General Flashcards

1
Q

DDx of scrotal masses

A

Benign:
- hydrocele
- epididymal cyst
- varicocoele
- epididymo-orchitis
- inguinal hernias
- benign epididymal tumours

Malignant:
- testicular cancer

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2
Q

Types of testicular cancers

A

Germ cell tumours (95%)

Non-germ cell tumours include: leydig cell tumours, sertoli cell tumours, secondary metastasis

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3
Q

What embryonic level does testicular cancer spread via lymphatic drainage?

A

T11-L4

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4
Q

Tumour markers for testicular cancer?

A

a-feto protein (AFP)

B-HCG

LDH -> usually elevated in metastatic disease

e.g high B-HCG and no AFP = most likely a choriocarcinoma

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5
Q

What is an orchidectomy?

A

removal of one or more testes

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6
Q

Testicular cancer staging

A
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7
Q

Testicular cancer risk factors

A
  • An undescended testicle
  • Family history of testicular cancer
  • HIV infection
  • Carcinoma in situ of the testicle
  • Having had testicular cancer before
  • Being of a certain race/ethnicity (Black and Asian-American men have higher incidence)
  • increased height
  • male infertility
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8
Q

Testicular cancer treatment

A

Orchidectomy followed by chemotherapy (if required) and retroperitoneal lymph node dissection (RPLND) if there is residual mass

If a seminoma then can also use radiation.

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9
Q

What do you expect to find on examination of testicular cancer?

A

A painless lump that is:
- non-tender
- reduced sensation
- arise from the testicle
- is a hard lump that is irregular
- non-fluctuant
- cannot transluminate the lump

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10
Q

Investigations for testicular cancer?

A

Scrotal US

Tumour markers - B-HCG, AFP, LDH (not as specific)

Stage tumour using a CT

Histopathological confirmation post orchidectomy (do not biopsy before removal due to risk of tumour seeding)

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11
Q

SEs of testicular cancer treatment

A

Infertility

Nerve damage around the testes (often cannot ejaculate due to damage to the sympathetic fibres)

Hypogonadism (may need to supplement with testosterone

Increased risk of cancer in the future

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12
Q

which testicular cancer is radioresistant

A

non-seminoma -> aggressive germ cell cancer arising from mixed cells. More aggressive than seminoma testicular cancer.

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13
Q

Risk factors for breast cancer?

A
  • Fx (oncogenes, BRCA1 or 2 mutation)
  • early menarchy and/or late menopause (increased length of oestrogen exposure)
  • age at first live birth (later birth age = increased risk)
  • nulliparity
  • hormone replacement therapy
  • atypical hyperplasia (abnormal cells on biopsy but not cancer)
  • high alcohol use
  • obesity (associated with increased estrogen)
  • high radiation exposure
  • smoking
  • low fibre, high fat diet
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14
Q

Breast cancer mammography screening vs diagnosis

A

Screening is a two place imaging to assess any abnormal masses within the breast

Diagnostic takes multiple images specific to one area/location of the breast to assess a concerning mass of interest. Usually part of triple testing (examination + history, imaging, biopsy)

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15
Q

What does Ki67 assess in breast cancer prognosis?

A

Looks at how quickly the tumours are growing. The higher the Ki67, the quicker it is growing.

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16
Q

what is the triple test approach in breast cancer?

A
  • Hx and examination
  • imaging (mammogram and/or US
  • non-excision biopsy (fine needle aspiration and/or core biopsy)
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17
Q

Invasive vs npn invasive breast cancers

A

Non-invasive:
- ductal carcinoma in situ (DCIS)
- lobular carcinoma in situ (LCIS)
Both have potential to become invasive breast cancers.

Invasive:
- invasive ductal carcinoma
- invasive lobular carcinoma

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18
Q

Benign DDx of breast lump

A

breast cyst

fibroadenoma

breast abscess

fat necrosis of the breast

solidary intraductal papilloma

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19
Q

What is Paget’s disease of the nipple?

A

malignant cells/paget cells involved in DCIS extend within the ductal system -> infiltrate the skin of the nipple without crossing the basement membrane -> causes itching and oozing of the nipple -> usually poorly differentiated.

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20
Q

Lifetime risk of breast cancer and ovarian cancer in women with the BRCA1 gene mutation?

A

85% breast cancer and 40% ovarian cancer

Prophylactic surgery is a mastectomy and a bilateral salpingo oorophorectomy

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21
Q

What cancer is the BRCA2 gene associated with?

A

higher risk of breast and ovarian cancer, as well as pancreatic cancer, melanoma, sarcoma and prostate cancer (in males)

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22
Q

Difference between transudate vs exudate?

A

Transudate is low protein fluid associated with liver cirrhosis, CCF, hypoproteinemia. Does not contain inflammatory cells.

Exudate in a high protein fluid associated with cancer, pancreatitis, abscess/peritonitis, bowel ischemia, BO

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23
Q

Difference between sclerotic vs lytic bone metastasis?

A

Sclerotic (aka osteoblastic) refers to distant tumour deposits from a primary tumour into the bone. It causes osteogenesis. A
Associated with prostate cancer, and TCC (a rare kidney cancer).

Lytic bone metastasis is when tumour cells dissolve bone and make it less dense. It causes osteolysis. Associated with renal cancer, thyroid cancer, melanoma and lung cancer. Also breast cancer but is can be mixed

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24
Q

Tumours most associated with bone metastasis?

A

Breast cancer
Prostate cancer
Melanoma
Kidney/renal cancer
Lung cancer
Thyroids

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25
Q

Best imaging modality to assessing bone metastasis?

A

CT followed by MRI

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26
Q

What is the aim of adjuvant vs neoadjuvant therapy in cancer treatment?

A

Adjuvant ‘mops’ up any cancer cells after the main treatment (e.g. radiation post mastectomy). This decreases the rate of local recurrence and micro-metastasis

Neoadjuvant is aimed to reduce tumour size prior to main treatment (e.g. chemotherapy to reduce breast cancer size prior to mastectomy).

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27
Q

What is the arterial supply of the breast?

A

internal thoracic, axillary, and intercostal arteries

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28
Q

what is the venous drainage of the breast?

A

internal thoracic, axillary and intercostal veins

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29
Q

What is the lymphatic drainage of the breast?

A

lymph fluid drains into the axillary nodes (75%), parasternal nodes (20%), and posterior intercostal nodes (5%)

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30
Q

Where does breast cancer metastasis main occur?

A

occurs through haematogenous and lymphatic spread -> into the lymph nodes, bone, liver, lungs, and brain (LBLBL)

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31
Q

S&S of breast cnacer

A

Signs:
- breast asymmetry
- nipple retraction/inversion
- colour/skin changes e.g. erythema, peau d’orange
- lymphadenopathy - swollen lymph nodes (esp. of the axilla)
- lymphedema of the arm
- signs of metastasis such as bone pain

Symptoms:
- painless lumps (hard, uneven borders)
- bloody discharge from the nipples

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32
Q

Tumour marker for breast cancer?

A

CA.15-3

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33
Q

Ovarian cancer tumour markers?

A

CA 125

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34
Q

Why is core needle biopsy preferred of fine needle biopsy for breast cancer diagnosis?

A

Core needle biopsy allows for moledular typing, fine needle does not

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35
Q

What is a sentinel node biopsy?

A

Radioactive substance or blue dye is injected into the tumour and will travel to affected lymphnodes. Lymph node with metastatic disease can then be identified and assessed whether lymph node dissection is required.

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36
Q

What chemotherapy agents are typically used in the treatment of breast cancer?

A

FEC
Fluorouracil, epirubicin, and cyclophosphamide

Add docetaxel if there is lymph node involvement.
Can be given before (neoadjuvant) or after surgery (adjuvant).

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37
Q

What hormonal therapy is used in breast cancer?

A

If ER positive:
- Premenopausal: use tamoxifen (an estrogen receptor antagonist in the breast, and estrogen receptor agonist in bone and uterus). This means it will prevent osteoporosis but it increases the risk of endometrial cancer (and VTE).
Tamoxifen is effective in reducing local recurrence, mortality and contraletal breast cancer

  • Postmenopausal: use aromatase inhibitors to reduce the production of oestrogen which decreases cancer growth, but also causes menopausal symptoms.

