react with myocardial antigens

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18
Q

main pathogen of infection preceeding rheumatic fever ?

A

Lancefield group A strep is the main pathogen.

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19
Q

what is criteria for rheumatic fever ?

A

Jones criteria

eviednce group A strep infection + 2 major criteria or 1 major + 2 minor criteria

Major criteria:
Carditis
Arthritis
Sydenham’s chorea
Erythema marginatum
Subcutaneous nodules

Minor criteria:
Fever
Raised CRP/ESR
Migratory arthralgia
Prolonged PR
Prev. rheumatic fever
Malaise
Tachycardia

Evidence of GAS infection:
Positive throat culture
Elevate AsO
Recent scarlet fever

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20
Q

rheumatic fever important histology to know

A

Histology: Beady fibrous vegetations (verrucae), Aschoff bodies (small giant-cell granulomas) and Anitschkov myocytes (regenerating myocytes).

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21
Q

treatment for rheumatic fever ?

A

NSAIDs (e.g. ibuprofen) are helpful for treating joint pain

Aspirin and steroids are used to treat carditis

Prophylactic antibiotics (oral or intramuscular penicillin) are used to prevent further streptococcal infections and recurrence of the rheumatic fever. These are continued into adulthood.

Monitoring and management of complications

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22
Q

in infective endocarditis, the Bacteraemia secondary to:

A
  • Poor dental hygiene (Strep. Viridans)
  • IVDU
  • Soft tissue infection
  • Dental treatments
  • Cannulas/lines
  • Cardiac and valvular surgery/pacemakers
  • Previously damaged valve e.g. post-rheumatic fever
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23
Q

difference between acute and subacute infective endocarditis ?

A

Acute:
- staph aureus / strep pyogenes
high virulence
vegetation is larger and more localised
spread is to the aorta

Subacute:
Strep. viridans, Staph. epidermis, HACEK* (culture -ve), Coxiella, Mycoplasma,candida
Low
Friable, soft thrombi. A few mm in size.
Chordae

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24
Q

what valve in infective endocarditis ?

A

Usually mitral/aortic valve unless IVDU when right-sided valves involved.

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25
Q

what is the common cardiac murmur in infective endocarditis ?

A

New murmur (MR/AR usually)

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26
Q

what criteria for diagnosing infective endocarditis

A

Duke Criteria:

Major:
○ Positive blood culture growing typical IE organisms or 2 positive cultures >12hrs apart
○ Evidence of vegetation/abscess on echo or new regurgitant murmur

Minor:
○ Risk factor (e.g. prosthetic valve, IVDU, congenital valve abnormalities)
○ Fever >38
○ Thromboembolic phenomena
○ Immune phenomena
○ Positive blood cultures not meeting major criteria

Diagnosis:
● 2 major
● 1 major + 3 minor
● 5 minor

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27
Q

how to manage infective endocarditis ?

A

Treatment: Start with broad spectrum Abx once cultures taken. Then treat according to sensitivities.

Subacute: Benzylpenicillin + gentamicin; or vancomycin for 4 weeks.

Acute: Flucloxacillin for MSSA, rifampicin + vancomycin + gentamicin for MRSA. (S. aureus IE is very nasty so make sure there is cover for this).

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28
Q

give path, cause, and murmur for these valve diseases:

aortic stenosis

A

Narrowed aortic valve high velocity, high pressure flow

Calcification (old age), congenital bicuspid valve

Crescendo-decrescendo, radiates to carotids

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29
Q

give path, cause, and murmur for these valve diseases:

aortic regurg

A

Incompetent aortic valve blood flows back into LV after systole

Infective endocarditis, dissecting aortic aneurysm, LV dilation, connective tissue disease e.g. Marfans, Ank Spon

Early diastolic, with collapsing pulse

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30
Q

give path, cause, and murmur for these valve diseases:

mitral stenosis

A

Narrowed mitral valve high velocity, high pressure flow. Back pressure in left atrium dilatation

Rheumatic fever

Mid diastolic, opening click

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31
Q

give path, cause, and murmur for these valve diseases:

mitral regurg

A

Incompetent mitral valve blood flows back into left atrium during systole

Infective endocarditis, connective tissue disease, post-MI, rheumatic fever, left ventricular dilation (functional MR)

Pansystolic,Radiates to axilla

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32
Q

histology chronnic bronchitis

A

Dilatation of the airways, goblet cell hyperplasia and hypertrophy of mucous glands

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33
Q

histology of bronchiectasis

A

Permanent fibrotic dilatation of the bronchi

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34
Q

histology of asthma

A

SM cell hyperplasia, excess mucus (goblet cell hypertrophy), inflammation
Whorls of shed epithelium (Curschmann spirals), eosinophils, Charcot-Leyden crystals

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35
Q

histrology of emphysema

A

Loss of the alveolar parenchyma distal to the terminal bronchiole

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36
Q

what is Interstitial Lung Disease and how does it present ?

A

inflammation and fibrosis of pulmonary tissue - features of restrictive lung disease (FEV1/FVC > 70%)

chronic shortness of breath
fine end inspiratory crackles
ground glass / honeycomb appearance on CT CAP

causes can be: idiopathic pulmonary fibrosis, drug induced. sarcoid., eosinophillic, smoking related

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37
Q

outline stages of lobar pneumonia

A

Lobar pneumonia* – Fibrinosuppurative consolidation.

