Histopathology Flashcards
(281 cards)
1
Q
Name some organisms that cause gynaecological infection, and give a brief description for each
A
- Candida albicans: yeast. Causes vulvovaginitis, classically with thick, cottage-cheese discharge
- Gardnerella: Gram -ve rod, causes BV. Classically grey, fishy-smelling watery discharge. ‘Salt + pepper’, ‘clue cells’ appearance on microscopy
- Trichomonas: protozoa. Classically greenish, frothy discharge. Swab posterior fornix + wet slide microscopy.
- Chlamydia trachomatis: obligate intracellular gram -ve. Usually asymptomatic, can lead to PID
- Neisseria gonorrhoea: gram -ve diplococci.
- HPV, HSV (covered elsewhere)
2
Q
Which pathogens can cause PID? Where do they typically come from?
A
- Gonorrhoea, chlamydia: STI, ascending infection from lower GUT
- Staph, Strep, Clostridium: abortions
3
Q
What are some complications of PID?
A
Peritonitis, adhesions -> BO, infertility, sepsis
4
Q
What is salpingitis? What are the complications?
A
Infection/inflammation of the Fallopian tubes. Can lead to tubo-ovarian abscess, hydrosalpinx, infertility, ectopic pregnancy
5
Q
Describe the relationship between cervical cancer and HPV.
A
95% of cervical carcinomas are associated with HPV infection, specifically 16+18.
*Low risk types: 6+11
Most people will clear HPV infection, but some will have persistent infection. This can progress to intraepithelial neoplasia -> carcinoma
6
Q
How does HPV affect epithelia cells?
A
E6 and E7 genes inactivated the tumour suppressor genes p53 (E6) and Rb (E7). This prevents apoptosis.
7
Q
What are the 2 states of HPV infection?
A
Latent: dormant in basal cells. No active viral replication (replicates with the cell replication). No visible infection, must use molecular methods
Productive: active viral replication. Characteristic ‘halo cells’/koilocytes
8
Q
Which area of the cervix is usually affected by carcinoma? Why does this matter?
A
Squamocolumnar junction/ transition zone. This is where cells are sampled for screening.
9
Q
What are the two common types of cervical carcinoma, and what are their precursors? How are these graded?
A
Cervical cancer is usually squamous cell carcinoma (precursor CIN), but can also be adenocarcinoma (precursor CGIN).
Cervical intraepithelial neoplasia is a type of dysplasia, which means the cells are abnormal (increased mitoses, large nuclei:cytoplasm) without invading the basement membrane.
If it affects the lower 1/3 cells -> grade 1
2/3 -> grade 2.
Full thickness -> grade 3
Invading basement membrane -> carcinoma in situ
10
Q
Describe the process of cervical screening (post sampling).
A
Cells are sampled and smeared on a slide for microscopy.
They are first tested for high-risk HPV types using ‘Hybrid Capture II’ DNA test (uses RNA probes).
If there are high-risk variants found, then the sample goes to cytology
11
Q
What is the commonest uterine tumour? How common is it?
A
Leiomyoma (fibroid). Affects about 20% of women >35 yrs
12
Q
What are the types of leiomyoma?
A
Submucosal, intramural, subserosal
13
Q
A malignant tumour of the myometrium is ____. Describe briefly.
A
Leiomyosarcoma. Rare, affects older women (PMB), poor prognosis.
14
Q
What are the risk factors for endometrial hyperplasia? What is the potential consequence?
A
High oestrogen states: obesity, nulliparity, PCOS, HRT use
Can lead to endometrial carcinoma (typically affecting younger women)
15
Q
What are the types of endometrial carcinoma? Describe them (subtypes, epidemiology, etc)
A
Type 1 (85%): oestrogen dependent, associated with endometrial hyperplasia. Affects younger women, esp. obese. Low grade. Subtypes: endometrioid, mucinous, secretory. Mutations: PTEN, Kras, P13KCA, etc.
Type 2 (15%): Older women, PMB, high grade + invasive. Subtypes: serous, clear cell. Mutations: serous- p53, clear cell- PTEN
16
Q
How is endometrial cancer staged?
A
FIGO. 1- uterus 2- cervix 3- ovaries, vagina, pelvic nodes 4- anywhere else
17
Q
Define gestational trophoblastic disease. What are the types?
A
A spectrum of diseases in which there is abnormal proliferation of trophoblastic cells (placental) in the uterus.
Includes partial and complete moles, invasive mole, and choriocarcinoma
18
Q
What is a molar pregnancy? Describe the different types
A
An abnormal fertilised egg implants in the uterus, with proliferation of abnormal trophoblasts. Complete/partial occur in about 1/1000 pregnancies.
Complete- risk of malignant transformation in 2.5%, risk of invasive mole in 10%
Complete mole: fertilisation of EMPTY egg. Either duplication of sperm or fertilised by 2 sperm –> 46XX/XY
Partial mole: normal egg gets fertilised by 2 sperm/1 sperm with two sets of DNA –> 69XXY/XYY. This is dispermy/diandry
19
Q
How can molar pregnancy present?
A
Spontaneous miscarriage, very high hCG
20
Q
What is a choriocarcinoma? What are the RFs?
A
Very rare (1 in 20-30,000 pregnancies), very aggressive type of cancer arising from placental trophoblasts. 50% arise from molar pregnancies. Also RFs: previous abortion/miscarriage
21
Q
What is endometriosis? What are the proposed theories of pathogenesis?
A
Benign growth of endometrial tissue outside of the uterus.
1) Retrograde menstruation: endometrial tissue –> tubes into peritoneum
2) Metaplasia of peritoneum to endometrial cells
22
Q
What is adenomyosis?
A
Growth of endometrial tissue within the myometrium.
Causes painful, heavy periods.
23
Q
What are the types of ovarian cysts?
A
Functional cysts: follicular, corpus luteum cyst, theca luteal
Endometrioma/chocolate cyst: related to endometriosis. Filled with old blood -> brown, tarry
PCOS: multifollicular ovaries
24
Q
What is the classification of ovarian tumours?
A
Primary: epithelial (carcinomas), sex cord stromal (fibroma, thecoma, GCs), germ cell (teratoma/dermoid cyst, embryonal, dysgerminoma), non-specific (lymphomas, sarcomas)
Secondary: lymphomas, Krukenberg tumours, mets (GI, breast)
25
What are the risk factors for ovarian cancer?
Nulliparity, older age, early menarche, late menopause, FHx, inflammation (PID), HRT
26
Describe the two types of ovarian carcinoma
Type 1: low grade, usually arise from precursors eg. cysts, endometriosis. Associated w/ Kras, BRAF, P13KCA mutations. Includes: low grade serous, mucinous, endometrioid, clear cell
Type 2: high grade, aggressive, caught late. No precursor lesion. Usually serous, associated w/ p53 mutation
27
Describe the following types of ovarian epithelial tumour: serous, mucinous, endometrioid, clear cell carcinoma
Serous: most common. Usually cystic, bilateral. Can be benign, borderline, or malignant
Mucinous: 10-20% of tumours. Mucin-secreting epithelium (similar to GI/cervical)
Endometrioid: associated with endometriosis. Better prognosis than serous/mucinous.