May consider ovarian function suppression via radiotherapy, oophorectomy or medical (triptorelin)

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38
Q

Contraindications for hormonal therapy n breast cancer treatment?

A

Pregnancy

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39
Q

Which target therapy is used in HER2 positive cancers?

A

Trastuzumab (aka Herceptin) is a monoclonal antibody that targets HER2

Can cause gastrointestinal upset and is cardiotoxic

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40
Q

What are some complications of a full axillary node dissection?

A

Damage to the long thoracic nerve -> winging of the scapula
Damage to the thoracodorsal nerve
Lymphodema
Shoulder stiffness, pain, numbness
Risk of infection to the surgical area

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41
Q

What does HER2 stand for?

A

Human epidermal growth factor receptor

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42
Q

Tipple negative breast cancer risk factors?

A
  • age (more common in younger patients)
  • race - more common in African-American
  • being premenopausal
  • young age of first pregnancy
  • obesity
  • BRCA1 mutation
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43
Q

What age group are mammograms freely offered to in Australia?

A

Every two years for people aged 50-74yrs

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44
Q

Prevention vs treatment of VTE

A

Prevention = enoxaparin 40mg subcut

Treatment = enoxaparin 1.5mg/kg subcut daily. Can also start oral anticoagulant such as warfarin.

Use IV heparin is kidney impairment.

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45
Q

Causes of increased ALP?

A

hyperparathyroidism, Paget disease, osteoblastic bone tumours, osteomalacia, rickets, healfing fractures, liver disease, hyperthyroidism

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46
Q

What is an annular pancreas?

A

Head and neck of the pancreas wraps around the duodenum -> get gastric distention and vomiting

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47
Q

What is pancreas divisum

A

Abnormaility in pancreatic duct/drainage -> leads to chronic pancreatitis

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48
Q

Causes of acute pancreatitis?

A

Alcohol use
Biliary tract disease
Obstruction due to neoplasms
Iatrogenic (ERCP_
Drugs (frusemide)
Trauma

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48
Q

Causes of acute pancreatitis?

A

Alcohol use
Biliary tract disease
Obstruction due to neoplasms
Iatrogenic (ERCP_
Drugs (frusemide)
Trauma

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49
Q

Pathophysiology of acute pancreatitis?

A

Acina cell injury via multiple mechanisms (obstruction, inflammation, drugs, ischemia, premature activation of enzymes) -> premature activation of pancreatic enzymes -> autodigestion of the pancreas (proteases, lipases, and elastases).

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50
Q

Cullens vs gray turners sign?

A

Cullens is around the umbillicus and grey turner is the flanks (bruising in pancreatitis due to internal retroperitoneal haemorrhage)

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51
Q

Acute pancreatitis signs and symptoms:

A
  • severe abdominal pain
  • elevated serum lipase
  • bloody abdominal fluid (due to small vessel haemorrhage due to elastase)
  • ARDS
  • electrolyte disturbances and renal failure
  • Shock
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52
Q

Acute pancreatitis treatment

A

Usually pancreatic rest and supportive treatment is all that is required. Very severe cases where infective necrosis is present will require surgery and empiric ABx.

Give pain relief
NBM until pain free and has bowel sounds
Give IV fluids/resusc

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53
Q

Chronic pancreatitis sequale

A

Recurrent mild pancreatitis leads to chronic injury and scarring of the pancreas. Leads to loss of function and acini. Ressults in pancreatic insufficiency (weight losss, malnutrition, diarrhea/steatorrhea, diabetes mellitis)

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54
Q

What does I GET SMASHED stand for?

A

I = idiopathic

G = gallstones
E = ethanol
T = trauma

S = steroids
M = mumps or malignancy
A = autoimmune
S = scorpion sting
H = hypertrigliceridemia or hypercalcemia
E = ERCP
D = drugs (diuretics, NSAIDs)

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55
Q

Diagnostic criteria for acute pancreatitis?

A

Abdominal pain suggestive of acute pancreatitis

Raised serum lipase -> 3 times the upper limit (can also do amylase but not as specific)

characteristic findings of acute pancreatitis on CT

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56
Q

What would be seen on abdominal CT in acute pancreatitis?

A
  • pancreatic enlargement
  • oedema
  • fat stranding
  • free fluid
  • complications including necrosis, pseudocyst, abscess
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57
Q

Treatment of acute pancreatitis?

A

Pancreatic rest
Fluid administration (normal saline)
Pain relief (morphine or fentanyl)
ABs have limited role unless pancreatic necrosis (occurs due to haemmaorhage and damage to the blood vessels) or an abscess is present.
Recommence food when patient is pain free and tolerating food.

Also consider the underlying cause and treat. e.g ERCP if gallstone obstruction

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58
Q

Why can hypocalcemia result from acute pancreatitis?

A

The pancreatic lipase breask down peripancreatic and mesenteric fat. Get release of fatty acids that bind calcium which results in hypocalcemia.

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59
Q

Causes of chronic pancreatitis?

A

excessive alcohol consumption

idiopathic pancreatitis

ductal obstruction

other causes include CF, AI, hereditary conditions.

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60
Q

Are serum amylase and lipase usually raised in chronic pancreatitis?

A

They are usually normal due to fibrosis and atrophy of the pancreas

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61
Q

What is the foecal pancreatic elastase test helpful for?

A

Identifies pancreatic exocrine insufficiency in chronic pancreatitis.
Faecal elastase will be low in pancreatic insufficiency

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62
Q

Treatment/management of chronic pancreatitis?

A

Lifestyle:
- reduce risk factors such as excessive alcohol use, smoking

Identify diabetes and manage

Pain management using analgesia

Pancreatic enzyme replacement therapy

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63
Q

Indication for cholecystectomy?

A
  • symptomatic cholelithiasis with or without complications
  • asymptomatic cholelithiasis in patients who are at an increased risk of gallbladder cancer or gallstone complications
  • cholecystitis
  • gallbladder polyps >0.5 cm
  • porcelain gallbladder
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64
Q

What is Strasberg’s classification of bile duct damage during surgery?

A
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65
Q

What is Charcot’s triad?

A

Presenting feautres of acute cholangitis (NOT CHOLECYSTITIS) including fever, abdominal pain, and jaundice.

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66
Q

What is Reynold’s pentad?

A

Occurs in suppurative cholangitis where patients have fever, abdominal pain, jaundice, confusion, and hypotension.

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67
Q

Treatment of acute cholangitis?

A

Monitor for sepsis and treat with empiric ABs (gent, amp, met) before commencing targeted therapy once cultures are returned.

Establish biliary draining (usually via ERCP)

Supportive therapy (e.g pain, nausea, fluids)

Cholecystectomy if gangrenous

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68
Q

What is Ranson’s criteria for acute pancreatitis?

A
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69
Q

Mild vs moderate vs severe acute pancreatitis?

A

Mild = no organ damage, no local or systemic complication

Moderate = transient organ failure that resolves within 48hr and/or local or systemic complication without persistent organ failure

Severe = persistent organ failure that may involve one or more organs.

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70
Q

Cholangitis vs cholecystitis

A

Cholangitis = inflammation of the bile duct

Cholecystitis = inflammation of the gallbladder. Murphy’s sign will be positive

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71
Q

What are gallstones made up of?

A

Usually cholesterol, calcium, and bilirubin.
Usually radiopaque.
Will create an acoustic shadow behind it.

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72
Q

Cholelithiasis vs choledocholithiasis

A

Cholelithiasis = gallstone in the gallbladder

Choledocholithiasis = gallstones within the bile duct

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73
Q

Risk factors for gallstones

A

Six F’s = female, fat, forty, fertile, fair skinned, family hx

Modifiable:
- physical inactivity
- low fibre intake
- hypercholesterolemia
- rapid weight loss (bariatric surgery patients)

Non-modifiable:
- liver cirrhosis
- Crohn’s disease (inflamed terminal ileum impairs bile acid recirculation)
- presence of gallstones
- comorbidities such as T2DM, cirrhosis, jaundice

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74
Q

Empiric ABs used for cholecystitis

A

Gentamicin + ampicillin

If chronic biliary obstruction then add metronidazole

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75
Q

Treatment for cholecystitis?