Stages:

1.Consolidation;
2. Red Hepatisation (neutrophilia);
3. Grey Hepatisation (Fibrosis);
4. Resolution
Typically high virulence organisms (Strep. Pneumoniae – rust coloured sputum)

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38
Q

which lung cancer has strongest correlation with smoking ?

A

squamous cell carcinoma

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39
Q

which lung cancer has associations with PTHrP secreion ?

A

squamous cell carcinoma

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40
Q

where in the lung is squamous cell carcinoma most commonly?

A

proximal bronchi (ie central)

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41
Q

what lung cancer is most common in women and non smokers?

A

adenocarcinoma

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42
Q

where in the lung do you find adenocarcinoma ?

A

peripherally

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43
Q

where do you find small cell carcinoma in the lung ?

A

proximal bronchi (central)

has a strong relationship to smoking

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44
Q

which lung cancer is associated with SIADH ?

A

small cell carcinoma

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45
Q

which lung cancer is associated with ectopic ACTH secretion ?

A

small cell carcinoma

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46
Q

flushing + diarrhoea + bronchoconstriction

A

carcinoid syndrome ( release of serotonin)

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47
Q

how to stage lung cancer ?

A

Staging – most important prognostic factor:

  • Tumour (T1-4) – based on size and invasion of pleura, pericardium
  • Lymph node metastasis (N0-2) - N0 – lymph node not involved by tumour, N1 or N2 - lymph nodes involved. 1 vs 2 depends on extent of involvement
  • Distant metastasis (M0 or 1) - M1 – tumour has spread to distant sites
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48
Q

what is Mesothelioma:

A

Arise from either parietal or visceral pleura. It spreads widely within the pleural space and usually associated with extensive pleural effusion, chest pain and dyspnoea.

There is a long latent period of 25-45 years for development of asbestos-related mesothelioma.

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49
Q

“iron laden macrophages “

A

history for acute intra alevolar fluid

Pulomary oedema

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50
Q

CXR Findings in pulomary oedema

A
  • CXR findings: Alveolar opacification (batwing appearance), Kerley B-lines, (cardiomegaly suggesting a cardiac cause), fluid in horizontal fissure.
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51
Q

Squamous cell
oesophageal carcinoma associated with….

A

alochol and smoking

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52
Q

signet ring cell carcinoma

A

gastric cancer

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53
Q

how does coeliac present ?

A

Symptoms (of malabsorption): Steatorrhoea, abdo pain, bloating, n&v, ↓wt, fatigue, IDA, failure to thrive, rash (dermatitis herpetiformis).

Also associated with hyposplenism so may need extra vaccines.

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54
Q

gold standard Ix for coeliac disease

A

Gold standard Ix: Upper GI endoscopy and duodenal biopsy (villous atrophy, crypt hyperplasia, increased intraepithelial lymphocytes) while eating gluten.
NB normal villous:crypt ratio is ~ 2:1.

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55
Q

gold standard Ix for hirschprung’s disease

A
  • Gold standard Ix: Full thickness biopsy – hypertrophied nerve fibres, no ganglia
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56
Q

what is Carcinoid Syndrome

A
  • Diverse group of tumours of enterochromaffin cell origin, Produce 5-HT (serotonin)
  • Commonly found in the bowel (but also lung, ovaries, testes)
  • Usually slow growing
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57
Q

how are cancers of colon / rectum classified ? important histo risk factors ?

A

Classified based on architecture as tubular, tubulovillous or villous.

  • Large size is most important risk factor for malignancy, in addition to degree of dysplasia and increased villous component.
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58
Q

what type of cancer is colorectal cancer ?

A

98% are adenocarcinoma, 45% in rectum

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59
Q

Familial adenomatous polyposis (FAP) - what is it?

A
  1. 70% AD mutation in APC tumour suppressor gene (C5q1), 30% AR mutation in DNA mismatch repair genes.
  2. Present 10-15yrs - >100 adenomatous polyps required for diagnosis, usually 100-1000s seen. ALL will → adenocarcinoma if left untreated by 30yrs therefore most have prophylactic colectomy.
  3. Increased risk of neoplasia elsewhere, e.g.: ampulla of Vater and stomach
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60
Q

Cholecystokinin

A

responsible for stimulating digestion of fat and protein. Made by I-cells in the duodenum. Causes release of digestive enzymes

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61
Q

different endocrine function of the different cells of the pancreas

A

Alpha cells: glucagon increases blood glucose
Beta cells: insulin decreases blood glucose
Delta cells: somatostatin regulates the above cells
D1: a vasoactive peptide, stimulates the secretion of H20 into pancreatic system
PP: pancreatic polypeptide, self regulates secretion activities

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62
Q

scoring system for acute pancreatitis

A

Glasgow scale

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63
Q

causes of acute pancreatitis

A

‘I GET SMASHED’: Idiopathic, Gallstones, Ethanol, Trauma, Steroids, Mumps, Autoimmune, Scorpion venom, Hyperlipidaemia, ERCP, Drugs e.g. thiazides

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64
Q

what bloods good to assess for pancreatitis

A
  • NB: Amylase only transiently increased. Serum lipase is more sensitive.
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65
Q

marker for pancreatic cancer ?

A

CA19.9 >70IU/mL

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66
Q

what surgery for pancreatic cancer ?

