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Histopathology Flashcards

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)
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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
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3
Q

What are some complications of PID?

A

Peritonitis, adhesions -> BO, infertility, sepsis

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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

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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

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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.

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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

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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.

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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

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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

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11
Q

What is the commonest uterine tumour? How common is it?

A

Leiomyoma (fibroid). Affects about 20% of women >35 yrs

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12
Q

What are the types of leiomyoma?

A

Submucosal, intramural, subserosal

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13
Q

A malignant tumour of the myometrium is ____. Describe briefly.

A

Leiomyosarcoma. Rare, affects older women (PMB), poor prognosis.

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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)

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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

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16
Q

How is endometrial cancer staged?

A 
FIGO.
1- uterus
2- cervix
3- ovaries, vagina, pelvic nodes
4- anywhere else
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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

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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

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19
Q

How can molar pregnancy present?

A

Spontaneous miscarriage, very high hCG

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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
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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

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22
Q

What is adenomyosis?

A

Growth of endometrial tissue within the myometrium.

Causes painful, heavy periods.

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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

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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)

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25
Q

What are the risk factors for ovarian cancer?

A

Nulliparity, older age, early menarche, late menopause, FHx, inflammation (PID), HRT

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26
Q

Describe the two types of ovarian carcinoma

A

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

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27
Q

Describe the following types of ovarian epithelial tumour: serous, mucinous, endometrioid, clear cell carcinoma

A

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

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28
Q

Describe the types of germ cell tumours:

A

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.

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29
Q

What is a Krukenberg tumour?

A

Metastases from gastric/breast cancer, mucin-producing signet ring cell

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30
Q

Which genes are associated with familial ovarian cancers?

A

BRCA- serous carcinoma

HNPCC- endometrioid and mucinous carcinomas

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31
Q

What is the most common type of vulval cancer? What are the RFs?

A

Squamous cell carcinoma makes up 85% of cancers. It arises on the background of VIN (vulval intraepi neo)
RFs: HPV, lichen sclerosus, VIN

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32
Q

Describe the important histological landmark in the oesophagus and explain why this is clinically relevant

A
  • 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
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33
Q

What are the two types of Barrett’s oesophagus?

A 
Gastric metaplasia (no goblet cells)
Intestinal metaplasia (goblet cells)
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34
Q

What are the types of oesophageal carcinoma? Describe. How are they differentiated?

A
  • 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.
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35
Q

How do oesophageal varices form?

A
  • 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
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36
Q

Which layer of the stomach is breached by ulceration?

A

The muscularis mucosae

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37
Q

Describe the types of gastritis

A

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

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38
Q

What are the complications of gastritis?

A
  • Ulceration
  • Intestinal metaplasia -> dysplasia -> cancer
  • Lymphoma (B cell MALToma) from H pylori
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39
Q

What are the causes of gastric ulcers? What are the complications?

A
  • H pylori, alcohol, smoking, NSAIDs, stress
  • Complications: bleeding, anaemia, perforation, cancer

**Ulcers can become cancerous, but cancers can also ulcerate. BIOPSY every ulcer

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40
Q

What are the types of gastric cancer?

A

Usually adenocarcinomas (also lymphoma, SCC, GIST)

  • Intestinal: well-differentiated. Big glands with mucin
  • Diffuse: poorly differentiated. Signet ring cells, no glands. Linnitus plastica
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41
Q

Describe the different pathologies of the duodenum

A
  • 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
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42
Q

Describe the changes that occur in coeliac disease. How is it diagnosed?

A

-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

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43
Q

What are some complications of coeliac disease?

A
  • Poor growth, delayed puberty
  • Malnutrition, vitamin deficiency
  • Lymphoma (enteropathy associated T cell lymphoma)
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44
Q

How is an ulcer different to an erosion? What are the different types of gastric ulcers?

A
  • 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)
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45
Q

Which part of the pancreas is exocrine? Which is endocrine? What are their functions?

A
  • Exocrine: Acini. Secretes digestive enzymes

- Endocrine: Islets of Langerhans. Release insulin (b) and glucagon (a) to regulate blood glucose.

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46
Q

List the causes of acute pancreatitis

A 
Gallstones
Ethanol
Trauma, tumours
Steroids
Mumps
Autoimmune
Scorpion bites
Hypertriglyceridaemia, hypercalcaemia
ERCP
Drugs eg thiazides
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47
Q

How does duct obstruction lead to pancreatitis?

A

Bile ascends up the duct and damages acini causing enzyme release

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48
Q

___ are cells that indicate acute inflammation, while ___ indicate chronic inflammation

A

Neutrophils. Lymphocytes

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49
Q

Describe the pathogenesis of acute pancreatitis

A
  • 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)
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50
Q

Name the causes of chronic pancreatitis, and the histological appearance

A
  • Acute relapsing/persistent -> chronic
  • Common causes: alcohol, haemochromatosis, gallstones, abnormal anatomy, CF, tumours
  • Fibrosis and scarring, exocrine gland atrophy, duct dilatation, calcification (on Xray)
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51
Q

What is the autoimmune disease that causes pancreatitis?