A

Withhold oral feeds if going for surgery (then low fat diet)

Empiric ABs gent + amp +/- met

Cholecystectomy -> laparoscopic vs open

Percutaneous cholecystostomy or ERCP to remove gallstone in bile duct. Cholecystectomy better to prevent recurrence.

Supportive care -> fluids, analgesia (morphine), lifestyle modification post surgery such as low fat diet 1 week following surgery.

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76
Q

What is Mirizzi syndrome?

A

gallstone located in the Hartmann’s pouch causing compression of the adjacent hepatic structures. Can result in obstructive jaundice.

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77
Q

Diverticulitis risk factors?

A

advanced age

genetic risk factors

smoking

elevated BMI

cheotherapy

high red meat consumption

connective tissue diseases such as Marfan Syndrome or Ehlers-Danlos syndrome

chronic constipation

low fibre diet

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78
Q

Diverticulitis pathophysiology?

A

Formation of diverticulosis (most commonly in the sigmoid colon) due to weakening of the diverticular wall (age, vascular penetration) and increase in intraluminal pressure -> bacteria or faecal matter enters the diverticular -> results in inflammation/infection -> can form complications such as abscess or perforation.

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79
Q

Diverticulitis essentials of diagnosis + clinical features?

A

Essentials of diagnosis:
- fever
- left lower abdominal pain
- leukocytosis

Clinical features:
- low grade fever
- left lower quadrant pain
- altered bowel habits (usually contipation)
- acute abdomen would possibly indicate perforation or peritonitis.

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80
Q

Most common organisms involved in diverticulitis?

A

E.coli
enterococcus
bacteroides fragilis

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81
Q

Diverticulitis complications?

A

Perforation

Abscess formation

intestinal obstruction due to inflammatory related narrowing

Fistula formation (usually rectovesical fistula

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82
Q

What is the Hinchey classification?

A

I - pericolic abscess formation

II - pelvic, intra-abdominal, or retroperitoneal abscess

III- generalised purulent peritonitis

IV - generalised fecal peritonitis

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83
Q

Management of complicated diverticulitis?

A

Complicated diverticulitis:

  • in patient management with broad spectrum IV antibiotic
    • gentamicin, metronizadole, ampicillin IV
  • CT guided percutaneous drainage for abscesses of more than 4cm (Hirchey 1 or 2)
  • emergency colectomy in patients with generalised peritonitis → Hartmann’s procedure where part of the descending or sigmoid colon is removed and a stoma bag is attached (can be connected to the sigmoid colon later on). Performed in Hirchey 3 or 4 (purulent or faecal peritonitis)
  • patients should be nil by mouth and receive IV fluids
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84
Q

Definition of diverticulosis?

A

Herniation of the mucosa and submucosa through the muscular layer of the colon wall

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85
Q

Preferred imaging modality for suspected diverticulitis?

A

Abdominal and pelvic contrast CT

Use MRI or US if CT is contraindicated

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86
Q

Anterior vs posterior PUD rupture?

A

Anterior = arteries not impacted, more likely to result in free intra-peritoneal gas under the diaphragm.

Posterior = gastroduodenal artery likely to be perforated. Causes bleeding into the intra-peritoneal cavity.

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87
Q

Pain fibres involved in visceral vs parietal pain?

A

Visceral pain = c-fibres

Parietal/somatic pain = A and c-fibres (more localised)

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88
Q

Most common causes of acute abdomen?

A

GIT: appendicitis, large or small bowel obstruction, perforated peptic ulcer, diverticulitis, IBD, mesenteric adenitis

Liver, spleen, biliary:
- acute cholecystitis, acute cholangitis, acute hepatitis, spontaneous rupture of the spleen

Pancreatic:
- acute pancreatitis

Urinary:
- renal or ureteral colic, acute pyelonephritis, acute cystitis

Gynae:
- acute salpingitis, ruptured ovarian cyst, ruptured ectopic pregnancy

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89
Q

Types of colon polyps?

A

Non-neoplastic polyps include: hyperplastic polyps, inflammatory polyps, haemartomatous polyps. These polyps have a low potential to become malignant.

Neoplastic polyps include adenomas (e.g. tubular, tubulovillous, and villous adenomas) and serrated types. These polyps have moderate to high potential to become malignant if given enough time to grow.

Most CRC arise from dysplastic adenomatous polyps.

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90
Q

CRC staging

A

Staging:

TNM staging:

T part

  • T1 → invaded the submucosa
  • T2 → invaded the muscularis propria
  • T3 → invaded to the serosa/adventia or perirectal tissues
  • T4 → invaded into the peritoneum and surrounding tissues

N part

  • 0 → no lymph node involvement
  • 1 → invaded 1-3 local lymph nodes
  • 2 → invaded 4 or more local lymph nodes
  • 3 → distant lymph node metastasis

M part

  • 0 → no metastsis
  • 1 → metastasis
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91
Q

Lynch Syndrome vs FAP?

A

Lynch syndrome: accounts for 2-10% of CRC and is caused by a mutation of a MMR genes (esp MLH, MSH, PMS2). This leads to microsatellite instability and an increased risk of CRC. Condition is autosomal dominant.

Familial adenomatous polyposis: accounts for 1% of CRC. Affected patients have multiple precancerous adenomatous polyps with the onset of polyps at a mean age of 16. They have a 95% lifetime risk of developing CRC. Also autosomal dominant. Management includes polyp removal but will eventually require a protocholectomy and ileostomy.

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92
Q

CRC screening recommendations

A
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93
Q

CRC management:

A

Colon:
- colectomy (hemi, sigmoid, subtotal, total) with lymph node dissection indicated in all resectable tumours
- chemotherapy including FOLFOX (usually used as an adjuvant therapy)
- radiation is typically not used due to risk of radiation enteritis
- preoperative chemotherapy or immunotherapy considered for stage IV CRC

Rectal:
- surgical resection if possible
- neoadjuvant radiation may be used to decrease tumour size
- adjuvant chemotherapy considered

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94
Q

Mutation pathways involved in CRC

A
  • Chromosomal instability
    • Most common pathway
    • Abnormality to chromosomal segregation (M phase)
    • Mutation to APC, p53, DCC, K-Ras, B-Raf, C-Myc
    • Seen in most cases of CRC (FAP)
  • Microsatellite instability
    • Typically associated with mutations in mismatch repair enzymes including MSH2 and MLH1
    • Seen in Lynch Syndrome
  • Aberrant methylation
    • Abnormal patterns in epigenetic methylation. Usually hypermethylation which causes DNA to wrap tightly, leading to the silencing of genes.
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95
Q

Types of AF

A

paroxysmal = less than 1 week

persistent = >1week to 12mth

longstanding = 1yr

new onset

permanent = decision for no more control strategies

valvular = mitral stenosis or mechanical HV

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96
Q

Causes of AF

A

atrial dilatation -> HTN, valve dysfunction

sepsis

electrolytes abnormalities

thyroid - thyroidoxicosis or hyperthyroidism

alcohol

drugs - cocaine

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97
Q

Grave’s disease treatment?

A

anti-thyroid medications

radioactive iodine therapy -> thyroid takes up the radioactive iodine which progressively kills the thyroid cells to decrease its function

beta blockers - symptom control

surgery (partial or full thyroidectomy)

corticosteroids for poptosis

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98
Q

Prostate cancer vs BPH on

A
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99
Q

Prostate cancer symptoms

A

Early prostate cancer is typically asymptomatic and detected by early screening.

Lower urinary tract symptoms include:
- frequency
- urinary retention
- haematuria
- incontinence
- nocturia
- dribbling

Metastatic:
- bone pain, pathological fractures
- lymphadema

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100
Q

BPH complications

A

Urinary stasis -> recurrent UTIs and bladder calculi

Bladder wall hypertrophy and pseudodiverticula

Renal impairment -> pyelonephritis, hydroureteronephrosis

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101
Q

Prostate cancer risk factors

A

increasing age

Fx

genetics (BRCA1/2, lynch syndrome)

high BMI

smoking

chemical exposure (firefighters at greater risk)

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102
Q

Prostate cancer on DRE vs BPH?