A

Whipple’s procedure – surgical resection

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67
Q

Multiple Endocrine Neoplasia (MEN)**

go through the types

A
  • MEN 1= ‘PPP’ - Parathyroid hyperplasia/adenoma, Pancreatic endocrine tumour (often phaeochromocytoma), Pituitary adenoma.
  • MEN 2A- Parathyroid, Thyroid, Phaeochromocytoma
  • MEN 2B- Medullary Thyroid, Phaeochromocytoma, Acoustic Neuroma. Marfanoid phenotype
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68
Q

outline the pathophysiology of liver injury

A
  • A normal liver has hepatocytes with microvilli. Stellate cells which lie quiescent in the space of Disse (space between hepatocytes and sinusoid)
  • Chronic inflammation causes the loss of microvilli and activation of stellate cells, which produce collagen.
  • They become myofibroblasts that initiate fibrosis by deposition of collagen in the space of Disse.
  • Myofibroblasts contract constricting sinusoids and increasing vascular resistance.
  • Undamaged hepatocytes regenerate in nodules between fibrous septa
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69
Q

spotty necrosis

A

acute hepatitis

(small foci of inflammation and infiltrates)

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70
Q

causes of acute hepatitis

A

Acute Hepatitis
* Can either be caused by viruses (Hepatitis A to E) or by drugs

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71
Q

define liver cirrhosis

A

Diffuse abnormality of liver architecture that interferes with blood flow and liver function.

Histopathology of a cirrhotic liver:

Hepatocyte necrosis
Fibrosis
Nodules of regenerating hepatocytes
Disturbance of vascular architecture

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72
Q

The major causes of cirrhosis include:

A
  1. Alcoholic liver disease
  2. Non-alcoholic fatty liver disease
  3. Chronic viral hepatitis (hep B+/-D and C)
  4. Autoimmune hepatitis
  5. Biliary causes: Primary biliary cirrhosis & Primary sclerosing cholangitis
  6. Genetic causes:
    a) Haemochromatosis- HFE gene Chr 6
    b) Wilson’s disease- ATP7B gene Chr 13
    c) Alpha 1 antitrypsin deficiency (A1AT)
    d) Galactosaemia
    e) Glycogen storage disease
  7. Drugs e.g. methotrexate
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73
Q

size of regenerating nodules and are these 2 different types called and what can cause each ?

A

It can also be classified according to the size of the regenerating nodules into:

MICRONODULAR (nodules < 3mm) - uniform liver involvement
* Caused by: alcoholic hepatitis, biliary tract disease

MACRONODULAR (nodules > 3mm) - variable nodule size
* Caused by: viral hepatitis, Wilson’s disease, alpha1 antitrypsin deficiency

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74
Q

modified child’s pugh score is for what?

A

predicts survival

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75
Q

microscopic characteristics of alcholic hepatitis

A

hepatocyte ballooning
mallory denk bodies
micronodular sclerosis

76
Q

histology in primary billiary cholangitis

A
  • Histology: bile duct loss with granulomas [HIGH YIELD]
77
Q

which antibodies in primary biliary cholangitis ?

A
  • Anti-mitochondrial antibodies in > 90% [HIGH YIELD]
78
Q

which antibodies in primary sclerosing cholangitis

A

p-ANCA [HIGH YIELD]

79
Q

onion skinning fibrosis

A

primary sclerosing cholangitis

80
Q

USS and ERCP findings in primary sclerosing cholangitis

A
  • US scan: bile duct dilatation
  • ERCP: shows beading of bile ducts
81
Q

inheritance of haemochromatosis ?

A

Autosomal recessive [HIGH YIELD]

82
Q

inheritance of wilson’s disease ?

A

Autosomal recessive [HIGH YIELD]

83
Q

what stain in wilson’s

A

Copper stains with Rhodanine stain

84
Q

● Kayser Fleischer rings

A

wilson’s disease

85
Q

features pf haemochromatosis

A

● Skin bronzing (melanin deposition)
● Diabetes
● Hepatomegaly with micronodular cirrhosis
● Cardiomyopathy
● Hypogonadism
● Pseudogout

86
Q

features of wilson’s disease

A

● Liver disease: acute hepatitis, fulminant liver failure or cirrhosis
● Neuro disease: parkinsonism, psychosis, dementia (basal ganglia involvement)
● Kayser Fleischer rings: copper deposits in Descemet’s membrane in cornea

87
Q

treatment for haemochromatosis

A

Venesection
Desferrioxamine

88
Q

treatment for wilson’s

A

Lifelong penicillamine.

Good prognosis with early treatment but any neuro damage is permanent and may require liver transplant.

89
Q

what is Cholangiocarcinoma linked to ?

A

primary sclerosing cholangitis

90
Q

whta is the MOST COMMON malignant liver lesion

A

secondary tumours

91
Q

most common renal stone ?