A

IgG4 related disease- infiltration by IgG4 plasma cells -> fibrosis and inflammation

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52
Q

What are the types of pancreatic cancer? Describe the histological appearance

A

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.

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53
Q

What are the risk factors for gallstones? What are the types of stones?

A

RFs: female, middle aged, overweight/obese, high fat diet, high oestrogen eg. pregnancy, haemolysis
Cholesterol stones: radioluscent, single
Pigment stones: radio-opaque, multiple

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54
Q

Describe the microanatomy of the liver

A

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).

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55
Q

What is the cause of Gilbert’s syndrome?

A

Deficiency in UDP glucuronosyl transferase ->

unconjugated bilirubin remains tightly bound to proteins

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56
Q

Describe the structure of the nephron and the function of each part.

A

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
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57
Q

Immunofluorescence of renal histology can show ___

A

Immune deposits

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58
Q

What is the inheritance of PKD? Which genes are responsible? What is PKD associated with?

A

Autosomal dominant
PKD1 and 2
Berry aneurysms, liver cysts

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59
Q

Name some causes of ATN. What is the mechanism?

A

-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)

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60
Q

What is the cause of TIN?

A

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

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61
Q

How can renal diseases be classified?

A

By the part of the nephron affected:

  • Glomerulus: nephrotic and nephritic syndrome
  • Tubules and interstitium: ATN, TIN
  • Blood vessels: vasculitis, thrombotic microangiopathies
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62
Q

What are some features of glomerulonephritis?

A 
Haematuria and proteinuria 
Oliguria 
Hypertension
Red cell casts
Crescents (in rapidly progressive)
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63
Q

Name some causes of nephritic syndrome (at least 5)

A
  • 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
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64
Q

Describe the characteristics of post-streptococcal GN and how it is different to IgA nephropathy

A
  • 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
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65
Q

What are the types of rapidly progressive GN? How are they different?

A

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.

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66
Q

What is the defining characteristic of rapidly progressive GN?

A

Crescents in the glomerulus on light microscopy

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67
Q

What is the cause of Alport syndrome? What is the inheritance pattern? How does it present?

A

Mutation in Type IV collagen (alpha 5 chain)
X linked
Nephritic syndrome, SNHL, eye disorders

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68
Q

What is the cause of thin basement membrane disease? What is the inheritance pattern? How does it present?

A

Mutation in Type IV collagen (alpha 4 chain)
Autosomal dominant
Asymptomatic, microscopic haematuria with normal renal function

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69
Q

Name some causes of asymptomatic haematuria

A

Thin basement membrane disease
Alport syndrome
IgA nephropathy (Berger disease)

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70
Q

If a patient presents with a picture of severe nephritic syndrome, what would you consider as DDx? What investigations would you do?

A
  • 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
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71
Q

What are the features of haemolytic uraemic syndrome? TTP? What are the similarities in presentation?

A

-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

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72
Q

What is the pathophysiology of HUS and TTP? What are the causes?

A

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

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73
Q

Name some causes of nephrotic syndrome

A

Primary causes:

  • Minimal change disease (steroid-sensitive nephrotic syndrome)
  • Membranous glomerulonephritis
  • Focal segmental glomerulosclerosis

Secondary causes:

  • Amyloidosis
  • DM -> nodular glomerulosclerosis
  • SLE
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74
Q

Describe the features of minimal change disease

A
  • Common in children
  • Steroid sensitive
  • No immune complexes (no abnormality on light microscopy)
  • Loss of podocyte foot processes on electron microscopy
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75
Q

Describe the features of membranous glomerulonephritis

A
  • 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)
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76
Q

Describe the features of FSGS

A
  • Common in adults
  • Scarring of the glomerulus (light microscopy) with immune deposition
  • Somewhat responsive to steroids
  • Can be 2˚ to HIV
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77
Q

Describe the features of diabetic nephropathy

A
  • Common!! (30-40% of diabetics)
  • Microalbuminuria is key finding -> proteinuria, nephrotic syndrome
  • Nodular glomerulosclerosis (Kimmelstiel Wilson nodules)
  • Thickening of the BM
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78
Q

Describe the features of amyloidosis (in renal disease)

A
  • Apple green birefringence with Congo red stain
  • AA: associated with chronic inflammation eg. IBD, RA
  • AL: associated with myeloma, light chains
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79
Q

How does hypertension cause CKD?

A
  • Increased pressure leads to scarring, ischaemia etc
  • Shrunken kidneys with granular cortices
  • Nephrosclerosis
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80
Q

Name the different kinds of kidney stones? Describe some features of each.

A

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

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81
Q

Name some types of benign renal tumours and describe some features of each

A
  • 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.
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82
Q

Name some types of renal carcinoma and describe the features of each. How do they present?

A

-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.

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83
Q

The renal tumour common in children is called ___

A

Nephroblastoma (Wilm’s tumour)

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84
Q

Name the types of transitional cell carcinoma and describe the features of each.

