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AANIYA PATH > Aani: Histo general > Flashcards

Aani: Histo general Flashcards

1
Q

How do statins work?

A

Lower cholesterol by inhibiting HMG-coA reductase enzyme needed to make cholesterol in liver

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2
Q

What are the components of the atherosclerotic plaque?

A
  1. Fatty streak (muscle cells/macrophages)
  2. Fatty core (lipids)
  3. Fibrous cap (collagen ECM)
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3
Q

Differences in symptoms between left and right ventricular failures?

A

LVF: Lung symptoms e.g. orthopnoea, pulmonary oedema, pink exudate, SOB

RVF: Body symptoms e.g. Peripheral oedema, ascites

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4
Q

How does congestive heart failure affect the liver?

A

Dilates vessels and gives nutmeg liver appearance. This can lead to fibrosis

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5
Q

What are the types of cardiomyopathy?

A

Dilated - dilated vessels, weaker
Hypertrophic - Thickened & enlarged heart, esp heart wall & septum
Restrictive - Stiffer vessels

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6
Q

Causes of restrictive cardiomyopathy?

A

Amyloidosis/Sarcoidosis/Fibrosis

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7
Q

Causes of hypertrophic cardiomyopathy?

A

Inherited

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8
Q

Causes of dilated cardiomyopathy?

A

Alcohol/genetic/idiopathic/CHD/infection

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9
Q

Discuss genetics of hypertrophic cardiomyopathy?

A 
Mutations in sarcomeric proteins.
Examples of mutations:
Beta MHC (403 Arg - Gin).
MYBP-C 
Trop-T
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10
Q

What criteria is used for Acute Rheumatic Fever diagnosis?

A

Jones Criteria:

Joints (arthritis)
O is Heart (carditis)
Nodules (aschoff bodies)
Erythema Marginatum
Sydenham’s chorea (rapid jerky movements)
These are the major criteria.
Minor criteria include fever, malaise, high ESR and CRP, ASOT, tachycardia, joint pain

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11
Q

What are the name of the nodules found in the hearts of Rheumatic Fever pts?

A

Aschoff Bodies

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12
Q

Which valves are commonly affected in Rheumatic fever?

A

Mitral ONLY (70%). But can affect mitral and aortic.

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13
Q

When does rheumatic fever occur?

A

2-4 weeks following a Strep Pyogenes throat infection (lancefield group A). Group A B haemolytic strep (GAS)

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14
Q

How do you diagnose Rheumatic Fever?

A

Jones criteria along with raised ESR and raised ASOT (anti streptolysin O Abs).

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15
Q

Treatment of Rheumatic Fever?

A

Benzylpenicillin

or erythromycin if allergic)

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16
Q

Which histological features are present in Rheumatic Fever

A 
Aschoff bodies (granulomas)
Verrucae (beady vegetation)
Anitschkov myocytes (regenerating myocytes)
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17
Q

Which organism causes acute bacterial endocarditis?

A

Staph A
OR
Coagulase negative staph in prosthetic valve endocarditis)

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18
Q

Which organism causes subacute bacterial endocarditis?

A

Strep Viridans

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19
Q

Which valves are involved in bacterial endocarditis?

A

Usually mitral and aortic (left sided)

but in IVDU pulmonary and tricuspid (right sided)

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20
Q

Which criteria is used for Bacterial endocarditis diagnosis? Explain it

A

Dukes Criteria:
2 major
1 major and 3 minor
5 minor

Major:

  1. Persistent bacteraemia (>2 positive blood cultures)
  2. Vegetations on Echo
  3. Positive cultures for bartonella, coxiella or brucella

Minor:

  1. Evidence of immune complex formation e.g. janeway lesions
  2. Bacteraemia not enough for major
  3. Echo findings not enough for echo
  4. Fever >38 or high CRP
  5. Murmur or IVDU
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21
Q

How to treat infective endocarditis?

A

Benzylpenicillin and gentamycin

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22
Q

Describe the following murmur:

Mitral regurgitation

A

Pan systolic

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23
Q

Describe the following murmur:

Arotic regurgitation

A

Early diastolic

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24
Q

Describe the following murmur:

Mitral valve prolapse

A

Mid systolic click + late systolic murmur

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25
Q

Describe the following murmur:

Aortic Stenosis

A

Ejection systolic

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26
Q

Describe the following murmur:

Mitral stenosis

A

Diastolic

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27
Q

What is COPD?

A

Group of lung conditions commonly including Chronic Bronchitis and Emphysema

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28
Q

What is emphysema? Histology?

A

Air space enlargement and wall destruction.

You see loss of alveolar parenchyma distal to the terminal bronchioles

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29
Q

What is Chronic bronchitis? Histology? Diagnostic criteria?

A

Airway dilatation and increased mucus secretions.
On histology you see goblet cell hyperplasia and hypertrophy of mucus glands.
To diagnose you must have had a cough for at least 3 months for 2 consecutive years.

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30
Q

Causes of emphysema?

A

Asthma
Alpha 1 antitrypsin deficiency
Marfans (rare)

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31
Q

What are the histological findings in asthma?

A

Charcot Leyden crystals (seen in allergic disease)
And
Curschmann spirals (shed epithelium whirls)

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32
Q

CF: Genetics, inheritance

A

Autosomal Recessive
Defective CF transmembrane conductase regulator gene (CFTR) on Chr 7q31.2
= defective chloride ion transport

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33
Q

What are the types of interstitial lung disease?

A

Granulomatous (Caused by Tb, sarcoid, fungal, foreign bodies)
Fibrosing lung disease (caused by EAA, connective tissue, idiopathic). Recognising EAA early can prevent progression to fibrosis

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34
Q

Which part of the lung does asbestosis affect?

A

Lower lobe

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35
Q

What are the types of lung cancer in order of most common to least common?

A 
Squamous cell (type of non small cell)
Adenocarcinoma (type of non small cell) 
Small cell carcinoma
Large cell (type of non small cell)
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36
Q

RF for squamous cell carcinoma? Mutations?

A

Smoking

C-Myc/p53

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37
Q

Which lung tumour is most common in non-smokers? Which mutation is associated.

A

Adenocarcinoma

Associated with EGFR mutation

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38
Q

Histology of lung adenocarcinomas?

A

Glandular differentiation

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39
Q

Which paraneoplastic syndromes are associated with Small Cell Carcinoma?

A

ADH
ACTH
Lambert Eaton

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40
Q

Which paraneoplastic syndromes are associated with Squamous cell?

A

parathyroid- PTH

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41
Q

Which drug can be given in lung Adenocarcinoma?

A

Tyrosine Kinase inhibitor that targets the EGFR e.g. Tarceva

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42
Q

Which cells do you see in pulmonary oedema?

A

Iron laden macrophages (heart failure cells)

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43
Q

Causes of pulmonary oedema?

A

LVF
Hypoxia e.g. high altitude
Capillary damage

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44
Q

What are the complications of GORD?

A
  • Ulceration
  • Haemorrhage (melena, haematamesis)
  • Barrett’s oesophagus
  • Perforation
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45
Q

What could a pH monitor show in GORD?

