Concise Flashcards Sem 2B

1
Q

Give the names and functions of the fat-soluble vitamins.

A

Fat-soluble Vitamins = ADEK

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2
Q

Explain the results of deficiency of each of the vitamins.

A

Vitamin Deficiencies

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3
Q

Describe the pathogenesis of Wernicke-Korsakoff syndrome.

A
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4
Q

Describe some features of Wernicke-Korsakoff syndrome.

A

Wernicke’s Encephalopathy

  1. Occulomotor abnormalities – nystagmus, opthalmoplegia
  2. Ataxia of gait (cerebellum) – wide-based stance and slow-uncertian, short-stepped gait
  3. Derangement of mental function – confusion, apathy, disorientation

Korsakoff’s Psychosis

  1. Retrograde amnesia – inability to recall events that occurred before the onset of amnesia
  2. Anterograde amnesia – inability to acquire new information or make new memories
  3. Confabulation – unconscious creation of facts and experiences to fill gaps in memory
  4. Peripheral neuropathy, postural hypotension, tachycardia
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5
Q

Briefly list the types of long-term memory.

A

Types of Long Term Memory

Explicit (Declarative) Memory

  1. Facts (semantic)
  2. Events (episodic)

Implicit (Non-Declarative) Memory

  1. Priming - recognition or recall of words, objects or sounds improved by prior exposure to these stimuli
  2. Procedural – skills and habits
  3. Associative learning – classical and operant conditioning
  4. Non-associative learning – habituation and sensitisation
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6
Q

List the four main metabolic effects of alcohol.

A
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7
Q

List the 4 major causes of death due to alcohol.

A

Major causes of death due to alcohol

  1. Alcoholic liver disease
  2. Motor vehicle crash injury
  3. Cancer
  4. Suicide
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8
Q

List 4 criteria for which one or more needs to be met in a 12- month period to constitute alcoholism.

A

Alcoholism

  1. Recurrent substance use resulting in failure to fulfil major role obligations at work, school or home
  2. Recurrent substance use in situations in which it is physically hazardous (eg driving, using machinery)
  3. Recurrent substance-related legal problems
  4. Continued substance use despite having persistent or recurrent social or interpersonal problems caused or exacerbated by the effects of the substance
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9
Q

Describe two medications that can be given to treat alcoholism.

A

Alcoholism - Pharmacological Treatment

Disulfiram: alcohol dehydrogenase inhibitor

  • Requires a motivated patient and a dose supervision carer – begin >48 hours after last drink
  • Remains inert unless ethanol is taken
  • Within minutes of ethanol intake, the patient experiences headaches, dyspnoea, nausea, blurred vision, vomiting, sweating, weakness
  • Reaction is short-lived but can be severe/life threatening

Naltextrone: opiod antagonist

  • Blocks alcohol ‘high’ by blocking opoid receptors and → ↑ cravings
  • Decreases rate of relapse
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10
Q

List some of the features of simple withdrawal, withdrawal complicated by fits and delirium tremens.

A

Simple Withdrawal

  1. Tremor
  2. Sweating
  3. Nausea
  4. Vomiting
  5. Malaise
  6. Anxiety
  7. Agitation
  8. Depressed mood
  9. Tachycardia
  10. ↑ Blood pressure

Withdrawal Complicated by Fits → Grand mal tonic – clonal fits (usually only 1 fit during withdrawal)

Delerium Tremens

  1. Occurs 24h-7d after cessation
  2. Tremor & agitation
  3. Clouding of consciousness
  4. Disorientation
  5. Hallucinations
  6. Paranoid delusions
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11
Q

Give some advantages and disadvantages of MRI and CT.

A
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12
Q

List some contraindications to MRI.

A

Contraindications to MRI

  1. Aneurysm clips placed in the last 6 months
  2. Surgical clips placed in the last 6 weeks
  3. Neurostimulator devices
  4. Pacemaker or implantable defibrillator
  5. Cochlear implant
  6. Critical illness
  7. Claustrophobia
  8. Metallic ocular foreign body (welding history), metallic shrapnel
  9. Other metallic implanted devices such as insulin pumps
  10. Obesity (maximum table allowance is ~160kg)
  11. Pregnancy
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13
Q

List some general causes of anaemia.