Clear cell: strong association with endometriosis
28
Describe the types of germ cell tumours:
Germ cell tumours are common (20% of tumours), usually affecting young women.
Germ cell tumours can be dysgerminomas if they do not undergo differentiation, or embryonal if they do.
Embryonal includes: teratomas, choriocarcinoma, and endodermal/yolk sac tumours.
Teratomas are most common. Mature teratomas are benign, and usually cystic/solid with various tissues eg. hair, teeth. Immature teratomas are malignant.
29
What is a Krukenberg tumour?
Metastases from gastric/breast cancer, mucin-producing signet ring cell
30
Which genes are associated with familial ovarian cancers?
BRCA- serous carcinoma
| HNPCC- endometrioid and mucinous carcinomas
31
What is the most common type of vulval cancer? What are the RFs?
Squamous cell carcinoma makes up 85% of cancers. It arises on the background of VIN (vulval intraepi neo)
RFs: HPV, lichen sclerosus, VIN
32
Describe the important histological landmark in the oesophagus and explain why this is clinically relevant
- Z line is the site where squamous epithelium of the upper 2/3s transitions to columnar epithelium of the lower 1/3
- Metaplasia can occur in an oesophagus that is exposed to gastric acid (in GORD), causing squamous to become columnar (Barrett's oesophagus). This is seen as the Z line migrating higher.
- Metaplasia can -> dysplasia -> Ca IS -> carcinoma
33
What are the two types of Barrett's oesophagus?
```
Gastric metaplasia (no goblet cells)
Intestinal metaplasia (goblet cells)
```
34
What are the types of oesophageal carcinoma? Describe. How are they differentiated?
- Adenocarcinoma: lower 1/3, or rising from Barrett's oesophagus. Characterised by glands + mucin production. RFs GORD
- Squamous cell carcinoma: most common in middle 1/3. Characterised by intercellular bridges, keratin. RFs smoking, alcohol, African + Chinese.
35
How do oesophageal varices form?
- On the background of cirrhosis or portal vein thrombosis
- Increasing pressures in the portal circulation cause dilation of the anastomoses between portal + systemic
- One site is the oesophagus -> dilation, easily erode causing massive haemorrhage
36
Which layer of the stomach is breached by ulceration?
The muscularis mucosae
37
Describe the types of gastritis
Acute gastritis: caused by acute insult eg. NSAIDs, corrosives, infection. Erythematous, painful, swollen.
Chronic gastritis: caused by long term damage eg. chronic H pylori, autoimmune, chemical. The body is affected by autoimmune disease (pernicious anaemia), the antrum by chemical + bacterial.
Also more niche: CMV gastritis, IBD
38
What are the complications of gastritis?
- Ulceration
- Intestinal metaplasia -> dysplasia -> cancer
- Lymphoma (B cell MALToma) from H pylori
39
What are the causes of gastric ulcers? What are the complications?
- H pylori, alcohol, smoking, NSAIDs, stress
- Complications: bleeding, anaemia, perforation, cancer
**Ulcers can become cancerous, but cancers can also ulcerate. BIOPSY every ulcer
40
What are the types of gastric cancer?
Usually adenocarcinomas (also lymphoma, SCC, GIST)
- Intestinal: well-differentiated. Big glands with mucin
- Diffuse: poorly differentiated. Signet ring cells, no glands. Linnitus plastica
41
Describe the different pathologies of the duodenum
- Duodenitis + ulceration: usually H pylori or NSAIDs, smoking, acid production. Can lead to gastric metaplasia (no mucin). Always benign ulcers
- Infections: Giardia, CMV
- Coeliac disease
42
Describe the changes that occur in coeliac disease. How is it diagnosed?
-Villous atrophy (normal ratio of villi: crypt is 2:1)
-Crypt hyperplasia
-Infiltration of lymphocytes
Diagnosis: anti-tTG (+IgA level), anti-EMA, BIOPSY IS NECESSARY
43
What are some complications of coeliac disease?
- Poor growth, delayed puberty
- Malnutrition, vitamin deficiency
- Lymphoma (enteropathy associated T cell lymphoma)
44
How is an ulcer different to an erosion? What are the different types of gastric ulcers?
- Ulcer: into the submucosa (eg. thru muscularis mucosa) vs erosions don't (thru the lamina propria only)
- Acute vs chronic (differentiated by scarring + fibrosis in chronic)
45
Which part of the pancreas is exocrine? Which is endocrine? What are their functions?
- Exocrine: Acini. Secretes digestive enzymes
| - Endocrine: Islets of Langerhans. Release insulin (b) and glucagon (a) to regulate blood glucose.
46
List the causes of acute pancreatitis
```
Gallstones
Ethanol
Trauma, tumours
Steroids
Mumps
Autoimmune
Scorpion bites
Hypertriglyceridaemia, hypercalcaemia
ERCP
Drugs eg thiazides
```
47
How does duct obstruction lead to pancreatitis?
Bile ascends up the duct and damages acini causing enzyme release
48
___ are cells that indicate acute inflammation, while ___ indicate chronic inflammation
Neutrophils. Lymphocytes
49
Describe the pathogenesis of acute pancreatitis
- Duct obstruction/acinar damage leads to enzyme release
- Enzymes cause autolysis of the pancreas + inflammation
- Lipases cause fat necrosis + Ca binds causing saponification (yellow-white areas)
50
Name the causes of chronic pancreatitis, and the histological appearance
- Acute relapsing/persistent -> chronic
- Common causes: alcohol, haemochromatosis, gallstones, abnormal anatomy, CF, tumours
- Fibrosis and scarring, exocrine gland atrophy, duct dilatation, calcification (on Xray)
51
What is the autoimmune disease that causes pancreatitis?
IgG4 related disease- infiltration by IgG4 plasma cells -> fibrosis and inflammation
52
What are the types of pancreatic cancer? Describe the histological appearance
Ductal carcinoma (majority). Arise from ductal lesions, usually affecting head of the pancreas. Kras mutations in almost all. Mucin secreting glands in desmoplastic stroma.
Acinar. Eosinphilic cytoplasm.
NETs: include insulinomas, gastrinomas, etc. Stain with chromogranin. Occur in the tail of the pancreas.
53
What are the risk factors for gallstones? What are the types of stones?
RFs: female, middle aged, overweight/obese, high fat diet, high oestrogen eg. pregnancy, haemolysis
Cholesterol stones: radioluscent, single
Pigment stones: radio-opaque, multiple
54
Describe the microanatomy of the liver
Liver is made up of lobules shaped like hexagons
-Each hexagon has a central vein and portal triads at the corners (triad = hepatic artery, portal vein, bile duct)
-Blood flows through sinusoids from the outside in eg. towards the central vein
-Sinusoids are lined with discontinuous epithelium, separated from hepatocytes by the Space of Disse
-3 zones: 1 by the portal triad, 3 by the central vein
Zone 1 most oxygenated, zone 3 most metabolically active (most liver enzymes).
55
What is the cause of Gilbert's syndrome?