A

Low (acidic) from stomach contents

High (alkalotic) from bile- this shows worse disease

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46
Q

What happens in Barrett’s oesophagus?

A

Metaplasia of oesophageal squamous epithelium into mucin-secreting collumnar epithelium. The SC junction moves proximally towards mouth.

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47
Q

RFs for GORD?

A

Smoking
Obesity
Male

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48
Q

Which type of cancer is Barrett’s ass. with? Location? What are the steps from metaplasia?

A

Adenocarcinoma of the oesophagus, therefore in the distal 1/3 of oesophagus.
Metaplasia –> dysplasia (in situ) –> Carcinoma

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49
Q

Which types of oesophageal cancer are there? Talk about each?

A
  1. Adenocarcinoma: Lower 1/3. Ass. with barrett’s oesophagus. Mucin producing.
  2. Squamous cell carcinoma: Middle of oesophagus most common. Ass. with smoking and alcohol. Common in eastern world. Keratin producing therefore blockage symptoms e.g. dysphagia.
    Afrocaribbians
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50
Q

Which cells would you expect to see in acute gastritis?

Chronic gastritis?

A

Acute: neutrophils
Chronic: lymphocytes and plasma cells

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51
Q

What can happen when you have Helicobacter Pylori infection in stomach?

A
  1. Gastritis (acute or chronic) which can lead to ulcers
    Metaplasia –> dyplasia can lead to:
  2. MALT and/or
  3. Adenocarcinoma
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52
Q

Which ulcers are worse with food?

A

Stomach ulcers.

Duodenal ulcers are relieved by food

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53
Q

How does H.Pylori cause MALT?

A

Chronic antigen stimulation causes B cell proliferation which can cause a mutation. These are B cell marginal zone lymphomas

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54
Q

Which ulcer is relieved by food?

A

Duodenal ulcer. However it worse at night

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55
Q

Which peptic ulcer is more common?

A

Duodenal (4 x)

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56
Q

Which cells are involved in Coeliac’s? Which HLA status?

A

T cells

DQ2 and DQ8

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57
Q

What is the gold standard for diagnosing Coeliac?

A

Duodenal biopsy

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58
Q

Which rash do Coeliac pts get?

A

Dermatitis Herpetiformis

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59
Q

Which ethnic group get Coelic (EMQ)?

A

Irish women

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60
Q

What is Hirschprung’s disease?

A

Missing ganglion in myenteric plexus so poor gut motility (80% males)

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61
Q

What is the first sign of Hirschprung’s disease?

A

Delayed passage of meconium (not within first 48 hours of life)

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62
Q

Genetics of Hirschprung’s?

A

RET protooncogene Chromosome 10

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63
Q

Signs of Intussusception vs Pyloric stenosis?

A 
Intissusception:  Telescoping of a segment of bowel (the intussusceptum) into another
Episodic Crying
Colic pain/draws legs up
red current stool
palpable sausage shape mass (RLQ)
Bile stained vomit
Dance's sign (empty RLQ on uss)

Pyrloric stenosis:
No bile
Projectile vomiting
Palpable mass in LUQ

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64
Q

What causes C.Diff and what happens?

A

Use of cephalosporin and ciproflox Abx.

Causes pseudomembranous colitis

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65
Q

Diagnosing C.Diff? Tx?

A

Stool sample. Treat with metronidazole

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66
Q

Which part of the colon is affected in Diverticular disease?

A

Left Colon 90%.

Right sided in asians (cos we’re always right)

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67
Q

RFs for diverticulosis?

A

Old age
Smoking
NSAIDs
Low fibre diet

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68
Q

Name for a connection between two epithelial surfaces e.g. when ulcers connect in Crohn’s?

A

Serpentine Ulcer

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69
Q

Describe the appearance of the gut in Crohn’s? Which abnormalities do you get?

A

Skip lesions –> cobblestone appearance

Ulcers called Aphthous ulcers (Rose-thorn ulcers). Often in mouth.

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70
Q

Symptoms of Crohn’s?

A

Fever
Abdo pain
Intermittent Diarrhoea
Malabsorption

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71
Q

Is Crohn’s Deep or superficial?

A

Deep

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72
Q

Is UC deep or superficial?

A

Superficial

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73
Q

Which part of the bowel can UC affect?

A

UC starts at rectum and ascends proximally but is continuous. Crohn’s is skip lesions but can affect any part of the GI tract.

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74
Q

When is the small bowel affected in UC?

A

When severe colitis causes backwash ileitis

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75
Q

Symptoms of UC?

A

Bloody & mucus-y diarrhoea
Crampy abdo pain
Relieved by defacation

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76
Q

Complications of Crohn’s?

A 
Polly Skipped For Ages
Perforation
Stritctures
Fistulae
Abscesses
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77
Q

Complications of UC?

A

Toxic megacolon

Adenocarcinoma

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78
Q

Complications of UC?

A

Toxic megacolon
Adenocarcinoma
Haemorrhage

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79
Q

Differences in investigations for Crohn’s VS UC?

A 
Crohn's will more likely have missing vitamins e.g. B12
Do barium contrast for Crohn's
Crohn's will have ASCA
UC will have pANCA Abs
Rectal biopsy useful for UC
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80
Q

Which test can be done to differentiate IBD and IBS?

A

Faecal calprotectin testing

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81
Q

Which treatments are used in UC and Crohn’s?

A

Corticosteroids e.g. Prednisolone, hydrocortisone
5 Amino-salicylic-Acid (5-ASA)
Immunosuppressants e.g. Azathioprine, DMARDs e.g. Methotrexate
Abx e.g. Metronidazole

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82
Q

How to treat mild and severe Crohn’s

A
  1. Mild: prednisolone or hydrocortisone
  2. Severe: IV hydrocortisone and metronidazole or 5- ASA (mesalazine or sulphasalazine)

Additional for maintaining remission: Azathioprine, methotrexate, mercaptopurine

TNf alpha inhibs: infliximab or adalimumab

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83
Q

How to treat mild and severe UC?

A

Mild: Prednisolone and mesalazine or sulphasalazine (5 ASA)
(ASA in children)
Severe: admit, IV hydrocortisone + Prednisolone
Azathioprine 2nd line

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84
Q

What is carcinoid syndrome?

A

Carcinoid syndrome is a paraneoplastic syndrome comprising the signs and symptoms that occur secondary to carcinoid tumors. Release of 5-HT serotonin.

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85
Q

Which cells are involved in carcinoid syndrome?

A

Excess circulating serotonin is usually manufactured by ENTEROCHROMAFFIN cell-originated carcinoid tumors in the small bowel or appendix.

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86
Q

Symptoms of carcinoid syndrome?

A 
Abdo pain
Bronchochonstriction
Flushing (after coffee/alcohol)
Diarrhoea 
If severe can progress to Carcinoid crisis
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87
Q

Symptoms of carcinoid crisis?

A 
Vasodilation
Hypotension
Tachycardia
Bronchoconstriction
Hyperglycaemia
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88
Q

How to investigate for carcinoid syndrome?

