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Path - Things to Go Over > Histo > Flashcards

Histo Flashcards

1
Q

What is the typical chemotherapy regime used for non-resectable pancreatic cancer?

A

FOLFIRINOX

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2
Q

What is the most likely abnormality that will be found on his echocardiogram to explain his permanent atrial fibrillation and poor success at cardioversion?

A

Dilated left atrium

NOTE: Being in AF means you’re more likely to stay in AF. This is often due to atrial dilatation.

May develop heart failure.

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3
Q

Classification of AF

A

Permanent AF - Easiest. Always in AF despite optimal rhythm control (DCCV or antiarrhythmics)

Persistent AF - Remains in AF >7 days but not tried maximal rhythm control yet

Paroxysmal AF - Intermittent AF, lasts <7 days.

AF is also either primary AF (patient has no reversible cause of AF other than e.g. structural heart disease) or secondary AF (patient is in AF because they have a severe infection or have binged alcohol)

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4
Q

What further imaging is indicated for a confirmed transient ischaemic attack of the anterior circulation when neurological symptoms have resolved?

A

Carotid Ultrasound

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5
Q

Best investigation for pancreatic cancer

A

Appropriate first line investigation is CT

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6
Q

Neuroendocrine tumours

A

Insulinomas - Whipple’s triad of symptoms
Gastrinoma - Zollinger-Ellison syndrome + gastric ulceration

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7
Q

For patients with a confirmed anterior circulation TIA, next appropriate management?

A

imaging of the carotids (USS Carotid Dopplers) to consider them for a carotid endarterectomy

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8
Q

Which class of lupus nephritis on biopsy may show complete sclerosis of nearly all glomeruli?

A

Class VI

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9
Q

What is the most common type of breast cancer in the UK?

A

Invasive ductal carcinoma

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10
Q

A nephrologist is investigating an elderly gentleman with nephrotic syndrome.

A renal biopsy revealed normal histology when viewed under a light microscopy. There were no immune complexes detected in the biopsy either. There was no amyloid deposition.

Urinary Bence Jones Protein and serum electrophoresis were normal.

The patient responded well to steroids and their renal function is normal.

What is the most likely primary cause of the nephrotic syndrome?

A

Minimal change disease, as no depositon

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11
Q

What cancer is associated with the presence of “oat shaped cells” on biopsy?

A

small cell lung cancer

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12
Q

A 23 year old man visits their GP with a positive pregnancy test, which he did for a joke. A repeat pregnancy test in the surgery is also positive.

He denies any sexual activity in the last year.

What is the possible underlying diagnosis?

A

Testicular cancer

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13
Q

A 83 year old man is started on bicalutamide for treatment of his metastatic prostate cancer.

What is the method of action of bicalutamide?

A

Androgen antagonist

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14
Q

Head trauma causing loss of consciousness followed by a lucid interval before the patient deteriorates is a classical history of what cerebral pathology?

A

Extradural haemorrhage

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15
Q

What is the first line chemotherapy drug for treating prostate cancer in the UK?

A

Docetaxel

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16
Q

A 18 year old woman was stabbed in the groin at a party. Arterial blood flow was observed from the wound on scene. Haemostasis was achieved by bystanders.

She was stabilised on scene and transferred to hospital by air ambulance.

She lost an estimated 6 units of blood, however the air ambulance transfused one unit on scene and bolused two litres of 0.9% sodium chloride.

You perform an A-E assessment in the emergency department 30 minutes later. She is unconscious but tachypneic. You note the presence of a new, soft, systolic murmur.

Given the history, what type of murmur is this likely to be?

A

Flow murmur - Innocent

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17
Q

What condition is the presence of waxy casts in urine associated with?

A

Chronic Kidney disease

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18
Q

Other than zinc, what is the first line pharmacological treatment for Wilson’s disease?

A

Trientine

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19
Q

What is the name given to areas of regenerating mucosa which project into the lumen of the bowel, which may be visualised during a colonoscopy of a patient with ulcerative colitis?

A

pseudopolyp

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20
Q

A 55 year old gentleman with newly diagnosed bipolar disorder is seen by a psychiatrist. An ECG is performed as part of the workup for starting lithium, a mood stabiliser.

His past medical history includes an anterior STEMI 4 months ago.

The ECG shows ST elevation in leads V2, V3, V4 and V5. He denies chest pain, breathlessness or any other symptoms.

What is the diagnosis?

A

Ventricular aneurysm

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21
Q

What is persistent ST elevation post MI suggest? What are they at risk of?

A

Persistent ST elevation post myocardial infarction in the absence of chest pain or other ischaemic features is suggestive of the development of a ventricular aneurysm.

These patients are at high risk of ventricular free wall rupture and subsequent death. It is diagnosed through an echocardiogram or cardiac MRI.

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22
Q

A 68-year-old woman presents to her GP with a non-tender, hard lump with irregular borders in her left breast. She denies any nipple discharge, weight loss or malaise.

She was in a car accident 6 months ago and sustained significant bruising to the chest wall.

She undergoes triple assessment. Ultrasound shows a solid mass with indistinct margins.

The biopsy report is lost however the system recorded that the specimen was benign.

What condition may explain the lump?

A

Fat necrosis

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23
Q

What is the most common type of lung cancer in the UK?

A

Adenocarcinoma

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24
Q

A 83 year old woman was admitted to hospital for a severe chest infection. At the time of admission, her CURB-65 was 4. Her blood pressure was 80/40

She was diagnosed as having an acute kidney injury.

What is the likely cause of the AKI?

A

ATN secondary to sepsis and hypoperfusion

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25
Q

What condition is characterised by microangiopathic haemolytic anaemia, thrombocytopenia and stroke-like symptoms in an adult?

A

Thrombotic Thrombocytopenic Purpura

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26
Q

What histopathological description is given to cells that have lost their intercellular connections between neighbouring cells?

An example could be the loss of desmosomal connections in pemphigus vulgaris.

A

Acantholysis

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27
Q

What monoclonal antibody therapy targets human epidermal growth factor receptor 2 and is used in the treatment of breast cancer?

A

Trastuzumab

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28
Q

poor prognostic marker in breast cancer

A

Presence of HER2 is a poor prognostic marker (but does allow for treatment with trastuzumab - a monoclonal antibody therapy)

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29
Q

good prognostic marker in breast cancer

A

Presence of oestrogen receptor or progesterone receptor is good as it predicts response to oestrogen deprivation therapy.

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30
Q

eczema of nipple then areola

A

Paget’s disease of breast

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31
Q

oedema + pitting of breast

A

peau d’orange

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32
Q

What protein is defective in adult polycystic kidney disease?

A

Polycystin-1

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33
Q

What is the most common cause of a pulmonary embolus?

A

DVT

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34
Q

What is the most common histochemical stain used to visualise cells for light microscopy, such as that used for diagnosis of cancers?

A

Haematoxylin and eosin stain

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35
Q

A 55 year old woman presents to her GP with a number of painful fluid filled blisters in her mouth and on her body. They are relatively large, approximately 2-3cm on the body. She says they itch intermittently.

She feels well in herself and her type 1 diabetes is well controlled.

When you run your finger over the surface of one of the blisters on her arm, the roof of the blister easily comes away.

A biopsy reveals acantholytic cells, however the basal keratinocytes remain attached to the basement membrane.

What is the diagnosis?

A

Pemphigus vulgaris

NOTE: Pemphigus vulgaris presents with painful fluid filled blisters on the body and in the mouth, with acantholytic cells on biopsy. The roof of the blister easily comes away with light pressure.

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36
Q

The ECG leads II, III and aVF represent which region of the heart?

A

Inferior wall

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37
Q

What sign, which may be visible around the nails, is seen in Graves’ disease and is due to periosteal bone growth in the nail bed?

A

Thyroid acropachy

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38
Q

An 84 year old Asian woman presented to the ED with chest pain of 10 hours duration, which began while watching television. The pain was 9/10 and did not radiate. She reported being under extreme stress since the death of her 50 year old son a week ago.

An ECG revealed ST elevation in V2 and V3. Chest X ray was normal. Troponin and electrolytes were normal. Percutaneous Coronary Intervention was unremarkable with no occlusions and no evidence of atherosclerotic disease.

An echocardiogram showed apical akinesis with an ejection fraction of 36%. There was hypertrophy of the interventricular septum.

What is the diagnosis?

A

Takotsubo’s cardiomyopathy

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39
Q

What type of bladder cancer is associated with chronic cystitis?

A

sqaumous cell carcinoma

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40
Q

A 20-year-old man with cystic fibrosis presents to his GP with a chronic productive cough, that has been getting worse over the last two years. He is known to be colonised with pseudomonas aeruginosa.

His BMI is 18.5. Temperature in the surgery was 36.8c.

Examination revealed coarse crackles at the bases which shifted upon coughing.

Chest x ray was reported as showing tram-track opacities.

What is the diagnosis?

A

Bronchiectasis

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41
Q

CXR - tram track opacities
CT - signet ring sign

A

Bronchiectasis

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42
Q

Degeneration of neurons in the substantia nigra is implicated in the pathogenesis of what synucleinopathy?

A

Idiopathic Parkinson’s disease

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43
Q

What condition is the presence of epithelial casts in urine associated with?

A

Acute tubular necrosis

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44
Q

What is the most appropriate treatment for non-small cell lung cancer that is present in both lungs?

A

Palliative care

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45
Q

What paraneoplastic syndromes are small cell lung cancers associated with?

A

Associated with SIADH (15% of patients), Cushing’s syndrome (5%), Lambert-Eaton Myasthenic syndrome (3%) and acromegaly

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46
Q

Kimmelstiel WIlson Nodules

A

Diabetes Nephropathy

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47
Q

Most common renal cancer

A

Renal cell carcinoma

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48
Q

Most common CNS tumour

A

Glioblastoma multiforme

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49
Q

Sarcoid histological finding

A

non-caseating epithelioid cell granuloma

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50
Q

PKD inheritance

A

AD

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51
Q

What cells are found in granulomas?

A

Activated epitheloid amcrophages

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52
Q

What disease are eosinophils involved in?