Deficiency in UDP glucuronosyl transferase ->
| unconjugated bilirubin remains tightly bound to proteins
56
Describe the structure of the nephron and the function of each part.
Glomerulus: podocytes, fenestrated epithelium, BM
-Filters blood
Tubules:
- Proximal tubule: actively reabsorbs electrolytes
- Loop of Henle: triple transporter, creates counter-current for concentration of urine
- Distal tubule: resorption of Na by aldosterone, controls pH
- Collecting duct: water resorption by ADH to control BP
57
Immunofluorescence of renal histology can show ___
Immune deposits
58
What is the inheritance of PKD? Which genes are responsible? What is PKD associated with?
Autosomal dominant
PKD1 and 2
Berry aneurysms, liver cysts
59
Name some causes of ATN. What is the mechanism?
-Ischaemia (due to pre-renal cause eg hypovolaemia)
-Toxins
-Contrast
-Drugs (aminoglycosides)
Damage to tubular epithelial cells, loss of brush border -> shed and block tubules -> increase pressure in nephron -> AKI (decreased output + clearance)
60
What is the cause of TIN?
Tubulo-interstitial nephritis is caused by immune injury. Can be caused by infection (pyelonephritis) or acute interstitial nephritis by RSVP (Rifampicin, Sulfa drugs, 5 Ps- penicillin, phenytoin, PPIs, pain relief (NSAIDs) and pee pills (diuretics)
-> immune mediated inflammation, granuloma formation
61
How can renal diseases be classified?
By the part of the nephron affected:
- Glomerulus: nephrotic and nephritic syndrome
- Tubules and interstitium: ATN, TIN
- Blood vessels: vasculitis, thrombotic microangiopathies
62
What are some features of glomerulonephritis?
```
Haematuria and proteinuria
Oliguria
Hypertension
Red cell casts
Crescents (in rapidly progressive)
```
63
Name some causes of nephritic syndrome (at least 5)
- Post-streptococcal GN
- IgA nephropathy (Berger disease)
- Rapidly progressive GN (anti-GBM, immune complex mediated, Pauci-immune eg. vasculitis)
- Alport syndrome
- Thin basement membrane disease
64
Describe the characteristics of post-streptococcal GN and how it is different to IgA nephropathy
- Post-strep: occurs weeks after infection (usually Grp A). Granular immune complex deposits (IgG and C3).
- IgA nephropathy: occurs days after infection (URTI), presenting with frank haematuria. More common, can reoccur. Granular IgA deposits. Oxford classification
* Both can lead to Type 2 rapidly progressive (crescentic) GN
65
What are the types of rapidly progressive GN? How are they different?
Type 1: anti-GBM antibodies (Goodpasture). Linear deposits on fluorescence microscopy. Can have lung involvement - haemoptysis
Type 2: immune complex deposition (SLE, IgA neph, post-infectious). Granular deposits.
Type 3: Pauci immune (Wegener's, MPA). No deposits. Vasculitis esp. rashes, lungs. c/p-ANCA +ve.
66
What is the defining characteristic of rapidly progressive GN?
Crescents in the glomerulus on light microscopy
67
What is the cause of Alport syndrome? What is the inheritance pattern? How does it present?
Mutation in Type IV collagen (alpha 5 chain)
X linked
Nephritic syndrome, SNHL, eye disorders
68
What is the cause of thin basement membrane disease? What is the inheritance pattern? How does it present?
Mutation in Type IV collagen (alpha 4 chain)
Autosomal dominant
Asymptomatic, microscopic haematuria with normal renal function
69
Name some causes of asymptomatic haematuria
Thin basement membrane disease
Alport syndrome
IgA nephropathy (Berger disease)
70
If a patient presents with a picture of severe nephritic syndrome, what would you consider as DDx? What investigations would you do?
- Rapidly progressive GN: serology for anti-GBM antibodies (Type 1), ANCAs (Type 3), anti-dsDNA + complement + throat swab/ASOT titre (Type 2)
- Consider renal biopsy for light microscopy, immunofluorescence
71
What are the features of haemolytic uraemic syndrome? TTP? What are the similarities in presentation?
-HUS: MAHA (mostly renal), low platelets, AKI
-TTP: HUS + neurological dysfunction + fever
Both have:
HA -> anaemia, jaundice. High bilirubin and LDH, reticulocytosis, fragmented RBCs
Thrombocytopenia: petechiae, bleeding
72
What is the pathophysiology of HUS and TTP? What are the causes?
ADAMTS13 causes widespread fibrin deposition in vessels
-> lots of tiny thrombi which damage RBCs and platelets
Caused by E coli O157:H7 (HUS), ADAMTS13 deficiency, drugs, radiation, APS
73
Name some causes of nephrotic syndrome
Primary causes:
- Minimal change disease (steroid-sensitive nephrotic syndrome)
- Membranous glomerulonephritis
- Focal segmental glomerulosclerosis
Secondary causes:
- Amyloidosis
- DM -> nodular glomerulosclerosis
- SLE
74
Describe the features of minimal change disease
- Common in children
- Steroid sensitive
- No immune complexes (no abnormality on light microscopy)
- Loss of podocyte foot processes on electron microscopy
75
Describe the features of membranous glomerulonephritis
- Common in adults
- Subepithelial immune deposits
- Glomerular BM thickening on light microscopy
- 'Spikey' appearance on electron microscopy
- Associated with antibody to PLAR2
- Can be 2˚ to SLE, infection, malignancy (exclude)
76
Describe the features of FSGS
- Common in adults
- Scarring of the glomerulus (light microscopy) with immune deposition
- Somewhat responsive to steroids
- Can be 2˚ to HIV
77
Describe the features of diabetic nephropathy
- Common!! (30-40% of diabetics)
- Microalbuminuria is key finding -> proteinuria, nephrotic syndrome
- Nodular glomerulosclerosis (Kimmelstiel Wilson nodules)
- Thickening of the BM
78
Describe the features of amyloidosis (in renal disease)
- Apple green birefringence with Congo red stain
- AA: associated with chronic inflammation eg. IBD, RA
- AL: associated with myeloma, light chains
79
How does hypertension cause CKD?
- Increased pressure leads to scarring, ischaemia etc
- Shrunken kidneys with granular cortices
- Nephrosclerosis
80
Name the different kinds of kidney stones? Describe some features of each.
Calcium oxalate: most common. Caused by excess calcium. Radio-opaque
Uric acid: associated with hyperuricaemia, gout.
Triple stones: Mg ammonia phosphate. Staghorn shape. Associated with UTI. Radioluscent
81
Name some types of benign renal tumours and describe some features of each
- Papillary adenoma: small epithelial tumour. Associated with Trisomy 7, 17. <15mm
- Oncocytoma: brown, scar in the centre. Pink granular cytoplasm. If lots- associated with Birt-Hogg-Dube syndrome
- Angiomyolipoma: Mesenchymal cells eg. vessels, muscle, fat. Associated with tuberous sclerosis.
82
Name some types of renal carcinoma and describe the features of each. How do they present?
-Clear cell carcinoma: golden tumour. Lots of clear cells.