A

Urinary 24 hour 5HIAA measurement (metabolite of 5HT (seratonin))

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89
Q

Treatment for carcinoid syndrome?

A

Octreotide (somatostatin analogue)

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90
Q

Which genes are implicated in neoplastic colon polyps?

A

APC gene
K-Ras activation
LOF of p53

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91
Q

What types of non neoplastic colon tumours are there?

A
  1. Juvenille Polyposis - in infants (bleeding)
  2. Peutz Jeghers - many polyps . Freckles seen around mouth. Increased risk of malignancy
  3. Hyperplastic polyps - shedding of epithelium. Seen on 50-60 y/o
  4. Pseudopolyps e.g. IBD
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92
Q

Which tumour suppressor is linked to Peutz-Jegher’s syndrome?

A

LKB1 loss

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93
Q

Which staging is used in colorectal cancer?

A

Dukes staging

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94
Q

Which type of carcinoma are most colorectal cancers?

A

Adenocarcinoma (98%)

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95
Q

Why are NSAIDs protective in Colorectal cancer?

A

NSAIDs inhibit the cyclooxygenase (COX)-1 and COX-2 enzymes, which are involved in the synthesis of prostaglandins and so reduce inflammation

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96
Q

Which chemo is given in colorectal cancer in palliation?

A

5 Flurouracil

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97
Q

Surgical treatment options for colorectal cancers?

A

Less than 2cm from anal sphincter? Abdominoperoneal resection (removes whole rectum anus and sigmoid colon)

More than 2cm from anal sphincter? Anterior resection - removes tumour and can create an anastamosis with anus.

Ascending colon cancer/prox transverse? Right hemicolectomy

Descending colon cancer/distal transverse? Left hemicolectomy

Transverse colon cancer? Extended right hemicolectomy

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98
Q

Which familial colon syndromes are there?

A

FAP
Gardners
HNPCC

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99
Q

What is FAP? Which gene?

A

Familial Adenomatous Polyposis
Over 100 polyps needed to diagnose this.
Most will become adenocarcinoma before age 30 so do prophylactic colectomy
AD C5q1 mutation on APC gene

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100
Q

What is Gardners syndrome?

A

Like FAP but with extra-intestinal features e.g. dental caries and osteomas

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101
Q

What is HNPCC?

A

Hereditary Non Polyposis Colorectal Cancer i.e. Lynch Syndrome
Fast progression to cancer. Associated with extra-colonic cancers e.g. ovarian, stomach etc.

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102
Q

Which hormones regulate pancreatic enzyme release? Which cells are they released from?

A

Cholecystokinin (CCK) - released from I cells of duodenum

Secretin - released from S cells of duodenum

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103
Q

Which cells of the pancreas release which hormones?

A

Alpha: Glucagon
Beta: Insulin
Delta: Somatostatin (regulates insulin and glucagon)

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104
Q

What is metabolic syndrome?

A

It is a cluster of conditions that increase your risk of heart disease, diabetes and stroke.

It includes:
Hypertension >140/90
High BMI (central obesity) >94 cm in men and 80cm in women
Dyslipidaemia
Microalbuminaemia
Fasting blood glucose high
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105
Q

What is the criteria for diagnosing diabetes mellitus?

A

Random plasma glucose >11.1 mmol/l

Fasting plasma glucose >7 mmol/l

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106
Q

Macrovascular complications of DM?

A

Cardiac - MI
Renal - Glomerulonephritis/pyelonephritis
Cerebral - Cerebrovascular accident

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107
Q

Microvascular complications of DM?

A

Diabetic retinopathy

Peripheral vascular - poor healing ulcers e.g. diabetic foot

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108
Q

Causes of acute pancreatitis?

A 
Idiopathic
Gallstones
Ethanol
Trauma/tumours
Scorpion venom
Mumps
Autoimmune
Steroids
Hyperlipidaemia
ERCP
Drugs e.g. thiazides
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109
Q

Pain in acute pancreatitis (features)?

A

Sharp epigastric
Relieved by sitting forward
Radiates to the back
(Vomiting)

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110
Q

Which cells will you see in autoimmune pancreatitis?

A

IgG4+ plasma cell

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111
Q

Acinar cell carcinoma histological features?

A

Eosinophils
Granular cytoplasm
Lipase and trypsin immunoreactivity

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112
Q

What is Schmid Triad?

A

Triad presentation seen in Acinar Cell carcinoma:

  • fat necrosis
  • polyarthritis
  • eosinophilia
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113
Q

What blood results would you expect in Pancreatic carcinoma of the head? including liver enzymes and tumour markers.

A 
High bilirubin
Low Hb
High calcium
High ALP/GGT
High Ca19.9 > 70IU/mL
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114
Q

Which specific signs could you see in Pancreatic carcinoma of the head?

A
  1. Trousseau’s syndrome - Thrombophlebitis (vessel inflammation due to blood clots) Ass. with pancreatic, gastric and lung cancer
  2. Troisier’s Sign (virchow’s node)
  3. Courvoisier’s sign (painless jaundice + palpable gallbladder)
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115
Q

Which kinds of neuroendocrine tumours are there?

A

Functional (hormone excess) and non-functional (picked up incidentally).
Functional: Gastroma; Zollinger-Ellison syndrome (HIGH ACID)
Insulinoma
Glucagonoma

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116
Q

What is MEN and what are the types?

A

Multiple Endocrine Neoplasia
MEN 1
MEN 2A
MEN 2B

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117
Q

What is MEN1?

A

Endocrine neoplasia of the:

  1. Anterior Pituitary
  2. Parathyroid
  3. Pancreas
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118
Q

What is MEN2A?

A

Thyroid
Parathyroid
Phaeochromacytoma

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119
Q

What is MEN2B?

A

Medullary Thyroid Carcinoma
Phaeochromacytoma
Commonly marfinoid features and mucosal neuromas - tongue bubbles

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120
Q

Which mutation leads to MEN2?

A

RET Protooncogene

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121
Q

Which multiple endocrine neoplasm affects the pancreas?

A

MEN1

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122
Q

Which multiple endocrine neoplasm presents with marfinoid features?

A

MEN2B

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123
Q

Which multiple endocrine neoplasm has the highest chance of developing medullaty thryoid carcinoma?

A

MEN2B

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124
Q

Which multiple endocrine neoplasm affects the parathyroid and the thyroid?

A

MEN 2A

it can present with phaeocromacytoma

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125
Q

What is the name given to outpouchings of gallbladder epithelium into the gallbladder muscle layer?

A

Rokitansky–Aschoff sinuses

Not necessarily abnormal but ass. with cholecystitis

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126
Q

What is the portal tract of the liver made up of?

A

Bile duct
Portal vein
Hepatic artery

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127
Q

Which liver cells in the hepatic lobule are most metabolically active?

A

Perivenular cells near the centre of the lobule, around the hepatic central vein. Zone 3

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128
Q

Which liver cells in the hepatic lobule receive the most O2 and nutrients?