A

Causes of Anaemia

  1. Blood loss - acute (trauma), chronic (GIT lesions, gynaecologic disturbances
  2. Impaired RBC production
    • Defective Hb production - iron deficiency, chronic disease
    • Defective DNA synthesis – B12/folate deficiency
    • Stem cell failure – aplastic anaemia
    • Bone marrow replacement – e.g. infiltration by malignant disease
    • Inadequate erythropoietin stimulation – chronic renal failure
    • Other nutritional/toxic factors: scurvy, protein malnutrition, chronic liver disease, hypothyroidism
  3. Increased haemolysis
    • Intrinsic RBC abnormalities – haemoglobinopathies (sickle cell/thalassaemia), membrane defects, enzyme deficiency (G-6-Pase), acquired defects
    • Extrinsic causes - autoimmune haemolytic anaemia, haemolytic disease of the newborn, blood transfusion reactions, drug-induced immune haemolytic anaemia, infections (malaria, mycoplasma), snake venom, lead poisoning, physical trauma, hypersplenism
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14
Q

Outline the process of iron absorption.

A

Process of Iron Absorption

  1. Cytochrome B on the brush border converts Fe3+ to Fe2+ (vitamin-C dependent)
  2. Fe2+ is transferred over the brush border by DMT-1
  3. Some Fe2+ is converted back to Fe3+ and stored as ferritin
  4. The rest of the Fe2+ is transferred into the interstitium by ferroportin (FP)
  5. Fe2+ is then converted to Fe3+ by hephaestin (HP) or ceruloplasmin (copper-dependant)
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15
Q

List 7 functions of iron.

A

Functions of Iron

  1. Oxygen transport (haemoglobin)
  2. Cellular respiration (TCA cycle, electron transfer chain etc.)
  3. DNA synthesis
  4. Neurotransmitter synthesis
  5. Hormone synthesis
  6. Embryogenesis (myelin synthesis)
  7. Host defence (neutrophil killing)
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16
Q

Outline the regulation of iron metabolism.

A

Regulation of Iron Metabolism

  1. Haemochromatosis Protein (HFE) - reduces cellular uptake of transferrin
    • Binds transferrin receptor (TfR) and halves its binding capacity for transferrin
    • Also regulates release of Hepcidin by the liver
  2. Hepcidin - regulates iron absorption
    • Released by the liver in response to ↑transferrin:Fe complexes
    • Inhibits ferroportin on entrocytes → buildup of iron in enterocytes → ↓absorption
    • Also inhibits DMT-1 and Cytochrome B → ↓uptake of iron into enterocytes
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17
Q

List five general causes of iron deficiency.

A

Causes of Iron Deficiency

  1. Blood loss (occult GIT bleeding and menstruation)
  2. Pregnancy (loss of iron to the foetus)
  3. Rapid growth (especially 0-2 years)
  4. Malabsorption
  5. Dietary insufficiency
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18
Q

List 8 symptoms of iron overload.

A

Iron Overload Symptoms

  1. Weakness
  2. Abdominal pain
  3. Muscle aches
  4. Finger joint pain
  5. Dyspnoea on exertion
  6. Bronze colour
  7. Hepatomegaly; cirrhosis
  8. Pancreatic fibrosis, diabetes mellitus
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19
Q

Summarise α and β- Thalassaemia.

A
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20
Q

Summarise the pathogenesis of β-Thalassaemia.

A
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21
Q

Summarise the pathogenesis of sickle cell anaemia.

A
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22
Q

List some clinical features of homozygotic sickle cell anaemia.

A

Homozygotic Sickle Cell Anaemia - Clinical Features

  1. Severe haemolytic anaemia
  2. Patients present between 6 months – 3 years
  3. 90% survive to 20 years, 50% survive > 50 years
  4. Splenomegaly
  5. Continuous fibrosis → autosplenectomy by adulthood
  6. Defects in complement pathway → septicaemia/meningitis
  7. Pain crises – episodes of hypoxic injury and infarction
  8. General hypoxia → impairment of growth & development
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23
Q

List 8 possible causes of an increase in Prostate Specific Antigen (PSA).

