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Medicine MD2 > Week 2 > Flashcards

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
Q

What is the treatment for melanoma?

A

Surgical excision

Imiquimod topical treatment

Sentinel node biopsy

Ipilimumab - stage III melanoma

Radiotherapy

Chemotherapy

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26
Q

What is present on hx and examination of multiple myeloma?

A

Anaemia - SOB, pallor, syncope, fatigue

Bone pain (often back)

Febrile

Renal failure

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27
Q

What are some investigations and their findings in multiple myeloma?

A

Urine electrophoresis - hypogammaglobinemia, albuminuria

Skeletal assessment - osteopenia

Bone marrow aspirate - plasma cell infiltration

Serum calcium - hypercalcaemia

FBE - anaemia

Creatinine elevated

Low albumin

28
Q

What are some differential diagnoses of monoclonal gammopathy?

A
29
Q

What is smouldering myeloma?

A

Early asymptomatic face of myeloma - evidene on bone marrow biopsy - doesn’t require active treatment straigh away

30
Q

What are some complications of myeloma?

A

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
Q

What are some treatment options for multiple myeloma?

A

Dexamethasone pre transplant

DVT prophylaxis (aspirin, enoxaparin)

Stem cell collection

Transplant - autologous or allogenic

Bisphosphonates and analgesics for bone disease

32
Q

What are the 3 broad cell lineages of lymphoma?

A

B lymphocyte

T lymphocyte

Hodgkin

33
Q

What is non-hodgkin lymphoma?

A

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
Q

What are some risk factros for hodkin lymphoma?

A

EBV

Family History

Young adult from higher SES

35
Q

How is hodgkin lymphoma staged?

A
36
Q

What are the treatment options for Hodgkins lymphoma and the complications?

A

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
Q

What are the signs and symptoms of diffuse large B cell lymphoma?

A

Painless swelling in the neck, armpit or groin (caused by lymphadenopathy)

Extra nodal lymphadenopathy causing abdo pain, diarrhoea or bleeding

Constitutional symptoms

38
Q

What are the prognostic factors for diffuse large B cell lymphoma?

A

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
Q

What is the treatment for diffuse large B cell lymphoma?

A

Rituximab chemotherapy

Radiation

Stem cell transplant

Methotrexate chemotherapy if cancer has infiltrated spinal cord

40
Q

What are INR/PT and APTT tests used for?

A

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
Q

What are the features of vWF disease?

A

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
Q

What are the features of immune thrombocytopenia?

A

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
Q

What are the features of haemophilia A?

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
Q

What are the features of haemophilia B?

A

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
Q

What are some risks for prostate cancer development?

A

High fat diet

Hormonal influence

Black men have highest incidence

Age > 50

Family history

Elevated PSA

46
Q

What is the clinical presentation of prostate cancer?

A

Nocturia

Urinary frequency

Urinary hesitancy

Dysuria

Abnormal DRE - asymmetrical nodular prostate

47
Q

What are the differentials of a raised PSA?

A

Prostate cancer

Benign prostatic hyperplasia

Prostatitis

48
Q

What are the roles of biopsy and DRE in prostate cancer diagnosis?

A

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
Q

What are the treatment options for localised prostate cancer?

A

Surveillance - 3monthly PSA, 6monthly DRE

Prostatectomy

Radiotherapy

50
Q

How would disease recurrence post radical treatment for localised prostate cancer be picked up?

A

Rise in PSA (but slight rise is also seen with cessation of neoadjuvant treatment)

Gleason score > 8

51
Q

What are the salvage options post radical treatment for localised prostate cancer?

A

Radiotherapy

Prostatectomy - good level of control but higher risk of incontinence, impotence and rectal damage

Cryotherapy

High intensity focused US

Adjuvant hormonal therapy

52
Q

What are the treatment options for metastatic prostate cancer?

A

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
Q

What are the causes of diarrhoea?

A

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
Q

What are the differences b/w small and large bowel diarrhoea?

A

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
Q

What is the pathology of ulcerative colitis?

A

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
Q

What is the clinical presentation of ulcerative colitis?

A

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
Q

What are the complications of ulcerative colitis?

A

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
Q

What is the treatment for ulcerative colitis?

A

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
Q

What is the epidemiology of Chron’s?

A

Peaks in 20s and 70s

Genetics, dietary factors and immune response play a role

60
Q

What is the pathology of Chrons?

A

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
Q

What is the clinical presentation of chrons?

A

Abdo pain

Diarrhoea

Vomiting

Weight loss

Fissures and abscesses

Clubbing

Large joint arthritis

Conjunctivitis

62
Q

What are the complications of chrons?

A

Increased risk of GI malignancy - adenocarcinoma arising in distal ileum with poor prognosis

63
Q

What are the management options for chrons?

A

Smoking cessation

Low residue diet

Low fat diet

Treatment of vitamin deficiencies

Prednisolone

Azathioprine

Methotrexate

Infliximab

Surgery

64
Q

What is the action of aspirin?

A

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
Q

What is the action of warfarin?

A

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
Q

What is the action of heparin?

A

Binds to antithrombin leading to reduced thrombin and factor 8a activation

67
Q
A

Medicine MD2 (3 decks)

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