A

Prostate cancer:
- hard, enlarged, asymmetrical/bumpy nodular mass, loss of median sulcus

BPH:
- enlarged, non-tender smooth, can still feel median sulcus

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103
Q

Investigations for suspected prostate cancer?

A
  • DRE
  • prostate specific antigen (PSA) levels. PSA is a serine protease produced only by the prostate gland. Therefore it is an organ specific marker. It is elevated in benign and malignant conditions.
  • multiparametric MRI (mpMR)I of the prostate
  • transrectal US of the prostate (also used to guide a prostate biopsy)
  • perform prostate biopsy if there is clinical suspicion of prostate cancer. Need to give prophylactic ABx to prevent prostatitis.
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104
Q

True or false…

5-alpha reductase inhibitors can suppress PSA production?

A

True -> therefore needs to be taken into account if screening patient for prostate cancer in they are on 5-alpha reductase inhibitors for BPH

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105
Q

What is the Gleason system used for?

A

Grading cell differentiation in prostate cancer.

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106
Q

How is prostate cancer staged?

A

TNM staging

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107
Q

Prostate cancer treatment?

A

Watchful waiting - if a slow growing tumour, limited life expectancy. Still check PSA and perform DRE regularly.

Active surveillance - regular monitoring with DRE, PSA, biopsies, mpMRI

Radiotherpay

Radical prostatectomy

Androgen deprivation therapy (aims to decrease testosterone levels via medical or surgical castration.

Chemotherapy - usually an adjunct to androgen deprivation therapy. Docetaxel most commonly used.

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108
Q

Prostate cancer DDx

A

BPH

UTI/cystitis

overactive detrusor muscle

Prostatitis

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109
Q

What type of cancer is prostate cancer?

A

usually adenocarcinoma arising from gland cells.

Other types include small cell carcinomas.

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110
Q

Sites of metastatic spread in prostate cancer?

A

bone

liver

lungs

lymph nodes

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111
Q

Current australian recommendations for prostate screening?

A

no recommendations. Controversial as to whether PSA screening and DRE are beneficial. Informed patient decision making is encouraged.

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112
Q

BPH management?

A

non-pharm:
- medication reconcilliation, reduced fluid intake, reduced caffeine intake, reduced alcohol intake, bladder emptying techniques.

Pharm:
- a-blockers relax SM of the neck of bladder and internal urethral sphincter -> this improves urine outflow e.g tamsulosin, doxazosin

  • 5a-reductase inhibitors decrease conversion of testosterone to DHT -> this decreases prostate growth. e.g. finasteride
  • antimuscarinics to inhibit the PSns muscarinic receptors in the detrusor smooth muscle. Causes a decrease in muscle tone.

Phosphodiesterase type 5 inhibitors reduces tone in the detrusor muscle, prostate, and urethra.

Surgical:
TURP (transurethral resection of the prostate) is gold standard therapy. Indicated when pharmacology is insufficient or contraindicated. It is resection of the hyperplastic tissue around the urethra.
Can causes sexual dysfunction, retention, stricture and the BPH may be recurrent.

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113
Q

What 4 counter-regulatory hormones increase in DKA?

A

cortisol
glucagon
growth hormone
epinephrine

Remember all of these hormones will oppose insulin

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114
Q

What is pyrexia of unknown origin?

A

A temperature of > 38.3°C recorded on multiple occasions that lasts for > 3 weeks with no clear etiology despite appropriate diagnostics on 3 outpatient visits, 3 days in the hospital, or 1 week of invasive ambulatory investigation.

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115
Q

inheritance pattern for FAP

A

autosomal dominant inheritance -> mutation to the APC gene

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116
Q

What is CEA?

A

carcinoembryonic antigen -> found in increased amounts in blood in people who have colon cancer

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117
Q

Foregut artery and nerve supply

A

mouth to ampulla

coeliac artery

coeliac plexua

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118
Q

midgut artery and ner supply

A

ampulla to distal third of the transverse colon

SMA

superior mesenteric plexus

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119
Q

hindgut artery and nerve supply

A

distal transverse colon to rectum

IMA

inferior mesenteric plexua

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120
Q

visceral pain felt based on foregut, mid gut and hind gut origin

A

foregut = epigastrium

midgut = periumbilical

hindgut = suprapubic

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121
Q

what does murphys, mcburnerys, rovsing’s and grey turners sign each indicate?

A

murphy’s = cholecystitis

tender over mcburney’s = appendicitis

roving’s sign (RIF tenderness on palpation of the LIF) = suggests free fluid in pelvis

Grey-turner’s sign = retroperitoneal bleeding (occurs in pancreatitis)

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122
Q

Ranson’s criteria for pancreatitis diagnosis?

A

raised lipase (3 x upper limit of normal)

epigastric pain

CT proven pancreatic stranding

Need 2/3

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123
Q

mild, moderate and severe acute pancreatitis?

A

mild = no organ failure and no local or systemic complications

moderate = transient organ failure that last less than 48 hours

severe = persistent organ failure for more than 48hrs

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124
Q

Pancreatic cells that produce lipase?

A

Acinar cells (also produces other enzymes)

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125
Q

Types of seminoma and non-seminoma germ cell testicular cancers?

A

Seminoma

Non-seminoma:
- choriocarcinoma
- terotoma
- yolk sac carcinoma
- embyronal carcinoma
- mixed

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126
Q

DAPT loading dose and continuous dose?

A

Loading:
Aspirin = 300mg

Clopidogrel = 300mg

Therapeutic/prophylactic:
Aspirin = 100mg

Clopidogrel = 75mg

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127
Q

Ruptured abdominal aortic aneurysm classic triad of symptoms?

A
  • hypotension
  • sudden onset of severe abdominal and/or back pain
  • tender pulsatile abdominal mass
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128
Q

What is micardis?

A

Telmestartan

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129
Q

what surgery can be offered in AAA?

A

endovascular aneurysm repair - risk of a persistent endoleak
or
open surgical repair.

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130
Q

AAA risk factors?

A

male
smoking (biggest one)
advanced age
HTN
hyperlipidemia
atherosclerosis
FHx

131
Q

what percentage of AAA’s have a palpable pulse when >5cm?

A

80%

132
Q

Some of the risk factors for AKI post surgery?

A

Decreased blood flow to kidneys -> hypovolemia, dehydration, blood loss, vasodilation due to anaesthetic, blood being directed away from kidneys and the the areas of surgical trauma/intervention.

Clamping of the aorta -> decreases blood flow to the kidneys

iatrogenic -> trauma during surgery, nephrotoxin agents, contrasts,

Inflammation within the body

133
Q

why are DVTs more likely in pancreatic cancer patients?

A

because pancreatic carcinomas cause an increase expression of tissue factor.

134
Q

Which medications are included in A PINCH

A

antibiotics
potassium
insulin
narcotics
chemotherapy
heparin

135
Q

common drug interactions drugs?

A

warfarin
erythromycin
verapamil
warfarin
st johns wort
statins

136
Q

Features of acute cholecystitis on US

A

Positive sonographic murphy’s sing

Increased density/opacity of stone with posterior acoustic shadowing

Gallbladder wall thickening

137
Q

What is Bouveret syndrome that is a complication of acute cholecystitis?

A

gastric outlet obstruction caused by large gallstones that reach the duodenal bulb and get lodged there through a biliodigestive fistula.

138
Q

What is a low AFP in pregnancy indicate?

A

trisomy 21, 18, 13

139
Q

What tumours is AFP raised in?

A

hepatocellular carcinoma and testicular cancer

140
Q

What is courvoisier sign?

A

a painless and enlarged gallbladder (palpable). Can occur in pancreatitc cancer.

141
Q

types of oesophageal cancer?

A

SCC and adenocarcinoma (associated with Barrett’s oesophagus)

142
Q

oesophageal cancer surgery options:

A

transhiatal
trans thoracic
three field
minimally invasive

143
Q

Why can the virchow’s node be enlarged in GIT cancers?

