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Week 2 Flashcards

1
Q

What increases the risk of breast cancer?

A

Nulliparous Earlier menarche Late menopause Interrupted pregnancy Obesity First degree relative

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2
Q

What decreases the risk of breast cancer?

A

Breastfeeding Late menarche Early menopause Normal BMI Childbirth Oopherectomy

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3
Q

What are the issues with breast cancer surgical management?

A

Mastectomy - emotional wellbeing of patient, reconstructive surgery option Lymph node clearance - risk of lymphedema, pain, loss of function and Oopherectomy - egg conservation, early menopause

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4
Q

What are the options for adjuvant systemic therapy for breast cancer?

A

Chemotherapy - tumours >1cm, ER -ve OR pre surgery to shrink tumour Endocrine - tamoxifen (ER/PR), herceptin (HER2 +ve), aromatase inhibitor (block androgen conversion to oestrogen) Radiotherapy - tumour >5cm, lymph node involvement, adjuvant to breast conservation surgery, risk of burns, secondary cancer, toxicity

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5
Q

What are the fertility issues in a premenopausal woman undergoing cancer treatment?

A

Chemotherapy can cause premature ovarian failure or amennorhea Consider fertility preservation on diagnosis of breast cancer

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6
Q

What lifestyle factors may have altered the natural history of breast cancer?

A

Alcohol - 2-5 alcoholic drinks per day increases risk of breast cancer 150% Overweight/obese - increased oestrogen release from adipose tissue Lack of physical activity Less children and lower breastfeeding duration OCP Depo injections HRT Older population Later pregnancy (> 30) Smoking More radiation exposure (CT)

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7
Q

When is a breast cancer relapse more common?

A

Within 5 years of diagnosis ER +ve cancer

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8
Q

What is this and what are the risk factors for formation?

A

Solar/Actinic keratosis - sun exposure, age, albinism, male, light skin, HPV, immunocompromised

p53 mutation leads to damaged keratinocytes that cannot undergo apoptosis

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9
Q

What are some features on history of solar keratosis and how is it diagnosed?

A

Pruritis, bleeding, hx of sun damage

Diagnose via dermatoscopy and skin biopsy

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10
Q

What is the treatment for solar keratosis?

A

Cryotherapy

Topical steroids

Phototherapy

Dermabrasian

Sun protection (future, and reduce progression to SCC)

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11
Q

What is this and what are the risk factors for development?

A

Squamous Cell Carcinoma - sun damage, previous skin cancer, ionising radiation, burns, arsenic, tar, HPV, immunocompromised, age, fair skin

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12
Q

What is evident on history of an SCC and how is it diagnosed?

A

Bleeding, crusting, pruritis, poor lesion healing, tender, skin mobile over other structures

Diagnose via biopsy (risk of invasion and metastases)

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13
Q

What is the treatment for SCC?

A

Bowens (SCC in situ) - cryotherapy, photohterapy, curretage, fluorouracil (topical), Mohs, radiotherapy

Invasive - surgical excision, Mohs (high risk on face - need 6mm margins)

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14
Q

What is this condition and what are the risk factors for development?

A

Basal Cell Carcinoma

Risks - UV exposure, radiation, arsenic, transplant history, +40

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15
Q

What are the features of a history of BCC and how is it diagnosed?

A

History - pearly nodular lesion, bleeding, ulcerated, telangiectasia, crusts and non-healing wounds

Diagnosis - biopsy and dermatoscopy (often diagnosable by appearance and hx)

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16
Q

What is the treatment for BCC?

A

Vismodegib (reduces tumour load)

Surgical excision

Curettage and cautery

Radiotherapy

Cryotherapy

Mohs

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17
Q

What is this condition and what are the risk factors for development?

A

Seborrheic Keratoses

Risks - sun exposure, age, fair skin, family history

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18
Q

What is the history of seborrheic keratoses and how is it diagnosed?

A

Stuck on lesion, wart like, raised, painless, itchy

Diagnosis with dermoscopy and biopsy ( may progress to Bowen’s and SCC)

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19
Q

What is the treatment for seborrheic keratoses?

A

Corticosteroids

Curettage or cautery

Cryotherapy

Laser/dermabrasion

Tretinoin

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20
Q

What is this condition and what are the risk factors?