-Papillary carcinoma: fragile brown tumour >15mm. Associated with cystic disease.
-Chromophobe: solid brown tumour. Central scar,
Present with renal mass, painless haematuria.
83
The renal tumour common in children is called ___
Nephroblastoma (Wilm's tumour)
84
Name the types of transitional cell carcinoma and describe the features of each.
- Non-invasive papillary. Frond-like
- Infiltrating
- Flat carcinoma in situ
85
Urinary schistosomiasis is associated with which type of cancer?
Squamous cell carcinoma
86
What is BPH? What are the presenting features?
Benign prostatic hyperplasia- androgen mediated growth of prostatic tissue -> nodule formation
Lower urinary tract symptoms: difficulty urinating, frequency, nocturia, retention, dribbling
87
What is the treatment of BPH?
Alpha1 blockers: Tamsulosin
5a reductase inhibitors: Finasteride
TURP
88
What is the main type of prostate cancer? What are the risk factors?
Prostatic adenocarcinoma
| RFs: older age, black, FHx of prostate/breast cancer
89
Describe how prostate cancer is graded.
Gleason score: 2 areas, grade from 1-5 and add
90
Name the types of testicular tumours and describe their features
```
Germ cell tumours (95%):
-Seminoma: most common, 30s. Clear cells, 'fried egg' appearance, lymphocytes. High hCG
-Teratoma: varied components
-Embryonal carcinoma: 2nd commonest
-Yolk sac tumour: high AFP
-Choriocarcinoma
Associated with undescended testes.
Non germ cell (5%): Leydig cell, Sertoli cell
```
91
Name some benign testicular pathology
- Varicocoele
- Hydrocoele
- Epididymitis
92
What are the most common types of pituitary adenoma (in order)?
Prolactinoma
Non-functioning
ACTH secreting
GnRH secreting
93
Describe the histological appearance of thyroid tissue
Epithelial cells with large pink globs (colloid)
94
Which cells produce calcitonin?
Parafollicular C cells
95
What are some causes of a thyroid goitre?
- Iodine deficiency
- Grave's disease
- Puberty
- Multinodular goitre
- de Quervain's
- Hashimoto's
96
An ovarian tumour that causes thyrotoxicosis is ?
Struma ovarii. A type of teratoma
97
What are some histological features of Hashimoto's?
Lymphocytes (chronic inflammation)
| Hurthle cells
98
What are the types of thyroid cancer? How common are they? Briefly describe
Papillary: 80%. Clear nuclei, psamomma bodies
Follicular: 15%. Well demarcated. Early metasases.
Medullary: 5%. Affect C cells, producing calcitonin -> amyloid (stain with Congo red). Associated with MEN2.
Anaplastic: <5%. Elderly, poor prognosis.
99
What are the causes of 1˚ hyperparathyroidism (in order of frequency)?
Parathyroid adenoma
Parathyroid hyperplasia
Parathyroid carcinoma
100
How do the adrenals change in different causes of Cushings/adrenal failure?
Cushings disease/ectopic ACTH: hyperplasia
Exogenous steroids: atrophy
Adrenal failure: atrophy
101
What is the adrenal complication of sepsis with DIC?
Waterhouse-Friedrichson syndrome
102
What are the different MEN syndromes?
1 (3 Ps): parathyroid hyperplasia, pituitary adenoma, pancreatic NETS
2A (2 Ps): parathyroid hyperplasia, phaeo, medullary thyroid cancer
2B: medullary thyroid cancer, phaeo, Marfanoid body
103
Describe the characteristic features of SLE.
| How is it diagnosed?
```
Need 4/11 criteria:
Serositis
Oral ulcers
Arthritis
Photosensitivity
Blood disorders
Renal
ANA +ve
Immune phenomena (anti-dsDNA)
Neuro symptoms
Malar rash
Discoid rash
```
104
Which antibodies are +ve in SLE?
ANA (anti-nuclear)
anti-dsDNA
anti-Sm
105
Which test can show immune complex deposition? Which conditions can this be used in?
Immunofluorescence
| SLE, post-strep GN etc
106
Which cardiac conditions are associated with SLE?
Pericarditis, Libman-Sacks endocarditis
107
What is scleroderma? What are the two types?
Scleroderma is an auto-immune multisystem condition characterised by skin fibrosis (collagen)
Limited/cutaneous (CREST) vs diffuse
108
Describe the characteristics of limited scleroderma
```
+Anti-centromere antibodies
Skin changes on face/limbs
Calcinosis
Raynaud's
Esophageal dysmotility
Sclerodactyly
Telangiectasia
```
109
Describe the characteristics of diffuse scleroderma
+Anti-Scl-70
Skin changes anywhere on the body
Widespread organ involvement: renal, pulmonary fibrosis, vascular etc
110
Name the features of dermatomyositis and polymyositis
Anti-Jo1 +ve
Proximal muscle weakness, raised CK
DM: heliotrope rash, Gottron's papules
111
What is the key pathology in sarcoidosis?
Non-caseating granulomas (histiocytes)
112
Describe the classic presentation of sarcoidosis + other features
```
Young, F, Afro-Caribbean
SOB, dry cough -> bilateral hilar lymphadenopathy
+skin: lupus pernio, nodules, erythema nodosum
Lymphadenopathy
Eye involvement
Blood dyscrasias
Hypercalcaemia
Cardiac: arrhythmia, heart block
```
113
Name some investigation findings in sarcoidosis
- CXR: bilateral hilar lymphadenopathy
- Raised Ca
- Raised ACE
- Raised ESR
114
Name some types of vasculitis and briefly describe (antibodies, presentation, etc)
Large vessel:
- Takayasu's: 'pulseless disease'. Japanese F.
- Temporal arteritis: temporal headache, jaw claudication, PMR. Older F. High ESR. Giant cells + skip lesions.
Medium vessel:
- Kawasaki: children. CRASH and burn. High ESR. Coronary aneurysms.
- PAN: renal involvement/gut ischaemia, no lungs. Microaneurysms- 'rosary beads'.
Small vessel:
- GPA: cANCA +. Triad: upper resp, lower resp, kidneys.
- eGPA: pANCA +. Asthma, allergic rhinitis, eosinophilia.
- MPA: pANCA +. Pulmonary renal syndrome.
- HSP: IgA. Children. Preceding URTI. Lower limb purpuric rash, arthritis, abdo pain, renal.
115
cANCA is + in which conditions? pANCA is + in which?
cANCA: GPA
pANCA: eGPA, MPA
116
What is the difference between macrophages and lymphocytes on microscopy?
Lymphocyte: big nucleus, very little cytoplasm
Macrophage: big nucleus, lots of cytoplasm. Bigger than lymphocytes
117
What are macrophages are associated with?
Late acute inflammation
| Chronic inflammation- granulomas
118
What is a granuloma? What does it look like histologically?
An organised collection of activated macrophages.
Lots of epithelioid macrophages (activated- lots of cytoplasm)
Can have Langerhans giant cells
119
What tells you that you have a good sputum sample from the alveoli?
Pigmented macrophages
120
What are the histological characteristics of squamous cell carcinomas vs adenocarcinomas?