A

Causes of Increased PSA

  1. Benign prostatic hyperplasia (BPH)
  2. Prostate cancer – lower % free PSA than BPH
  3. Ejaculation – increases PSA for 6-48 hours
  4. Urinary tract infection
  5. Urinary retention
  6. Prostatitis
  7. Prostatic massage (e.g. DRE – take blood first)
  8. Prostatic needle biopsy
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24
Q

Comment on the accuracy/quality of PSA testing.

A

PSA Testing

  • Low specificity (91%)– organ-specific, but not cancer-specific
    • Significant overlap with PBH and prostate cancer (but BPH is generally lower)
    • Many false positives leading to unnecessary prostatic biopsies
  • Low sensitivity - not all men with prostate disease have elevated PSA
    • Many false negatives – many cases missed
    • For PSA >4.0 ng/mL, sensitivity is ~91%
    • For PSA <4.0 ng/mL, sensitivity is ~56%
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25
Q

Summarise the actions of different tumour supressors.

A

Tumour Suppressors

  1. p21
  2. p16
  3. p53
  4. pRB
  5. p14ARF
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26
Q

For each cyclin, state which cyclin- dependent kinase they bind to and what their function in the cell cycle is.

A

Cyclins DEAB

  • Cyclin D → CDK4 or CDK6
  • Cyclin E → CDK2
  • Cyclin A → CDK2
  • Cyclin B → CDK1
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27
Q

List the 5 pathologic zones of the prostate and state where most hyperplasia and carcinoma occurs.

A

Zones of the Prostate

  1. Peripheral zone (PZ)
    • Most carcinomas originate here
  2. Central zone (CZ)
    • Cancers here (2.5%) are more likely to invade seminal vesicles
  3. Transitional zone (TZ)
    • Most hyperplasias originate here = BPH
  4. Periurethral zone
  5. Fibromuscular stroma (non-glandular)
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28
Q

Outline the pathogenesis of BPH (4 steps).

A

Pathogenesis of BPH

  1. Stromal cells produce 5α-reductase
  2. 5α-reductase converts testosterone to dihydroxytestosterone (DHT)
    • DHT is ~10x as potent as testosterone
  3. DHT stimulates transcription of growth factors by stromal cells (autocrine) and epithelial cells (paracrine)
    • Oestrogen also binds androgen receptors, enhancing the response
  4. Hyperplastic stromal and epithelial tissues compress the prostatic urethra, leading to bladder outflow obstruction
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29
Q

List some symptoms of BPH.

A

Symptoms of BPH

  1. Urinary frequency, urgency, hesitancy
  2. Weak flow of urine, small volume voided
  3. Nocturia
  4. Interrupted stream
  5. Incomplete bladder emptying
  6. Dribbling
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30
Q

List some general carcinogenic agents.

A

Carcinogenic Agents

  • Chemicals - vinyl chloride, tobacco smoke (polycyclicaromatic hydrocarbons)
  • Viruses – HPV, hepatitis B, Epstein-Barr, herpes simplex
  • Ionizing (UV, X-rays, gamma rays) and non-ionising (α/β particles, neutrons, protons) radiation
    • Immediate effects – death, bone marrow failure, GIT effects
    • Late effects – leukaemia, thyroid cancer, lung/breast etc. cancer
  • Exogenous hormones – e.g. oestrogens in plastics
  • Bacteria, fungi, and parasites e.g. H. pylori
  • Miscellaneous agents (asbestos, metals)
31
Q

Contrast benign and malignant neoplasms in terms of:

  • Cell size and shape
  • Anaplasia
  • Differentiation
  • Rate of Growth
  • Local invasion
  • Metastasis
A
32
Q

List 10 types of urinary casts and what their presence is suggestive of.

A

Urinary Casts

  1. Hyaline casts
  2. Granular casts
  3. Waxy casts
  4. Fatty casts
  5. Pigment casts
  6. Crystal casts
  7. RBC casts
  8. WBC casts
  9. Bacterial casts
  10. Epithelial casts
33
Q

List some possible causes of tubulointerstitial nephritis.

A

Causes of Tubulointerstitial Nephritis

  1. Infections – pyelonephritis
  2. Toxins – drugs, analgesics, heavy metals
  3. Metabolic diseases – urate nephropathy, hypokalemic nephropathy
  4. Obstruction – of urinary tract
  5. Neoplasms – multiple myeloma
  6. Immune reactions
34
Q

Outline some major types of glomerulonephritis and whether they present with non-specific symptoms, nephritic syndrome or nephrotic syndrome.