A

Parasitic infections and Hodgkin’s disease

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53
Q

Histological features of squamous cell carcinomas

A

keratin production, intercellular bridges, do NOT form glands

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54
Q

Histological features of adenocarcinomas

A

form glandular epithelium AND mucin glands that can SECRETE substances

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55
Q

Histological features of transitional cell carcinomas

A

stretchy epithelium

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56
Q

Histochemical and immunohistology stain

A

Histochemical stain – result from the chemical reaction between stain and the tissue
Immunohistology stain – antibodies against a specific antigen

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57
Q

Most common cancer in men

A

Prostate

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58
Q

Most common cancer overall

A

Breast

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59
Q

Most deadly cancer in men and women

A

Lung

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60
Q

What type of necrosis occurs in MIs? Why?

A

Coagulative (dry) occurs in MI’s  blockage of blood vessel to heart  muscle gets a wedge of infarction that is dry, doesn’t liquify  just dies

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61
Q

What type of necrosis occurs in strokes? Why?

A

Liquefactive (wet)  occurs in strokes  brain is high fat organ  similar process to coagulative as stroke is like an MI of brain but as lipid rich organ  liquefactive. Can also occur in organs involving proteolytic enzymes

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62
Q

What type of necrosis is usually due to pseudomonas?

A

Gangrenous

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63
Q

What type of necrosis occurs due to TB?

A

Caseous  granuloma (cordoned off, inflamed tissue)  has cell death inside (“cheese-like”)  seen in TB, non-caseating  sarcoidosis

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64
Q

What type of necrosis occurs in acute pancreatitis?

A

Saponification  fat necrosis binds with calcium to form soap crystals within dead tissue  ACUTE PANCREATITIS

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65
Q

What type of necrosis occurs in AID, vasculitis or malignant hypertension?

A

Fibrinoid  cell death within a vessel due to inflammation in AID or vasculitis, malignant hypertension  fibrin leaks out of cell and deposits out of the cell  fibrin deposition around vessel wall

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66
Q

Epithelial anatomy and what happens in BArrets

A

Epithelial anatomy:
- PROXIMAL 2/3RD SQUAMOUS EPITHELIUM  WHITE
- DISTAL 1/3RD COLUMNAR EPITHELIUM  PINK
- JOINED BY THE SQUAMOUS COLUMNAR JUNCTION  Z LINE

Barret’s  After chronic GORD can get metaplasia in the oesophagus from squamous epithelial to columnar which have goblet cells  upward movement of the SCJ

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67
Q

Difference between gastric and intestinal metaplasia

A
  • GASTRIC METAPLASIA  WITHOUT GOBLET CELLS
  • INTESTINAL TYPE METAPLASIA  WITH GOBLET CELLS
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68
Q

Most common oesophogael cancer in developed world? RFs? Anatomical location?

A
  • ADENOCARCINOMA (MOST COMMON OESOPHAGAEL CANCER IN DEVELOPED WORLD)
    o RFS: BARRETS, SMOKING, OBESITY
     LOCATED IN DISTAL 1/3RD OF OESOPHAGUS due to GORD
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69
Q

Most common oesophogael cancer in developing world? RFs? Anatomical location?

A
  • SQUAMOUS CELL CARCINOMA  MOST COMMON IN DEVELOPING WORLD
    o RFS: SMOKING, ALCOHOL
     LOCATED IN THE MIDDLE 1/3RD OF OESOPHAGUS (upper 2/3rds)

NOTE: THINK S’ –> squamous occurs due to smoking, superiorly

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70
Q

What GI condition can pernicious anaemia cause? What can this lead to?

A

can cause AI gastritis, can also cause atrophy leading to malabsorption

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71
Q

What bacteria can cause chronic gastritis?

A

H.Pylori in antrum

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72
Q

Difference ebtween gastritis and ulcer

A

ULCERS BREACH THROUGH MUSCULARIS MUCOSA INTO SUBMUCOSA

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73
Q

Most common cause of gastric ulcer

A

H.pylori

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74
Q

Most vulnerable area in GI tract to H.pylori, why?

A

DUODENUM IS MOST VULNERABLE TO H. PYLORI AS INCREASED ACID PRODUCTION LEAKS INTO DUODENUM CAUSING GASTRIC METAPLASIA (WITHOUT GOBLET CELLS)
NB: Intestinal type metaplasia  with goblet cell

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75
Q

What cancers can H.pylori lead to?

A

Adenocarcinoma via metaplasia
Gastric MALToma

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76
Q

What are duodenal ulcers caused by?

A

 H.PYLORI
 GIARDIA LAMBLIA  MOST IMPORTANT

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77
Q

What is Whipple’s disease caused by? How does it present? What does this lead to?

A

CAUSED BY TROPHERYMA WHIPPELII  CAUSED DUODENAL ULCERS AND GASTRITIS
Leads to malabsorption in the small intestine

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78
Q

Atrophic gastritis is caused by

A

Pernicious anaemia

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79
Q

Most common cause of stomach cancer

A

adenocarcinoma

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80
Q

Histopathological sign of gastric adenocarcinoma

A

Signet ring cells

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81
Q

What type of cell is gastric MALToma mediated by?

A

B cells as it is a lymphoma, presents in the stomach

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82
Q

Difference in type of cells between acute and chronic inflam

A

acute - neutrophils
chronic - lymphocytes

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83
Q

What are 100% of duodenal ulcers due to?

A

H.pylori

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84
Q

What cancer can occur in the small intestine? What is it due to?

A

Enteropathy associated T cell lymphoma (EATL), due to untreated coeliac leading to INCREASED EPITHELIAL LYMPHOCYTES

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85
Q

How does gastric MALToma differ from EATL?

A

Gastric MALToma occurs in stomach and is due to B cells, caused by H.Pylori
EATL occurs in small intestine and is due to T cells, caused by untreateed coeliac

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86
Q

Type of tropical enteropathy that causes malabsorpiton and jejunitis

A

Tropical sprue

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87
Q

Histological findings of coeliac

A

Crypt hyperplasia, villous atrophy and increased epithelial lymphocytes

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88
Q

First test to do before checking for antibodies in coeliac, why?

A

Serum IgA levels

Coeliac antibodies are IgA

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89
Q

Where to do biopsy in coeliac? Why?

A

Terminal duodenum as no brunners glands

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90
Q

Antibodies in coeliacl

A

If IgA normal: ANTI- TISSUE TRANSGUTAMINASE AND ANTI-ENDOMYSIAL

If IgA deficient: IgG anti-gliadin

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91
Q

Histological findings of crohns

A
  • SKIP LESIONS WITH COBBLESTONE MUCOSA
  • TRANSMURAL INFLAMMATION
  • NON-CASEATING GRANULOMAS
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92
Q

How does smoking differ in crohn’s and UC?

A

Smoking makes crohn’s much worse, makes UC ebtter

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93
Q

Most common type of IBD

A

US

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94
Q

Histological finding of UC

A
  • INFLAMMATION CONFINED TO MUCOSA
  • SHALLOW ULCERS
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95
Q

Complications of UC

A
  • Toxic megacolon
  • Adenocarcinoma
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96
Q

What extra-intestinal disease is UC associated with?

A

PSC

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97
Q

Areas of regenerating mucosa in UC that project into lumen of th e bowel

A

Pseudopolyps

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98
Q

Treatment of C.Diff

A

Oral vanco

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99
Q

What causes diverticular disease? What does it lead to?

A

Low fibre diet causing high intraluminal pressure which causes outpouchings at weak points in the bowel walls (weak outpouchings are known as TAENIA COLI)

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100
Q

weak outpouchi9ngs in diverticular disease AKA

A

taenia coli

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101
Q

Where do most outpouchings occur in diverticular disease?

A

sigmoid

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102
Q

Difference in presentaiton of volvulus between children and elderly

A

NB: IN CHILDREN  VOLVULUS AFFECTS SMALL BOWL, IN ELDERLY  SIGMOID COLON

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103
Q

Most common cause of colitisd by infection

A
  • VIRAL:
    o CMV
     SEEN IN IMMUNOSUPPRESSED
     OFTEN IBD AS TREATMENT IS IMMUNOSUPPRESSED
  • BACTERIAL
    o SALMONELLA
  • PROTOZOA
    o ENTAMOEBA HISTOLYTICA
  • FUNGAL
    o CANDIDA
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104
Q

Most common type of colorectal cancer, most common location?

A

MAJORITY OF COLORECTAL CANCERS ARE ADENOCARCINOMAS  MOST IN RECTUM

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105
Q

Area most affected by ischaemic colitis

A

ACUTE MESENTERIC ISCHAEMIC OCCURS IN WATERSHED ZONES  SPLENIC FLEXURE AND RECTOSIGMOID

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106
Q

Tumour marker of colorectal cancer

A

Carcinoembryonic antigen (CEA)

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107
Q

Where are enterochromaffin cells msot commonly found? What do they lead to?

A

ENTEROCHROMAFFIN CELLS MOST COMMONLY FOUND IN THE BOWEL, lead to carcinoid tumours

NOTE: therefore most commonly carcinoid tumours develop from the bowel

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108
Q

Carcinoid syndrome triad

A
  • BRONCHOCONSTRICTION
  • FLUSHING
  • DIARRHOEA
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109
Q

What is carcinoid syndrome caused by ?

A

BY EXCESS OF SERETONION (5-HYDROXYTRYPTAMINE (5-HT))

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110
Q

Diagnostic test for carcinid syndrome

A

24 HOUR URINE 5-HYDROXYINDOLEACETIC ACID (5-HIAA)

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111
Q

Treatment of carcinoid sydnrome

A

OCTREOTIDE  SOMATOSTATIN ANALOGUE

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112
Q

Polyp factors that demonstrate a high likelihood of transformation to cancer include:

A
  • Size of polyps
  • Quantity of polyps
  • Proportion of villous component (villous more so than tubular)
    o TUBULAR
    o TUBULOVILLOUS
    o VILLOUS  MOST LIKELY TO BECOME CANCER
  • Dysplasia
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113
Q

Villous or tubular, which ore likely to lead to colorectal cancer?