A

because tumour embolisation travels via the thoracic duct which drains in the left supraclavicular node. This indicated stage 4 disease (advanced disease).

Also enlarged in lymphma, breast, oesophageal, pelvic, and testicular cancers.

144
Q

which type of gastric cancer is H.pylori associated with?

A

Gastric lymphomas -> arise from mucosa associated lymphoid tissue (MALT)

145
Q

Oesophageal cancer S&S?

A
  • progressive dysphagia
  • retrosternal discomfort
  • systemic symptoms:
    • weight loss, fatigue, fever, night sweats
  • signs of anemia → fatigue, SoB
  • persistent cough
  • Horner’s syndrome → infiltrates local nerves/fibres
146
Q

hematemesis vs hemoptysis?

A

hemoptysis = blood from the respiratory system

Hematemesis = blood from the GIT

147
Q

RF for oesophageal cancer

A
  • smoking
  • GORD → barrett’s → adenocarcinoma
  • high alcohol consumption
  • male
  • advanced age
  • consumption of hot foods/liquids
  • achalasia
  • obesity
  • poor diet
148
Q

pathophysiology of Barrett’s oesophagus?

A

Reflux esophagitis → stomach acid damages mucosa of distal esophagus → nonkeratinized stratified squamous epithelium is replaced by nonciliated columnar epithelium and goblet cells (intestinal metaplasia, Barrett metaplasia)

149
Q

Therapeutic dose of panadol for adults and children?

A

Adult: oral 0.5-1g every 4-6hrs. Maximum 4g daily

Children: oral 15mg/kg every 4-6hrs

150
Q

Features of a SBO on x-ray

A
  • predominately central dilated bowel loops (peripheral in LBO). Dilation >3cm
  • Air-fluid levels noted in erect position (>2.5cm width)
  • dilation of small bowel loops present -> small bowel anatomical folds of the small bowel become more apparent
  • minimal air distal to site of obstruction
151
Q

Common mechanical causes of a SBO?

A

bowel adhesions

incarcerated hernia

volvulus

Crohn’s disease (strictures)

152
Q

What is ileus?

A

When there is a functional inability of bowel contraction to cause propulsion of food through the GIT. Can occur post operatively.

153
Q

Common causes of LBO?

A

CRC
Diverticulitis
Volvulus
Adhesions from previous surgery
IBD -> strictures
foreign body

154
Q

What is the minimum creatinine clearance that enoxaparin can be used. And what medication should be used alternatively if the creatinine clearance reaches the minimum?

A

15ml/min

Use heparin -> 5000 units

Can use 20mg subcut enoxaparin if CrCl is between 15-30ml/min

155
Q

What is the aimed INR in warfarin therapy for VTE?

A

between 2-3

156
Q

What is prothrombinex and what is it used for?

A

For patients who require reversal of anticoagulation therapy and the the prevention/treatment of bleeding patients with low levels of factor II, IX, or X.
Can be used prophylactically in surgery for patients who are on warfarin and require immediate surgery.
Obviously increases risk of VTE

157
Q

How is fresh frozen plasma used in bleeding patients?

A

Helps to replace coagulation factors in bleeding patients. i.e. helps to replenish what is lost. Not as potent as prothrombinex.

158
Q

Alteplase for PE treatment dose?

A

100mg IV infusion over two hours

159
Q

Alteplase for thrombolysis in stroke dose?

A

0.9mg/kg over 60mins

160
Q

What feature is found on an ECG in a PE?

A

S1Q3T3

161
Q

Management of AF?

A

Hemodynamically unstable:
- DCCV (direct current cardioversion)

Stable:
- treat cause (infection, hyperthyroid)
- AV nodal blockers
- rate vs rhythm control (rate = BBlockers, CCBs, digoxin - not in HF) (rhythm = amiodarone, cardioversion)

162
Q

Management for atrial flutter

A

Aim for rhythm control

163
Q

Which cranial nerves sit laterally within the brainstem?

A

Every CN that does NOT divide into 12 (except 11)
i.e. 5, 7, 8, 9, 10.

So 5, 7, 8 for lateral pontine strokes

And 9, 10 for lateral medulla (hoarse voice and dysarthria)

164
Q

The 4 S pathways that lie lateral in the brainstem?

A

spinocerebellar tracts (ataxia)
spinothalamic tract (pain and temperature)
Spinotrigeminal tract (pain and temp in the face)
Sympathetic pathway (Horner’s syndrome)

165
Q

Structures that sit medially in the brainstem?

A

Motor tracts (corticospinal)
Medial lemniscus
Cranial nerves that divide evenly into 12 PLUS CN11 (3, 4, 6, 12)

166
Q

Benedict vs Weber’s syndrome?

A

Benedict = lesion to CN3, medial lemniscus, red nucleus
- occulomotor nerve palsy contralateral loss of proprioreceptoion and vibration, involuntary movements (ataxia and tremor)

Webers = CN3, corticospinal and corticobulbar
- occulomotor nerve palsy, contralateral hemiparesis

167
Q

Outline the types of Salter Haris Fractures?

A
168
Q

What does the ectoderm, mesoderm and endoderm become?

A

Ectoderm: skin and nervous system

Mesoderm: bone, muscle and connective tissue

Endoderm: linings of the digestive and respiratory system, as well as organs including the pancreas

169
Q

What are the three histological subtypes of CRC?

A

Adenocarcinoma (most common)

Mucinous adenocarcinoma

Signet ring cell carcinoma

170
Q

CRC prognosis based on staging

A
171
Q

Electrolyte changes in vomiting patient?

A

Hypokalemia
Hypochloremia
Hyponatremia

172
Q

Name a NOAC that can be used in the treatment of a VTE and its dose and frequency

A

Apixaban 10mg oral twice daily for 7 days, then 5mg twice daily
for the treatment of a VTE.
Use 2.5mg daily in the prevention of a VTE.

If post hip surgery then don’t use apixaban. Instead, use dabigatran 150mg oral twice daily.

173
Q

Complicated vs uncomplicated gallstone disease?

A

Uncomplicated = biliary colic in the absence of complications

Complication = gallstone related complications
- cholecystitis, cholangitits, gallstone pancreatitis, gallstone ileus (gallstone causes obstruction of the small bowel), Mirizzi syndrome

174
Q

3 reasons for emergency surgery for UC?

A

Viscus perforation
Severe rectal bleeding  uncontrollable and causing hemodynamic compromise
Toxic megacolon

175
Q

What is small bowel syndrome?

A

Where the small bowel is not able to adequately absorb nutrients, fluids, and electrolytes. Common post-surgery.

176
Q

Causes of post-surgical AKI or decreased renal output?

A

PRERENAL:
Physiological response to surgery including release of cytokines and increased stress response -> increases ACTH release from the AP -> increase cortisol and aldosterone release -> increased Na+ and H2O reabsorption in the distal convoluted tubule -> decreased urine output.
Also, Post-op hypotension (decreased CO, vasodilatation and hypovalemia) causes baroreceptor stimulation to increase ADH release -> increased H2O reabsorption in collecting ducts -> decreased urine output

Hypovolemia post-surgery: dehydration -> decreased renal perfusion causes decreased GFR and urine output

RENAL:
Nephrotoxic substances (e.g. contrast, ABx, NSAIDs) or direct renal damage during surgery

POST-RENAL:
e.g. catheter obstruction, BPH

**Also UTI post-surgery likely due to catheter

177
Q

Features of a good screening test?

A

Screening is intended for a target population where they do not have symptoms of the disease

178
Q

What are WHO’s principles of early detection of disease?

A

Disease:
- must target a disease and look at a particular population group
- disease has an early latent period
- justify early detection of disease through its health burden

Test: (good screening test)
- high sensitivity and specificity
- detects disease while asymptomatic
- simple to perform and cost affective
- safe to perform
- reproducible in a variety of settings
-

Treatment:
- there must be an effective treatment for the disease
- improved survival if treated early -> i.e. treatment via screening better than treatment via clinical diagnosis

179
Q

What is the CEA (carcinoembryonic antigen) used for?

A

Monitoring and recurrence of CRC

180
Q

What cancer is CA 19.9 elevated in?