A

Zone 1, periportal

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129
Q

What is the name of the structure that contains the portal tracts in the liver?

A

Sinusoids

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130
Q

What kind of cells feature in all adenocarcinomas?

A

Mucin-secreting Glands

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131
Q

Which tumour marker is high in HCC?

A

AlphaFetoProtein (AFP)

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132
Q

Causes of cholangiocarcinoma?

A

Bild duct cancer. Adenocarcinoma so mucin-secreting
Lynch syndrome 2 (HNPCC)
Primary Sclerosing Cholangitis
Parasitic infection

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133
Q

What happens when there is increased resistance to blood flow through the liver?

A

This creates portal hypertension so there is intra and extra hepatic shunting.
Intra: Bypassing of hepatocytes straight from portal vein to central hepatic vein.
Extra: Oesophageal varices and haemorrhoids

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134
Q

What is alpha1anti-trypsin associated with?

A

Liver cirrhosis

COPD - Emphysema

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135
Q

Which liver cell stores Vitamin A?

A

Stellate Cell

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136
Q

Describe the stages of liver cirrhosis?

A
  1. Hepatocyte damage and necrosis
  2. Inflammation activates stellate cells in the space of disse that become myefibroblasts and initiate fibrosis by depositing collagen in the space of disse
  3. Some hepatocytes regenerate and form nodules]
  4. There is disruption of the liver architecture

Cirrhosis is reversible if treated aggressively

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137
Q

What causes micronodular cirrhosis?

A

<3mm nodules (AnuBear is small)
Alcoholic hepatitis
Biliary tract disease

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138
Q

What causes macronodular cirrhosis?

A

> 3mm nodules
Viral hepatits
Alpha 1 antitrypsin deficiency
Wilson’s disease

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139
Q

At what raised portal pressure do the dilation symptoms/changes begin?

A

10-12 mmHg

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140
Q

What are the main categories of liver cirrhosis?

A

ANA Got Big Veins

  1. Alcoholic
  2. Non Alcoholic fatty liver disease (NAFLD)
  3. Viral Hep
  4. Genetic
  5. Auto-immune hep
  6. Billiary causes
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141
Q

What are the types of alcoholic liver cirrhosis?

A

Alcoholic steatosis
Alcoholic hepatitis
Alcoholic cirrhosis

142
Q

What do you see in alcoholic hepatitis?

A

key cells are neutrophil polymorphs

You see mallory denck bodies and hepatocyte ballooning

143
Q

Types of NAFLD?

A

Steatohepatitis
Simple steatosis

Similar to alcoholic liver disease but seen in FAT non-alcoholics. Due to high levels of lipids.
Common in pts with metabolic syndrome

144
Q

Auto-immune hepatitis HLA Ass?

145
Q

Types if auto-immune hepatitis?

A

type 1 and type 2
Type 1: ANA, anti SMA and anti-actin
Type 2: Anti LKM

146
Q

Billiary causes of hepatic cirrhosis?

A

Primary Billiary Cholangitis (PBC) and Primary Sclerosing Cholangitis (PSC)

147
Q

Key features of PBC

A

Primary Billiary Cholangitis (PBC): B in it, Big (opposite). These ones try to trick you.
Auto-immune destriction of intra-hepatic bile ducts
Anti Mitochondrial Abs seen
Loss of bile ducts seen (no duct dilatation) so NOT big.
Raised ALP and IgM

148
Q

Key features of PSC

A

Primary Sclerosing Cholangitis (PSC): S in it, Small (opposite).
Auto-immune fibrosis of intra and extra hepatic bile ducts.
Autoantibodies seen
DILATED bile ducts , BIG
Raised ALP and pANCA
Diagnose via ERCP - will show beading of bile ducts because multifocal strictures are created and there is dilatation of preserved bile duct
High risk of progression to cholangiocarcinoma

149
Q

What are the genetic causes of liver cirrhosis?

A

Haemochromatosis
Wilson’s disease
Alpha 1 antitrypsin deficiency

150
Q

What gene is mutated in haemochromatosis?

A 
HFE gene (can be screened for) on Cr 6
Human haemochromatosis protein
151
Q

What happens in haemochromatosis?

A

Increased gut iron absorption which deposits in the liver, heart, kidneys, skin etc. This causes damage to the parenchyma

152
Q

How to test for haemochromatosis?

A
  • Iron in the liver- prussian blue stain

- Iron studies. high serum Fe, high serum ferritin, low TIBC

153
Q

Treatment of haemochromatosis?

A

Desferrioxamine

Venesection

154
Q

Wilson’s disease mutation?

A

ATP7B

Chr 13

155
Q

What happens in wilson’s disease? Symptoms?

A 
Caeruloplasmin is not created so copper cannot be excreted into the bile. This leads to a build up of copper so it gets deposited in the brain and liver. It also spills out into blood and goes into kidneys.
Itchiness
Yellowness
Tremors/Psychosis/Dementia
Vom
Ascites
Kayser Fleischer Rings
156
Q

Investigations for Wilson’s disease?

A

Rhodanine stain
Mallory bodies & steatosis on microscopy
Copper tests:
Low serum copper (because of low caeruloplasmin)
High urinary copper
Low caeruloplasmin

157
Q

What is the opposite of Wilson’s disease?

A

Menke’s disease (complete deficiency in copper) due to ATP7A mutation

158
Q

Which part of the brain is most affected in Wilsons disease?

A

Lenticular nuceli - they appear brown because of the copper deposition

159
Q

Treatment of Wilson’s disease?

A

Penacillamine FOR LIFE

160
Q

When should you suspect A1AT?

A

When there is cirrhosis in combination with emphysema. In children you get neonatal jaundice

161
Q

Histology/Ix of A1AT?

A
  • Intracytoplasmic Inclusions of A1AT which stain with Periodic acid schiff staining technique
  • No alpha globulin band on electrophoresis
162
Q

Side effects of cyclophosphamide?

A

Haemhoragic cyctitis
Bladder cancer
Infertility

163
Q

Types of bladder cancer?

A

Transitional cell
Squamous ce
Adenocarcinoma

164
Q

Which is the most common type of bladder cancer?

A

Urothelial carcinoma/Transitional cell carcinoma (TCC)

165
Q

RFs for transitional cell bladder carcinoma?

A

Smoking

Aromatic amines

166
Q

Symptoms of transitional cell carcinoma?

A 
Painless haematuria
Urgency
Frequency
Pyelonephritis
Hydronephritis
167
Q

Diagnosis of bladder cancer?

A

Cystoscopy and biopsy

168
Q

Which organism is ass. with squamous cell carcinoma?

A

Schistosomiasis

169
Q

Symptoms of Benign Prostatic Hyperplasia and reasons why these symptoms occur?

A 
Retention
Dribbling
Frequency
Nocturia
The enlarged prostate presses/blocks the bladder
170
Q

Treatment of BPH?

A
  1. Alpha blocker e.g. Doxazosin
  2. TURP Transurethral resection of prostate
  3. 5alpha reductase inhibitor e.g. Finasteride
171
Q

How to grade and investigate prostate cancer?