A

Melanocytic Naevi

Overgrowth of hair cells and melanocytes - often congenital - round or oval shaped pigment patches, may have excess hair growth, rough surface, often become darker and more hairy in puberty

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21
Q

What is the treatment for melanocytic naevi and what is the risk of no treatment?

A

Observation

Surgery

Dermabrasion

Shave excision

Chemical peel

Laser therapy

No Treatment - risk is development to malignant melanoma (mainly related to size of naevi)

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22
Q

What is this and what are the risk factors for development?

A

Malignant Melanoma

Risks: UV exposure, > 100 naevi, > 5 dysplastic naevi, previous extreme sun burn, fair skinned (fitzpatrick I or II), blue eyes, red hair, immunosuppression, hx of skin cancer, xeroderma pigmentosum

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23
Q

What are the features on history that make melanoma likely and how is it diagnosed?

A

ABCDE - asymetrical, irregular borders, multiple colours, diameter >6mm, evolving lesion

Spontaneous bleeding or ulceration

Constitutional symptoms

Bluish veil - dermal fibrosis

Diagnosed via biopsy and dermatoscopy

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24
Q

How is melanoma staged and how does this affect prognosis?

A

Stage 0 (in-situ melanoma): >98%

Stage I (Breslow’s depth <1 mm and no nodal or metastatic disease): 90% to 95%

Stage II (localised disease, intermediate to thick depth): 45% to 78% (78% for non-ulcerated melanoma of depth 1 to 4 mm; 45% for an ulcerated melanoma >4 mm depth)

Stage III (nodal metastases): 69% (non-ulcerated melanoma of any depth with a single positive node) to 26% (ulcerated melanoma of any depth with 4 or more positive nodes)

Stage IV (metastatic): without treatment, overall prognosis is bleak, ranging from 3% to 10% depending on the extent and sites of metastasis. New drugs are changing this, with 20% having long-term survival with ipilimumab, and newer drugs await long-term follow-up data.