A

Pancreatic cancer and CRC

181
Q

What cancer is Bence-Jones protein elevated in?

A

Multiple myeloma -> highly sensitive and specific. Found in urine. Also called M-protein (monoclonal protein)

182
Q

Prevalence vs incidence?

A

Prevalence = TOTAL number of cases of a disease during a particular period of time

Incidence = number of NEW cases of a disease during a particular period of time

183
Q

Mortality rate?

A

Number of deaths caused by a disease over a period of time / the number of people at risk of dying in the same period

184
Q

Describing a gallstone on US?

A

Hyperechoic circular mass with posterior acoustic shadowing.

May have gallbladder wall thickening in cholecystitis

185
Q

Define delirium?

A

Acute confusional state with an organic cause -> dehydration, sepsis, toxins.

Characterised by a cognitive disturbance of attention and awareness.

Delirium is the most common surgical complication among older patients.

186
Q

What are the predisposing and precipitating factors of delirium?

A

Predisposing:
- change of environment (noise, cold, sleep deprived, hungry, thirsty)
- pre-existing conditions (co-morbidities, substance abuse - withdrawal, dementia, polypharmacy

Precipitating:
- full bladder
- pain
- hypoxia (big one to remember)
- alcohol or drug withdrawal
- sepsis
- metabolic -> electrolyte disturbance, BSL (high, low), acidotic
- endocrine -> thyroid conditions

187
Q

DDx for BPH?

A
  • Prostate cancer
  • UTI
  • Neurogenic bladder
  • Urethral stricture
188
Q

TURP complications

A

— Bleeding
— Urethral stricture or bladder neck contracture
— Perforation of the prostate capsule with extravasation
— Retrograde ejaculation (75%)
— Erectile dys unction (5%–10%)
— Urinary incontinence (< 1%)

189
Q

DDx for prostate cancer?

A
  • Urinary obstruction, eg, urethral stricture, stone, bladder neck contracture
  • Prostatitis
  • Benign prostatic hyperplasia
  • Prostatic stones
  • Bladder cancer
190
Q

Normal PSA levels?

A

4ng/ml (greater then 10 is suggestive of metastatic disease)

191
Q

Would serum alkaline phosphatase be elevated in metastatic prostate cancer?

A

yes - osteoblastic cancer

192
Q

Which BRCA gene is involved in an increased risk of CRC?

A

BRCA1

BRCA2 involved in prostate cancer

193
Q

Types of peripheral vertigo?

A

benign paroxysmal positional vertigo (dix hallpikes)

labyrinthitis (vestibular neuritis)

meniere’s disease (impaired endolymph absorption)

194
Q

List some poor prognostic factors in COPD?

A
  • frequent exacerbations (more than 3 times a year)
  • cachexia
  • signs of pulmonary hypertension
195
Q

treatment of COPD exacerbation?

A
  • oral ABx (amox and docy)
  • steroids (prednisolone 3-5 days)
196
Q

Organisms that causes acute exacerbation of COPD?

A

H. influenzae
Pseudomonas aeruginosa
Moraxella catarrhalis

197
Q

Triad involved in acute coagulopathy that increases bleeding?

A

coagulopathy + acidosis + hypothermia = increased bleeding

198
Q

Volume of fluid given to someone in hypovolemic shock?

A

20ml/kg of IV fluid bolus

199
Q

What is tranexamic acid used for?

A

To correct coagulopathy in bleeding patients

200
Q

IV mainetence fluids for adult?

A

25-30ml/kg/day

201
Q
A

ABG - hypoxia
D-dimer
Imaging -> TTE, V/Q scan, CTPA

202
Q

amiodarone dose and when in cardiac arrest?

A

3rd cycle if shockable rhythm and 300mg

203
Q

SIRS criteria?

A

TTTW

Tachycardia >90
Tachypnoea >20 or partial pressure of CO2 <32mmHg
Temperature >38 or <36
WCC >12,000 or <4,000

204
Q

What is serum tryptase used for?

A

Blood test investigation for suspected anaphylaxis. Will be elevated.

205
Q

What does electrical alternans on an ECG indicate?

A

Cardiac tamponade

206
Q

Treatment of melanoma

A

chemo - minimal benefit
radiotherapy - local regional disease such as brain met
surgical excision - only curative
some immunotherapies available

207
Q

Testicular torsion clinical features

A

Elevated testicle

Horizontal lie of the testis (bell clapper deformity

Absence of the cremasteric reflex

A negative Prehn sign (positive in epididymitis

Blue dot sign

208
Q

Best imaging modality for renal colic/stone?

A

Non-contrast CT of kidneys, ureter, and bladder

209
Q

Causes of elevated PSA?

A

BPH, prostatitis, UTU, urinary retention, catheterisation, or by prostate cancer

210
Q

What is Conn’s syndrome?

A

Hypoaldosteronism
- hyponatremia, hyperkalemia, hypertension

211
Q

Bare metal stents complications?

A

Increased risk of re-narrowing and clot formation. Leads to need of revascularisation due to increased risk of MI.
Patients should be put on DAPT (aspirin and clopidogrel) to reduce the risk of stent thrombosis.

212
Q

Medications used in drug eluting stents

A

antiproliferative drugs including paclitaxel or sirolimus

213
Q

Review arteries of the heart and ECG findings (Watt mentioned)

A
214
Q

Aspirin 1/2 life?

A

Half life is about 6hrs but it irreversibly inactivates platelets to prevent the synthesis of thromboxane A2. Platelet lifespan ~10days. Works for the lifetime of a platelet, therefore needs to be stopped 5-7 days prior to surgery.

215
Q

What is CHA2DS2-VAS used for?

A

To measure risk of arterial clot formation?

216
Q

Platelet plug formation? i.e. primary hemostasis
Watt

A

Adhesion - release of ADP, TXA, 5HT

Activation - change shape, secrete vWF, fibrinogen

Aggregation - to form platelet plug, and stimulation of the clotting cascade

217
Q

Normal platelet count

A

150-300 x10^9

218
Q

Platelet count in which spontaneous bleeding can occur?

A

<10

> 50 is usually ok for most operations

219
Q

What risk factors for blood clot formation would justify warfarin ‘bridging’?

A

AF + CHADS 5-6, or AF + CHADS-VASC7-8, or VTE in last 3mths, or recent embolic event, or a mechanical heart valve.

220
Q

Therapeutic vs prophylactic enoxaparin dose?

A

Therapeutic: treatment of VTE or bridging 1-1.5mg/kg daily

Prophylactic: 40mg subcut daily
20mg if CrCl between 15-30 ml/min

221
Q

Rivaroxaban (watt)

A

Inhibitor of factor Xa

Used in AF
absolute CrCl for its use is <15

222
Q

Apixaban (watt)

A

Factor Xa inhibitor

VTE treatment 10mg twice daily for 7 days then 5mg twice daily (oral)
VTE prophylaxis is 2.5mg daily (oral)

223
Q

Know about B-lactam antibiotics, how they work, and cell wall structure and shape

A
224
Q

Surgery with highest risk of SSI?

A

Colorectal -> gram -ves (E.coli, anaerobes)

225
Q

SSI risk factors?

A

Patient factors:
- age
- diabetes
- smoking
- obesity
- immunosuppression
- malnutrition
- length of hospital stay

Types of surgery:
- wound classification -> clean, clean contaminated, contaminated, dirty
- abscess
- foreign body
- open bowel
- should only be covered for 24hrs

Perioperative care factors:
- hair removal increases risk
- inadequate skin prep
- preop BSL control in diabetes
- inadequate or inappropriate prophylactic antibiotics (1hr before the first cut)

Intraoperative:
- open vs close theatre
- pressure in the OT (should be positive pressure)
- operation time

226
Q

Prophylaxis ABx for colorectal surgery?

A

Metronidazole 500mg IV + cefazolin 2g IV

227
Q

Prophylactic ABx for small bowel surgery?

A

Cefazolin 2g IV

228
Q

Tool to assess for c-spine damage?

A

NEXUS c-spine rules, and canadian c-spine rules

229
Q

What do yo expect to see on histology of cancer?