A

Grade: Gleason system
Investigate: Biopsy and PSA (high over 4ng/ml is indicative)

172
Q

Treatment of prostate cancer?

A
  1. Observe
  2. Prostatectomy
  3. Radiotherapy
173
Q

Types of testicular cancers and which is more common?

A

Germ cell 95% - Seminoma (most common), Yolk Sac tumour, Choriocarcinoma, Teratoma
Non germ cell 5% - Leydig cell, sertoli cell

174
Q

Biological markers for Germ cell teratomas?

175
Q

Causes of pre-renal AKI?

A

Hovolaemia, sepsis, renal artery stenosis

176
Q

Categorise renal causes of AKI

A

Glomerular
Tubular/interstitial
Vessels

177
Q

Overall symptoms of AKI?

A 
Reduced GFR
Acidosis
Hypertension/fluid overload
Hypocalcaemia
Hyperkalaemia
Uraemia
178
Q

What are the key features of nephrotic syndrome?

A

Proteinuria (>3.5g/day)

Hypoalbuminaemia (<30g/L)

179
Q

Primary causes of nephrotic syndrome?

A

Minimal change
membranous glomerular disease
Focal segmental Glomerulosclerosis (FSGS)

180
Q

Most common cause of nephrotic syndrome in kids?

A

Minimal Change

181
Q

What do you see on electron microscopy of Membranous Glomerular Disease?

A

Loss of podocyte foot processes. Spikes due to deposits.

On IF you see granular deposits along the GBM

182
Q

Which primary nephrotic syndrome cause has the worst prognosis?

A

Focal Segmental Glomerulosclerosis -50% chance of end stage renal failure in 10 years

183
Q

Secondary causes of nephrotic syndrome?

A

Diabetic nephropathy
Amyloidosis
SLE

184
Q

What are Kimmelstiel Wilson Nodules?

A

Diabetic glomerulosclerosis allows proteins through the glomerulus and they accumulate in the Bowman’s Capsule and form these nodules.
They are Periodic Acid Schiff Positive

185
Q

What are the differences between the types of Amyloidosis?

A

Type 1 is AA, serum amyloid associated protein. Ass. w/TB and chronic infection
Type 2 is AL, light chains- ass. with MM.

186
Q

What are the key features in nephritic syndrome?

A

Cocacola urine

Red and white casts in urine

187
Q

What are the causes of glomerulonephritis?

A 
thin CHIPS
Thin basement membrane
Crescentric glomerulonephritis
Hereditary (alports)
IgA nephropathy (berger)
Post-Strep GN
188
Q

Causes of crescentric GN?

A

Pauci immune
Anti-GBM
Immune complex mediated

189
Q

Talk about the 3 types of crescentric GN

A

GOOD CROISSANT PASTRIES
GBM
COMPLEX
PAUCI

ALL 3 will show crescents in glomeruli because of damage and cell accumulation in bowman’s space.

Pauci immune - ass. with pANCA and cANCA

Anti GBM - Goodpasture’s. Diagnostic test is fluroscopy, you’ll see a band of IgG on GBM. Abs against type 4 collagen a3

Immune complex mediated - will see granular deposition of IgG immune complexes in mesangium or GBM. Caused by SLE, IgA and Post infectious

190
Q

What is Alport’s syndrome?

A

Mutation in collagen type 4 alpha 5 chain
Affects kidneys, eyes and defness
Presents Age 5-20

191
Q

What is IgA nephropathy?

A

Also known as BERGER disease.
Commonest GN worldwide
IgA immune complex deposition. IgA will be v high.
Doesnt usually cause nephritic syndrome

192
Q

When does IgA nephropathy present

A

After upper resp tract infection and frank or microscopic haematuria

193
Q

What is thin basement membrane disease?

A 
Mutation in type 4 alpha chain 4 collagen
Causes thinning of GBM
Common 5% of people
AD
Doesnt usually cause nephritic syndrome
194
Q

What are the causes of Tubular/interstital damage that causes AKI?

A

ATN (caused by drugs/toxins/ischaemia)

and

Tubulointerstitial Nephritis 
(caused by acute or chronic pyelonephritis due to UTIs or caused by acute or chronic interstitial nephritis caused by hypersensitivity reaction to drugs)
195
Q

Which thrombotic microangiopathy is sometimes diarrhoea associated?

A

HUS

Caused by E.Coli 0157, often kids at petting zoo

196
Q

What are the causes of vessel damage AKI?

A

HUS and TTP
HUS - kids. confined to kidneys
TTP - adults. Systemic thrombi throughout circulation

197
Q

Causes of CKD?

A 
Diabetes
Glomerulonephritis
Pyelonephritis
Hypertension
Polycystic Kidney Disease
198
Q

What happen in polycystic kidney disease?

A

Cysts within the nephrons dilate and press onto the kidney and cause nephron loss. Can cause haematuria, flank pain and UTIs

199
Q

Which mutations are associated with polycystic kidney disease?

A

PKD1 on Chr 16 and PKD2 on Chr 4

200
Q

What else are Polycystic kidneys associated with?

A

Berry aneurysms in circle of Willis and cysts in liver (in PKD1)

201
Q

What is the name of the PID complication that causes peri-hepatic adhesions

A

Fitz Hugh Curtis syndrome

Violin string adhesions

202
Q

What are the types of endometrial carcinoma?

A

Endometroid 80% - oestrogen dependent PERIMENOPAUSAL women.

Non-endometroid 20% - Clear cell/serous/papillary unrelated to oestrogen excess. OLDER women.
In endometroid there is an accumulation of 4+ gene mutations

203
Q

RFs for vulvular carcinoma?

A 
VIN
Lichen sclerosis
Pagets disease of vulva
Smoking
HPV

80% are squamous cell
Labia Majorum is most common site

204
Q

Which form of gestational trophoblastic disease (GTD) is ass. with progression to cancer?

A

COMPLETE moles and choriocarcinoma (placental origin)

205
Q

What do choriocarcinomas secrete? Which cells secrete it?

A

bHCG (from synctiotrophoblasts)

206
Q

What are the types of ovarian tumours?

A

EGS
Epithelial
Germ Cell
Sex Cord

Epithelial: SCEM
Serous
Clear Cell
Endometroid
Mucinous

Germ Cell: DTC
Dysgerminoma
Teratoma
Choriocarcinoma

Sex Cord: FGS
Fibroma
Granulosa-theca cell
Sertoli-Leydig

207
Q

Which histo finding do you see in Serous ovarian tumours?

A

Psammoma Bodies

208
Q

Which type of Epithelial ovarian tumours are most common?

209
Q

What is the appearance of clear cell ovarian tumours?

A

Clear cytoplasm with hob like appearance

210
Q

What is the name of a stomach tumour that metastasises to the ovaries and what would you see?

A

Mucinous KRUKENBERG tumour. You would see signet ring cells (from gastric tumour)

211
Q

What is the name of the ovarian tumour with bits of different cells in them like teeth, hair, nails etc.

A

Cystic Teratoma or Dermoid Cyst

212
Q

Which syndrome is associated with ovarian fibromas? What is the syndrome?