A
35
Q

Outline some of the different ways patients with glomerular conditions will present.

A

Glomerular Conditions - Clinical Presentation

  1. Nonspecific → haematuria or polyuria
  2. Nephrotic syndrome→ proteinuria, hypoalbuminaemia, hyperlipidaemia, lipiduria
    • Leakage of large amounts of protein due to increased glomerular permeability
  3. Nephritic syndrome → proteinuria, haematuria, azotaemia, oliguria, hypertension, oedema
    • Leakage of protein and red blood cells due to renal inflammation
  4. Acute renal failure - acute nephritis, proteinuria
  5. Chronic renal failure - azotaemia → uraemia progressing for months to years
36
Q

List the 7 changes essential for malignant growth to occur, and give some examples of mutations.

A

Changes Essential for Malignant Growth

  1. Self-sufficiency of growth signals (↑oncogenes) – mutations in growth factors, GF receptors, RAS, MYC, cyclins, CDKs
  2. Insensitivity to growth-inhibitory signals (↓tumour suppressor genes)
    • BRCA1, BRCA2 (breast cancer)
    • APC (colorectal cancer)
    • p53 (many tumours)
    • Rb (retinoblastoma)
    • NF1 (neuofibromatosis)
  3. Evasion of apoptosis – mutations in Bax, Bcl, caspases
  4. Defects in DNA repair
  5. Potential for limitless replication - e.g. maintenance of telomere length
  6. Angiogenesis
  7. Invasion and metastasis
37
Q

Summarise the 4 steps in the process of haemostasis.

A

Haemostasis

  1. Vasoconstriction/Spasm
    • Direct trauma (local myogenic spasm), chemical signals from damaged cells (e.g. TXA2 from platelets), nervous reflexes (from pain impulses and sensory inputs)
  2. Platelet Plug Formation
    1. Adhesion: platelets bind to exposed collagen – aided by vWF (platelets)
    2. Activation: by exposed collagen - activated platelets secrete ADP and TXA2
    3. Aggregation onto the growing platelet plug
  3. Blood Coagulation – The Clotting Cascade
    • Prothr. activator catalyses prothrombin → thrombin - catalyses fibrinogen → fibrin
  4. Restoration of Normal Bloodflow
    • Clot lysed by Fibrinolysis - Plasminogen → plasmin → catalyses breakdown of fibrin
38
Q

List 3 endogenous substances that limit coagulation and describe their mechanism.

A

Endogenous Substances that Limit Coagulation

  1. Antithrombin III (ATIII) – binds to activated clotting factors (IIa, IXa, XIa, XIIa) and inactivates them – heparin increases ATIII activity
  2. Activated Protein C (APC) – activated by thrombin - inactivates factors V and VIII
  3. Protein S – cofactor for protein C on platelet surface
39
Q

Summarise the four major causes of disorders of haemostasis.

A

Disorders of Haemostasis

  1. Vessel Wall Abnormalities
  2. Platelet Deficiency (thrombocytopenia)
  3. Defective Platelet Function
  4. Abnormalities in Clotting Factors
40
Q

Summarise disseminated intravascular coagulation (DIC) and its pathogenesis.

A

Disseminated Intravascular Coagulation (DIC)

Summary

  • Excessive activation of coagulation, leading to formation of thrombi in the microvasculature
  • Occurs as a secondary complication of many different disorders
  • Presents with signs and symptoms related to tissue hypoxia/infarction or haemorrhage

Pathogenesis

  1. Release of tissue factor or thromboplastic substances into the circulation, or
  2. Widespread injury to endothelial cells
41
Q

Compare acute lymphoblastic and chronic lymphocytic leukaemia in terms of:

  • Cells composed of
  • Presentation
  • Clinical Features
A
42
Q

Summarise the types of lymphoid neoplasms their cells of origin.