SCC: keratin producing, intercellular bridges
AC: mucin producing, glands
121
What is histochemistry and what is immunohistochemistry?
Histochem: using stains to that produce a chemical rxn with specific molecules eg. Fontana stain for melanin, haematoxylin and eosin, Congo red for amyloid
Immunohistochem: using antibodies that bind to specific antigens eg. cytokeratin for epithelial
122
What are the different levels of breast cytology?
```
C1-5
C1: inadequate sample
C2: benign
C3: atypia
C4: suspicious of malignancy
C5: malignant
```
123
What is the gold standard method for diagnosing breast pathology?
Tissue biopsy with histopathology - can visualise the tissue architecture
124
What is duct ectasia? What is the typical presentation? What is the histological appearance?
Inflammation and dilation of the lactiferous ducts.
Post-menopausal women with nipple discharge. Can form chronic mass, similar to cancer on mammogram
Dilatation of the ducts, full of protein-rich material
125
Define acute mastitis. What is the typical presentation? What is the most common causative organism? What is the management?
Acute inflammation of the breast tissue caused by infection.
Associated with lactation. Painful, tender, hot, swollen breast. Unilateral.
Caused by Staph aureus usually
Mx: continue breastfeeding/expressing, antibiotics eg. fluclox.
126
Name some benign causes of breast lumps.
Fibrocystic breasts
Fibroadenoma
Duct papilloma
127
Describe fibrocystic changes in breasts
Lumpy breasts, may be tender. Very common
| Associated with hormonal changes, eg. menstrual cycle
128
Describe the features of breast fibroadenoma
- Mobile, round, rubbery non-tender benign mass
- Young women
- Consists of glandular and stromal cells
129
Describe Phyllodes tumour
- Potentially aggressive type of fibroadenoma. Very dense. Can become malignant.
- Affect older women, enlarging mass
130
Describe ductal papilloma (breast)
- Benign papillary growth (epithelial cells in frond-like structure) within ductal system
- Common. In middle aged F. May be asymp or have bloody discharge
131
What is a radial scar (breast)?
Benign sclerosing lesion with central scarring in a stellate pattern. Due to incorrect repair mechanism.
-Stellate pattern on mammogram + histology
132
Name some different types of pre-malignant breast disease
Proliferative conditions (with risk of malignancy):
- Epithelial hyperplasia: not technically precursor. Slight increased risk. Frond-like growth.
- Flat epithelial atypia: increased risk. Well-circumscribed ducts.
- in situ lobular neoplasia: increased risk. Solid proliferation.
DCIS (ductal carcinoma in situ): intraductal. Microcalcification on mammogram. Atypical cells.
LCIS (lobular CIS): no sign on mammogram.
133
What is the most common type of breast cancer? What are the subtypes?
Carcinoma
- Ductal
- Lobular: single-file cells (Indian file)
- Tubular: tubular structure, small
- Mucinous: lots of mucin
- Basal-like: assoc with BRCA. Lymphocyte infiltration. CK (cytokeratin) 5/6+ stain.
134
What is the classic method of diagnosing breast pathology?
Clinical examination
Mammogram/USS
FNA + cytology
135
What are some signs + symptoms of breast cancer?
- Firm non-tender fixed lump
- Peau d'orange
- Nipple inversion
- Discharge
- Skin tethering
- Paget's disease of the breast (eczema of nipple)
136
Who is invited for breast screening?
Women aged 47-73 every 3 years -> mammogram
137
What are some markers of good prognosis in breast cancer? Why? Bad?
Good: ER/PR/HER2 positive. Will respond well to Tamoxifen and Herceptin
Bad: triple negative **HER2 is more aggressive, but more treatable.
138
Describe the basic skin histology
Epidermis: keratinised squamous epithelial cells (keratinocytes). 4 layers. Stratum corneum, granulosum, spinosum, basalis.
Dermis: contains vessels, pilosebaceous units, etc
SC fat
139
What are the different inflammatory patterns of skin? Briefly describe and give examples of conditions.
- Vesicobullous: form fluid filled vesicles/bullae eg. bullous pemphigoid.
- Spongioid: oedematous eg. acute eczema
- Psoriaform: thickened eg. psoriasis
- Lichenoid: plaque eg lichen sclerosis
- Vasculitic
- Granulomatous
140
What are some types of blistering skin conditions?
Bullous pemphigoid: autoimmune condition. IgG and C3 attack BM -> splitting at the dermis. Tense bullae.
Pemphigus vulgaris: autoimmune condition. IgG to desmosomes -> splitting of keratinocytes (acantholysis) Superficial and easily ruptured bullae. Also mucosal.
141
How are bullous pemphigoid and pemphigus differentiated?
Clinically- deep vs superficial
| Histology- immunofluorescence showing IgG and C3 on BM in pemphigoid, IgG in epidermis for pemphigus
142
What is eczema? What are the types?
Inflammation of the skin with dry itchy rash (synonymous with dermatitis)
Atopic dermatitis/eczema: affects face babies, flexural surfaces in adults. Dry, itchy, scaly rash.
Contact: Type IV hypersensitivity reaction to nickel, latex, etc.
Seborrheic dermatitis: inflammatory reaction to yeast - Malassezia furfur. Cradle cap in babies. Dandruff.
143
What is psoriasis? How does it present?
Chronic inflammatory skin condition (T cells) characterised by red scaly plaques. Associated with nail changes: onycholysis, pitting, subungual hyperkeratosis.
Chronic plaque psoriasis- extensor surfaces.
Guttate- rain drop pattern.
Pustular
144
What is the histology of psoriasis?
Parakeratosis (nuclei in stratum corneum), no granular layer, Munro's microabscesses (neutrophils)
145
Describe lichen planus
Inflammatory skin condition (T cells under epidermis)
Pruritic, purple papules and plaques with mother-of-pearl sheen and Wickam's striae
Can affect mucous membranes
146
What are some causes of erythema multiforme?
Usually infection > drugs
| HSV, mycoplasma. Antibiotics, NSAIDs, AEDs
147
What are Stevens-Johnson syndrome and toxic epidermal necrolysis?
Derm emergencies, blistering skin conditions that cover large areas of the body.
SJS: <10%
TEN: >30%
Usually caused by drug reaction eg. AEDs, sulphonamides
148
What is pityriasis rosea?
A rash that occurs after a viral illness
| Starts with a herald patch -> Christmas tree distribution
149
What is pyoderma gangrenosum?
A form of vasculitis presenting as an ulcer. A systemic manifestation of illness eg. malignancy, IBD, SLE, TB
150
Describe seborrheic keratosis
A benign skin growth. Stuck on mole/warty appearance.
| Keratin horns/horn cysts with proliferating epidermis on histology
151
Describe actinic keratosis
Premalignant lesion, develops on sun-exposed area. Can be rough and sandpaper scaly lesion, hyperkeratotic, etc.
152
Describe keratoacanthoma.
Premalignant dome-shaped nodule that grows rapidly and can spontaneously clear up. Similar to SCC
153
Describe Bowen's disease
Premalignant lesion, red scaly patch/macule. SCC in situ
154
Describe a BCC. What is another name for this condition?