A

o Calcium Oxalate

92
Q

prostate cancer type most common in men over 50

A
  • Adenocarcinoma is the commonest form in men over 50y.
92
Q

grading for prostate cancer

A

Gleason score

  • 1-5 based on differentiation (5 is worst – least differentiated and most aggressive)
  • Take a biopsy and classify the most common pattern seen and the worst pattern seen
  • Add these two numbers together to get a result out of 10
  • Expressed as X+Y=Z
93
Q

sx, histo, mx for benign prostatic hyperplasia

A
  • Dihydrotestosterone-mediated hyperplasia of prostatic stromal and epithelial cells, resulting in the formation of large nodules
  • Nodule formation compresses prostatic urethra leading to outflow tract obstruction
  • Symptoms: difficulty urinating, retention, frequency, nocturia, overflow dribbling
  • Histology: nodule formation, prostatic epithelial ducts with duct spaces
  • Management: TURP, 5α reductase inhibitors, alpha blocker (tamsulosin, aware of BP effects)
93
Q

staghorn calculi made from

A

o Magnesium Ammonium Phosphate

94
Q

what is a blood marker used in prostate cancer

A

prostate specific antigen (PSA)

95
Q

most common testicular tumours

A

Most testicular tumours are germ cell tumours – arising from germ cells in the testes. Commonly seen in men aged 20-45

intratubular germ cell neoplasia

96
Q

different types of germ cell testicular tumours and which is most common

A
  • Seminoma: most common type of germinal tumour. Peak age: 30s. Radiosensitive.
  • Teratoma: occur at any age from infancy to adult life. Regarded as malignant when occurs in the post-pubertal male. Chemo sensitive. Biologic markers for germ cell tumours: AFP, HCG, and LDH
  • Embryonal carcinoma – resembles embryonic tissue
  • Yolk sac tumour
  • Choriocarcinoma
97
Q

type of non germ cell tumour testicular

A

Leydig cell tumour (derived from stroma), Sertoli cell tumour (derived from sex cord)

98
Q

most common malignant renal cell carcinoma

A

clear cell

99
Q

give both benign and malignant renal tumours

A

benign
1. papillary adenoma
2. oncocytoma
3. angiomyolipoma

malignant
1. renal cell carcinoma - clear cell / papillary / chromophobe
2. nephroblastoma / Wilm’s tumour
3. transitional cell carcinoma

100
Q

most common bladder cacner ?

A

transitional cell tumour

101
Q

what type of bladder cancer more frequent in countries with endemic urinary schistosomiasis.

A

Squamous Cell Carcinoma:

102
Q

list the nephrotic and nephritic syndromes

A

Nephrotic syndrome:
* Primary
o Minimal change disease
o Membranous glomerular disease
o Focal segmental glomerulosclerosis
* Secondary – e.g. Diabetes, amyloidosis, SLE

Nephritic syndrome:
* Acute post-infectious (aka Post-streptococcal)
* IgA nephropathy (aka Berger Disease)
* Rapidly progressive glomerulonephritis
* Alport’s syndrome (aka Hereditary nephritis)
* Thin basement membrane disease (aka Benign familial haematuria)
As a general rule, the glomerular vessels are very delicate and so deposition of immune complexes (which may release inflammatory substances and cause further damage) will reduce their function.

103
Q

nephrotic syndrome triad

A
  1. Proteinuria (>3g/24h / protein:creatinine ratio >300mg/mmol)
  2. Hypoalbuminaemia (<30 g/L)
  3. Oedema
104
Q

periorbital swelling in children ?

A

minimal change disease

105
Q

frothy urine is due to ?

A

proteinuria

106
Q

why is it called minimal change disease ?

A

no changes under light microscope

but under electron microscope –> loss of podocyte foot processes

107
Q

features of nephritic syndrome

A

Syndrome characterised by: PHAROH
* Proteinuria (less than nephrotic syndrome)
* Haematuria (coke-coloured urine)
* Azootemia – (high urea and creatinine)
* Red Cell Casts (in urine – these are red cells that have clumped together & have leaked out into the tubules)
* Oliguria
* Hypertension

108
Q

muddy brown casts

A

acute tubular necrosis

109
Q

time frame of post-strep glomerulonephritis and what organism? compare it to IgA nephropathy

A

Occurs 1-3 weeks after streptococcal throat infection or impetigo (usually Lancefield Group A beta-haemolytic strep = Strep. pyogenes).

  • Presents 1-2 days (earlier than Acute postinfectious GN!) after an URTI with frank haematuria*
110
Q

what is HEREDITARY NEPHRITIS (ALPORT’S SYNDROME)

A
  • Hereditary glomerular disease caused by mutation in type IV collagen alpha 5 chain
  • X linked
  • Nephritic syndrome + sensorineural deafness + eye disorders (lens dislocation, cataracts)
  • Presents at 5-20yrs with nephritic syndrome progressing to ESRF
111
Q

differentials of asymptomatic haematuria in renal path

A

Asymptomatic Haematuria
If this appears in an SBA – the differentials include:
1. THIN BASEMENT MEMBRANE DISEASE (Benign familial haematuria)
2. IgA NEPHROPATHY (Berger disease)
3. ALPORT SYNDROME

IgA and Thin basement membrane are more common causes of asymptomatic haematuria than of nephritic syndrome. Differentiation between thin basement membrane and IgA is clinically difficult.
If there are no histological findings included in the questions clinical differences include IgA being more likely to cause frank haematuria, more likely to cause a change in renal function Cr raised) and slightly more common in the Asian population.

112
Q

causes of acute tubular necrosis

A

Causes:
* Hypovolaemia → Pre-renal ARF → Ischaemia of nephrons (EMQ: cured hypovolaemia but persistent ARF).
* Nephrotoxins – drugs (aminoglycosides, NSAIDs), radiographic contrast agents, myoglobin (e.g. secondary to rhabdomyolysis), heavy metals

Damage to tubular epithelial cells → cells shed and block of tubules as casts → 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.
Most common cause of acute renal failure

Histopathology: Necrosis of short segments of tubules

113
Q

how does Thrombotic thrombocytopaenic purpura presetn ?