A

villous

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114
Q

Inheritance of familial adenomatous polyposis? Where is mutation? Presents with?

A
  • AUTOSOMAL DOMINANT
  • APC TUMOUR GENE (on chromosome 5q21)
  • HUNDREDS TO THOUSANDS OF POLYPS
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115
Q

Gardner syndrome

A

FAP WITH EXTRA-INTESTINAL MANIFESTIONS WHICH INCLUDE OSTEOMAS AND DESMOID TUMOURS (BENIGN BONE TUMOURS)

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116
Q

Turcot syndrome

A

FAP WITH BRAIN TUMOURS

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117
Q

Most commonc cause of hereditary colorectal cancer

A

Hereditary nonpolyposis colorectal cancer (HNPCC), AKA lynch syndrome

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118
Q

Inheritance of Lynch syndrome? Where is mutation? Presents with?

A
  • AUTOSOMAL DOMINANT
  • VERY FEW POLYPS  HIGHER CHANCE OF PROGRESSION TO CANCERS
  • DNA REPAIR GENES ERROS
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119
Q

Differences between FAP and HNPCC

A
  • BOTH AUTOSOMAL DOMINANT
  • FAP
    o HUNDREDS TO THOUSANDS OF POLYPS
    o RECTOSIGMOID TUMOURS
  • HNPCC
    o HANDFUL OF POLYPS
    o PROXIMAL TO SPLENIC FLEXURE
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120
Q

What other cancers are Lynch ssyndfrome associated with?

A

ENDOMETRIAL (next most common after colorectal)
Ovarian
small bowel
gastric

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121
Q

Portal triad consists of

A

 Portal vein (posterolateral)
 Hepatic artery (medial)
 Bile ducts (lateral)

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122
Q

Zones of liver

A
  • Zone 1  closest to portal triad (periportal triad)  most oxygenated
    o ZONE AFFECTED FIRST BY TOXIC SUBSTANCES AND VIRAL HEPATITIS
  • Zone 2  mid zone
  • Zone 3  perivenular hepatocytes (most mature and metabolically active)
    o MOST SUSCPETIBLE ZONE TO ISCHAEMIC AS NEAREST TO THE HEPATIC VEIN WHICH IS LEAST OXYGENATED
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123
Q

Which zone in liver is affected first by toxic substances and viral hepatitis?

A
  • Zone 1  closest to portal triad (periportal triad)  most oxygenated
    o ZONE AFFECTED FIRST BY TOXIC SUBSTANCES AND VIRAL HEPATITIS
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124
Q

Which zone in liver is most suspceptible zone to ischaemic? why?

A
  • Zone 3  perivenular hepatocytes (most mature and metabolically active)
    o MOST SUSCPETIBLE ZONE TO ISCHAEMIA AND METABOLIC TOXINS AS NEAREST TO THE HEPATIC VEIN WHICH IS LEAST OXYGENATED
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125
Q

liver macropahge

A

Kuppfer cell

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126
Q

What test determines the proportion of conjugated vs unconjuated bilirubin? How does it work?

A
  • VAN DER BERGH
    o DIRECT REACTION  MEASURES CONJUGATED
    o INDIRECT  MEASURES UNCONJUGATED
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127
Q

What is itching in liver disease caused by? What type of liver disease causes it?

A

ITCHING IN LIVER DISEASE IS CAUSED BY UROBILINOGEN AND STERCOBILINOGEN
IN POST-HEPATIC LIVER DISEASE

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128
Q

Findings in portal hypertension

A
  • DISTENDED VEINS
  • ASCITES
  • SPLENOMEGALY  MOST COMMON FINDING DUE TO EXTRAHEPATIC SHUNTING
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129
Q

Most common finding in portal hypertension

A

Portal hypertension causes splenomegaly, NOT hepatomegaly  hepatomegaly may be seen as a result of hepatitis NOT portal HTN

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130
Q

Histology of acute hepatitis

A

spotty necrosis concentrated around the portal triad

NB: small foci of inflammation and necrosis with inflammatory infiltrates

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131
Q

What viruses can cause acute hepatitis?

A

HEPATITIS A AND E MORE LIKELY TO CAUSE ACUTE HEPATITIS

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132
Q

What viruses CANNOT cause chronic hepatitis?

A

Hep A and E

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133
Q

Which viruses cause chronic hepatitis/

A
  • VIRAL (B,C,D)
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134
Q

Histopathology of chronic hepatitis

A
  • INTERFACE HEPATITIS  PIECEMEAL NECROSIS  CAN’T SEE BORDER BETWEEN PORTAL TRACT AND PARENCHYMA DUE TO INFLAM
  • BRIDGING FIBROSIS FROM PORTAL VEIN TO CENTRAL VEIN  THIS IS A CRITICAL STAGE IN HEPATITIS TO CIRRHOSIS INTERFACE
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135
Q

Summary table of types Hep B antigens

A
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136
Q

Causes of micronodular cirrhosis

A
  • MICRONODULAR <3MM
    o CAUSES
     ALCOHOLIC HEPATITIS
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137
Q

How is cirrhosis classified ?

A

size of regenerating nodules
- MICRONODULAR <3MM
- MACRONODULAR >3MM

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138
Q

What is A1AT deficiency? What can it caues? Histopathological features?

A

 A1AT DEFICIENCY
* Caused by a failure to secrete it
* CAN CAUSE HEPATITS AND PNEUMONITIS (COPD)
* PERIPORTAL RED HYALINE GLOBULES USING PERIODIC ACID SCHIFF STAIN

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139
Q

Most common benign liver lesion

A

hemangioma

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140
Q

Association of hepatic adeoma

A

OCP

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141
Q

Pathophys of cirrhosis, difference between intra and extrahepatic shunting

A

INTRAHEPATIC SHUNTING  WHEN BLOOD GOES THROUGH LIVER BUT DOES NOT CONTACT HEPATOCYTES  NOT FILTERED

EXTRAHEPATIC SHUNTING  WHEN BLOOD BACKLOGS INTO SITES OF PORTOSYTEMIC ANASTOMSES  caused by portal HTN

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142
Q

Histology of alcoholic hepatitis

A
  • HEPATOCYTE BALLOONING AND NECROSIS
  • MALLORY DENK BODIES (FILAMENTS OF COLLAGEN)  STAIN BLUE - TRICHOME
  • PERICELLULAR FIBROSIS

NOTE: Mainly seen in zone 3

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143
Q

Histology of hepatic steatosis

A

fat droplets in hepatocytes

REVERSIBLE

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144
Q

Histology of alcoholic cirrhosis

A

micronodular cirrhosis

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145
Q

Histtology of NAFLD/NASH, what is it similar to?

A

ON HISTOLOGY: SIMILAR TO ALCOHOL HEPATITIS
- HEPATOCYTE BALLOONING AND NECROSIS
- MALLORY DENK BODIES (FILAMENTS OF COLLAGEN)  STAIN BLUE - TRICHOME

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146
Q

What is the most common cause of chronic liver disease in the west?

A

NAFLD/NASH

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147
Q

Who is PBC more common in? Blood findings? Abs? US? Histology?

A

More common in females
Blood findings:
- RAISED ALP
- RAISED CHOLESEROL
GET RAISED ANTI-MITOCHONDRIAL ANTIBODIES IN PBC
ON ULTRASOUND, NO BILE DUCT DILATATION IS SEEN
ON HISTOLOGY, SEE BILE DUCT LOSS WITH GRANULOMAS

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148
Q

Who is PSC more common in? Blood findings? Abs? US? On ERCP? Histology?

A

More common in males
Inflam and obliterative fibrosis of BOTH intrahepatic and extrahepatic ducts
MAIN ASSOCIATION IS WITH UC
Blood findings:
- HIGH ALP
GET RAISED P-ANCA IN PSC
ON ULTRASOUND, SEE BILE DUCT DILATATION (DON’T GET THIS IN PBC)
ON ERCP  BEADING OF BILE DUCTS  ‘BEAD ON STRINGS’
ON HISTOLOGY  ONION SKINNING FIBROSIS  ONCENTRIC FIBROSIS

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149
Q

Main association of PSC

A

UC

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150
Q

PSC is a major risk factor for

A

cholangiocarcinoma

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151
Q

Types of AIH and their respective antibodies

A
  • TYPE 1  ANTI-SMA, ANA
  • TYPE 2  ANTI-LKM (LIVER, KIDNEY, MICROSOMAL)
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152
Q

Inheritance of haemochromatosis? Gene affected? Stain used?

A

AUTOSOMAL RECESSIVE
HFE GENE ON CHROMOSOME 6 AFFECTED
STAIN USED IS PRUSSIAN BLUE

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153
Q

Complications of haemochromatosis

A

haemochromatosis (HaemoChromatosis Can Cause Deposits Anywhere)
o Hypogonadism
o Cancer (hepatocellular)
o Cirrhosis
o Cardiomyopathy
o Diabetes mellitus
o Arthropathy

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154
Q

Inheritance of WIlsons? Gene affected? Blood finding? Stain done? Management?