A
  • Non-invasive papillary. Frond-like
  • Infiltrating
  • Flat carcinoma in situ
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85
Q

Urinary schistosomiasis is associated with which type of cancer?

A

Squamous cell carcinoma

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86
Q

What is BPH? What are the presenting features?

A

Benign prostatic hyperplasia- androgen mediated growth of prostatic tissue -> nodule formation
Lower urinary tract symptoms: difficulty urinating, frequency, nocturia, retention, dribbling

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87
Q

What is the treatment of BPH?

A

Alpha1 blockers: Tamsulosin
5a reductase inhibitors: Finasteride
TURP

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88
Q

What is the main type of prostate cancer? What are the risk factors?

A

Prostatic adenocarcinoma

RFs: older age, black, FHx of prostate/breast cancer

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89
Q

Describe how prostate cancer is graded.

A

Gleason score: 2 areas, grade from 1-5 and add

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90
Q

Name the types of testicular tumours and describe their features

A 
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
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91
Q

Name some benign testicular pathology

A
  • Varicocoele
  • Hydrocoele
  • Epididymitis
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92
Q

What are the most common types of pituitary adenoma (in order)?

A

Prolactinoma
Non-functioning
ACTH secreting
GnRH secreting

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93
Q

Describe the histological appearance of thyroid tissue

A

Epithelial cells with large pink globs (colloid)

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94
Q

Which cells produce calcitonin?

A

Parafollicular C cells

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95
Q

What are some causes of a thyroid goitre?

A
  • Iodine deficiency
  • Grave’s disease
  • Puberty
  • Multinodular goitre
  • de Quervain’s
  • Hashimoto’s
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96
Q

An ovarian tumour that causes thyrotoxicosis is ?

A

Struma ovarii. A type of teratoma

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97
Q

What are some histological features of Hashimoto’s?

A

Lymphocytes (chronic inflammation)

Hurthle cells

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98
Q

What are the types of thyroid cancer? How common are they? Briefly describe

A

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.

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99
Q

What are the causes of 1˚ hyperparathyroidism (in order of frequency)?

A

Parathyroid adenoma
Parathyroid hyperplasia
Parathyroid carcinoma

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100
Q

How do the adrenals change in different causes of Cushings/adrenal failure?

A

Cushings disease/ectopic ACTH: hyperplasia
Exogenous steroids: atrophy
Adrenal failure: atrophy

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101
Q

What is the adrenal complication of sepsis with DIC?

A

Waterhouse-Friedrichson syndrome

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102
Q

What are the different MEN syndromes?

A

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

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103
Q

Describe the characteristic features of SLE.

How is it diagnosed?

A 
Need 4/11 criteria: 
Serositis
Oral ulcers
Arthritis 
Photosensitivity
Blood disorders
Renal 
ANA +ve
Immune phenomena (anti-dsDNA)
Neuro symptoms
Malar rash
Discoid rash
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104
Q

Which antibodies are +ve in SLE?

A

ANA (anti-nuclear)
anti-dsDNA
anti-Sm

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105
Q

Which test can show immune complex deposition? Which conditions can this be used in?

A

Immunofluorescence

SLE, post-strep GN etc

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106
Q

Which cardiac conditions are associated with SLE?

A

Pericarditis, Libman-Sacks endocarditis

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107
Q

What is scleroderma? What are the two types?

A

Scleroderma is an auto-immune multisystem condition characterised by skin fibrosis (collagen)
Limited/cutaneous (CREST) vs diffuse

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108
Q

Describe the characteristics of limited scleroderma

A 
\+Anti-centromere antibodies
Skin changes on face/limbs
Calcinosis
Raynaud's
Esophageal dysmotility
Sclerodactyly
Telangiectasia
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109
Q

Describe the characteristics of diffuse scleroderma

A

+Anti-Scl-70
Skin changes anywhere on the body
Widespread organ involvement: renal, pulmonary fibrosis, vascular etc

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110
Q

Name the features of dermatomyositis and polymyositis

A

Anti-Jo1 +ve
Proximal muscle weakness, raised CK
DM: heliotrope rash, Gottron’s papules

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111
Q

What is the key pathology in sarcoidosis?

A

Non-caseating granulomas (histiocytes)

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112
Q

Describe the classic presentation of sarcoidosis + other features

A 
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
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113
Q

Name some investigation findings in sarcoidosis

A
  • CXR: bilateral hilar lymphadenopathy
  • Raised Ca
  • Raised ACE
  • Raised ESR
114
Q

Name some types of vasculitis and briefly describe (antibodies, presentation, etc)

A

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
Q

cANCA is + in which conditions? pANCA is + in which?

A

cANCA: GPA
pANCA: eGPA, MPA

116
Q

What is the difference between macrophages and lymphocytes on microscopy?

A

Lymphocyte: big nucleus, very little cytoplasm
Macrophage: big nucleus, lots of cytoplasm. Bigger than lymphocytes

117
Q

What are macrophages are associated with?