A

Types of Lymphoid Neoplasms

  1. Lymphoid Neoplasms – the phenotype of the neoplastic cell resembles a stage of lymphocyte differentiation
    • Acute lymphoblastic leukaemia (ALL): proliferation of pre-B/T cells
    • Chronic lymphocytic leukaemia (CLL): proliferation of B cells
    • Lymphoma: proliferation of B/T/NK cells in tissues
  2. Myeloid Neoplasms – arise from haematopoietic stem cells that differentiate into myeloid lineages
    • Acute myeloid leukaemia (AML): accumulation of immature progenitor cells in bone marrow
    • Myelodysplastic syndromes : due to ineffective haematopoiesis
    • Chronic myeloid leukaemia (CML): accumulation of terminally differentiated myeloid cells
  3. Histiocytoses – proliferative lesions of macrophages and dendritic cells
43
Q

Compare Acute and Chronic Myelogenous Leukaemia in terms of:

  • Cells composed of
  • Presentation
  • Clinical Features
A
44
Q

Summarise the prognosis of the 4 major types of leukaemia.

A

Major Types of Leukemia - Prognosis

  1. Acute Lymphoblastic - ~95% of children will achieve full remission with aggressive chemotherapy, and ~80% are cured
  2. Chronic Lymphoblastic - extremely variable, median survival is 4-6 years
  3. Acute Myelogenous - difficult to treat, 60% of patients achieve full remission using chemotherapy, but only ~20% remain disease-free for 5 years
  4. Chronic Myelogenous - insidious onset and slow-progressing disease, without treatment, the median survival is 3 years
    • Allogenic bone marrow transplantation in young patients is curative in 75% of cases
45
Q

Summarise purine metabolism.

A

Purine Metabolism

46
Q

Summarise pyramidine metabolism.

A

Pyramidine Metabolism

47
Q

List some common side effects of chemotherapy.

A

Chemotherapy - Side effects

  • Bone Marrow: myelosuppression
    • Leukopenia, lymphocytopenia, thrombocytopenia, anaemia
    • Increased risk of infection
    • Impaired wound healing, haemorrhage
  • GIT: oral/intestinal ulceration → nausea, vomiting, diarrhoea
  • Hair roots: alopecia
  • Gonads: menstrual irregularities, amenorrhoea, infertility
  • Any tissue: predisposition to future cancer (disruption of DNA)
  • Foetus: teratogenesis
48
Q

Explain two limitations of chemotherapy, that are overcome by combination therapy.

A

Overcoming Limitations of Chemotherapy

  1. Toxicity
    • Most drugs are cytotoxic – kill normal cells as well as cancer cells
  2. Resistance
    • Inability of tumour cells to undergo apoptosis in response to drug-mediated DNA damage
    • Alteration of the drug target, ↑expression of the drug target, ↑rate of repair following damage
    • ↓ drug uptake, ↑ drug efflux/clearance, ↓ activation of prodrug
49
Q

Explain some of the difficulties a rural doctor might face.

A

Difficulties faced by a rural doctor

  • Being the ‘outsider’ when entering into the community – local rules
  • Isolation
  • Difficult for spouse & children – lack of family support, difficulty in making friends
  • Often a low standard of working environment
  • Extended on-call period
  • Boundaries between personal and professional relationships may become blurred
50
Q

Describe 7 rural barriers to healthcare.

A

Rural Barriers to Healthcare

  1. Decreased access to healthcare
    • Geographical remoteness
    • Limited resources (e.g. imaging/pathology)
    • Lower proportion of people with private healthcare
    • Difficulty attracting local specialists
    • Shortage of nursing homes
  2. Lower socioeconomic status
  3. Harsher environments
  4. Sparse infrastructure
  5. Poor uptake of health promotion messages
  6. Increased occupational hazards
  7. Attitudes towards safety and more frequent indulgences in risky behaviour
51
Q

State the path of milk in the mammary glands, from the alveoli to the nipple.

A

Path of Milk

  1. Alveoli
  2. Intralobular ducts
  3. Terminal interlobular ducts
  4. Lactiferous ducts
  5. Lactiferous sinuses
52
Q

What 4 muscles are deep to the breast?

A
  1. Pectoralis major
  2. Pectoralis minor
  3. Parts of serratus anterior
  4. External oblique
53
Q

Briefly explain the lymphatic drainage of the breast.

A

Lymphatic Drainage of the Breast.

  • Lateral: anterior axillary nodes (75%)
  • Medial: parasternal nodes
54
Q

For each of the structures of the glandular and ductal systems of the mammary gland, state the type of epithelium involved and the function of the structure.

A

Mammary Gland

55
Q

Describe the hormonal control of mammogenesis.