Also known as Rodent ulcer.
Pearly papule with rolled edge, telangectasia.
Does not metastasise, but can be locally invasive
155
Describe a SCC.
Malignant neoplasm of SCs. Rough scaly patches with varying appearance, invading into the dermis. Can be ulcerated, nodular, crusty.
156
Name some melanocytic conditions
Melanocytic naevi (moles): benign proliferation of melanocytes.
Malignant melanoma: malignant neoplasm of melanocytes
-Lentigo: flat, slow growing
-Superficial spreading
-Nodular
-Acral lentiginous: palms/soles/subungual
157
How are melanomas assessed?
ABCDE
- Asymmetry
- Borders (irregular)
- Colour (multiple)
- Diameter >5mm
- Evolution
158
Which part of the skin are melanocytes normally found? What is abnormal?
Stratum basale + dermis
| NOT normal to be moving up through the epidermis
159
How are skin cancers staged?
BCC + SCC: width
| Malignant melanoma: depth (Breslow's thickness)
160
What are the two main types of bone? Where are they found? What do they look like on histology?
Cortical: long bones. Lots of dense pink material.
Cancellous: vertebrae, pelvis. Pink + white areas of adipose and haem stem cells
161
What are the main cells involved in metabolism of bone?
Osteoclasts: breakdown bone. Have RANK
Osteoblasts: build bone. Have RANKL
162
What is metabolic bone disease? Give some examples
```
Disorder of bone turnover due to imbalance in chemical factors and hormones.
Osteoporosis
Osteomalacia/Rickets
Paget's disease of bone
Renal osteodystrophy
```
163
Name some causes of osteoporosis
```
Older age
Post-menopausal/early menopause/FHA
Steroid use
Chronic illness
FHx
```
164
Define osteoporosis and osteopenia. What is the presentation of osteoporosis?
Osteoporosis: T score
165
Explain the biochemistry in osteoporosis, osteomalacia and Paget's
- OP: normal Ca, normal Vit D, normal ALP, normal PTH
- OM: low/normal Ca, low Vit D, high ALP, high PTH
- Paget's: normal Ca, normal Phos, very high ALP
166
Brown cell tumours are characteristic of which condition?
Hyperparathyroidism
167
What are some types of fractures?
```
Simple
Compound
Greenstick
Comminuted
Impacted
```
168
What is Pott's disease? What does it look like on histology?
TB of the spine
| Inflammatory cells with granulomas, Langerhans cells
169
Which joints are commonly affected by osteoarthritis? Rheumatoid arthritis?
OA: Knees, hips, DIPs and PIPs
RA: hands and feet (DIP sparing), elbows, ankles etc
170
What are the features of rheumatoid arthritis?
Morning stiffness
Swan-neck and Boutonnière deformity
Ulnar deviation of fingers, radial of wrist
Anaemia, raised ESR, RF, anti-CCP
171
What are the histological features of OA and RA?
OA: cartilage degeneration, osteophytes
RA: inflammatory cells, thickening of synovial membranes, Grimley-Sokoloff cells
172
What is the difference between gout and pseudogout?
Gout: urate crystals, negative birefringence
Pseudogout: calcium pyrophosphate crystals, positive birefringence
173
What is the most common type of bone tumour?
Metastases
174
Which tumours commonly metastasise to bone?
Adult: breast, prostate, lung, kidney, thyroid
Children: neuroblastoma, Wilm's
175
What are 3 types of primary malignant bone tumour?
Osteosarcoma
Chondrosarcoma
Ewing's sarcoma
176
Describe the features of osteosarcoma eg. presentation, histology
```
Commonly in young/teen men
Affects the knee, jaw
Xray: Codmann's sign (periosteal elevation), lytic lesions
Histology: stromal cells
Poor prognosis
```
177
Describe the features of chondrosarcoma eg. presentation, histology
Abnormal proliferation of cartilage
Usually older adults
Affects axial skeleton, long bones
Decent prognosis
178
Describe the features of Ewing's sarcoma eg. presentation, histology
Highly malignant small round cell tumour
Commonly in young people
Affects long bones and pelvis
Xray: periosteal reaction (onion skin appearance)
179
T/F. ALP is raised in malignant primary bone tumours
False. ALP is commonly raised in osteosarcoma, but normal in Ewing's sarcoma
180
What are the features of osteoarthritis? On exam and Xray.
Stiffness at the end of the day
Heberden's nodes (DIP) and Bouchard's nodes (PIP)
Xray: loss of joint space, osteophytes, subchondral sclerosis, subchondral cysts
181
Name some benign bone tumours
- Fibrous dysplasia: proximal femur. F. Assoc w/ McCune Albright syndrome
- Osteoma: bony outgrowths.
- Osteochondroma: end of long bones. Young M. Cartilage capped bony outgrowth
182
Spongiform changes in the brain are consistent with ___
Prion disease
183
Name some histological features of Alzheimer's disease
Intracellular neurofibrillary tangles (Tau protein)
Extracellular plaques (Amyloid-beta)
Cerebral amyloid angiopathy (buildup in vessels)
Neuronal loss
184
What is the pathogenesis of Alzheimer's disease?
Generalised brain atrophy due to:
- Beta amyloid builds up extracellularly (breakdown of APP), disrupts cell functioning
- Hyperphosphorylation of Tau -> accumulation -> cell death
185
How are Parkinson's and Alzheimer's staged histologically?
Braak stages- describes the location of the Tau protein/alpha-synuclein in the brain
186
Describe the histological features/pathogenesis of Parkinson's disease
Loss of dopaminergic neurons in the substantia nigra
| Intracellular alpha-synuclein accumulation -> Lewy bodies
187
What is the gold standard of diagnosis in Parkinsons?
Brain histology -> immunostaining for alpha-synuclein
188
What are some causes of Parkinsonism? How are they different/similar?
Parkinson's disease: a-synuclein, SN
Multisystem atrophy: a-synuclein, glial cells, cerebellum
Progressive supranuclear palsy: Tau (4R)
Corticobasal degeneration: Tau (4R)
189
Describe the pathogenesis/histological features of Pick's disease
Fronto-temporal atrophy: neuronal loss
Balloon neurons
Pick bodies- Tau protein (3R Tau)
190
Define dementia and neurodegenerative disease
Neurodegenerative disease: a progressive condition leading to neuronal loss
Dementia: global impairment in cognitive function without impairment of consciousness
191
What is the presentation of different types of dementia?
Alzheimer's disease: slowly progressive memory loss and impairment.
Lewy body: fluctuating cognition, psychological disturbance, visual hallucinations, Parkinsonism
Vascular: rapid, stepwise deterioration in function, BG of risk factors.
Pick's disease: dysexecutive syndrome, behavioural changes
192
What are the two causes of cerebral oedema?
Cytogenic: cellular injury
Vasogenic: disruption of the BBB
193
How does cerebral oedema appear on Xray?
Loss of gyri
194
What are the types of hydrocephalus? What is the pathogenesis of each?