A

AUTOSOMAL RECESSIVE
THE ATP7B GENE ON CHROMOSOME 13 IS AFFECTED
SEE LOW CAERUPLASMIN AND COPPER ON BLOODS
RHODANINE IS THE STAIN DONE FOR COPPER
NB: Treated with Zinc and Trientine (copper chelating agent)

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155
Q

Presentation of wilsons

A

Liver cirrhosis that presents in kids

Neuro signs

Kaiser Fleischer rings

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156
Q

Most common liver malignancy

A

Secondary mets from GI TRACT, BREAST OR LUNG

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157
Q

Tumour marker of hepatocellular carcinoma

A

AFP

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158
Q

causes of hepatic granulomas

A

PBC, drugs, TB, sarcoid

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159
Q

Most common tyype of gallstone

A

Cholesterol - radiolucent

Different from pigment stones which are radioopaque

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160
Q

Histology of chronic cholecystitis

A
  • DIVERTICULA OUTPOUCHING FROM GALLBLADDER – ROKITANSKY-ASCHKOFF SINUSES
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161
Q

Most common cause of chronic cholecystitis and gallbladder cancer

A

gallstones

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162
Q

Most common type of gallbladder cancer

A

adenocarcinomas

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163
Q

RFs for gallsotones

A

Fair, fat, femal,e fertile, forty

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164
Q

Most common cause of acute pancreatitis, second most common/

A

Gallstones, Ethanol

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165
Q

Causes of acute pancreatitis

A

THINK: I GET SMASHED

  • IDIOPATHIC
  • GALLSTONES - MOST COMMON
  • ETHANOL – 2ND MOST COMMON
  • TRAUMA
  • STEROIDS
  • MUMPS
  • AID
  • SCORPION STING
  • HYPERCALCAEMIA
  • HYPERLIPIDEMIA
  • ERCP
  • DRUGS  THIAZIDES
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166
Q

Pathogenesis of acute pancreatitis

A

Positive feedback of enzyme activation causing acinar necrosis causing further enzyme release and activation
Damage ranges from stromal oedema to haemorrhagic necrosis
Lipase release + pancreas tissue necrosis = saponification

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167
Q

Complications of acute pancreatitsi

A
  • Pseudocyst
  • Abscess
  • Shock
  • Chronic pancreatitis
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168
Q

Most common cause of chronic pancreatitis

A

Alcohol

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169
Q

Genetic conditions that can cause chronic pancreatitsi

A

Haemochromatosis
CF

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170
Q

Histology of chronic pancreatitsi

A
  • PARENCHYMAL FIBROSIS WITH LOSS OF PARENCHYMA
  • DUCT STRICTURE WITH CALCIFIED STONES
  • LOSE ACINAR CELLS FIRST
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171
Q

What antibodies seen in AI pancreatitis

A

IGG4 POSITIVE PLASMA CELLS

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172
Q

Histology of pancreatic carcinomas

A
  • Adenocarcinomas with mucin producing glands set in desmoplastic stroma
  • Gritty and grey macroscopically
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173
Q

Most common type of pancreatic cancer

A

Ductal adenocarcinoma

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174
Q

Most common secretory pancreatic tumour

A

insulinomat

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175
Q

most common site of pancreatic adenocarcinoma

A

Head of the pancreas

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176
Q

What is trousseau syndrome? What is it seen in?

A

OFTEN GET TROUSSEAU SYNDROME IN PANCREATIC ADENOCARCINOMA  SUPERFICIAL THROMBOPHLEBITIS  EARLY SIGN  ALSO SEEN IN GASTRIC AND LUNG

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177
Q

Where are neurodencorine tumours found?

A

FOUND IN TAIL OF PANCREAS, UNLIKE ADENOCARCINOMAS  FOUND IN HEAD

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178
Q

How does insuloma present?

A

hypoglycaemic attacks

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179
Q

How does gastrinoma present?

A

WITH ZOLLINGER ELLISON SYNDROME HIGH ACID OUTPUT  RECURRENT ULCERATION OF STOMACH  TYPICALLY FOUND IN PANCREAS OR DUODENUM

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180
Q

Triad of Zollinger Ellison syndrome

A

(1) gastric acid hypersecretion, sustained by (2) fasting serum hypergastrinemia causing (3) peptic ulcer disease and diarrhea

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181
Q

How does VIPoma present?

A

DIARRHOEA  VIP IS VASOACTIVE INTESTINAL PEPTIDE

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182
Q

How does glucagonoma present?

A

NECROLYTIC MIGRATING ERYTHEMA

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183
Q

Main stain for NE tumours? Alternatives?

A

MAIN STAIN FOR NE TUMOURS IS CHROMOGRANIN
CAN ALSO DO SYNAPTOPHYSIN. CD56 AND INDIVIDUAL HORMOMES (E.G. GASTRIN, INSULIN)

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184
Q

What are neurodenocrine tumours associated with?

A

MEN1

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185
Q

Triad of nephrotic syndrome

A

Peripheral oedema
proteinuria
low serum albumin

THINK: PPL

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186
Q

Important protein lost in nephrotic syndrome

A

Antithrombin III

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187
Q

What are all nephrotic syndromes treated with?

A

Steroids

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188
Q

Causes and histology of nephrotic syndrome

A

o MINIMAL CHANGE DISEASE
 HISTOLOGY  EFFACEMENT OF PODOCYTE FOOT PROCESSES

o FOCAL SEGMENTAL GLOMERULOSCLEROSIS (FSGS)
 HISTOLOGY  GLOMERULI WHICH ARE SCARRED

o MEMBRANOUS GLOMERULONEPHRITIS
 HISTOLOGY  SUBEPITHELIAL DEPOSITION OF IMMUN DEPOSITS

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189
Q

What is seen in the urine of nephrotic syndrome?

A

Fatty casts

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190
Q

Most common cause of nephropathy in kids, finding on electron microscopy? Management?

A

Minimal change disease, loss of foot processes, responds very well to steroids

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191
Q

Most common cause of nephropathy in adults

A

Membranous glomerulonpphropathy

192
Q

Histology of FSGS

A

FOCAL + SEGMENTAL SCARRING

193
Q

Histology of membranous glomerulonephropathy

A

. GET DIFFUSE BASEMENT MEMBRANE THICKNENING AND SPIKEY IMMUNE COMPLEXES ACROSS ALL OF BASEMENT MEMBRANE

194
Q

What is membranous glomerulonephropathy associated with?

A

SLE and anti-phospholipase A2 ABs.

195
Q

Most common cause of chronic renal failure

A

Diabetes, see Kimmelstiel Wilson nodules

196
Q

Most common cause of nodular glomerulosclerosis

197
Q

Histological progression of diabetic nephropathy

A
  • Stage 1- thickened BM on EM
  • Stage 2- increase in mesangial matrix but no nodules
  • Stage 3- nodular lesions- kimmelstiel wilson
  • Stage 4- advanced nodular glomerulosclerosis
198
Q

Pathophys of amyloidosis

A

Pathophysiology – XS proteins clump together to form beta sheets which make fibrils  deposit in EC space of tissues and cause damage

199
Q

Types of amyloidosis

A

AL amyloidosis – Amyloid ‘light’ as excess light chains e.g. MM
AA amyloidosis – chronic systemic inflam responses to infections, cancers and AI conditions  XS serum amyloid A which forms amyloid deposits in tissues

200
Q

Most common form of familial amyloidosis, where is amyloid typically deposited?

A

FAMILIAL MEDITERRANEAN FEVER
Amyloid deposition in FMF is predominantly in the KIDNEY

201
Q

What type of amyloidosis can occur in chronic renal failure patients? What protein is deposited?

A

Haemodialysis associated amyloidosis can occur in chronic renal failure patients, ESPECIALLY those on peritoneal dialysis
In this case, the protein deposited is BETA-2 MICROGLOBULIN

202
Q

Stain for amyloidosis, findings?

A

AMYLOID IS CONGO RED STAIN POSITIVE, +ve FINDING SHOWS APPLE GREEN BIREFRINGENCE IN POLARISED LIGHT

NOTE: Negative finding is pink/red

203
Q

Most common presentation of amyloidosis

A

npehrotic syndromc

204
Q

Histology of amyloidosis

A

DEPOSITION OF EXTRACELLULAR PROTEINACEOUS MATERIAL EXHIBITING BETA SHEET STRUCTURE

205
Q

Triad of nephritic syndrome

A

Hypertension Haematuria
Peripheral oedema

THINK: HHP

206
Q

What is seen in urine of nephriti syndrome

A

red cell casts

207
Q

most common glonerulonephritis in the world

A

IgA nephropathy

208
Q

Immunofluorescence of IgA nephropathy

A

IgA deposits in mesangium

209
Q

Important pattern of IgA neprhopathy

A

Typically 1-2 days after group A step  think IgA  acute

210
Q

Prognosis of IgA nephropathy

A

third get better, third get CKD, third need dialysis

211
Q

Difference between IgA nephropathy and post-streptococcal glomerulonephritis

A

BIG DIFF BETWEEN IGA AND POST STREP IS TIMING  IGA IS ACUTE (1-2 DAYS), POST-STREP IS WEEKS AFTER. IgA is deposited in mesangium in IgA nephropathy, IgG is deposited in basement membrane in post-strep glomerulonephropathy.

212
Q

immunofluorescence of post streptococcal glomeruloneprhtisi

A

Granular IgG deposits in basement membrane

213
Q

What is raised on blood findings in post-streptococcal glomerulonephritis?

A

Raised anti-streptolysin O titre, reduced C3

214
Q

Histology of acute crescenteric (rapidly progressive) glomerulonephritsi

A
  • CRESCENTS FROM PROLIFERATION OF CELLS IN BOWMANS SPACE SEEN ON LIGHT MICROSCOPY OF ALL
215
Q

What is rapidly progressive glomerulonephritis characterised by?

A

SEVERITY AND PRESENCE OF CRESCENTS (MACROPHAGES IN BOWMAN’S)

216
Q

Cauess of acute crescenteric glomerulonephritis

A
  • Anti-GBM disease (Goodpasture’s)
  • Immune complexes
  • Pauci-immune
    o ANTI-NEUTROPHIL CYTOPLASM ANTIBODIES PRESENT

NOTE: cANCA seen in polyangiitis with granulomatosis against proteinase 3, pANCA seen in microscopic polyangiitis against myeloperoxidase

217
Q

Summary slide showing types of rapidly progressive glomerulonephritsi

218
Q

What Abs in goodpasture’s syndrome? Against what?