A

Late acute inflammation

Chronic inflammation- granulomas

118
Q

What is a granuloma? What does it look like histologically?

A

An organised collection of activated macrophages.
Lots of epithelioid macrophages (activated- lots of cytoplasm)
Can have Langerhans giant cells

119
Q

What tells you that you have a good sputum sample from the alveoli?

A

Pigmented macrophages

120
Q

What are the histological characteristics of squamous cell carcinomas vs adenocarcinomas?

A

SCC: keratin producing, intercellular bridges
AC: mucin producing, glands

121
Q

What is histochemistry and what is immunohistochemistry?

A

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
Q

What are the different levels of breast cytology?

A 
C1-5 
C1: inadequate sample
C2: benign
C3: atypia
C4: suspicious of malignancy
C5: malignant
123
Q

What is the gold standard method for diagnosing breast pathology?

A

Tissue biopsy with histopathology - can visualise the tissue architecture

124
Q

What is duct ectasia? What is the typical presentation? What is the histological appearance?

A

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
Q

Define acute mastitis. What is the typical presentation? What is the most common causative organism? What is the management?

A

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
Q

Name some benign causes of breast lumps.

A

Fibrocystic breasts
Fibroadenoma
Duct papilloma

127
Q

Describe fibrocystic changes in breasts

A

Lumpy breasts, may be tender. Very common

Associated with hormonal changes, eg. menstrual cycle

128
Q

Describe the features of breast fibroadenoma

A
  • Mobile, round, rubbery non-tender benign mass
  • Young women
  • Consists of glandular and stromal cells
129
Q

Describe Phyllodes tumour

A
  • Potentially aggressive type of fibroadenoma. Very dense. Can become malignant.
  • Affect older women, enlarging mass
130
Q

Describe ductal papilloma (breast)

A
  • 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
Q

What is a radial scar (breast)?

A

Benign sclerosing lesion with central scarring in a stellate pattern. Due to incorrect repair mechanism.
-Stellate pattern on mammogram + histology

132
Q

Name some different types of pre-malignant breast disease

A

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
Q

What is the most common type of breast cancer? What are the subtypes?

A

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
Q

What is the classic method of diagnosing breast pathology?

A

Clinical examination
Mammogram/USS
FNA + cytology

135
Q

What are some signs + symptoms of breast cancer?

A
  • Firm non-tender fixed lump
  • Peau d’orange
  • Nipple inversion
  • Discharge
  • Skin tethering
  • Paget’s disease of the breast (eczema of nipple)
136
Q

Who is invited for breast screening?

A

Women aged 47-73 every 3 years -> mammogram

137
Q

What are some markers of good prognosis in breast cancer? Why? Bad?

A

Good: ER/PR/HER2 positive. Will respond well to Tamoxifen and Herceptin
Bad: triple negative **HER2 is more aggressive, but more treatable.

138
Q

Describe the basic skin histology

A

Epidermis: keratinised squamous epithelial cells (keratinocytes). 4 layers. Stratum corneum, granulosum, spinosum, basalis.
Dermis: contains vessels, pilosebaceous units, etc
SC fat

139
Q

What are the different inflammatory patterns of skin? Briefly describe and give examples of conditions.

A
  • 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
Q

What are some types of blistering skin conditions?

A

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
Q

How are bullous pemphigoid and pemphigus differentiated?

A

Clinically- deep vs superficial

Histology- immunofluorescence showing IgG and C3 on BM in pemphigoid, IgG in epidermis for pemphigus

142
Q

What is eczema? What are the types?

A

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
Q

What is psoriasis? How does it present?

A

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
Q

What is the histology of psoriasis?

A

Parakeratosis (nuclei in stratum corneum), no granular layer, Munro’s microabscesses (neutrophils)

145
Q

Describe lichen planus

A

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
Q

What are some causes of erythema multiforme?

A

Usually infection > drugs

HSV, mycoplasma. Antibiotics, NSAIDs, AEDs

147
Q

What are Stevens-Johnson syndrome and toxic epidermal necrolysis?

A

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
Q

What is pityriasis rosea?

A

A rash that occurs after a viral illness

Starts with a herald patch -> Christmas tree distribution

149
Q

What is pyoderma gangrenosum?

A

A form of vasculitis presenting as an ulcer. A systemic manifestation of illness eg. malignancy, IBD, SLE, TB

150
Q

Describe seborrheic keratosis

A

A benign skin growth. Stuck on mole/warty appearance.

Keratin horns/horn cysts with proliferating epidermis on histology

151
Q

Describe actinic keratosis

A

Premalignant lesion, develops on sun-exposed area. Can be rough and sandpaper scaly lesion, hyperkeratotic, etc.

152
Q

Describe keratoacanthoma.

A

Premalignant dome-shaped nodule that grows rapidly and can spontaneously clear up. Similar to SCC

153
Q

Describe Bowen’s disease

A

Premalignant lesion, red scaly patch/macule. SCC in situ

154
Q

Describe a BCC. What is another name for this condition?