A

PENTAD:
* MAHA
* Thrombocytopenia
* Renal failure
* Fever
* Neurological Sx e.g. confusion, seizures

114
Q

causes of acute renal failure

A

PRE-RENAL
* Most common cause of acute renal failure
* Caused by renal hypo-perfusion e.g. hypovolaemia, sepsis, burns, acute pancreatitis, and renal artery stenosis.

RENAL
* Acute Tubular Necrosis (ATN): commonest renal cause of ARF.
* Acute glomerulonephritis.
* Thrombotic microangiopathy.

POST-RENAL
* Obstruction to urine flow as a result of stones, tumours (primary & secondary), prostatic hypertrophy and retroperitoneal fibrosis

115
Q

chronic kidney disease stages

A

1 Kidney damage with normal renal function (often proteinuria) >90

2 Mildly impaired 60-89

3 Moderately impaired 30-59

4 Severely impaired 15-29

5 Renal failure (generally requires replacement therapy) <15 (or if being treated with renal replacement therapy)

116
Q

adult polycyctsic disease inheritance and which mutations

A
  • Autosomal dominant inheritance. 85% due to mutations in PKD1 on chromosome 16 (encoding polycystin-1), 15% due to mutations in PKD2 on chromosome 4 (encoding polycystin-2)
117
Q

‘wire loop capillaries’

lumpy-bumpy granular fashion

A

Lupus Nephritis
Depending on site and intensity of immune complex deposition clinical presentation may be: isolated urinary abnormalities, acute renal failure, nephrotic syndrome or progressive chronic renal failure.

Renal Histology: Immune complex deposition in capillaries  ‘wire loop capillaries’, deposition of immune complexes & complement in the GBM in a lumpy-bumpy granular fashion.
Class 1: Minimal mesangial disease, looks near normal on light microscopy

Class 2: Mesangial proliferative disease
Class 3: Focal subendothelial deposits
Class 4: Diffuse subendothelial deposits
Class 5: Subepithelial immune deposits (membranous disease)
Class 6: Advanced sclerosis (>90%)*

118
Q

define pelvic inflammatory disease

A

Pelvic Inflammatory Disease (PID / Salpingitis)
Infection ascending from vagina and cervix up to uterus and Fallopian tubes, leading to inflammation (endometritis, salpingitis) and the formation of adhesions.

119
Q

causes of PID (give organisms as well)

A
  • Ascending bacteria from lower genital tract - Neisseria gonorrhoea, Chlamydia trachomatis, enteric bacteria
  • Secondary to abortion/termination of pregnancy – S. aureus, Streptococcus, C. perfringens, Coliforms
120
Q

clinical features of PID

A

Clinically: bilateral lower abdo pain, deep dyspareunia, vaginal bleeding/discharge, fever, adnexal tenderness, and cervical excitation

121
Q

violin-string” peri-hepatic adhesions

A

PID causing…

10% have Fitz Hugh Curtis syndrome – formation of scar tissue along liver capsule - RUQ pain from peri-hepatitis + “violin-string” peri-hepatic adhesions [BUZZWORD]

122
Q

what is Fitz Hugh Curtis syndrome

A
  • 10% have Fitz Hugh Curtis syndrome – formation of scar tissue along liver capsule - RUQ pain from peri-hepatitis + “violin-string” peri-hepatic adhesions [BUZZWORD]
123
Q

complications of PID

A

Complications:
* 10% have Fitz Hugh Curtis syndrome – formation of scar tissue along liver capsule - RUQ pain from peri-hepatitis + “violin-string” peri-hepatic adhesions [BUZZWORD]
* Infertility
* ↑Risk of ectopic pregnancy
* Bacteraemia → SEPSIS
* Tubo-ovarian abscess
* Chronic PID
* Peritonitis
* Plical fusion – fimbrial ends of fallopian tubes adhere together

124
Q

define endometriosis

A

Endometriosis
Presence of endometrial glands or stroma in abnormal locations outside the uterus e.g. ovaries, uterine ligaments, rectovaginal septum, Pouch of Douglas, pelvic peritoneum

125
Q

clinical features of endometriosis

A

Clinically:
* Cyclical pelvic pain, dysmenorrhoea, deep dyspareunia, ↓fertility
* Cyclical PR bleeding, haematuria, bleeding from umbilicus (depending on site of endometrial deposits)
* Nodules/tenderness in vagina, posterior fornix or uterus; immobile and retroverted uterus in advanced disease

126
Q

chocolate cysts

A
  • Endometriomas = blood-filled “chocolate cysts” on ovaries [BUZZWORD]
127
Q

powder burns

A

endometriosis

Macroscopically:
* Red-blue to brown vesicles - “powder burns” [BUZZWORD]
* Endometriomas = blood-filled “chocolate cysts” on ovaries [BUZZWORD]
`

128
Q

bulky uterus

A

adenomyosis

Similar to endometriosis; presence of ectopic endometrial tissue deep within the myometrium