A

Meig’s syndrome.
Pleural effusion
Ovarian cancer
Ascites

213
Q

Describe Granulosa-Theca cell tumours of the ovaries?

A

Oestrogen producing- so look for oestrogenic effects e.g. breast enlargements, irregular menstruation

214
Q

Describe Sertoli-Leydig ovarian tumours?

A

they secrete androgens- look for defeminisation e.g. hirsutism, enlarged clitoris, deep voice

215
Q

How does the HPV virus cause cancer?

A

It has 2 proteins E7 and E6.
They inactivate tumour suppressor genes.
E6 does p53
E7 does Retinoblastoma

These changes cause increased proliferation

216
Q

Which strands of HPV are associated with cervical cancer?

217
Q

Describe the cell types of the cervix

A

Outer: squamous
Inner: Collumnar
Separated by squamou-collumnar junction (transformational zone)

218
Q

Which part of the cervix is susceptible to malignant change?

A

transformational zone

219
Q

Describe the grading of CIN

A

1: distal 1/3 dysplasia
2: lower 2/3
3: full thickness but BM intact

220
Q

RFs for cervical cancer

A 
Younger age at first sex
Multiple sexual partners
Smoking 
Multiparity
Immunosuppression
221
Q

Which type of cervical carcinoma is more common?

A

Squamous cell (80%) then 20% adenocarcinoma + others

222
Q

How do women get acute mastitis?

A

Staph infection via cracks in nipples - stasis of milk contributes. Pts get fever and red, painful, swollen breast

223
Q

Which type of mastitis is not associated with breastfeeding? Histology?

A

Periductal mastitis - seen in smokers. Histologically you see keratinizing squamous epithelium

224
Q

Which breast condition presents with thick white nipple secretions?

A

Duct ectasia. Caused by inflammation and dilatation of large breast ducts. Proteinaceous material inside - mimics appearance of cancer on mammography.

225
Q

How does fat necrosis occur in the breast? What do you see histologically?

A

Damage to adipose tissue in the breast causes infiltration of inflammatory cells and causes painless breast mass. You will see inflamm cells around the fat cells

226
Q

What are fibrocystic breast changes?

A

Benign Proliferative. Exaggerated response to normal hormones that causes small cysts in the breast -often fluid filled (green/yellow on FNA) and can be calcified. Cysts can rupture and cause fibrosis or fat necrosis.

227
Q

Which age do people get fibroadenomas? Give details about fibroadenomas.

A

20-30. Response to hormones, englarge during pregnancy. Calcify during menopause. Benign. Mobile.. Can shell out the large >3cm ones

228
Q

What does it mean if you see epithelial hyperplasia in the breast?

A

It is a risk for invasive carcinoma.

229
Q

What is the male equivalent of fibroadenoma?

A

It is an exaggerated response to oestrogen so you get gynaecomastia

230
Q

Which breast condition commonly causes bleeding from nipple?

A

Duct papilloma (peripheral ones don’t usually bleed but central ones do).
Ix: galactogram
Tx: excision

231
Q

Which condition can look like a star shaped cancer on mammogram?

A

Radial scar - scarring around glandular tissue in stellate pattern

232
Q

RFs for breast cancer?

A
  • Hormone exposure (E2) - early menarche, late menopause, OCP
  • Age
  • FH
  • Genetics BRCA1/BRCA2
  • Smoking
  • Obesity
233
Q

Which Chromosome loss causes low grade susceptibility?

A

16q loss and 1q gain

234
Q

What is the histological hallmark of ductal carcinoma in situ?

A

Punched out spaces that are regular and round

Microcalcifications

235
Q

What are the symptoms of a worrying breast malignancy?

A

Skin changes e.g. eczematous/paget’s breast/peau d’orange

  • hard fixed lump
  • nipple retraction
236
Q

Which breast cancer has sheets of atypical cells?

A

basal-like carcinoma

237
Q

Which breast cancer has lines of single file strands?

A

Invasive lobular (indian file)

238
Q

Which breast cancer has well formed tubules?

A

Tubular carcinoma

239
Q

Which receptors are screened for in neoplastic breast lesions?

A

HER2
E2 (oestrogen)
PR (progest)

240
Q

Which breast receptors are associated with a good prognosis? bad prognosis?

A 
E2/PR = good Will respond to tamoxifen
HER2 = bad
241
Q

Which treatment can you give against HER2 receptor?

A

Herceptin (trastuzumab)

242
Q

What is the key prognostic factor in breast cancer prognosis?

A

Axilliary LN presence

243
Q

What are the effects of tamoxifen?

A

Antagonist to breast E2 receptor but agonist to bone/uterus E2 receptor, so increased risk of uterine cancer (i.e. endometrial)

244
Q

What does basal-like breast carcinoma stain positive for?

245
Q

What are phyllodes tumours? Treatment?

A

Breast tumours mostly benign but can be malignant. Arise from breast stromal tissue
High cellularity & mitotic activity = more likely to be malignant.
>50 years old but also in young
Tx: Wide local excision

246
Q

What age is the national breast screening programme for?

247
Q

What FNA grade would you give to a DCIS? Invasive?

A

DCIS: B5a
Invasive: B5b

248
Q

When do you give thrombolytics in a stroke?

A

If its been less than 3 hours since the event

249
Q

What is the cause of most subarachnoid haemorrhages?

A

ruptured berry aneurysms

250
Q

Causes of raised intracranial pressure?

A

SOL - neoplasia, abscess, bleed
Cerebral oedema - hydrocephalus (accumulation of CSF; communicating = poor reabsorption of CSF into sinuses. non-communicating = blockage of aqueduct)
Tx: stent

251
Q

What is Kernig’s sign?

A

When thigh is flexed and knee at 90 degrees, extension of knee causes pain. It indicates SAH or meningitis

252
Q

What is often the first presentation of NF1?

A

Cafe Au Lait spots. Pts must have 3-5 to warrant investigation.

253
Q

What is neurofibromatosis?

A

AD

Cause lesions in the skin, nervous system and skeleton.

254
Q

Which Chr is the mutated NF1 gene on?

255
Q

Which Chr is the mutated NF2 gene on?

256
Q

Which brain tumours are seen in children?

A 
Medulloblastoma
Hairy cell (pilocytic astrocytoma)
257
Q

Which brain tumours are hairy cell?

A

Astrocytomas - pilocytic

258
Q

What is glioblastoma?

A

A type of astrocytoma.Quite bad.

Grade 4 - very invasive

259
Q

Which brain tumours are grade 4 on WHO grading?

A

Glioblastomas

Medulloblastomas

260
Q

Which codeletion is important for oligodendromas?

261
Q

What are the features of dementia?

A 
A global impairment of cognitive function without impairment of consciousness
Aphasia
Apraxia
Agnosia
Amnesia
262
Q

Which staging is used in Alzheimers disease?

263
Q

Alzheimer’s is associated with which proteins?