A

Anti-glomerular basement membrane against COL4-A3 (COLLAGEN TYPE IV)

219
Q

Difference between presentation of goodpasture’s and granulomatosis with polyangitis

A

: in goodpasture’s get pulmonary haemorrhages and NO NOSE INOLVEMENT unlike granulomatosis with polyangiitis

220
Q

Histology of goodpasture’s

A

LINEAR DEPOSITION OF IGG ON GBM

NOTE: Crescents on light microscopy

221
Q

Histology of immune complex glomerulonpehritis

A

Bumpy depositon of immune complexes in GBM or mesangium

NOTE: Crescents seen on light microscopy

222
Q

Histology of pauci-immune/ANCA associated glomerulonpehritis

A

no/scanty immune complexes

NOTE: Crescents on light microscopy

223
Q

How to differ between GPA and EGPA

A

: GPA  cavitating lesions, saddle shaped nose and glomerulonephritis - cANCA
eGPA  asthma, chronic rhinosinusitis and glomerulonephritis with same features as GPA (also eosinophils in blood - pANCA

224
Q

HUS triad

A

haemolytic anaemia (MAHA), acute renal failure, thrombocytopenia

225
Q

TTP pentad

A

haemolytic anaemia (MAHA), acute renal failure, thrombocytopenia, fever, neurlogic Sx

226
Q

renal deisease with deafness and ocular damage

A

alport syndrome

227
Q

Triad of alport syndrome

A

X linked gene causing problem with type IV collagen

228
Q

Triad of alprot syndrome

A

Npephritic syndrome, bilateral sensorineural deafness, lens dislocations

229
Q

Inheritance of benign familial haematuria? On histology?

A

AD gene causing problem with type 4 collagen, thin basement membrane

230
Q

Most common renal cause of AKI

A
  • ACUTE TUBULAR NECROSIS
231
Q

Causes of acute tubulointerstitial nephritis? Histology?

A

o DRUGS:
 ABX (e.g. gentamicin)
 PPIS
 NSAIDS
 DIURETICS

ATIN HISTOLOGY:
- EOSINIOPHILS  DRUG HYPERSENSITIVITY
- GRANULOMAS

232
Q

What is found in urine of acute tubular necrosis?

A

Brown casts, and epithelial casts

233
Q

What is seen in urine of acute interstitial nephritis?

A

White cell casts, or white cells in urine with no infection

NOTE: Think of it as an allergic reaction

234
Q

Most common causes of acute interstitial nephritis

A

Penicillins, allopurinol, NSAIDs

235
Q

Causative agent of HUS

A

E.coli 0157:H7

236
Q

What enzyme deficiecny in TTP

A

ADAMTS13 –> cleaves vwf, so left with platelet aggregation and fibrin depositon

237
Q

How many stages of lupus nephritis? how does it present?

A

6 stages

Silent –> nephrotic –> nephritis

238
Q

How is myeloma kidney different to amyloidosis causing nephrotic syndrome?

A

Myrloma kidney causes cast npehorpathy –> more common –> due to light chain deposition causing tubulointerstitial disease

80% of AL is due to multiple myeloma, but this causes light chain depositon in glomerulus

239
Q

Inheritance of PCKD? Mutation? Presentiation?

A

AD, due to mutation in PKD gene encoding polycystin-1

CAues haematuria and kidney failure

Extra renal manifestations are liver cysts (most common) and berry aneurysms (SAH)ost c

240
Q

Most common exta renal manifestation of PCKD

A

Liver cysts

NOTE: can also cause berry aneurysms

241
Q

Second most common childhood malignancy after ALL

A

Nephroblastoma

242
Q

oy of nephroblastoma

A

small round blue cells on microscopic appearance

243
Q

Most common type of renal cell carcinoma, give two other types

A
  • Clear cell (70%)
  • Papillary (15%)
  • Chromophobe (5%)

NOTE: Macroscopic appearance:
- Clear cell  golden yellow with haemorrhagic areas
- Papillary – friable brown
- Chromophobe  solid brown
Microscopic appearance:
- Clear cell  nests of epithelium with CLEAR (TRANSPARENT) CYTOPLASM
- Papillary  papillary tubopapillary growth patter OVER 5MM
- Chromophobe  sheets of large cells WITH DISTINCT CELL BORDERS

244
Q

Most common type of bladder cancer

A

transitional cell carcinoma

245
Q

What is squamoos cell carcinoma of bladder caused by?

A

SCHISTOMIASIS + CHRONIC CYSTITIS

246
Q

Most common form of prostate cancer in over 50s

A

ADENOCCARCINOMA  MOST COMMON MALIGNANT TUMOUR IN MEN  25% OF ALL MALE CANCERS, 1 IN 8 WILL GET IT

247
Q

precursor of prostate cancers

A

PROSTATIC INTRAEPITHELIAL NEOPLASIA (PIN)

248
Q

painless frank haematuria

A

bladder cancer

249
Q

Most common type of testicular cancer

250
Q

Most common manlignant tumour in men

251
Q

How to calculate gleason score?

A

The Gleason score is calculated by adding together the two grades of cancer cells that make up the largest areas of the biopsied tissue sample.

252
Q

most common tupe of renal stone, caused by?

A

Calcium oxalate, hypercalcaemiaW

253
Q

Composition of renal stone from proteus infection, caused by?

A
  • MAGENESIUM, AMMONIUM, PHOSPHATE (MAP/STRUVITE)  PROTEUS INFECTION
    o GIVE STAGHORN CALICULI

 CAUSED BY UREASE (ENZYME RELEASED BY BACTERIA)

254
Q

What causes uric acid stones?

A

Gout, Tumour Lysis syndrome

255
Q

How to remember stages of CKD?

A

NB: Think of it like a clock, with 120 at 12, 90 at 3, 60 at 6, 30 at 9. Means that anywhere between 90-120 is 1. Anywhere between 60-90 is 2. Anywhere between 30-60 is 3 (A+B) etc.

256
Q

Most common causes of CKD

A

Diabetes and HTN, diabetes is more common

257
Q

How does HPV transform cells? What proteins doe s it produce?

A
  • Producing 2 proteins which inactivate tumour suppressor genes:
    o E6  inactivates p53
    o E7  inactivates Rb (Retinoblastoma)
258
Q

What protein is associated with serous endometrial carcinoma n 90% of casse?

259
Q

Types of VIN, how to differentiate?

A

Usual type:
HPV 16/18
Smoking

Differentiated type:
Lichen sclerosis
PROGRESSION TO SCC

260
Q

Most common type of vulval carcinoma? Who does it present in?

A

SCC, presents in older women, associated with Lichen sclerosis

261
Q

Who does vulval adenocarcinoma present in?

A

Teenagers, associated with COCP use

MOST COMMON TYPE IS SCC - older women, lichen sclerosis

262
Q

How to differentiate between vulval SCC or adenocarcinoma?

A

SCC - older women, lichen sclerosis, most common
Adenocarcinom - teenagers, COCP

263
Q

Actauly pathological process of CIN

264
Q

What occurs in CIN?

A

Clomunar epithelium of endocervix becoems squamous (opposite to barrets)

265
Q

How to grade CIN? WHat stain is used?

A

CIN 1 (low grade) – up to one third of the thickness of the lining covering the cervix has abnormal cells. CIN 2 (high grade) – up to two thirds of the thickness of the lining covering the cervix has abnormal cells. CIN 3 (high grade) – the full thickness of the lining covering the cervix has abnormal cells.

Stain used is H&E

266
Q

Process of CIN to cancer

A

. Dysplasia  when cells are proliferating to create a disorganised structure. Neoplasia  new cell formation from dysplasia, continuation from dysplasia.
Cancer  INVASION OF BASEMENT MEMBRANE

267
Q

Most common type of cervical cancer

A

Squamous cell cancer

268
Q

Biggest RFs for SCC of cervix

A

HPV 16+18, COCP, smoking

269
Q

Most common type of end0ometrial cancer

A

Adenocarcinoma

270
Q

What is a fibroid? Who does it present in? Features?

A

Benign tumour of myometrium
Common 40% in women over 40, afro-carribean

Oestrogen dependent growth - enlarge during pregnancy, regress during menopause

271
Q

Fibroids aka

272
Q

What is seen on laparaoscopy of endometriosis?

A

Power burns, chocolate cysts, endometriomas

273
Q

Histology of endometriosis

A

Powder burns

274
Q

Subtypes of adenocarcinomas (most common type of endometrial carcinomas) - LEARN THIS SLIDE

275
Q

What is Fitz-Hugh Curtis syndrome due to? How does it present?

A

Fitx-Hugh Curtis syndrome due to PID which causes adhesions of liver capsue to peritoneum  peri-hepatic lesions  “violin strings”

276
Q

Types of epithelial ovarian tumours

A
  • EPITHELIAL (SURFACE-DERIVED) (THINK: SM EC)
    o SEROUS (Benign)  most common epithelial, columnar epithelium, psammoma bodies (round microscopic calcific collections)
    o MUCINOUS (Benign)  mucin secreting cells
    o ENDOMETRIOID (Malignant)  co-exist with endometrial cancer/endometriosis, CA125, tubular glands
    o CLEAR CELL (malignant)  ASx with endometrioma, clear cells, hobnail appearance
277
Q

Most common epithelial ovarian tumour

A

o SEROUS (Benign)  most common epithelial, columnar epithelium, psammoma bodies (round microscopic calcific collections)

278
Q

What type of ovarian tumour dco-exists with endometrial cancer/endometriosis?

A

Endometroid (malignant)

279
Q

What type of ovarian tumour is associatied with endometrioma?

A

o CLEAR CELL (malignant)  ASx with endometrioma, clear cells, hobnail appearance

280
Q

Histology of granulosa-theca cells

A

Cal-exner bodies

281
Q

What type of ovarian tumour secretes androgens?

A

Sertoli-leydig

282
Q

Most common benign ovarian tumour in under 30? Associated with?

A

o DERMOID CYST (Mature cystic teratoma) (Benign)  MOST COMON BENIGN OVARIAN IN UNDER 30  ASx with torsion, ROKITANSKY PROTUBERANCE

283
Q

Most common malignant ovarian tumour in younger women?

A

dysgerminoma

284
Q

What type of ovarian tumour secretes HCG?

A

Choriocarcinoma

285
Q

Most common type of cyst

A

Follicular, commonly regress after severeal menstrual cysts

286
Q

When is corpus lutem most common? What is it most likely to present with?

A

Corpus Lutem cyst most likely presents with intraperitoneal bleeds. COMMON IN EARLY PREGNANCE.

287
Q

Rokitansky protuerberance

A

Dermoid cyst

288
Q

Histology of serous cystadenoma

A

psamammoma bodies, caused by p53 mutation (E6 protein)

289
Q

What are mucinous cystadenomas associated with?