129
Q

outline adenomyosis - presentation etc

A

Adenomyosis
Similar to endometriosis; presence of ectopic endometrial tissue deep within the myometrium
Clinically: heavy menstrual bleeding, dysmenorrhoea, and deep dyspareunia.
BUZZWORDS: “Bulky uterus”, “Subendothelial linear striations”, “Globular uterus”.
Complications:
* Malignant transformation
* Red degeneration during pregnancy

130
Q

fibroids clinical presentation

A

Clinically:
* Heavy menstrual bleeding, dysmenorrhoea, pressure effects (urinary frequency, tenesmus)

  • Subfertility
  • In pregnancy: red degeneration of fibroids (haemorrhagic infarction → severe abdo pain), post-partum torsion
131
Q

most common type of endometrial cancer

A

Postmenopausal bleeding is endometrial cancer until proven otherwise
Adenocarcinomas (85%), squamous cell carcinoma (15%)

132
Q

Postmenopausal bleeding is …….. until proven otherwise

A

endometrial cancer

132
Q

staging for endometrial cancer

A

Staged with FIGO system:
* Stage 1 – Cancer ONLY in uterus
* Stage 2 – spread to CERVIX
* Stage 3 – spread to PELVIC AREA
* Stage 4 – METASTASIS to rectum/bladder/distal organs

133
Q

most common ovarian cyst ?

A

follicular cyst

  • Due to non-rupture of the dominant follicle/failure of atresia in a non-dominant follicle
  • Commonly regress after several menstrual cycles
134
Q

most common type of ovarian carcinoma

A

– 90% are epithelial ovarian cancers

135
Q

Histology: columnar epithelium, Psammoma bodies

in ovarian cancer

A

Serous cystadenoma (subtype of benign epithelial ovarian cancer)

136
Q

Most common benign ovarian epithelial tumour

A

serous cystadenoma

137
Q

Histology: mucin secreting cells [BUZZWORD]

in ovarian cancer

A

mucinous cystadenoma (subtype of benign epithelial ovarian cancer)

138
Q

Histology: clear cells, clear cytoplasm, Hobnail appearance

in ovarian cancer

A

clear cell

139
Q

Histology: tubular glands [BUZZWORD]

in ovarian cancer

A

endometrioid

140
Q

Most common ovarian tumours in younger women (15-21 yo)

what are they and outline /…. .

A

Shows differentiation toward somatic structures

Mature teratomas (dermoid cyst) 95% of teratomas: Benign; usually cystic;
Differentiation of germ cells into mature tissues (e.g. skin, hair, teeth, bone, cartilage); usually bilateral and asymptomatic.

Immature teratomas:
Malignant, usually solid;
Contains immature, embryonal tissues
Secrete AFP

141
Q

Histology: Call-Exner bodies [BUZZWORD]

in ovarian cancer

A

Granulosa-Theca cell tumour

(subset of sex cord/ stroma tumours )

Produce E2
Look for oestrogenic effects – irregular menstrual cycles, breast enlargement, endometrial/breast cancer
Histology: Call-Exner bodies [BUZZWORD]

142
Q

Histology: Mucin producing signet ring cells [BUZZWORD]

in ovarian cancer

A

Krukenberg tumour

Malignancy of the ovary that has metastasised from usually gastric / colonic cancer
Histology: Mucin producing signet ring cells [BUZZWORD]

143
Q

how to stage ovarian cancer ?

A

FIGO staging
* Stage I: ONLY in ovaries
* Stage II: spread to PELVIS
* Stage III: spread to ABDOMEN (including regional LN metastases)
* Stage IV: METASTASIS outside abdominal cavity

The true abdominal cavity consists of the stomach, duodenum (first part), jejunum, ileum, liver, gallbladder, the tail of the pancreas, spleen, and the transverse colon

144
Q

Risk of malignancy index (RMI)

A

– scoring system used to estimate the likelihood of a malignant cyst – cut-off score 200:
RMI = U x M x Ca-125
U = Ultrasound
* 1 Point for each feature: multilocular, evidence of solid areas, evidence of metastases, ascited and bilateral lesions
* Overall ultrasound score summarised between 0 and 3 with 0=no ultrasound features, 1=1 ultrasound feature and 3=2-5 ultrasound features

M = Menopause
* 1 point for premenopausal
* 3 points for post-menopausal
Ca-125
* Measured in iu/ml

145
Q

outline normal histology of cervix and and how CIN can progress and where

A

Normal cervical histology:
Outer cervix (continuous with vagina) covered by squamous epithelium; endocervical canal lined by columnar glandular epithelium. The squamocolumnar junction (SCJ) separates them.

Transformation zone (TZ): the area where columnar epithelium transforms into squamous cells (=squamous metaplasia). This is a normal physiological process. This area is susceptible to malignant change due to high rates of cell turnover
CIN: Dysplasia at the TZ as a result of infection by HPV 16 & 18.
Graded mild, moderate or severe dyskaryosis on cytology, but graded CIN 1-3 on histology (from biopsy).
* CIN 1 = dysplasia confined to deepest 1/3 of epithelium
* CIN 2 = lower 2/3
* CIN 3 = full thickness, but basement membrane intact

60-90% of CIN 1 reverts to normal over 10-23 months
30% of CIN 3 progress to cervical cancer over 10 years if left untreated

145
Q
A
145
Q

figo staging for cervical cacner

A

Staged using FIGO system
* Stage 0: CIN
* Stage I: ONLY
* Stage II: spread into UPPER 1/3 VAGINA
* Stage III: spread into PELVIC SIDE WALL and/or LOWER 1/3 VAGINA Stage IV: METASTASIS beyond pelvis to bladder/bowel

146
Q

CIN 1-3 on histology (from biopsy).