A

get answers to question. Some things include increased nucleus to cytoplasmic ratio, coarse chromatin, variable cell shapes and sizes.

230
Q

what should you ask for on a specimen for cytology?

A

microbiology, biochemistry,

231
Q

Difference between transudate and exudate (Watt)

A
232
Q

haemoglobin vs hematocrit?

A

Hb: is the measure of concentration of protein hemoglobin within RBCs. Requires the lysis of RBCs to release the hemoglobin. It is a concentration. Males are 14-18 g/dl, and females are 12-18 g/dl.

Hct: measures the % of RBC in total blood. It is a percentage. Male is about 45% and females are about 40%.

233
Q

Know about blood loss compensation (Watt)

A

including baroreceptors, chemoreceptors, SNS stimulation, osmoreceptors, RAAS, transcapillary fill

*look at the trauma tutorial

234
Q

SEs of blood transfusion? What does TACO and TRALI stand for?

A

anaphylaxis, fever, urticaria, ABO incompatibility (human error), infection (HIV, hep B)

TACO: transfusion related acute cardiac overload (BAD)

TRALI: transfusion related acute lung injury (immunological)

235
Q

How to know if an IV contrast on CT?

A

if the contrast in in the kidneys then been givenIV.
If the contrast is in the stomach then likely given an oral contrast.

Mention if a coronal or sagittal plane. May be in the osce (Watt)

236
Q

What is a smiths fracture?

A

low energy, volarly (palmer side) displaced, extra-articular fracture

237
Q

What is a Colles’ fracture?

A

low energy, dorsally displaced, extra-articular

238
Q

Compartment syndrome symptoms?

A

pain out of proportion
swelling
cool limb distally
redness/erythema
tingling/change in sensation
motor weakness
weak or absent pulse (bad)

239
Q

Garden classification of NOFs?

A
240
Q

What is the Pauwels classification used for?

A
241
Q

Describe 3 significant findings on this CT image?
What is the diagnosis?

A

Superficial haematoma on the left side of the head

Biconvex haemorrhage

Midline shift to the right

Diagnosis: extradural haematoma (aka epidural haematoma)

242
Q

If hit near the temple (over the pterion), which artery is likely to be damaged?

A

The middle meningeal artery (involved in 75% of extradural haematomas)

243
Q

What is the diagnosis? What is a salient feature?

A

Subdural haematoma (between the dura mater and the arachnoid mater).

Salient feature: crescentric shape of haemorrhage. Some midline shift.

244
Q

2 types of haemorrhagic strokes (based on location)?

A

subarachnoid (10% of all strokes) (bleeding between the arachnoid mater and the pia mater)

intracerebral haemorrhage

245
Q

What is the most common cause of a subarachnoid stroke??

A

ruptures of a saccular “berry” aneurysm

246
Q

Virchow’s triad components?

A

hypercoagulability
blood stasis
enodthelial injury

247
Q

Does heparin induce thromboctopenia occur with unfractionated or low molecular weight heparin?

A

unfractionated heparin

248
Q

CD15 and CD30 are markers for which cancer?

A

Hodgkin’s lymphoma

249
Q

How does acidosis affect coagulation?

A

Impairs enzymatic activation of coagulation factors, therefore get impaired coagulation.

250
Q

Does calcium assist in coagulation?

A

Yes (it acts as a co-factor)

251
Q

Will blood transfusions cause calcium depletion?

A

Yes, depleted during the storage process of the blood. Therefore should replace calcium in patients

252
Q

MoA for tranexamic acid?

A

Inhibits plasminogen from converting to plasmin. Plasmin is then not able to break down fibrin.

253
Q

TACO vs TRALI?

A

TACO:
- transfusion associated circulatory overload

TRALI:
- transfusion related acute lung injury

Usually within 6hrs of transfusion and has a high mortality.
Not related to poor crossmatching.
Patients with co-morbidities.

Cannot treat - can only give supportive management

254
Q

What does cryoprecipitate contain?

A

fibrinogen, vWF, fibrinnectin, factor 8, factor 13.

Takes the insoluble proteins from FFP

255
Q

What does prothrombinex contain?

A

factors II, IX, X

used in the reversal of warfarin and in haemophilia B (IX)

**Works quickly, is short acting

256
Q

Know about cranial bleeds (Skyring)

A
257
Q

Know about Pagets disease in respect to breast cancer (Skyring)

A
258
Q

What family hx is relevant in people with breast cancer?

A

Only 5% of breast cancer is familial

Increased risk:
- FDR <40 = 2x risk
- 2 FDR or SDR <60yr
- close relative bilateral breast cancer
- close male relative with breast cancer

259
Q

BRCA1 lifetime risk of breast and ovarian cancer

A

85% breast and 40% ovarian.

Increases the risk of triple negative cancer

260
Q

Which cancers is BRCA2 associated with

A

pancreatic cancer, melanoma, sarcoma, prostate cancer. Also ovarian cancer

261
Q

Type of inheritance of BRCA1/2?

A

autosomal dominant

262
Q

What is screened for in the new born guthrie test?

A

phenylketonuria
primary congenital hypothyroidism
cystic fibrosis
galactosaemia

263
Q

WHO principles or early detection relates to:
the disease/condition
test
treatment

Outline what is required for each

A

The disease/condition:
- needs to have a ‘burden of disease’
- there is a recognisable latent or early symptomatic stage
- the natural history of the condition should be adequately understood

The features of a good screening test:
- accurately detects the target condition while it is still asymptomatic
- cost effective
- sensitive and specific
- reproducible in a variety of setting
- safe to perform

The treatment:
- effective treatment is available
- early detective with treatment improves surviival
- benefits of screening outweights any harm

264
Q

What does CEA stand for?

A

chorioembryonic antigen

265
Q

How are tumour markers used?

A

screen fir malignancy
prognosis
determine the success of treatment
monitor recurrence

266
Q

What is required for consent?

A

Consent needs to be:
- specific to the treatment
- patient must be competent
- patient must be informed
- must be freely given

Patient requires:
- Benefits
- Risks
- Information
- Alternative treatments
- Natural progression of the disease

267
Q

Dose of apixaban for VTE treatment?

A

renal clearance > 25ml/min

268
Q

Does of apixaban for the prevention of VTE?

A

2.5mg oral daily

269
Q

Apixaban dose for atrial fibrillation?

A

5mg twice daily. If valvular AF, then use warfarin and adjust to INR of 2-3

270
Q

What is the drug class of enoxaparin?

A

low molecular weight heparin

271
Q

Name some anticoagulants and the doses required for the prevention of VTE

A
272
Q

what is neologism?

A

a new word or expression

273
Q

Classification of wounds?

A

clean wounds
clean contaminated wound
contaminated wounds
dirty wounds

274
Q

Which bacteria do gentamicin, metronidazole, cephazolin, and ampicillin cover?

A

cephazolin = gram +ve and skin flora

ampicillin = gram positive

metronidazole = anaerobes

gentamicin = wide spectrum but gram -ve in particular (does not cover an +ve)

275
Q

What are some predisposing and precipitating factors for post-op delirium?

A

Predisposing factors:
- change in environment
- pre-existing health conditions including dementia, polypharmacy, malnutrition, visual/hearing impairment

Precipitating:
- full bladder
- pain
- sepsis/infection
- hypoxia
- endocrine changes
- metabolic

276
Q

Initial assessment of a post-op patient with low urine output?

A

check operation notes - includes information about blood loss, fluid replacement during surgery

patient history - any medical conditions

ask patient about symptoms - SoB, full bladder, thirsty

check fluid chart - know input vs output

examination - assess fluid overload or dehydration

277
Q

Outline the body’s response during surgery that leads to decreased urine output?

A
  • stress response and release of cytokines: increase in SNS which causes vasoconstriction and reduced GFR. Also get increased cortisol which increases aldosterone release. Aldosterone causes increased sodium and water reabsorption in the DCT and CD.
  • decreased blood volume: baroreceptor response also increases SNS response, and activates the RAAS, which leads to increased aldosterone release
  • Will also have loss of serum H2O, which increases osmolality. This causes an increase in ADH which increasees H2O reabsorption in the CD.
278
Q

What are the two major types of stents?