A

Pseudomyxoma peritonei

290
Q

What type of ovarian tumours have clear cells with clear cytoplasm and a hobnail appearance on histology?

A

Clear cell ovarian tumours

291
Q

What mutation causes mucinous cystaenomas?

A

KRAS mutation

292
Q

Difference between serous cystadenoma and mucinous cystadenoma in terms of mutations

A

P53 MUTATION CAUSES SEROUS CYSTADENOMA, KRAS MUTATION CAUSES MUCINOUS OVARIAN CYSTADENOMA

293
Q

Difference between male and female teratomas

A

MALE TERATOMAS ARE NROMALLY MALIGNANT, UNLIKE FEMALES WHICH ARE NORMALLY BENIGN

294
Q

What do immature teratomas secrete?

295
Q

What type of ovarian cancer is seen in TUrners? How does it present?

A

DYSGERMINOMA IS SEEN IN TURNERS, PRESENTS WITH RAISED HCG AND LDH

296
Q

Relationship between dysgerminoma and seminoma

A

Dysgerminoma is female counterpart to testicular seminoma (both most common for respective sex0

297
Q

What hormone do granulosa theca cells produce?

298
Q

What is seen on histology of Krukenberg tumours?

A

Mucin producing signet ring cells

299
Q

Tumour markers produced by germ cell testicular tumours

A
  • AFP
  • BHCG
  • LDH
300
Q

RFs for testicular cancer

A
  • UNDESCENDED TESTICLES
  • KLEINEFELTERS
301
Q

Triple assessment summary

A

NB: Mammogram not very useful when breast is firmer (at a younger age). FNA is when you put needle into offending area and take a biopsy  used for cystic leisons. Core biopsy is when you take a “punch” out and biopsy that  solid lesions

302
Q

On histology of mastitis

A

abundance of neutrophils

303
Q

Managemnt of mastitis

A

Conservative for first 24 hours with warm compress, analgesia and continue breastfeeding

No improvement in 24 hours - oral ABx - Fluclox

304
Q

Most common organism for mastritis

A

Staph aureus

305
Q

Breast abscess presents with? Management?

A

Fluctuant swelling, swinging fevers. Give IV Abx and incision and draiange

306
Q

Most common breast lesion that presents with discharge

A

papilloma

duct ectasia second most common

307
Q

a sub/peri-areolar mass that presens in smokers with yellow-green discharge

A

Duct ectasia

308
Q

What is fat necrosis often preceded by?

A

Trauma, radiotherapy

309
Q

A breast mass that is unilateral and occurred after trauma

A

fat necrosis

310
Q

Most common benign breast condition

A

Fibroadenoma

311
Q

Most common breast lump in women 20-40

A

fibroadenoma

312
Q

Single 1-5cm, unilateral, spherical, well dermarcated, firm/rubbery. painless, mobile breast mass AKA breast mouse

A

Fibroadenoma

313
Q

Peripheral intraductal papilloma presents with

A

subareolar mass

314
Q

central intraductal paipilloma presents with

A

blood or clear nipple discharge

315
Q

Difference between discharge in duct ectasia and papilloma

A

NB: GREEN/YELLOW DISCHARGE  DUCT ECTASIA, BLOOD-STAINED DISCHARGE  INTRADUCTAL PAPILLOMA/CANCER. SMALL BUT IUMPORTANT RISK OF PROGRESSING TO DUCTAL CARCINOMA IN SITU AND THEREFORE INVASIVE CARCINOMA  USUALLY EXCISED.

316
Q

central, fibrous, stellate area

A

Radial scar

317
Q

What is radial scar often confused for on mammography?

318
Q

What is phyllodes tumour structurally similar to?

A

Fibroadenomas - but malignant version

319
Q

Artichoke appearance, frond-like, branching

A

Phyllodes (means leaf) tumour

320
Q

Lumpiness in breasts which changes according to cycle

A

Fibrocystic breast disease

321
Q

Well dermarcated, fluctuant, transilluminable, clear nipple discharge

A

fibrocystic disease

322
Q

RED FLAGS FOR FIBROCYSTIC DISEASE

A

FNA is blood stained, core biopsy reveals complex chystic contents

323
Q

Summary table for breast conditions

324
Q

What cancers does BRCA increase the risk of?

A

BRCA INCREASES THE RISK OF: (THINK: BOPP)
- BREAST CANCER
- OVARIAN CANCER
- PANCREATIC CANCER
- PROSTATE CANCER

325
Q

How does pagest disease present? What can it develop from? What to look for on mammography?

A

ECZEMA OF NIPPLE THEN AREOLA  NEVER GET ECZEMA ON NIPPLE NORMALLY  CAN DEVELOP FROM DUCTAL CARCINOMA IN SITU

LOOKING FOR MICROCALCIFICATIONS

326
Q

Where is lobular carcinoma in situ detected? Why? What does it lack?

A

ALWAYS DETECTED ON BIOPSY AS NO MICROCALCIFICATION
NB: LACK PROTEIN E-CADHERIN

327
Q

What does ductal carcinoma in situ appear as on mammogram? What can it lead to?

A

APPEAR AS AREAS OF MICROCALCIFICATIONS ON MAMMOGRAM  TYPICALLY FOUND ON SCREENING UNLESS GET PAGETS
NB: PAGETS CAN DEVELOP FROM DUCTAL

328
Q

Summary slide showing different types of breast cancers

329
Q

What receptors are tested for in breast cancer? Why?

A

HER2 RECEPTORS ARE TESTED FOR IN BREAST CANCER  HERCEPTIN/TRASTUZUMAB USED TO TREAT (MONOCLONAL Ig TO HER2)  HERCEPTIN HAS A DIRECT TOXIC AFFECT ON MYOCARDIUM SO MUST MONITOR LVEF

330
Q

What receptors have the best prognosis in breast cancer? Why?

A

ER/PR HAVE BEST PROGNOSIS AS RESPONSE VERY WELL TO TAMOXIFEN  TAMOXIFEN IS USED TO TREAT ER/PR POSITIVE CANCER

331
Q

What mutation is asssociated with male breast canceers?

A

BRCA2 IS ASSOCIATED WITH MALE BREAST CANCERS

332
Q

Most significant prognostic factor in breast cancer

A

AXILLARY LN INVOLVEMENT  BEST PROGNOSTIC FACTOR IS NO INVASION OF LYMPH NODES

333
Q

Most common cause of ischaemic stroke

A

Atherosclerosis

334
Q

Most common cause of haemorrhagic stroke

335
Q

Difference between stroke and TIA

A

Stroke lasts more than 24 hours, TIA resolves within 24 hours

336
Q

Type of necrosis in stroke

A

Liquefactive, both ischaemic and haemorrhagic cause it

337
Q

Most common cause of stroke

A

Ischaemic, due to atherosclerosis

338
Q

Difference between ischaemia and infarction

A

Ischaemia - lack of o2 supply to tissue
Infarction - death of tissue due to lack of o2 supply

339
Q

MOST COMMON SITE OF INTRA-PARENCHYMAL HAEMORRHAGE? Cause?

A

MOST COMMON SITE OF INTRA-PARENCHYMAL HAEMORRHAGE IS IN THE BASAL GANGLIA

CAUSE IN OVER 50% OF CASES IS HYPERTENSION

340
Q

Cause of SAH? Most common site?

A

CAUSED BY BERRY ANEURYSM IN CIRCLE OF WILLIS
- MOST COMMON SITE OF BERRY ANEURYSM IS THE INTERNAL CAROTID ARTERY BIFURCATION

341
Q

What causes prinzmetal angina?

A

coronary artery spasms

342
Q

hypoattenuation around the circle of willis

A

Haemorrhagic stroke

343
Q

What kidney condition is association with ruptured berry aneurysms?

A

PCKD - AD - defect in polycystin 1

344
Q

Initial investigation for haemorrhagic stroke? If _ve?

A

Non-contrast CT head, if neg do LP at 12 hours to look for xanthochromia and oxyhaemoflobin

345
Q

Difference between extradural and subdural haemorrhage

346
Q

Fracture of pterio caused by trauma, rupture of middle meningeal artery and lemon shape on CT

A

extradural haemorrhage

347
Q

Rupture of bridging vein in an elderly aclholicc on anti coag with a banana shape on CT

A

Subdural haemorrahage

348
Q

Common sign on examination of skull fracture

A

Straw coloured otorrhoea and rhinorrhoea

349
Q

BATTLES SIGN

A

BLEEDING BEHIND EAR SHOWING SKULL BASE FRACTURE

350
Q

CONTUSIONS

A

BRAIN IN COLLISION WITH SKULL AND GET SURFACE BRUISING  IF PIA MATER TORN DURING THIS COLLISION  BECOMES A LACERATION, NOT CONTUSION

351
Q

CHRONIC TRAUMATIC ENCEPHALOPATHY

A

EFFECTS ON BRAIN OF REPEATED TRAUMA TO HEAD

352
Q

Straw coloured fluid from nose or ears

A

traumatic brain inury

353
Q

Summary slide for traumatic brain injury

354
Q

Most common primary brain tumour in adults

A

Meningioma

355
Q

Most common form of brain tumour

A

Seccondary - from lung, skin and breast

356
Q

Most common brain tumour in children

A

Pilocystic astrocytoma

357
Q

Second most common brain tumour in children

A

Medulloblastoma

358
Q

Histology of pilocystic astrocytoma

A
  • PILOID HAIRY CELLS
  • ROSENTHAL FIBRES
359
Q

Mutation in what for pilocystic astrocytoma

360
Q

MRI fidnings of pilocytic astrocytoma

A
  • WELL CIRCUMCISED
  • CYSTIC
  • ENHANCING LESION
  • FOUND IN CEREBELLUM
361
Q

Summary slide of astrocytomas

362
Q

Summary slide of brain cancer buzzworlds

363
Q

Most common benign CNS tumour

A

Meningioma - psammoma bodies

364
Q

5 A’s of alzheimer

A

Amnesia
Apreaxia
Aphasia
Agnosia
Anomia

365
Q

Most common dementia

A

Alzheimer’s

366
Q

Order of prevalence of dementia

A

Alzheimer’s
Vascular
Lewy body
Frontotemporal

367
Q

Imaging of AD

A
  • CORTICAL ATROPHY
  • WIDENED VENTRICLES
  • NARROWED GYRI
  • WIDENED SULCI
368
Q

Aetiology of Alzheimer’s

A

Accumulation of beta-amyloid plaques
Hyperphophorylation of TAu

369
Q

Histology of lewy body demtnia

A
  • ALPHA SYNUCLEIN
  • UBIQUITIN
  • LEWY BODIES
370
Q

Waht staging for alzheimer’s

A

BRAAK staging

371
Q

Histology of pick’s disease

A
  • FRONTO-TEMPORAL ATROPHY
  • MARKED GLIOSIS AND NEURONAL LOSS
  • BALLOON NEURONES
  • TAU POSTIVE PICK BODIES
    NB: TAU IS STAINED POSITIVELY IN PICKS DISEASE AND IS LINKED TO CHROMOSOME 17:
372
Q

Dementia Buzzwords

A

NB: vascular  atherosclerotic build up of plaques  progeressive deterioration in cognition. Pick’s disease (frontotemporal dementia) can lead to extremities of weird Sx  gambling, inappropriate sexual advances.