A
  • CIN 1 = dysplasia confined to deepest 1/3 of epithelium
  • CIN 2 = lower 2/3
  • CIN 3 = full thickness, but basement membrane intact
147
Q

what separates endo cervix and ecto cervix ? Normal cervical

A

histology:
Outer cervix (continuous with vagina) covered by squamous epithelium; endocervical canal lined by columnar glandular epithelium. The squamocolumnar junction (SCJ) separates them.

Transformation zone (TZ): the area where columnar epithelium transforms into squamous cells (=squamous metaplasia). This is a normal physiological process. This area is susceptible to malignant change due to high rates of cell turnover
CIN: Dysplasia at the TZ as a result of infection by HPV 16 & 18.

148
Q

what is the triple assessment in breast

A

Triple assessment comprises:
1. Clinical Examination
2. Imaging – USS/mammography – decision based on density of breast tissue –dense=USS, less dense=mammography – general age cut-off 35
3. Cytology and histology –
* Cytopathology (obtained via fine needle aspiration (FNA)) – cells spread across a slide, stained and Coded from C1 (inadequate sample), C2 (benign), C3 (atypia), C4 (suspicious of malignancy) to C5 (malignant)
* Histopathology (obtained via core biopsy) – intact tissues removed showing architectural and cellular detail and coded B1 (normal), B2 (benign), B3 (uncertain), B4 (suspicious) to B5 (malignant). B5a = DCIS, B5b = invasive carcinoma
o NOTE: histopathology = gold-standard for diagnosis of breast cancer. Normal breast histology is a ductal-lobular system lined by inner glandular epithelium

149
Q

outline the non neoplastic breast conidtionns

A

Acute Mastitis**
* Presentation: painful, red breast, hot to touch and fever
* Either lactational (more common) or non-lactational
* Lactational is usually secondary to S. aureus infection (often polymicrobial) via cracks in the nipple & due to stasis of milk
* FNA cytology shows an abundance of neutrophils [BUZZWORD]
* Management: continued expression of milk + antibiotics +/- surgical drainage
* Non-lactational – keratinising squamous metaplasia block lactiferous ducts leading to peri-ductal inflammation and rupture.

Fat Necrosis
* Inflammatory reaction to damaged adipose tissue (typically obese, middle-aged women).
* Presents as painless breast mass/skin thickening/mammographic lesion (may mimic carcinoma displaying skin tethering/niplle retraction)
* Causes – trauma, radiotherapy, surgery, nodular panniculitis
* Cytology – empty fat spaces , histiocytes and giant cells [BUZZWORDS]

150
Q

breast mouse

A

fibroadenoma

151
Q

breast histo

empty fat spaces , histiocytes and giant cells

A

fat necrosis

152
Q

breast histo / cytology

shows an abundance of neutrophils

A

acute mastitis

153
Q

breast cytology

Nipple discharge – proteinaceous material and macrophages

A

duct ectasia

154
Q

breast histo

papillary mass within a dilated duct lined by epithelium

A

intraductal papiloma

155
Q

breast histo

central, fibrous, stellate area

A

radial scar

156
Q

branching”/”leaf-like fronds”/”artichoke appearance

A

phyllodes tumour

(breast)

157
Q

breast histo

dilated large ducts which may become calcified

A

fibrocystic disease

158
Q

different histo for invasive breast carcinoma

A

Invasive breast carcinoma (80%) – malignant epithelial tumours which infiltrate within breast, capacity to spread to distant sites.
* They can be histologically subcategorised into ductal, lobular, tubular and mucinous.
* Invasive ductal = carcinoma that cannot be subclassified into another group. Most common. Big, pleiomorphic cells [BUZZWORD] – invasive cells move intro stroma
* Invasive lobular = cells aligned in single file chains/strands.
* Tubular carcinomas = well-formed tubules [BUZZWORD] with low grade nuclei. Rarely palpable as <1cm.
* Mucinous carcinoma = cells produce abundant quantities of extracellular mucin [BUZZWORD] which dissects into surrounding stroma.

159
Q

common site of intraparenchymal haemorrhagic stroke

A
  • Common site= basal ganglia
160
Q
  • Commonest form of adult brain tumours
A

Secondary tumours are metastatic lesions from other parts of the body

161
Q

Most common, aggressive primary brain tumour in adults

A

Glioblastoma multiforme (G4) - BAD

162
Q

2 most common brain tumours in children

A
  1. astrocytoma
  2. medulloblastoma
163
Q

Brown’s tumours

A

primary hyperPTH

164
Q

causes of osteomyletis in all these grousp

adults
children
sickle cell patients
immunocompromsied
congenital

A

Adults=
S. aureus
Vertebrae, jaw (2o to dental abscess) and toes (2o to diabetic skin ulcer)

Children= Haemophilus influenza, Group B strep

Sickle Cell = Salmonella
`
Immunocompromised =TB

Congenital = Syphilis
.

165
Q

Onion skinning of periosteum

A

ewing’s sarcoma

166
Q

Histology: Parakeratosis

A

psoriasis

167
Q

most common type of psoriasis ?