A

bare metal stents and drug eluting stents.

ideally required to be on DAPT for at least 6 weeks for BMS and 6mths of DES.

279
Q
A
280
Q

Outline the process of platelet plug formation?

A

tissue damage leading to endothelial and collagen exposure –> platelet adheres –> release of receptor stimulants including thrombin, ADP –> get platelet activation –> secreting of vWF and other activating agents –> platelet aggregation –> formation of platelet plug.
Also further activation of the clotting cascade.

281
Q

BPH management?

A

5-alpha reductase, and tamsulosin (alpha-1 inhibitor for urinary retention)

282
Q
A
283
Q

How long after taking aspirin should you wait before performing surgery?

A

5-7 days

284
Q

When does bridging of an anticoagulant need to occur?

A

when the patient is a high srgical risk of bleeding and also a high risk of TE event

285
Q

During bridging of warfarin, what does the INR need to be one the day of surgery?

A

<1.5

286
Q

When do you commence enoxaparin during warfarin bridging?

A

commence when INR is </= 2. Also, use treatment dose (1.5mg/kg daily, or 1mg/kg x2 daily), not the prophylactic dose of 40mg subcut.

287
Q

When to stop taking warfarin prior to surgery?

A

take last dose 6 days prior to surgery so there are 5 days of not taking warfarin prior to the surgery.

288
Q

Advantages and disadvantages of warfarin?

Also disadvantages and advantages of DOACs?

A

Advantages of warfarin:
well known/studied anticoagulant

Disadvantages of warfarin:
requires monitoring
drug interactions
crosses the placenta (teratogenic)
high bleeding risk

Advantages of DOACs:
no monitoring
minimal drug interactions
fixed dosage
decreased risk of major bleeding compared with warfarin

Disadvantages:
short half-life -> therefore, even a single missed dose will impair anticoagulatory effect
not effective if mechanical heart valve

289
Q

What coagulation factors does prothrombinex replace?

A

Prothrombinex®-VF contains the concentrated human coagulation factors II, IX and X and low levels of the factors V and VII

290
Q

What does HAS-BLED stand for? And what is it assessing?

A

Risk of bleeding in a patient with AF

291
Q

vessel responsible for majority of extra-dural haematomas?

A

middle meningeal artery

292
Q

What is this?

A

cutaneous lupus

293
Q

What is Gilbert syndrome?

A

It is a diagnosis of exclusion -> will have completely normal investigations but patient will present as jaundice. It is an autosomal recessive condition where the liver is not able to metabolise billirubin at an adequate rate during times of physical stress (illness, drugs, alcohol). As a result, there is a build up of unconjugated billirubin in the blood, resulting in jaundice.

294
Q
A

know the gallstone image. This is choledocoliathesis

295
Q
A

Cutaneous larva migrans

Cutaneous larva migrans is the correct answer. It is most commonly caused by cat or dog hookworm larvae. The parasite is typically confined to the epidermis as it lacks the collagenase necessary to break through the basement membrane. Most infections are localized in the lower extremity as it is a common site of larval penetration. The eruption appears to migrate as the larvae move up to a few centimeters daily.

296
Q

Is lobular carcinoma in situ detected on mammogram screening?

A

no - usually detected on biopsy

297
Q

DDx of an itchy nipple?

A

CONTACT DERMATITIS
ATOPIC DERMATITIS
INFECTION – bacterial, fungal
PSORIASIS
MALIGNANCY – SCC, Paget’s disease

298
Q

chemo used in breast cancer?

A

FEC = fluorouracil, epirubicin and cyclophosphamide

299
Q

Tamoxifen MoA, use, and side effects?

A

used in ER positive breast cancer. Competitive ER antagonist in the breast, but it increased oestrogen sensitivity in other tissues. Increases the risk of endometrial cancer.

300
Q

How does a flail chest occur?

A

results from 2+ ribs being fracture in 2 or more places. Impairs movement during inspiration and expiration

301
Q

Management of a tension pneumothorax?

A

A-E assessment
thoraccentesis 2nd intercostal space mid-clavicular line

302
Q

Which genes are mutated in Lynch syndrome?

A

MLH1, MSH2, MSH6, PMS2, EPCAM

303
Q

Which gene in mutated in peutz-jeghers syndomr?

A

STK11

304
Q

Does a blood transfusion cause a left or right shift in the oxygen dissociation curve?

A

Causes a left shift as the RBCs lose 2,3 DPG and O2, meaning the transfused blood cell want to hold onto the O2. Therefore, does not improve oxygen delivery to tissues.

305
Q

MOA of heparin?

A

Potentiates the actions of anti-thrombin to prevent the convervsion of prothombin to thrombin.

306
Q

Management of compartment syndrome?

A
307
Q

Management of BPH?

A

Non-pharm:
Medication review - e.g. anti-histamines can contribute to urinary retention
Lifestyle: no caffeine or large amounts of fluid before bed
Bladder retraining and double voiding

Pharm:
alpha blockers including tamsulosin (increases risk of patient falls)
5-alpha reductase inhibitor e.g. finasteride
antimuscarinics

Surgical:
TURP (transurethral resection of the prostate)

308
Q

Method for investigating peripheral vascular disease?

A

History and exam (ask about intermittent claudication, Buerger’s)
ABI
Angiography
Dublex US - if angiogram is contraindicated (e.g. contrast allergy)

309
Q

DONT forget to mention DRE for every GIT exam (if relevant)

A
310
Q

How many eye tests for a cranial nerve exam?

A

7
acuity
eye fields
blind spot
fundus
accommodation
eye movement
light - direct and consensual response

311
Q

Causes of a hypertensive crisis?

A
  • anti-hypertensive medication non-adherence
  • MAOIs (especially if eating cheese)
  • pre-eclampsia
  • hyperthyroidism
  • pheochromocytoma (catecholamine secreting tumour of the adrenal medulla)
312
Q

Criteria for PE or DVT?

A

Well’s criteria

313
Q

location of DVT in legs?

A

Above-knee (proximal) DVT if present in the popliteal, superficial femoral (despite the name, still a deep vein), deep femoral, common femoral or external iliac veins

Below knee (distal) DVT if present in the soleal or peroneal veins

314
Q

Investigating DVT?

A

Doppler US

UEC to assess which choice of treatment
D-dimer

315
Q

What is Homan sign?

A

Positive in DVT - pain on dorsiflexion of the foot of the affected leg?

316
Q

Features of DVT?

A

general features:
non-compressible venous segment
loss of phasic flow on Valsalva manoeuvre
absent colour flow if completely occlusive
lack of flow augmentation with calf squeeze
increased flow in superficial veins

acute thrombus:
increased venous diameter
soft/deformable intraluminal material
smooth surface
free-floating edge (uncommon)

chronic post-thrombotic change:
normal or decreased venous diameter
rigid intraluminal material
irregular surface
synechiae or bands
calcifications (rare)
+/- acute thrombus

317
Q

Lesion thickness is the strongest predictor of prognosis in patients with a primary cutaneous melanoma

A
318
Q

NBCSP features?

A

the use of iFOBT as the screening test
provision of iFOBT screening at no cost to participants
distribution of invitations and screening tests by mail
analysis of screening in a central laboratory
follow-up of positive test results, mostly by colonoscopy, through the usual care pathway backed up by a central reminder service
central collation of data and reporting of NBCSP outcomes via regular reports

319
Q

Which gastric cancer is highly aggressive and often spreads to the ovaries?

A

Signet ring cell carcinoma (SRCC) is an aggressive and poorly differentiated gastric adenocarcinoma that occurs in the stomach in 90% of cases

320
Q

SLE antibodies?

A

anti-nuclear antibodies (ANA), anti-dsDNA antibodies, and anti-Sm antibodies

321
Q

Antiphospholipid antibodies?

A

lupus anticoagulant, anti-cardiolipin, anti-β2-glycoprotein

322
Q

Review HRT options

A
323
Q

What are the anti-thyroid antibodies?

A

TSH receptor antibodies (Graves disease)
Thyroid peroxidase antibodies (Hashimotos)
Thyroglobulin antibodies (can be both but not always)

324
Q
A
325
Q
A