373
Q

What physiological change ioccurs in parkinsons?

A

Reduced stimulation of cortex by basal ganglia due to dopaminergic loss in substantia nigra

374
Q

How does multiple system atrophy differ to parkinsons?

A

DUE TO ALPHA YNUCLEIN IN THE GLIAL CELLS NOT NEURONES

375
Q

What do you stain for in Parkinson’s

A

alpha synuclein

376
Q

Summary slide showing parkinsonian Sx

A

NB: MSA  postural hypotension, PSP  diplopia when they look up, may be described as issues with cranial nerve in exam qns

377
Q

Pathophys of parkinsons

378
Q

Types of hydrocephalus? How do they differ?

A

NON-COMMUNICATING  OBSTRUCTION IN PASSAGE OF FLUID
- MOST COMMON SITE OF OBSTRUCTION IS IN THE CEREBRAL AQUEDUCT

COMMUNICATING  CSF CAN STILL FLOW BETWEEN THE VENTRICLES, WHICH REMAIN OPEN

379
Q

Most common site of obstruction in non-communicating hydrocephalus

A

Cerebral aqueduct

380
Q

How do both types of hydrocephalus differ in presentation?

A

Both types occur due to too much CSF in ventricles.

Communicating  obstruction in outflow of CSF  in neonates.

Non-communicating  reduced absorption of CSF into veins  meningitis (if get fibrosis of meninges)

381
Q

Worst type of herniation

A

tonsillar worst one  get cerebellum impinging on brainstem  can cause coma and arrest.

382
Q

What are the two types of cerebral oedema? How do they differ?

A

2 types of cerebral oedema  vasogenic and cycotoxic. Vasogenic  disruption in interface between blood & brain  too much fluid coming in, but can’t remove from brain parenchyma into blood. Cytotoxic  damage due to toxins or ischaemia  brain tissue can die and swell  oedema

383
Q

TARGET SIGN ON IMAGING IN BRAIN

A

cavernous angioma

384
Q

what is calcium stored in the bone as?

A

calcium hydroxyapatite

385
Q

Types of bones

A
  • CORTICAL
    o LONG BONES
  • CANCELLOUS
    o VERTEBRAE AND PEVLIC
386
Q

Gold standard site for bone histology

A

Iliac crest

387
Q

X-ray features of osteoarthritis

A

Loss of joint space
Osteophytes
Subchondral sclerosis
Subchondral cysts

388
Q

Histology of RA

389
Q

What is the genetic predisposition of RA? Pathophys?

390
Q

Pathophys of osteomyelitis

391
Q

How do gout and pseudogout differ on imaging?

392
Q

How to differentiate gout and pseudgout crystals

A

GOUT CRYSTALS  NEGATIVE BIREFRINGENET NEEDLE SHAPED MONOSODIUM URATE CRYSTALS

PSEUDOGOUT CRYSTALS  RHOMBOID SHAPED AND POSITIVELY BIREFRINGENT:

393
Q

Summary slide for fibrous dysplasia

394
Q

What is fibrous dysplasia associated with? What is the triad?

A

ASSOCIATED WITH MCCCUNE-ALBRIGHT SYNDROME (IF POLYOSTOTIC)  TRIAD OF:
- FIBROUS DYSPLASIA
- CAFÉ AU LAIT SPOTS
- PRECCOIOUS PUBERTY

395
Q

X ray of fibrous dysplasia

A
  • SOAP BUBBLE OSTEOLYSIS AND SHEPHERDS CROOK DEFORMITY IF IN PROXIMAL FEMUR
396
Q

Histology of fibrous dysplasia

A

CHINESE LETTERES  MISSHAPEN BONE TRABECULAE

397
Q

histology and Xray findings of osteochondroma

A

ON HISTOLOGY  BONY PROTUBERANCE CAPPED IN CARTILAGE (THINK: OSTEO(BONE) CHOND(CARTILAGE) ROMA))

ON X-RAY  MUSHROOM CAP ON BONE

398
Q

Bone tumour with cotton wool or popocorn calcifications at the ends

A

endochromas

399
Q

Most common bone tumours

400
Q

Most common primary bone sarcoma

A

osteosarcomaX

401
Q

X ray findings of osteosarcoma

A
  • ELEVATED PERIOSTEUM (CODMANS TRIANGLE)
  • SUNBURST APPEARANCE
402
Q

How to differ osteosarcoma and chondrosarcoma?

A

ALP STAINING POSITIVE IN OSTEOSARCOMA, COMPARED TO NEGATIVE IN EWINGS

403
Q

Onion skinning of periosterum

A

ewings sarcoma

404
Q

What is the only tumour that can be diagnosed genetically? How?

A

EWINGS SARCOMA IS THE ONLY BONE TUMOUR WHICH CAN BE DIAGNOSED GENETICALLY:
- T11:22 TRANSLOCATION

405
Q

Summary slide showing malignant bone tumours

406
Q

Layers of the epidermis

A
  • Stratum corneum
  • Stratum lucidum
  • Stratum granulosum
  • Stratum spinosum
  • Stratum basale
  • Basement membrane
407
Q

Dermatology definitions (learn if have time)

A

Hyperkeratosis – INCREASE in size of stratum corneum and keratin
Parakeratosis – INCREASE in RETAINED nuclei in stratum corneum
Acanthosis – INCREASE in stratum spinosum
Acantholysis – REDUCE in cohesion between keratinocytes
Spongiosis – INTERcellular oedema
Actinic – Damaged by the sun

408
Q

Examples of pre-malignant derm neoplasms and how to differentiate

A

Actinic Keratosis - HAVE A SANDPAPER LIKE TEXTURE
Keratacanthoma - dome shaped nodule with necrotic crusted centre
Bowen’s disease - flat, red with scaly patches and is stand alone.

409
Q

Precursors to squamous cell carcinoma of skin& how to differntiate

A

BOWENS DISEASE AND ACTINIC KERATOSIS ARE PRECURSORS TO SCC  DIFFERENCE BETWEEN THEM IS BOWENS DISEASE IS FULL THICKNESS

410
Q

Histology of actinic keratosis

A

Histology has the acronym SPAIN (Solar Elastosis, Parakeratosis, Atypia/dysplasia/Inflam/NOT full thickness)

411
Q

Intra epidermal squamous cell acncer

A

Bowens disease

412
Q

Difference between bowens disease and squamous cell carcinoma

A

SCC IS BOWENS DISEASE THAT HAS SPREAD THROUGH THE BASEMENT MEMBRANE

413
Q

How does a basal cell carcinoma appear? AKA? Histology?

A

Appears with a pearly surface and telangiectasia
ALSO KNOWN AS A RODENT ULCER
ON HISTOLOGY: Mass of basal cells pushing down into dermis. Palisading (alignment of nuclei in outermost layer)

414
Q

Melanoma histology? Staining? Prognosis?

A

Histology:
- ATYPICAL MELANOCYTES
- INITIALL RADIAL GROWTH PHASE, THEN VERTICAL PHASE
- BUCKSHOT APPEARANCE IN VERTICAL PHASE
NB: STAIN FOR MELANIN IS FONTANA
WORST PROGNOSIS IS DUE TO BRESLOW THICKNESS, >4MM  50% 5 YEAR SURVIVAL

415
Q

Summary slide of skin cancers

416
Q

Images of skin cancers

417
Q

Squamous cell carcinoma in situ

A

Marjolin’s ulcer

418
Q

In chronic atopic dermatitis, skin becomes leathery and thick , known as?

A

Lichenification

419
Q

Mutation in what gene causes eczema

420
Q

How to atopic and contact dermatitsi differ in hypersensitivity

A

Atopic - T1
Contact - T4

421
Q

What cell is increased in atopic dermatitsi?

A

eosinophils

422
Q

Histology of eczema

A

Spongiosis  fluid collection in epidermis

Thickening of epidermis

423
Q

How does SJS present? What presents similarly? How to differntiate?

A

TYPE IV HYPERSENSITIVITY REACTION AGAINST EPIDERMIS AND MUCOSA WHICH CAN LEAD TO SKIN NECROSIS THAT CAN BE WIPED OFF
TO DIFFERENTIATE BETWEEN SJS AND TOXIC EPIDERMAL NECROLYSIS LOOK AT AMOUNT OF BODY AFFECTED  SJS IS <10%, TEN IS >30%

424
Q

Chronic plaque psoriasis presents with? Where?

A

salmon pink, well-demarcated red plaques with silver scales. It appears on the extensors of knees, elbows and scalp.

425
Q

Auspitz sign means what? Seen in what?

A

rubbing plaque leads to pinpoint bleeding, seen in plaque psoriasis

426
Q

When does guttate psoriasis present? Triggered by what? How does it present?

A

Guttate psoriasis presents in CHILDHOOD, typically triggered by a STREP THROAT 2 WEEKS AGO  Appears as small spots, with a rain drop plaque distribution over trunk and limbs

427
Q

Who does flexural psoriasis in? How does it present?