A

TAU protein becomes hyperphosphorylated (you see intracellular neurofibrillary tangles of tau protein)
B amlyoid protein accumulates to form extracellular senile plaques

264
Q

Which Braak stages would be clinical azlheimer’s?

265
Q

Which dementias involve the Tau protein?

A

Frontotemporal dementia including Picks disease (Accumulation of pick bodies made of tau protein)
And Alzheimer’s

266
Q

What causes the loss of colour in Parkinson’s?

A

Neuromelanin loss in substantia nigra, caused by dopaminergic metabolism

267
Q

What are lewy bodies?

A

Aggregates of protein Alpha Synuclein

268
Q

Which neuro condition involve Alpha Synuclein?

A
  1. Parkinson’s
  2. lewy body dementia
  3. Multiple System Atrophy - but pathology is in the glial cells
269
Q

Which proteins are seen in MS? (multiple sclerosis)

A

MBP and PLP
Myelin Basic Protein and
Proteo-lipid Protein

270
Q

What is MS?

A

Autoimmune demyelination of neurones - needed for axon conduction

271
Q

How does PTH increase calcium?

A

PTH binds to osteoblasts which upregulate the RANK ligand so more RANK can bind to RANK receptor which leads to osteoclast differentiation and survival.
Osteoclasts bind to bone and digestive enzymes break down collagen 1. and release calcium from bone

272
Q

How is calcium release from bone regulated?

A

PTH releases it

OPG (osteoprotegerin) competes with RANK to control levels of calcium release.

273
Q

Which drug can protect against osteoporosis?

A

Denosumab - mimics OPG

274
Q

What type of crystals do you get in gout?

A

Urate crystals

275
Q

What type of crystals do you get in pseudogout?

A

Calcium Pyrophosphate crystals

276
Q

Management of gout?

A

Acute: Colchine
LT: Allopurinol

277
Q

Which organisms cause osteomyelitis?

A

Neonates: Group B Strep, H. Influenza
Adults: Staph A, E.Coli, Kleb
Rare: syphilis, lyme disease (borrelia burgdoferi by ixodes dammini), TB (Pott’s disease)

278
Q

Featyres of osteoarthritis?

A 
Heberden's nodes (DIPS) 
Bouchards nodes (PIPS)
279
Q

Which Abs are in RA?

A

Rheum factor IgM alone

or IgG in immune complexes

280
Q

Which cells are seen in histology of RA?

A

Grimley-Sokoloff Cells (if you have Rh Arth you might wanna hide it by wearing GRIM SOCKs)

281
Q

Which age and joint is affected in osteosarcomas?

A

Adolescence

Knee

282
Q

Which are the malignant bone tumours?

A

OCE
Osteosarcoma
Chondrosarcoma
Ewing’s Sarcoma

283
Q

Describe the features of Ewing’s sarcoma

A

VERY malignant
<20 years (Harry was <20 when Hedwig died)
There is onion skinning of the periostium
T11:22 translocation (Harry was 11 when he got Hedwig)
CD99+ve
Long bones

284
Q

Describe the features of Osteosarcoma

A 
Malignant 
<30 years 
Knee
ALP +
Codman's triangle
Sunburst appearance
OSTIN THE COD IN THE SUN
285
Q

Describe the features of Chondrosarcoma

A

> 40 years
Axial skeleton - pelvis etc
Malginant chondrocytes
Lytic lesions with fluffy calcifications

286
Q

When there is fluffy calcification on Xray what could it be?

A

Chondrosarcoma

Enchondroma

287
Q

Describe features of enchondroma

A

Benign tumours of cartilage
Affects hands and feet
Cotton wool calcifications on Xray
Middle aged

Ollier’s syndrome: multiple enchondromas
Maffuci’s syndrome: Multiple enchondromas and haemangiomas

288
Q

Describe the features of Osteochondroma

A

Mimics cartilage around the bone- cartilage capped bony outgrowths seen

289
Q

Describe the features of Fibrous dysplasia

A

Bone replaced by fibrous tissue
Can present with cafe au lait spots if Albright syndrome
Chinese letters on histology
Soap bubble osteolysis and Shepherds crook deformity

290
Q

Which bone disease is borderline malignant/benign?

A

Giant Cell. You get osteoclast type multinucleate giant cells

291
Q

What are the types of inflammatory dermatoses?

A

Spongiotic
Psoriasiform
Vescicular Billous
Granulomatous

292
Q

What are the types of spongiotic dermatitis? What is the histology?

A

Contact (type 4 hypersensitivity reaction to jewellery etc)
Atopic (eczema)
Seborrhoeic (inflam reaction to yeast Malassezia) -cradle cap

Histology:
Sponginess
Inflammatory infiltrates
Chronic; Acanthosis, crusting

293
Q

What is the sign when you rub a rash and you get pinpoint bleeding?

A

Auspitz’ sign in psoriasis (i was 15 when diagnosed, went to Autzwits when i was 15)

294
Q

When lesions form at sites of trauma in psoriasis, what is it called?

A

Koebner’s phenomenon

295
Q

What nail/hand changes do you get in psoriasis?

A 
POSHA
Pitting
Onchylosis
Subungual Hyperkeratosis
Arthritis
296
Q

Histo features in psoriasis?

A

Loose granulocell layer, parakeratosis, neutrophils instead of eosinophils

297
Q

Describe lichen planus?

A 
Saw tooth ridges, hyperkeratosis
Purple
Puritic
Papules
Plaques
Mother of pearl sheen
Wickham Striae
Inner surface of wrists or mouth
298
Q

Causes of erythema multiforme rash?

A

HSV 1

Mucoplasma Pmneumoniae

299
Q

Describe erythema multipforme

A

Target lesions
Subepidermal bullae
Seen in HSV1/mycoplasma. Drug reactions e.g. Antimalarials, penicillin

300
Q

What are the 3 forms of Vesicular Bullous skin inflammations and where are they in the layers of the skin?

A

Dermatitis Herpatiformis -Subepidermal
Pemphigoid - Subepidermal
Pemhigus Vulgaris - Intraepidermal

301
Q

Differences between pemphigus and pemphigoid?

A

Pemphigus is superficial and intraepidermal They are easily ruptured and you see IgG deposits intrcellularly.

Pemphigoid is deep and subdermal. They are NOT easily ruptured and are big/balloon like.

302
Q

What are the malignant skin neoplasms?

A

Basal cell carcinoma (does not kill)

Small cell carcinoma (metastatic!)

303
Q

What is the name for a squamous cell carcinoma that doesn’t metastasize (in situ)?

A

Bowen’s disease

304
Q

Describe the basal cell carcinoma?

A

Rodent ulcer
Slow growing
Pearly surface with telangiectasia and rolled edge
Basiloblue cells

305
Q

Describe squamous cell carcinoma?

A

Flat/red/scaly/sun-exposed areas
Spreads through BM into dermis
Atypia
Nuclear crowding

306
Q

Which stain is used for Melanomas?

A

Fontana Stain

307
Q

Which scale is used for melanomas?