A

Also known as Rodent ulcer.
Pearly papule with rolled edge, telangectasia.
Does not metastasise, but can be locally invasive

155
Q

Describe a SCC.

A

Malignant neoplasm of SCs. Rough scaly patches with varying appearance, invading into the dermis. Can be ulcerated, nodular, crusty.

156
Q

Name some melanocytic conditions

A

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
Q

How are melanomas assessed?

A

ABCDE

  • Asymmetry
  • Borders (irregular)
  • Colour (multiple)
  • Diameter >5mm
  • Evolution
158
Q

Which part of the skin are melanocytes normally found? What is abnormal?

A

Stratum basale + dermis

NOT normal to be moving up through the epidermis

159
Q

How are skin cancers staged?

A

BCC + SCC: width

Malignant melanoma: depth (Breslow’s thickness)

160
Q

What are the two main types of bone? Where are they found? What do they look like on histology?

A

Cortical: long bones. Lots of dense pink material.
Cancellous: vertebrae, pelvis. Pink + white areas of adipose and haem stem cells

161
Q

What are the main cells involved in metabolism of bone?

A

Osteoclasts: breakdown bone. Have RANK
Osteoblasts: build bone. Have RANKL

162
Q

What is metabolic bone disease? Give some examples

A 
Disorder of bone turnover due to imbalance in chemical factors and hormones. 
Osteoporosis
Osteomalacia/Rickets
Paget's disease of bone
Renal osteodystrophy
163
Q

Name some causes of osteoporosis

A 
Older age
Post-menopausal/early menopause/FHA
Steroid use
Chronic illness
FHx
164
Q

Define osteoporosis and osteopenia. What is the presentation of osteoporosis?

A

Osteoporosis: T score

165
Q

Explain the biochemistry in osteoporosis, osteomalacia and Paget’s

A
  • 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
Q

Brown cell tumours are characteristic of which condition?

A

Hyperparathyroidism

167
Q

What are some types of fractures?

A 
Simple
Compound
Greenstick
Comminuted
Impacted
168
Q

What is Pott’s disease? What does it look like on histology?

A

TB of the spine

Inflammatory cells with granulomas, Langerhans cells

169
Q

Which joints are commonly affected by osteoarthritis? Rheumatoid arthritis?

A

OA: Knees, hips, DIPs and PIPs
RA: hands and feet (DIP sparing), elbows, ankles etc

170
Q

What are the features of rheumatoid arthritis?

A

Morning stiffness
Swan-neck and Boutonnière deformity
Ulnar deviation of fingers, radial of wrist
Anaemia, raised ESR, RF, anti-CCP

171
Q

What are the histological features of OA and RA?

A

OA: cartilage degeneration, osteophytes
RA: inflammatory cells, thickening of synovial membranes, Grimley-Sokoloff cells

172
Q

What is the difference between gout and pseudogout?

A

Gout: urate crystals, negative birefringence
Pseudogout: calcium pyrophosphate crystals, positive birefringence

173
Q

What is the most common type of bone tumour?

A

Metastases

174
Q

Which tumours commonly metastasise to bone?

A

Adult: breast, prostate, lung, kidney, thyroid
Children: neuroblastoma, Wilm’s

175
Q

What are 3 types of primary malignant bone tumour?

A

Osteosarcoma
Chondrosarcoma
Ewing’s sarcoma

176
Q

Describe the features of osteosarcoma eg. presentation, histology

A 
Commonly in young/teen men
Affects the knee, jaw
Xray: Codmann's sign (periosteal elevation), lytic lesions
Histology: stromal cells
Poor prognosis
177
Q

Describe the features of chondrosarcoma eg. presentation, histology

A

Abnormal proliferation of cartilage
Usually older adults
Affects axial skeleton, long bones
Decent prognosis

178
Q

Describe the features of Ewing’s sarcoma eg. presentation, histology

A

Highly malignant small round cell tumour
Commonly in young people
Affects long bones and pelvis
Xray: periosteal reaction (onion skin appearance)

179
Q

T/F. ALP is raised in malignant primary bone tumours

A

False. ALP is commonly raised in osteosarcoma, but normal in Ewing’s sarcoma

180
Q

What are the features of osteoarthritis? On exam and Xray.

A

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
Q

Name some benign bone tumours

A
  • 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
Q

Spongiform changes in the brain are consistent with ___

A

Prion disease

183
Q

Name some histological features of Alzheimer’s disease

A

Intracellular neurofibrillary tangles (Tau protein)
Extracellular plaques (Amyloid-beta)
Cerebral amyloid angiopathy (buildup in vessels)
Neuronal loss

184
Q

What is the pathogenesis of Alzheimer’s disease?

A

Generalised brain atrophy due to:

  • Beta amyloid builds up extracellularly (breakdown of APP), disrupts cell functioning
  • Hyperphosphorylation of Tau -> accumulation -> cell death
185
Q

How are Parkinson’s and Alzheimer’s staged histologically?