A
  • Chronic plaque psoriasis (MOST COMMON) – with salmon pink plaques and silver scales affecting extensor aspects of knees, elbows and scalp
168
Q

what is guttate psoriasis ?

A
  • Guttate psoriasis – “rain-drop” plaque distribution, often in children on trunk, usually seen 2 weeks post Group A Beta-haemolytic Strep infection (GABHS)
169
Q

types of bullous disease we need to know about ?

A

Bullous pemphigoid**

IgG Abs and C3 (complement) bind to hemidesmosomes (adhesion molecules) of basement membrane → epidermis lifts off and fluid accumulates in the space

SUBepidermal bulla Large tense bullae on erythematous base.

Often on flexural surfaces (forearms, groin and axillae). ELDERLY.

Bullae do not rupture as easily as pemphigus. EOSINOPHILIA

Linear deposition of IgG along basement membrane

Pemphigus vulgaris**

IgG Abs bind to desmoglein 1 & 3 (adhesion molecules) between keratinocytes in stratum spinosum → acantholysis

INTRAepidermal bulla Bullae are easily ruptured  raw red surface.

Found on skin AND mucosal membranes. Nikolsky’s sign +ve.
Mucosal involvement.
Intraepidermal bulla

Netlike pattern of intercellular IgG deposits

Acantholysis

170
Q

important prognistic factor for melanoma

A

o Breslow thickness = most important prognostic factor based off depth (every mm worsens prognosis…)

171
Q

most common types of melanoma ?

A

▪ Superficial spreading (MOST COMMON) – irregular borders with variation in colour

▪ Nodular (2nd COMMONEST) – can occur on all sites, more common in the younger age group

172
Q

Salmon pink rash
+
oval macules in Christmas tree distribution

A

Pityriasis Rosea

  • Salmon pink rash appears first (=herald patch) followed by oval macules in Christmas tree distribution
  • Appears after HHV-6 and HHV-7 infections.
  • Remits spontaneously
173
Q

scalp tenderness, temporal headache, jaw claudication –> then proceed to outline this condition

A

temporal arteritis (GCA)

high ESR / age > 50

Overlap with polymyalgia rheumatica (PMR)
Investigation: ESR (1st) temporal artery biopsy (definitive)
Histology: Granulomatous transmural inflammation + giant cells + skip lesions
Management: oral Pred IMMEDIATELY

174
Q

how does Granulomatosis with polyangiitis** present ?

A

(wegner’s)

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

cANCA +ve

175
Q

how does Eosinophilic granulomatosis with polyangiitis present ?

A

Asthma, allergic rhinitis
Eosinophilia
Later systemic involvement

pANCA +ve

176
Q

how does Henoch Schonlein Purpura present ?

A

IgA mediated vasculitis
In children 3-15 yrs
Preceding URTI → glomerulonephritis
Triad of:
* Purpuric rash on lower limb extensors + buttocks
* Abdo pain
* Arthralgia

176
Q

how does Microscopic polyangiitis present ?

A

Pulmonary renal syndrome:
* Pulmonary haemorrhage
* Rapidly progressive glomerulonephritis

pANCA +ve

177
Q

different types of amyloid what are they associated with ?

A

PRIMARY (AL amyloidosis)
* Most common
* Deposition of Ig light chains
* Most associated with multiple myeloma (although most don’t have multiple myeloma)
* Most have monoclonal Ig, free light chains in serum and urine (Bence Jones) and increased bone marrow plasma cells

SECONDARY (AA amyloidosis)
* Amyloid formed from serum amyloid A = acute phase protein, therefore build up occurs secondary to chronic infections / inflammation
o E.g. autoimmune diseases (60%): RA, ankylosing spondylitis, IBD
o E.g. chronic infections: TB osteomyelitis, IVDU (skin infections)
o Non-immune: renal cell carcinoma, Hodgkin’s

178
Q

clinicnal features of amyloid and why ?

A

Clinical features: caused by amyloid deposits in various organs:
* KIDNEY: nephrotic syndrome = most common presentation
* HEART: restrictive cardiomyopathy, conduction defects, heart failure, cardiomegaly
* LIVER/SPLEEN: hepatosplenomegaly
* TONGUE: macroglossia in 10%
* NEUROPATHIES: including carpal tunnel

 Think of amyloid proteins either constricting the organ or depositing and making it bigger

179
Q

sarcoidosis - features and histo

A

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

Histology: non-caseating granulomas; also get Schaumann and asteroid bodies (inclusions of protein and calcium)
* More severe disease in Afro-Caribbeans
* F>M, 40-60yrs
* Lungs most commonly involved
* Often detected at routine CXR → bilateral hilar lymphadenopathy (ddx TB, lymphoma, bronchial ca)
* Also see pulmonary infiltrates → fine nodular shadowing in mid zones
* Most seek help with insidious shortness of breath, cough, chest pain and night sweats

High-yield content:
o Bilateral hilar lymphadenopathy on CXR
o Non-caseating granulomas on histology
o High calcium, high ACE
o Treated with steroids

180
Q

what ix in sarcoidosis ?

A

Investigations:
* ↑Ca2+ (ectopic 1-alpha hydroxylase release by activated macrophages),
* ↑ESR,
* ↑ACE
* Transbronchial biopsy → non caseating granuloma
* Spirometry → restrictive,

Dylan's flashcards (14 decks)

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