A

Breslow’s thickness

308
Q

Describe malignant melanomas

A 
Keratinocytes in dermis = bad
Vertical growth of melanocytes into dermis
Buckshot appearance (pagetoid cells)
309
Q

How to test for malignant melanoma?

A

Fontana stain

Biopsy will show + melanin

310
Q

What are the conditions when there are patches of skin detachment and how do you define each one?

A

Stephen Johnsons Syndrome (<10% of skin)

Toxic Epidermal Necrolysis (TEN) >30%

311
Q

What happens in SJS/TEN?

A

Drug reaction - fly like symptoms then rash and blistering

Drugs e.g. Lamotrigine and Abx

312
Q

What is the name of the sign in SJS/TEN where there is prominent mucosal involvement?

A

Nikolsky’s sign

the little girl was a polish girl called Nikola

313
Q

Describe pityriasis Rosea

A 
Salmon pink rash
Starts with a herald patch 
Christmas tree distribution
Face usually unaffected
After viral illness
Resolves from 12 weeks to 5 months
314
Q

What do you see on Immunoflurescence if you have MIXED connective tissue disease?

A

Speckled pattern of ANA appearance

315
Q

Which HLA is ass. with SLE?

A

HLA DR3 (or DR2)

316
Q

Which HLA is ass. with Scleroderma?

A

HLA DR5 / HLA DRw8

317
Q

Which Abs do you see in SLE?

A 
ANA
Anti-dsDNA
Anti-Smith (only 30% have it but if they have it it's SLE)
Anti-histone (for drug related SLE)
Anti-Phospholipid
318
Q

Symptoms of SLE?

A 
SOAP BRAIN MD - need 4/11
Serositis (lung/heart/abdo)
Oral ulcers
Arthritis
Photosensitivity
Blood (pancytopaenia)
Renal involvement (proteinuria - nephrotic)
ANA +
Immune cells e.g. Anti dsDNA, anti phospholipid
Neuro symptoms
Malar rash
Discoid rash
319
Q

What do you see on SLE histology?

A

LE bodies
Libman Sack endocarditis
Onion skin lesions

320
Q

Difference between limited and diffuse scleroderma?

A 
Limited = CREST (scleroderma only on fingers)
Diffuse = Scleroderma anywhere, widespread organ involvement and skin is tight esp over chest
321
Q

Which Abs do you see in each of the sclerodermas?

A

Limited: Anti centromere
Diffuse: Anti topoisomerase/Anti-Scl-70 and Anti-fibrillarin

322
Q

What do you see on limited scleroderma histology?

A

Onion skin thickening of arterioles

323
Q

RFs for SLE?

A

Female
40 years old
Afro carabbean

SLE is a type 3 hypersensitivity i.e. immune complex mediated

324
Q

What is CREST?

A 
Calcinosis
Raynauds
Esophageal dysmotility
Scleroderma 
Telangiectasia
325
Q

What actually is scleroderma?

A

Thickening of skin due to excess collagen deposits- causes symptoms in crest e.g. oesophageal dysmotility

326
Q

Order of colour change in raynauds?

A

When Blood Returns
White
Blue
Red

327
Q

Which Ab is seen in polymyositis and dermatomyositis?

328
Q

What is myositis? What investigations can you do?

A

Inflammation of the muscles

Raised creatinine Kinase and abnormal EMG

329
Q

Cutaneous features of dermatomyositis?

A

Heliotrope rash and Gottron papules

330
Q

What are all the vasculitides?

A

Large vessel:

  1. Takaysu’s arteritis
  2. Temporal arteritis

Medium vessel:

  1. Kawasaki’s
  2. Polyarteritis Nodosa (PAN)
  3. Buerger’s disease

Small vessel:

  1. Wegener’s granulomatosis
  2. Churg Strauss
  3. Henoch schonlein purpura
  4. Microscopic polyangiitis
331
Q

In which vasculitis conditions do you get a non-palpable temporal artery?

A

Temporal arteritis AND takayasu’s arteritis

332
Q

What are the key features of takayasu’s arteritis?

A

Japanese women
pulseless disease
Bruits, claudication

333
Q

Histology of temporal arteritis?

A

Giant cells
High ESR
Skip lesions

334
Q

Features of Kawasaki’s disease?

A 
<5 years
Conjunctivitis
Rash
Adenopathy
Strawberry tongue
Hands and feet red
Fever >5 days
335
Q

Features of Wegeners?

Which Ab?

A 
Triad:
ENT (epistaxis, saddle nose, sinusitis)
Upper resp tract: haemorrhage/cavitation
Kidneys: cresentric glomerulonephritis
cANCA
Anti PR3
336
Q

Features of Churg Strauss?

A 
Vasculitis
Asthma - think eosinophilia init
Granulomas with Eosinophilia - this is what causes the 
pANCA
Anti MPO
337
Q

Features of microscopic polyangiitis

A 
Pulmonary renal syndrome: same as Wegeners without URT signs
-Pulmonary haemorrhage
-Glomerulonephritis
pANCA 
Anti MPO
338
Q

Age of Henoch Schonlein Purpura?

339
Q

What happens in Henoch Schonlein Purpura (HSP)?

A 
Preceded by a URTI
palpable Purpuric rash over limbs and buttocks
Abdo pain
Glomerulonephritis
Arthritis
Orchitis (testicular inflammation)
340
Q

Which stain is used to detect amyloidosis?

341
Q

What do you see under polarised light in amyloidosis?

A

Apple green birefringence

342
Q

Features of amyloidosis?

A 
Macroglossia
Carpel tunnel syndrome
Nephrotic syndrome
Hepatosplenomegaly
Heart Failure
343
Q

Most common familial amyloidosis?

A

Familial medetarranean fever -VERY high IL1 production

344
Q

What causes amyloidosis?

A

Deposition of misfolded amyloid proteins in normal tissue disrupting function. Beta pleated sheet configeration

345
Q

What are the different types of amyloidosis?

A
  1. Primary- AL - light chains, bence jones proteins, ass. with MM (most dont have MM)
  2. Secondary AA (systemic, serum AA)
    RA, TB, IBD associated
  3. Familial
  4. Haemodialysis ass.- deposition of beta 2 microglobulin
346
Q

What are the histological features of sarcoidosis?

A

Non-caseating granulomas
Shaumann bodies
Asteroid bodies

347
Q

What are Shaumann bodies?

A

Calcium and protein inclusions inside of Langhans giant cells as part of a granuloma.

348
Q

Mnemonic for Sarcoidosis features?

A 
HAHA JC SMELLS
Hepatosplenomegaly
ACE (high)
Hilar lymphadenopathy
Anterior uveitis 
Joints
Calcium (high)
Skin nodules
Myocardial involvement 
Erythema nodosum
Lupus pernio
Leukopenia
Shaumann bodies
349
Q

Which patient group is Sarcoidosis often seen in?

A

Afrocarrabeans, females

350
Q

How do you diagnose sarcoid?

A 
High ESR
High Calcium
Calciurea
High ACE
Bronchial biopsy - granulomas, asteroid bodies, giant cells, shaumann bodies
CXR: lymphadenopathy

AANIYA PATH (31 decks)

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