A

Braak stages- describes the location of the Tau protein/alpha-synuclein in the brain

186
Q

Describe the histological features/pathogenesis of Parkinson’s disease

A

Loss of dopaminergic neurons in the substantia nigra

Intracellular alpha-synuclein accumulation -> Lewy bodies

187
Q

What is the gold standard of diagnosis in Parkinsons?

A

Brain histology -> immunostaining for alpha-synuclein

188
Q

What are some causes of Parkinsonism? How are they different/similar?

A

Parkinson’s disease: a-synuclein, SN
Multisystem atrophy: a-synuclein, glial cells, cerebellum
Progressive supranuclear palsy: Tau (4R)
Corticobasal degeneration: Tau (4R)

189
Q

Describe the pathogenesis/histological features of Pick’s disease

A

Fronto-temporal atrophy: neuronal loss
Balloon neurons
Pick bodies- Tau protein (3R Tau)

190
Q

Define dementia and neurodegenerative disease

A

Neurodegenerative disease: a progressive condition leading to neuronal loss
Dementia: global impairment in cognitive function without impairment of consciousness

191
Q

What is the presentation of different types of dementia?

A

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
Q

What are the two causes of cerebral oedema?

A

Cytogenic: cellular injury
Vasogenic: disruption of the BBB

193
Q

How does cerebral oedema appear on Xray?

A

Loss of gyri

194
Q

What are the types of hydrocephalus? What is the pathogenesis of each?

A

Communicating: impaired resorption of CSF at the villi

Non-communicating: obstruction in the ventricular system

195
Q

What is the consequence of raised ICP? What are the different types?

A

Herniation

  • Transtentorial: under tentorium
  • Tonsillar: thru foramen magnum
  • Subfalcine: under the falx cerebri
196
Q

Define stroke. What are the types? What is not considered a stroke?

A

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
Q

What is a TIA? What is the risk of stroke?

A

Rapidly developing loss of focal/global cerebral function lasting <24 hours
1/3 will have significant infarction within 5 years

198
Q

Where do haemorrhagic strokes most commonly occur? What are the risk factors?

A

Basal ganglia

Hypertension, FHx, AVMs

199
Q

What is the difference between a cavernous angioma and an AVM?

A

AVM: has parenchyma wrapped around. Tends to bleed at higher pressure
Cavernous angioma: no parenchyma. Bleeds at lower pressure

200
Q

What is the cause of a subarachnoid haemorrhage?

A

Berry aneurysm

201
Q

What are the risk factors for cerebral infarction?

A

Cerebral atherosclerosis
Hypertension, smoking, DM, hypercholesterolaemia
Also AF + PFO

202
Q

What is the acute management of stroke/TIA?

A

Aspirin, dipyridamole

Thrombolysis (<3 hours from onset)

203
Q

How do the different types of stroke present (ACA, MCA, PCA)?

A

ACA: contralateral leg paresis + sensory loss
MCA: contralateral arm and face paresis + sensory loss, aphasia
PCA: contralateral visual field loss etc

204
Q

What are the ways of classifying traumatic brain injuries? Give examples

A

Missile (gunshot) vs non-missile (fall, RTA)
Acceleration and deceleration (RTA)
Rotational (boxing)

205
Q

What are some signs of basal skull fracture?

A

Raccoon eyes (periorbital)
Battle’s sign (mastoid)
CSF rhinorrhoea

206
Q

What is the difference between contusion and concussion?

A

Contusion: bruise to brain from hitting skull
Concussion: type of TBI, characterised by cognitive impairment

207
Q

What are some inherited conditions that are associated with brain tumours?

A

NF1+2
Tuberous sclerosis
vHL

208
Q

What is the best investigations for brain tumours?

A

T1 weighted MRI with and without contrast

209
Q

What is the management of brain tumours?

A

Medical: chemo (high grade gliomas), RDx

Surgery

210
Q

How are CNS tumours graded? Staged?

A

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
Q

Which are the most common primary CNS tumour? Name some types.
What is the second most common?

A

Gliomas eg. astrocytoma, glioblastoma multiforme

Meningioma 2nd.

212
Q

Which types of brain tumour are commonly seen in children? Where do they occur? What are the key histological features?

A 
Pilocytic astrocytoma (a type of glioma): cerebellar. Hairy cells, Rosenthal fibres. 
Medulloblastoma (embryonal cell): cerebellar. Small round blue cells. Wright rosettes.
213
Q

Which type of glioma is most common in adults? How can it arise?

A 
Glioblastoma multiforme (grade IV)
de novo mutation or secondary to progressive astrocytoma
214
Q

Which cancers most commonly metastasise to the brain?

A

Lung
Breast
Malignant melanoma
Renal cell

215
Q

Where is the site of the lesion in atherosclerosis?

A

Sub-intimal eg. endothelial lining

216
Q

Describe the process of atheroma formation

A
  • 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
Q

What are some risk factors for atherosclerosis?

A

T2DM, hypertension, hyperlipidaemia, smoking, FHx

218
Q

What are the consequences of atherosclerosis?