Communicating: impaired resorption of CSF at the villi
| Non-communicating: obstruction in the ventricular system
195
What is the consequence of raised ICP? What are the different types?
Herniation
- Transtentorial: under tentorium
- Tonsillar: thru foramen magnum
- Subfalcine: under the falx cerebri
196
Define stroke. What are the types? What is not considered a stroke?
A rapidly developing loss of focal/global cerebral function lasting >24 hours
-Ischaemic: due to loss of blood supply
-Haemorrhagic: due to rupture of small vessels
NOT a stroke: infarction due to tumour, extradural or subdural bleed
197
What is a TIA? What is the risk of stroke?
Rapidly developing loss of focal/global cerebral function lasting <24 hours
1/3 will have significant infarction within 5 years
198
Where do haemorrhagic strokes most commonly occur? What are the risk factors?
Basal ganglia
| Hypertension, FHx, AVMs
199
What is the difference between a cavernous angioma and an AVM?
AVM: has parenchyma wrapped around. Tends to bleed at higher pressure
Cavernous angioma: no parenchyma. Bleeds at lower pressure
200
What is the cause of a subarachnoid haemorrhage?
Berry aneurysm
201
What are the risk factors for cerebral infarction?
Cerebral atherosclerosis
Hypertension, smoking, DM, hypercholesterolaemia
Also AF + PFO
202
What is the acute management of stroke/TIA?
Aspirin, dipyridamole
| Thrombolysis (<3 hours from onset)
203
How do the different types of stroke present (ACA, MCA, PCA)?
ACA: contralateral leg paresis + sensory loss
MCA: contralateral arm and face paresis + sensory loss, aphasia
PCA: contralateral visual field loss etc
204
What are the ways of classifying traumatic brain injuries? Give examples
Missile (gunshot) vs non-missile (fall, RTA)
Acceleration and deceleration (RTA)
Rotational (boxing)
205
What are some signs of basal skull fracture?
Raccoon eyes (periorbital)
Battle's sign (mastoid)
CSF rhinorrhoea
206
What is the difference between contusion and concussion?
Contusion: bruise to brain from hitting skull
Concussion: type of TBI, characterised by cognitive impairment
207
What are some inherited conditions that are associated with brain tumours?
NF1+2
Tuberous sclerosis
vHL
208
What is the best investigations for brain tumours?
T1 weighted MRI with and without contrast
209
What is the management of brain tumours?
Medical: chemo (high grade gliomas), RDx
| Surgery
210
How are CNS tumours graded? Staged?
WHO classification based on histology. I + II are low-grade
I: benign
II: death >5 years
III: death <5 years
IV: death <1 year
They are NOT staged (except medulloblastoma)
211
Which are the most common primary CNS tumour? Name some types.
What is the second most common?
Gliomas eg. astrocytoma, glioblastoma multiforme
| Meningioma 2nd.
212
Which types of brain tumour are commonly seen in children? Where do they occur? What are the key histological features?
```
Pilocytic astrocytoma (a type of glioma): cerebellar. Hairy cells, Rosenthal fibres.
Medulloblastoma (embryonal cell): cerebellar. Small round blue cells. Wright rosettes.
```
213
Which type of glioma is most common in adults? How can it arise?
```
Glioblastoma multiforme (grade IV)
de novo mutation or secondary to progressive astrocytoma
```
214
Which cancers most commonly metastasise to the brain?
Lung
Breast
Malignant melanoma
Renal cell
215
Where is the site of the lesion in atherosclerosis?
Sub-intimal eg. endothelial lining
216
Describe the process of atheroma formation
- Endothelial injury
- LDL enters the sub-intimal space
- Macrophages migrate into the sub-endothelial space and phagocytose cholesterol esters -> foam cells
- Apoptosis of foam cells -> necrotic core
- Formation of the fibrous cap, thickening of SM cells
217
What are some risk factors for atherosclerosis?
T2DM, hypertension, hyperlipidaemia, smoking, FHx
218
What are the consequences of atherosclerosis?
Obstruction (at 70% stenosis) -> ischaemia
| Rupture -> thrombosis, embolus
219
What are the types of ischaemic heart disease? Which are ACS? What is the cause?
Stable angina: the only one that is non-ACS
Unstable angina, STEMI, NSTEMI
Caused by increased ratio of demand : supply eg. obstruction due to atherosclerosis
220
What is an MI? What are some causes of MI?
MI: myocardial necrosis due to prolonged ischaemia
Plaque rupture
Vasospam eg cocaine use
221
Which area of the myocardium is affected by obstruction of the LAD? RCA? LCx?
LAD: anterior wall + septum, apex
RCA: posterior wall + septum
LCx: lateral LV, not the apex
222
Describe the changes that occur in the myocardium after MI
Hyperacute (within hours): no visible changes
Acute (by 24 hours): pale, oedematous
Within days: haemorrhage, phagocytes
By 1-3 weeks: granulation tissue, fibroblasts + collagen
By 4-6 weeks: fibrosis + scarring
223
What are the complications of MI?
```
Death
Arrhythmia
Rupture
Tamponade
Heart failure
Valve problems eg. mitral incompetence
Aneurysm
Dressler's syndrome
Embolus
Recurrence
```
224
What can cause sudden cardiac death? Which is most common?
Plaque rupture/atherosclerosis. Most common
HOCM
Cardiac failure
225
What are the types of heart failure? How do they present?
Congestive: both sides. Mix of symptoms
Right HF: oedema, HSmegaly
Left HF: SOB, PND, exertional dyspnoea
226
What are the types of cardiomyopathy? Describe the histology and causes of each.
Dilated: floppy, enlarged chambers. Idiopathic, alcohol, thyroid disease, pregnancy, haemochromatosis
Hypertrophic: thickened walls. Familial.
Restrictive: stiffening of ventricles, big atria. Sarcoidosis, amyloidosis.
227
Which valves are classically affected in rheumatic valve disease?
Left-sided eg mitral, aortic
228
What are the most common valve disorders? What is the cause?
```
Mitral prolapse (regurg): very common
Aortic stenosis: due to calcification. Very common
```
229
Which valves are commonly affected in IE? What is the exception?
Left-sided.
| Except for IVDU- they classically get tricuspid vegetations
230
What are the histological features of infective endocarditis?
Aschoff bodies (granulomas)
Anitschkov myocytes
Vegetations/verrucae
231
What is the difference between a true aneurysm and a pseudoaneurysm?
True: dilatation of all layers of the vessel
Pseudoaneurysm: disruption of the vessel wall leading to collection of blood between the tunica media and adventitia
232
What is pulmonary oedema? What are the causes?
Fluid accumulation in the alveolar space
- LHF
- Alveolar injury eg. drugs, pancreatitis
- High altitude
233
What are the conditions of acute lung injury/diffuse alveolar damage? What are they caused by?
ARDS and hyaline membrane disease (neonatal RDS).
Adults: many
-Infection
-Aspiration
-Shock
-DIC
Neonates: insufficient surfactant production
234
What is the pathophysiology of ARDS?
Diffuse alveolar damage -> congestion + exudate -> protein deposits and granulation -> fibrosis
235
Define asthma.