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25
What is the treatment for melanoma?
Surgical excision Imiquimod topical treatment Sentinel node biopsy Ipilimumab - stage III melanoma Radiotherapy Chemotherapy
26
What is present on hx and examination of multiple myeloma?
Anaemia - SOB, pallor, syncope, fatigue Bone pain (often back) Febrile Renal failure
27
What are some investigations and their findings in multiple myeloma?
Urine electrophoresis - hypogammaglobinemia, albuminuria Skeletal assessment - osteopenia Bone marrow aspirate - plasma cell infiltration Serum calcium - hypercalcaemia FBE - anaemia Creatinine elevated Low albumin
28
What are some differential diagnoses of monoclonal gammopathy?
29
What is smouldering myeloma?
Early asymptomatic face of myeloma - evidene on bone marrow biopsy - doesn't require active treatment straigh away
30
What are some complications of myeloma?
Bone pain Vertebral fracture Hypercalcaemia Anaemia Thrombocytopenia (linked to - tumour infiltration of bone marrow, renal impairment and myelosuppressive effects of chemotherapy) Leukopenia Renal failure Recurrent infections
31
What are some treatment options for multiple myeloma?
Dexamethasone pre transplant DVT prophylaxis (aspirin, enoxaparin) Stem cell collection Transplant - autologous or allogenic Bisphosphonates and analgesics for bone disease
32
What are the 3 broad cell lineages of lymphoma?
B lymphocyte T lymphocyte Hodgkin
33
What is non-hodgkin lymphoma?
Heterogeneous group of malignancies in the lymph system - B and T cell lymphomas. Cancer arising when B and T lymphocytes undergo a malignant change and multiply in an uncontrolled way - form tumours in lymph nodes and around the body. Majority are B lymphocyte derived
34
What are some risk factros for hodkin lymphoma?
EBV Family History Young adult from higher SES
35
How is hodgkin lymphoma staged?
36
What are the treatment options for Hodgkins lymphoma and the complications?
Chemotherapy Radiotherapy Immunotherapy Complications * Radiotherapy thyroid abnormalities (hypothyroid, Graves, thyroid cancer) * Radiation and chemotherapy secondary malignancies, heart disease, pulmonary toxicity, ovarian dysfunction, testicular dysfunction, impaired immunity
37
What are the signs and symptoms of diffuse large B cell lymphoma?
Painless swelling in the neck, armpit or groin (caused by lymphadenopathy) Extra nodal lymphadenopathy causing abdo pain, diarrhoea or bleeding Constitutional symptoms
38
What are the prognostic factors for diffuse large B cell lymphoma?
Stage Age ECOG Status: 0 - no symptoms, 1 - symptoms but ambulatory, 2 - bedridden for less than half the day, 3 - bedridden half the day or longer, 4 - chronically bedridden and needs ADL assistance Elevated LDH Extranodal sites
39
What is the treatment for diffuse large B cell lymphoma?
Rituximab chemotherapy Radiation Stem cell transplant Methotrexate chemotherapy if cancer has infiltrated spinal cord
40
What are INR/PT and APTT tests used for?
INR/PT - test of extrinsic clotting, used to measure warfarin effect levels, normal level is between 0.8-1.2 and with warfarin is 2-3, mechanical valve 2.5-3.5 APTT - characterises blood coagulation/clotting, measure of intrinsic clotting time
41
What are the features of vWF disease?
Most common inherited bleeding disorder vWF is important for platelet adhesion and factor VIII transport Autosomal dominant - decreased concentration of vWF If severe there may be mucosal bleeding Blood often normal except for reduction in platelets and APTT prolonged Diagnosis via immunoassay Treat with tranexamic acid, infusion or nasal spray to release stored vWF
42
What are the features of immune thrombocytopenia?
Low platelets not associated with systemic disease Chronic in adults but usually self limiting and acute in children Spleen size normal Treatment - corticosteroids, splenectomy, immunosuppression, thrombopoietin receptor agonist drugs Signs & Symptoms - petechiae, purpura, mucosal bleeding Diagnosis - FBE with platelets elevated
43
What are the features of haemophilia A?
X-linked recessive condition, deficiency of factor VIII Low factor VIII levels predispose to bleeding Bleeds into joints (haemarthroses) cause chronic deformity, swelling and pain Increase in haematuria and intracranial haemorrhage Investigations - prolonged APTT, factor VIII assay Contraindication for IM injections, use of NSAIDs
44
What are the features of haemophilia B?
X-linked recessive condition - deficiency of factor IX Severely affected patients develop haemarthroses Recombinant factor IX for treatment Prophylactic treatment can be given once or twice weekly
45
What are some risks for prostate cancer development?
High fat diet Hormonal influence Black men have highest incidence Age \> 50 Family history Elevated PSA
46
What is the clinical presentation of prostate cancer?
Nocturia Urinary frequency Urinary hesitancy Dysuria Abnormal DRE - asymmetrical nodular prostate
47
What are the differentials of a raised PSA?
Prostate cancer Benign prostatic hyperplasia Prostatitis
48
What are the roles of biopsy and DRE in prostate cancer diagnosis?
Biopsy is required to see if prostate cancer is present and to give an idea of how aggressive the cancer is, PSA alone is not diagnostic of prostate cancer DRE - can be used to distinguish between prostate cancer and BPH, but is not recommended as a standard test for patients who have no symptoms of prostate cancer (may lead to unnecessary prostate biopsy)
49
What are the treatment options for localised prostate cancer?
Surveillance - 3monthly PSA, 6monthly DRE Prostatectomy Radiotherapy
50
How would disease recurrence post radical treatment for localised prostate cancer be picked up?