A

Obstruction (at 70% stenosis) -> ischaemia

Rupture -> thrombosis, embolus

219
Q

What are the types of ischaemic heart disease? Which are ACS? What is the cause?

A

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
Q

What is an MI? What are some causes of MI?

A

MI: myocardial necrosis due to prolonged ischaemia
Plaque rupture
Vasospam eg cocaine use

221
Q

Which area of the myocardium is affected by obstruction of the LAD? RCA? LCx?

A

LAD: anterior wall + septum, apex
RCA: posterior wall + septum
LCx: lateral LV, not the apex

222
Q

Describe the changes that occur in the myocardium after MI

A

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
Q

What are the complications of MI?

A 
Death
Arrhythmia
Rupture
Tamponade
Heart failure
Valve problems eg. mitral incompetence
Aneurysm
Dressler's syndrome
Embolus 
Recurrence
224
Q

What can cause sudden cardiac death? Which is most common?

A

Plaque rupture/atherosclerosis. Most common
HOCM
Cardiac failure

225
Q

What are the types of heart failure? How do they present?

A

Congestive: both sides. Mix of symptoms
Right HF: oedema, HSmegaly
Left HF: SOB, PND, exertional dyspnoea

226
Q

What are the types of cardiomyopathy? Describe the histology and causes of each.

A

Dilated: floppy, enlarged chambers. Idiopathic, alcohol, thyroid disease, pregnancy, haemochromatosis
Hypertrophic: thickened walls. Familial.
Restrictive: stiffening of ventricles, big atria. Sarcoidosis, amyloidosis.

227
Q

Which valves are classically affected in rheumatic valve disease?

A

Left-sided eg mitral, aortic

228
Q

What are the most common valve disorders? What is the cause?

A 
Mitral prolapse (regurg): very common
Aortic stenosis: due to calcification. Very common
229
Q

Which valves are commonly affected in IE? What is the exception?

A

Left-sided.

Except for IVDU- they classically get tricuspid vegetations

230
Q

What are the histological features of infective endocarditis?

A

Aschoff bodies (granulomas)
Anitschkov myocytes
Vegetations/verrucae

231
Q

What is the difference between a true aneurysm and a pseudoaneurysm?

A

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
Q

What is pulmonary oedema? What are the causes?

A

Fluid accumulation in the alveolar space

  • LHF
  • Alveolar injury eg. drugs, pancreatitis
  • High altitude
233
Q

What are the conditions of acute lung injury/diffuse alveolar damage? What are they caused by?

A

ARDS and hyaline membrane disease (neonatal RDS).
Adults: many
-Infection
-Aspiration
-Shock
-DIC
Neonates: insufficient surfactant production

234
Q

What is the pathophysiology of ARDS?

A

Diffuse alveolar damage -> congestion + exudate -> protein deposits and granulation -> fibrosis

235
Q

Define asthma.

A

Chronic inflammatory airway disorder characterised by airway hyperresponsiveness, chronic inflammation and reversible obstruction.

236
Q

What are the histological changes in asthma both acute + chronic?

A

Acute: inflammation with eosinophils + mast cells, oedema, bronchospasm
Chronic: smooth muscle hypertrophy, mucus plugging with goblet cell hyperplasia, airway narrowing

237
Q

What are the two main pathological processes in COPD? Describe the histology of each

A

Chronic bronchitis: goblet cell hyperplasia -> mucus

Emphysema: permanent alveolar loss due to chronic activation of phagocytes, bullae

238
Q

Describe the location of emphysema in that caused by smoking and alpha-1 antitrypsin deficiency

A
  • Smoking: centrilobular

- A1 antitrypsin: panacinar

239
Q

What is bronchiectasis? What are some causes?

A

Permanent enlargement of the bronchi with inflammation and fibrosis

  • Recurrent chest infections
  • CF
  • PCD
  • Amyloidosis
240
Q

What is the pathophysiology of CF?

A

Mutation in the CFTR gene on Chromosone 7q3
Most frequent is D F508
Causes buildup of viscous secretions eg. lungs, pancreas

241
Q

What are some complications of pneumonia?

A

Empyema
Pneumothorax
Pleural effusion
Abscess formation

242
Q

Owl’s eye inclusions are typical of which pathogen? What does this mean?

A

CMV. Very large nuclei

243
Q

What is pneumoconiosis?

A

Occupational lung disease caused by chronic inhalation of mineral dust/inorganic particles eg. miners, silicon

244
Q

What is extrinsic allergic alveolitis?

A

Occupational lung disease caused by inhalation of organic particles eg. Pigeon fancier’s lung, Farmer’s lung

245
Q

What are the main types of lung cancer? Which is most common?