A

Flexural psoriasis occurs in the elderly. It occurs on creases in the skin, in the groin, submammary, nasal cleft.

428
Q

Parakeratosis

A

PSORIASIS - increase in retained nuclei in stratum corneum

429
Q

Pathophys of psoriasis

A

T4 T cell hypersensitivity reaction within the epidermis
T cell recruitment and release of inflammatory cytokines e.g. TNF - alpha
Keratinocyte hyperproliferation
Epidermal thickening

430
Q

Summary slide of psoriasis types

431
Q

Difference between bullous pemphigoid and pemphigus vulgaris

A
  • BULLOUS PEMPHIGOID:
    o TENSE ON ERYTHEMATOUS BASE  DO NOT RUPTURE
  • PEMPHIGUS VULGARIS:
    o EASILY RUPTURED  RAW RED SURFACE
    o NIKOLSKY +VE  THIN TOP LAYER OF SKIN WILL SHEAR OFF, LEAVING SKIN PINK AND MOIST  USUALLY VERY TENDER
432
Q

Summary table showing difference between bullous pemphigoid, pemphigus vulgaris and pemphigus folicaeous

433
Q

Pathophys of atherogenesis

A
  • Endothelial Injury
  • LDL gets enters subintimal space and gets trapped
  • LDL oxidised
  • Oxidised LDL gets taken up by macrophages via scavenger receptor becoming FOAM CELLS
  • Foam cells apoptose causing cholesterol core
  • Increase in adhesion molecules on endothelium results in MORE MACROPHAGES AND T CELLS
  • Vascular smooth cells form fibrous cap
434
Q

Types of blood flow and there properties

A

LAMINAR BLOOD FLOW IS ANTI-ATHEROGENIC, TURBULENT IS ATHEROGENIC

435
Q

Complications of an MI

A
  • Death
  • Arrythmia
  • Rupture
  • Tamponade
  • Heart Failure
  • Valvular disease
  • Aneurysm of ventricle (persistent ST elevation following MI)
  • Dresslers syndrome
  • Embolism
  • Recurrence
436
Q

skin fidnings in sarcoidosis

A

erythema nodosum (IBD, sarcoidosis), lupus pernio (lesion affecting the nose), skin nodules

437
Q

What is uveoparotid fever? WHat is AKA? Presents with?

A

Eye manifestation of sarcoidosis

NB: UVEOPARATOID FEVER IS ALSO KNOWN AS HEERFORDT SYNDROME. IT CAN CAUSE BILATERAL UVEITIS, PAROTID ENLARGEMENT AND POTENTIALLY A FACIAL NERVE PALSY

438
Q

Most common valve disease post MI

A

MITRAL REGURG IS MOST COMMON VALVE DISEASE POST MI  CAUSED BY PAPILLARY MUSCLE RUPTURE OR NECROSIS

439
Q

Persistent ST elevation post MI

A

VENTRICULAR ANEURYSM  CAN DEVELOP FOR OVER A MONTH AFTER

440
Q

Difference between pericardial effusion and tamponade

A

DIFFERENCE BETWEEN PERICARDIAL EFFUSION AND TAMPONADE IS TAMPONADE OBSTRUCTS THE CONTRACTILITY OF THE HEART

441
Q

Most common causes of pericarditis by type

A
  • FIBRINOUS  MI
  • GRANULOMATOUS  TB
  • PURULENT  STAPHYLOCOCCUS
442
Q

Nutmeg liver

A

APPEARANCE OF THE LIVER DUE TO CHRONIC HEPATIC VEIN CONGESTION  BECOMES CARDIAC CIRRHOSIS OVER TIME (NOTE: PPQ)

443
Q

Haemosiderin laden macrophages in lungs

A

MACROPHAGES WHICH HAVE TAKEN ONTO RBCS IN LUNGS AFTER ALVEOLAR HAVE BURST  AKA HEART FAILURE CELLS

444
Q

Histology of rheumatic fever

A
  • BEADY FIBROUS VEGETATIONS
  • ASCHKOFF BODIES
  • ANITSCHOW MYOCYTES
445
Q

Management of rheumatic fever

A

TREATED WITH BENZYLPENICILLIN

446
Q

Diagnosis of Rheumatic fever is by what criteria?

A

Diagnosis:
- JONES CRITERIA:
o GROUP A STREP INFETION AND 2 MAJOR CRITERIA
o GROUP A STREP INFECTION AND 1 MAJOR + 2 MINOR

Major Criteria (CASES):
- Carditis
- Arthritis
- Sydenhams chorea  jerky, uncontrollable and purposeless movements of the body
- Erythema marginatum  skin rash specific to rheumatic fever  pink, pale centre surrounded by a red, raised border
- Subcut Nodules

Minor Criteria (FRAPP):
- Fever
- Raised ESR or CRP
- Arthralgia
- Prolonged PR interval
- Previous Hx of Rheum Fever

447
Q

Lung cancer htat affects proximal bronchi

A

small cell and squamous

448
Q

lung cancer that affects distal bronchi

A

adenocarcinomas

449
Q

Most common gene affected in HOCM

A

beta myosin heavy chain

450
Q

Hypertrophy occurs where in HOCM?

451
Q

Most common cause of restrictive cardiomyopathy

A

Amyloidosis

452
Q

Cardiac complication of SLE and APML, presents with?

A

Libmen sacks endocarditis. warty vegtations on endocardium that are sterile and platelet rich

453
Q

Organisms which cause acute endocarditis

A
  • STAPH AUREUS
  • STREP PYOGENES
454
Q

Organisms which cause subacute endocarditis

A
  • STREP VIRIDANS
  • STAPH EPIDERMIS
  • HACEK
    o HAEMOPHILUS
    o AGGREGATIBACTER
    o CARDIOBACTERIUM
    o EIKENELLA
    o KINGELLA
455
Q

Difference between acute and subacute infective endocarditis

A

NB: Acute infective endocarditis develops suddenly and may become life threatening within days. Subacute infective endocarditis (also called subacute bacterial endocarditis) develops gradually and subtly over a period of weeks to several months but also can be life threatening

456
Q

Most common valvular problems in IE

A

MITRAL AND AORTIC REGURG

457
Q

Most common murmur in IE

A

REGURG  MITRAL MOST COMMON, BUT IF IVDU  TRICUSP

458
Q

Diagnosis of IE is with what criteria?

A

Diagnosis of IE:
- DUKES CRITERIA
o 2 MAJOR
o 1 MAJOR AND 3 MINOR
o 5 MINOR

Major Dukes Criteria:
- POSITIVE BLOOD CULTURE GROWING TYPICAL IE ORGANISM
- VEGETATIONS ON ECHO/NEW REGURG MURMUR

Minor Dukes criteria:
- RF
- Fever
- Thromboembolic phenomena
- Immune phenomena
- Positive blood cultures that don’t meet major criteria

459
Q

Immune phenomena in IE

A
  • ROTH SPOTS  EYES
  • OSLER NODES  RED, PAINFUL NODES ON HANDS OR FEET
  • HAEMATURIA FROM GLOMERULONEPHRITIS
460
Q

Thromboembolic phenomena of IE

A
  • JANEWAY LESIONS
  • SEPTIC ABSCESSES
  • MICROEMBOLI
  • SPLINTER HAEMORRHAGES
  • SPLENOMEGALY
461
Q

most specific antibody in SLE

A

anti-smith (ribonucleoproteins)

462
Q

What does anti-histone antibody indicate in SLE?

A

INDICATES THAT IT IS DRUG INDUCED LUPUS FROM HYDRALAZINE

463
Q

Histology of scleroderma

A
  • INCREASED COLLAGEN DEPOSITION
  • FIBROSIS
  • ARTERIOLE ONION SKINNING APPEARANCE
464
Q

Differences between diffuse and limited systemic sclerosis

A
  • DIFFUSE:
    o WIDESPREAD SX INCLUDING RENAL + CARDIO
    o CAN LEAD TO PULMONARY FIBROSIS
  • LIMITED:
    o CONFINED TO FACE AND DISTAL ASPECTS OF LIMBS  DISTAL TO KNEE AND ELBOW
    o TYPICALLY CREST
    o CAN LEAD TO PULMONARY HTN
465
Q

Skin manifestations in myosiits

A
  • GOTTRONS PAPULES  CALLOUSES/REDDENING ON KNUCKLES
  • HELIOTROPE RASH  REDDENING AROUND EYES AND FACE
466
Q

Presentation of Giant cell arteritis

A
  • OVER 50
  • PRECEDING POLYMYALGIA RHEUMATICA
  • HEADACHE OVER EYE
  • VISION DIFFICULTY
  • ENLARGED TEMPORAL ARTERY
467
Q

Histology of giant cell arteritis

A
  • GRANULOMATOUS TRANSMURAL INFLAM
  • GIANT CELLS
  • SKIP LESIONS
468
Q

Blood finding of giant cell arteritis? management?

A

HIGH ESR, NEEDS TEMPORAL ARTERY BIOPSY AND URGENT STEROIDS

469
Q

What is polyarteritis nodosa associated with? What does it normally affect?

A

NORMALLY AFFECTS THE RENAL AND MESENTERIC ARTERIES
ASSOCIATED WITH HEPATITTIS B

470
Q

What investigations are done for polyarteritis nodosa? What do they show?

A

Investigations include an angiogram  SHOWS MICROANEURYSMS ON ANGIOGRAPHY (“STRING OF PEARLS”/ROSARY BEAD APPEARANCE)

471
Q

On histolofy of polyarteritis nodosa

A

FIBRINOID NECROSIS & NEUTROPHIL INFILTRATION

472
Q

Where is biopsy taken for polyarteritis nodosa?

A

Sural nerve (a superficial nerve in the calf of the leg

473
Q

Presentation of thromboangiitis obliterans? Investigations?

474
Q

Cytoplasmic ANCA (cANCA) is against

A

Proteinase 3

475
Q

perinuclear ANCA (pANCA) is against

A

myeloperoxidase

Path - Things to Go Over (6 decks)

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