Rise in PSA (but slight rise is also seen with cessation of neoadjuvant treatment) Gleason score \> 8
51
What are the salvage options post radical treatment for localised prostate cancer?
Radiotherapy Prostatectomy - good level of control but higher risk of incontinence, impotence and rectal damage Cryotherapy High intensity focused US Adjuvant hormonal therapy
52
What are the treatment options for metastatic prostate cancer?
Prostatectomy Adjuvant radiotherapy * External beam radiotherapy - high energy x-ray beams directed at prostate * Brachytherapy - radioactive material inserted into prostate Hormone therapy * Androgen deprivation therapy (5 alpha reductase inhibitor) * Orchidectomy * LH receptor agonist injections (block testosterone synthesis) Chemotherapy
53
What are the causes of diarrhoea?
Secretory - secretion of chloride and water * Increased electrolyte secretion * Cholera * E.coli * Pancreatic cholera * Villous adenoma Osmotic - increased amounts of poorly absorbable osmotically active solutes in the gut lumen * Maldigestion * Disaccharidase deficiency * Lactose intolerance Exudative - due to exudation of mucous, blood and protein from site of active inflammation into bowel lumen * IBD - Ulcerative colitis Infectious * Shigella * Entamoeba histolytica Malabsorption Motility Disorder - abnormal intestinal motility with decreased contact b/w luminal contents and mucosal surfaces * IBS * Thyrotoxicosis
54
What are the differences b/w small and large bowel diarrhoea?
Large * Increased frequency of defecation * Small quantities * Urgency and tenesmus (needing to go again soon after defecation) * Mucous * Red blood may be present * Weight loss rare * Left iliac fossa pain Small * Normal or slightly increased frequency * Large quantity of bulky or watery faeces * No urgency or tenesmus * Dark black melena with bleeding * Weight loss may be present * Central abdominal pain
55
What is the pathology of ulcerative colitis?
Continuous inflammation, worse distally and rectum is almost always involved - inflammation in mucosa and submucosa Inflammation leads to excess mucous production and triggers diarrhoea
56
What is the clinical presentation of ulcerative colitis?
Bloody diarrhoea Mucous and pus in stool Abdo discomfort Tenesmus (with rectal involvement) Malaise and anorexia Clubbing Mouth ulcers Arthralgia Iritis Erythema nodosum - painful itchy raised lumps in skin (legs most common) Pyoderma gangrenosum - pussy dead tissue, black necrotising mass, most common on legs or around a stoma Primary sclerosing cholangitis
57
What are the complications of ulcerative colitis?
Toxic Megacolon - deeper layer of bowel becomes affected and colon enlarges and may perforate - colon diameter \> 6cm Acute attack - tachycardia, heavy bleeding, pyrexia Dysplasia - two sites is reason for surgery to avoid malignancy
58
What is the treatment for ulcerative colitis?
Corticosteroids - hydrocortisone, prednisolone, dexamethasone (many side effects so not used for long term management - good for inducing remission but not for maintaining) Amino-salicylate - help to maintain remission (5-ASA), may be nephrotoxic, thought to work by trapping ROS to reduce inflammation Immunosuppressant's (azathioprine, cyclosporin) - may be used in severe cases of UC that don't respond to other treatments Surgery * Restorative proctocolectomy - total removal of colon and rectum but preservation of anus for anastomosis (usually anastomosis occurs later to reduce morbidity and mortality) * Complete proctocolectomy and permanent ileostomy - generally in elderly patients
59
What is the epidemiology of Chron's?
Peaks in 20s and 70s Genetics, dietary factors and immune response play a role
60
What is the pathology of Chrons?
Causes skip lesions where part of bowel sit unaffected between affected sections Most commonly ileocaecal Often causes malabsorption due to stricturing and fibrosis of the small intestine (leads to shortening)
61
What is the clinical presentation of chrons?
Abdo pain Diarrhoea Vomiting Weight loss Fissures and abscesses Clubbing Large joint arthritis Conjunctivitis
62
What are the complications of chrons?
Increased risk of GI malignancy - adenocarcinoma arising in distal ileum with poor prognosis
63
What are the management options for chrons?
Smoking cessation Low residue diet Low fat diet Treatment of vitamin deficiencies Prednisolone Azathioprine Methotrexate Infliximab Surgery
64
What is the action of aspirin?
Aspirin moves into the stomach and moves through the endothelium (endothelium produces prostacyclin) then the aspirin moves into the platelets in the gastric blood supply and permanently binds to COX – preventing thromboxane production (thromboxane vascoconstricts). Platelets don’t have a nucleus so they cannot resynthesise COX therefore cant form thromboxane, endothelial cells have a nucleus so they can produce more COX – leading to normal prostacyclin (vasodilator and platelet inhibitor) production – shifting the system towards vasodilation and anti coronary heart disease (less platelet activation for clotting and increased vessel diameter). This only happens for low dose of aspirin, because at a low dose the platelets can take up all of the aspirin from the stomach, but in a high dose aspirin would move to other cells.
65
What is the action of warfarin?
Vitamin K reductase inhibitor - prevents reduction of vitamin K, and therefore prevents activation of factors 2, 7, 9 and 10 - to reduce coagulation Reversed by vitamin K Increased by vitamin K deficiency or aspirin addition
66
What is the action of heparin?
Binds to antithrombin leading to reduced thrombin and factor 8a activation
67

Medicine MD2 (3 decks)

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