A

95% are carcinomas

  • Squamous cell 30%
  • Adenocarcinoma 30%
  • Small-cell 20%
  • Large cell 20%
246
Q

Describe the location and histology of squamous cell carcinoma of the lungs

A

Location: usually proximal, large airways
Histology: keratin, intercellular bridges

247
Q

Describe the location and histology of adenocarcinoma of the lungs

A

Location: peripheral, alveolar
Histology: glands, mucin-producing
Tend to metastasise early

248
Q

Describe the location and histology of small cell carcinoma of the lungs

A

Location: central, proximal bronchi
Histology: neuroendocrine cells. May stain with chromogranin. Associated with paraneoplastic syndrome.

249
Q

Name some paraneoplastic syndromes that may occur with small cell lung cancer

A
  • Hyperparathyroidism: PTHrP
  • Cushing’s: ACTH
  • SIADH: ADH
  • Carcinoid syndrome: serotonin
250
Q

What is amyloidosis?

A

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
Q

What are the types of amyloidosis? Describe them

A

AA amyloid: derived from serum amyloid A. Associated with chronic inflammation eg. RA, IBD
AL amyloid: derived from light chains eg. MM

252
Q

What is the purpose of hepatic stellate cells?

A

Store Vitamin A

Transform into fibroblasts and lay down collagen

253
Q

Describe cirrhosis

A

Chronic liver disease characterised by diffuse inflammation, fibrosis, nodular regeneration, and abnormal vascular architecture

254
Q

What are the main causes of cirrhosis?

A 
Alcoholism
NAFLD
Viral hepatitis
Autoimmune hepatitis
PBC and PSC
255
Q

How is cirrhosis classified?

A

Based on the size of nodules eg.

  • Micronodular: alcohol, biliary tract disease
  • Macronodular: viral hepatitis
256
Q

How is prognosis in cirrhosis determined?

A

Child-Pugh score:

  • Albumin
  • Bilirubin
  • Clotting
  • Distension (ascites)
  • Encephalopathy
257
Q

What is the histological feature of acute hepatitis?

A

Spotty necrosis

258
Q

What are the histological features of chronic hepatitis?

A

Piecemeal necrosis, fibrosis

259
Q

Describe the spectrum of liver disease

A

Steatosis/acute hepatitis -> fibrosis -> compensated cirrhosis -> HCC or decompensation -> death

260
Q

What are the histological features of alcoholic liver disease?

A

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
Q

T/F. Alcoholic and non-alcoholic steatosis look the same on histology

A

True!

262
Q

What is the histological appearance of PBC?

A

Bile duct loss with granulomas

263
Q

What is the histological appearance of PSC?

A

Bile duct fibrosis, strictures (NOT inflammation)

264
Q

What are some inherited causes of cirrhosis?

A
  • Haemochromatosis
  • Alpha1 antitrypsin
  • Wilson’s
265
Q

What stain can be used in Wilson’s?

A

Rhodanine

266
Q

What tests diagnose Wilson’s?

A

Serum Cu: Low
Serum caeruloplasmin: Low
Urinary Cu: High
Biopsy with rhodanine stain

267
Q

Which antibodies are found in autoimmune hepatitis? PBC?

A

AI hepatitis: anti-SMA

PBC: AMA

268
Q

T/F. Alpha1 antitrypsin defiency causes low levels in the liver

A

False. The pathology is misfolding of the proteins, leading to buildup in the hepatocytes and deficiency in the blood.

269
Q

Name some types of liver tumours. Which are most common?

A

Benign: haemangioma (commonest benign), adenoma
Malignant: metastases (commonest malignant), hepatocellular carcinoma, hepatoblastoma, cholangiocarcinoma

270
Q

Hepatic adenomas are associated with ___

A

The COCP

271
Q

Cholangiocarcinoma is associated with ___

A

PSC, worms, cirrhosis

272
Q

What is the most common site of volvulus?

A

Sigmoid colon

273
Q

Describe the pathology of diverticular disease

A

Outpouchings of the colon at weak points. Usually affects sigmoid

274
Q

Pseudomembranouscolitis is another term for ___

A

C difficile infection

275
Q

What are the types of bowel ischaemia? Briefly describe.

A

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
Q

Describe the classical findings in Crohn’s

A 
Skip lesions 
Transmural inflammation
Cobblestone appearance on endoscopy
Rose thorn ulcers
Granulomas
Fistulae, fissures, abscesses
277
Q

Describe the classical findings of ulcerative colitis

A

Continuous lesions
Mucosal inflammation (partial thickness)
Ulceration
Pseudopolyps

278
Q

T/F. Colonic adenomas have no association with carcinoma

A

False. Adenomas may progress to carcinoma. They should be removed. They also typically occur in areas that carcinoma may later appear

279
Q

What are some hereditary conditions that predispose to colonic polyps?

A

Peutz-Jeghers: hamartomatous polyps, freckles on lips
FAP: APC gene mutation. 100s of polyps, early cancer
HNPCC (Lynch syndrome): early cancers

280
Q

How is colorectal carcinoma staged?

A 
TNM or Duke's staging:
A: confined to bowel lumen
B: invasive
C: LN mets
D: distant mets
281
Q

HNPCC is also associated with ___

A

Ovarian cancer, endometrial cancer

Pathology (6 decks)

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