A

Hormonal Control of Mammogenesis

  1. Growth and branching of the ductal system and stroma is stimulated by:
    • Oestrogen
    • Growth hormone
    • Prolactin
    • Insulin
    • hCG
    • Placental lactogens (hCS)
  2. Development of alveolar tissue is stimulated by progesterone
    • Synergised by oestrogen and other hormones
  3. Prolactin levels are increased
    • Prolactin stimulates milk production
    • This is inhibited by oestrogen and progesterone until after parturition
56
Q

List some of the physiological effects of menopause.

A

Menopause

  1. Reduction in size of breasts and uterus
  2. Mood changes, anxiety, depression
  3. Hot flashes – intense heat, sweating, tachycardia
  4. ↑risk of cardiovascular disease
  5. Memory loss – anecdotal but no studies
  6. Vaginal dryness
  7. Dry skin
  8. Insomnia
  9. Fatigue
  10. ↑ risk of osteoporosis
57
Q

Explain the triple assessment for diagnosis of breast cancer, and state its sensitivity and specificity.

A

Triple Assessment of Breast Cancer Diagnosis

  1. Clinical – inspection and palpation
  2. Radiological – mammography, ultrasound, CT
  3. Pathological – fine needle aspiration, histological assessment

Sensitivity: 99.6%

Specificity: 62%

58
Q

List 14 risk factors for breast cancer.

A

Breast Cancer - Risk Factors

  1. Gender – 99% of cases occur in women (1% in men)
  2. Age – peaking at 75-80 years
  3. Age at menarche – menarche at 11 years old → 20% increased risk
  4. Age at 1st live birth - giving birth <20 years → 1/2 risk vs. nulliparous
  5. First-degree relatives with breast cancer
  6. History of atypical hyperplasia
  7. Race – risk of developing invasive carcinoma in the next 20 years:
    • Non-hispanic white women 1 in 15, African Americans: 1 in 20, Asian/Pacific islanders: 1 in 26, Hispanics: 1 in 27
  8. Estrogen exposure – postmenopausal hormone therapy (↑risk by ~1.5)
  9. Breast density – high breast radiodensity
  10. Radiation exposure – cancer therapy, atomic bomb, nuclear accidents
  11. Carcinoma of contralateral breast or endometrium
  12. Geographic – rates in the USA and Europe 4-7x higher than other areas
  13. Obesity – ↓ risk in obesity; ↑ risk with postmenopausal obesity
  14. Not breastfeeding – the longer a woman breastfeeds the lower the risk
59
Q

For each major histological subtype of breast cancer, state how often each occurs and explain their histological appearance and how they present clinically.

A

Histological Subtype of Breast Cancer

  1. In situ ductal carcinoma (DCIS)
  2. In situ lobular carcinoma (LCIS)
  3. Invasive ductal cancer
  4. Invasive lobular cancer
  5. Other invasive cancer
60
Q

Describe 3 options of hormonal therapy for ER+ breast cancers.

A

Treatments for ER+ (oestrogen receptor positive) cancers

  1. Selective Oestrogen Receptor Modulators (SERMS)
    • Tamoxifen
    • Raloxifene
    • Selectively antagonise/agonise E receptors → ↓ growt
  2. LHRH agonists (GNRH agonists)
    • ↓ LH and FSH → ↓oestrogen
    • Effective in premenopausal women
  3. Selective aromatase inhibitors (steroidal/non-steroidal)
61
Q

List some major prognostic indicators for breast cancer.

A

Prognostic Indicators for Breast Cancer

  1. Invasive vs. In situ
    • The majority of women with DCIS are cured
  2. Distant metastasis – cure is unlikely, but long-term remissions are possible
  3. Lymph node metastasis – the most important diagnostic factor
    • No nodal involvement – 10-year survival rate is 70%-80%
    • 1-3 nodes involved – 35-40%
    • >10 nodes involved – 10-15%
  4. Tumour size
  5. Locally advanced disease – into skin or skeletal muscle
  6. Inflammatory carcinoma – breast swelling and skin thickening
    • 3-year survival rate is only ~3-10%
62
Q

Describe a commonly used strategy for breaking bad news.