Chronic inflammatory airway disorder characterised by airway hyperresponsiveness, chronic inflammation and reversible obstruction.
236
What are the histological changes in asthma both acute + chronic?
Acute: inflammation with eosinophils + mast cells, oedema, bronchospasm
Chronic: smooth muscle hypertrophy, mucus plugging with goblet cell hyperplasia, airway narrowing
237
What are the two main pathological processes in COPD? Describe the histology of each
Chronic bronchitis: goblet cell hyperplasia -> mucus
| Emphysema: permanent alveolar loss due to chronic activation of phagocytes, bullae
238
Describe the location of emphysema in that caused by smoking and alpha-1 antitrypsin deficiency
- Smoking: centrilobular
| - A1 antitrypsin: panacinar
239
What is bronchiectasis? What are some causes?
Permanent enlargement of the bronchi with inflammation and fibrosis
- Recurrent chest infections
- CF
- PCD
- Amyloidosis
240
What is the pathophysiology of CF?
Mutation in the CFTR gene on Chromosone 7q3
Most frequent is D F508
Causes buildup of viscous secretions eg. lungs, pancreas
241
What are some complications of pneumonia?
Empyema
Pneumothorax
Pleural effusion
Abscess formation
242
Owl's eye inclusions are typical of which pathogen? What does this mean?
CMV. Very large nuclei
243
What is pneumoconiosis?
Occupational lung disease caused by chronic inhalation of mineral dust/inorganic particles eg. miners, silicon
244
What is extrinsic allergic alveolitis?
Occupational lung disease caused by inhalation of organic particles eg. Pigeon fancier's lung, Farmer's lung
245
What are the main types of lung cancer? Which is most common?
95% are carcinomas
- Squamous cell 30%
- Adenocarcinoma 30%
- Small-cell 20%
- Large cell 20%
246
Describe the location and histology of squamous cell carcinoma of the lungs
Location: usually proximal, large airways
Histology: keratin, intercellular bridges
247
Describe the location and histology of adenocarcinoma of the lungs
Location: peripheral, alveolar
Histology: glands, mucin-producing
Tend to metastasise early
248
Describe the location and histology of small cell carcinoma of the lungs
Location: central, proximal bronchi
Histology: neuroendocrine cells. May stain with chromogranin. Associated with paraneoplastic syndrome.
249
Name some paraneoplastic syndromes that may occur with small cell lung cancer
- Hyperparathyroidism: PTHrP
- Cushing's: ACTH
- SIADH: ADH
- Carcinoid syndrome: serotonin
250
What is amyloidosis?
A condition characterised by the deposition of abnormal proteins that are resistant to degradation. Can be many different proteins, always in a beta-pleated sheet structure.
251
What are the types of amyloidosis? Describe them
AA amyloid: derived from serum amyloid A. Associated with chronic inflammation eg. RA, IBD
AL amyloid: derived from light chains eg. MM
252
What is the purpose of hepatic stellate cells?
Store Vitamin A
| Transform into fibroblasts and lay down collagen
253
Describe cirrhosis
Chronic liver disease characterised by diffuse inflammation, fibrosis, nodular regeneration, and abnormal vascular architecture
254
What are the main causes of cirrhosis?
```
Alcoholism
NAFLD
Viral hepatitis
Autoimmune hepatitis
PBC and PSC
```
255
How is cirrhosis classified?
Based on the size of nodules eg.
- Micronodular: alcohol, biliary tract disease
- Macronodular: viral hepatitis
256
How is prognosis in cirrhosis determined?
Child-Pugh score:
- Albumin
- Bilirubin
- Clotting
- Distension (ascites)
- Encephalopathy
257
What is the histological feature of acute hepatitis?
Spotty necrosis
258
What are the histological features of chronic hepatitis?
Piecemeal necrosis, fibrosis
259
Describe the spectrum of liver disease
Steatosis/acute hepatitis -> fibrosis -> compensated cirrhosis -> HCC or decompensation -> death
260
What are the histological features of alcoholic liver disease?
Fatty changes/steatosis: fat droplets
Alcoholic hepatitis: balloon cells, Mallory Denk bodies, fibrosis. Specifically in zone 3 (close to central vein)
Cirrhosis: micronodules, fibrosis
261
T/F. Alcoholic and non-alcoholic steatosis look the same on histology
True!
262
What is the histological appearance of PBC?
Bile duct loss with granulomas
263
What is the histological appearance of PSC?
Bile duct fibrosis, strictures (NOT inflammation)
264
What are some inherited causes of cirrhosis?
- Haemochromatosis
- Alpha1 antitrypsin
- Wilson's
265
What stain can be used in Wilson's?
Rhodanine
266
What tests diagnose Wilson's?
Serum Cu: Low
Serum caeruloplasmin: Low
Urinary Cu: High
Biopsy with rhodanine stain
267
Which antibodies are found in autoimmune hepatitis? PBC?
AI hepatitis: anti-SMA
| PBC: AMA
268
T/F. Alpha1 antitrypsin defiency causes low levels in the liver
False. The pathology is misfolding of the proteins, leading to buildup in the hepatocytes and deficiency in the blood.
269
Name some types of liver tumours. Which are most common?
Benign: haemangioma (commonest benign), adenoma
Malignant: metastases (commonest malignant), hepatocellular carcinoma, hepatoblastoma, cholangiocarcinoma
270
Hepatic adenomas are associated with ___
The COCP
271
Cholangiocarcinoma is associated with ___
PSC, worms, cirrhosis
272
What is the most common site of volvulus?
Sigmoid colon
273
Describe the pathology of diverticular disease
Outpouchings of the colon at weak points. Usually affects sigmoid
274
Pseudomembranouscolitis is another term for ___
C difficile infection
275
What are the types of bowel ischaemia? Briefly describe.
Ischaemic colitis -> ischaemia leading to inflammation and sepsis. Bloody diarrhoea, systemic signs, thumbprint on AXR, +lactate, LDH and CK
Acute mesenteric ischaemia (infarction): similar to ischaemic colitis but less common. Typically periumbilical pain.
Chronic mesenteric ischaemia (angina): postprandial pain
276
Describe the classical findings in Crohn's
```
Skip lesions
Transmural inflammation
Cobblestone appearance on endoscopy
Rose thorn ulcers
Granulomas
Fistulae, fissures, abscesses
```
277
Describe the classical findings of ulcerative colitis
Continuous lesions
Mucosal inflammation (partial thickness)
Ulceration
Pseudopolyps
278
T/F. Colonic adenomas have no association with carcinoma
False. Adenomas may progress to carcinoma. They should be removed. They also typically occur in areas that carcinoma may later appear
279
What are some hereditary conditions that predispose to colonic polyps?
Peutz-Jeghers: hamartomatous polyps, freckles on lips
FAP: APC gene mutation. 100s of polyps, early cancer
HNPCC (Lynch syndrome): early cancers
280
How is colorectal carcinoma staged?
```
TNM or Duke's staging:
A: confined to bowel lumen
B: invasive
C: LN mets
D: distant mets
```
281
HNPCC is also associated with ___
Ovarian cancer, endometrial cancer