A

Strategy for Breaking Bad News = SPIKES

  • S – Setting → Basic communication and facilitation skills, be available, ensure privacy, involve significant others – e.g. family, close friends
  • P – Perception → Ask the patient what they already know or suspect, determine the patient’s perception of the seriousness of the situation as well as their comprehension
  • I – Invitation → Obtain a clear invitation to share information; determine the level of detail the patient wants, leave option to request information open
  • K – Knowledge → Warn that bad news is coming, start at the same level of the patient’s comprehension, give information in small chunks, check that content is understood
  • E – Empathy → Identify emotion/cause of emotion, respond to show a connection has been made
  • S – Strategy and Summary → Summarise major points, ensure that patient understands Strategise – make a clear contract for the next meeting
63
Q

Explain the concept of classical conditioning.

A

Classical Conditioning

  • A neutral conditioned stimulus is repeatedly paired with an unconditioned stimulus which invokes a conditioned response
  • Over repeated trials the neutral stimulus eventually evokes a similar response
  • E.g. Pavlov’s dog – the sound of footsteps (CS) began to evoke salivation (CR) in dogs anticipating food (UCS)
64
Q

Explain the concept of operant conditioning.

A

Operant Conditioning

  • Actions which result in reinforcement are strengthened and more likely to occur
    • Positive reinforcement – e.g. more parental attention with symptoms of anxiety
    • Negative reinforcement – removal of a negative stimulus e.g. avoiding school to avoid bullying
  • Actions which result in punishment are weakened and less likely to occur
    • Punishment – presentation of a negative stimulus
    • Negative punishment – removal of a reinforcer e.g. removing pocket money
65
Q

What specifically are the main causes of morbidity and death in young people?

A

Morbidity & Mortality - Young People

  • Mental health problems are the major burden of disease (50%) in young people
    • Primarily anxiety disorders
    • Affective disorders
    • Substance abuse disorders
  • Injury is the leading cause of death (2/3)
    • Suicide (27%)
    • Transport accidents (45%)
66
Q

List some of the changes that occur during adolescence.

A

Changes that occur during adolescence:

  • Peers and Parents
  • Autonomy
  • Education & Vocation
  • Sexuality
  • Body image & identity
67
Q

What are three main features of anxiety in general?

A

Anxiety - Clinical Features

  1. Cognitive experience of dread
  2. Associated physiological changes
  3. Behavioural attempts to escape or avoid
68
Q

Identify some cognitive and behavioural manifestations of anxiety.

A

Cognitive & Behavioural Manifestations of Anxiety

  • Hypervigilance – rapid and global scanning for threats
    • If a threat is detected, the anxious person’s attention focuses narrowly and intensely on it
  • Selective attention – narrowing of attention that occurs in response to a threat
    • External e.g. lightning – someone with a storm phobia will constantly watch the skies
    • Internal e.g. heart beat – someone with hypochondriasis will pay close attention for skipped beats
    • Excessive self-focus is the basis for abnormal behaviour and experience
    • Alcohol inhibits self-focussing – can reduce anxiety in social situations
  • Avoidance Behaviour
    • Initially, intense relief with avoidance of a feared situation - reinforcing
    • In the long term, avoidance strengthens the belief and maintains the anxiety
69
Q

List some physiological manifestations of anxiety.

A

Physiological Manifestations of Anxiety

  1. Dizziness
  2. Confusion – impairment of concentration, new learning, recall
  3. Syncope
  4. Hyperreflexia (twitching)
  5. Tremors; restlessness
  6. Diarrhoea, upset stomach
  7. Pupillary mydriasis
  8. Tachycardia; palpitations
  9. Hyperhidrosis (excess sweating)
  10. Hypertension
  11. Urinary frequency, hesitancy, urgency
70
Q

State the 3 diagnostic criteria for Obsessive Compulsive Disorder (OCD).

A

OCD - Diagnostic Criteria

  1. Presence of obsessions (pervasive and intrusive thoughts, impulses, images) and/or compulsions (repetitive behaviours or mental acts that must be applied rigidly)
  2. The person must realise that the obsession and/or compulsions are excessive and unreasonable
  3. The obsessions and/or compulsions cause marked distress, are time consuming (>1hour/day), or significantly interfere with day‐to‐day functioning
71
Q

Identify 4 pharmacological treatment options for anxiety.

A

Anxiety - Pharmacological Treatment Options

  1. Antidepressants
    • Selective serotonin reuptake inhibitors (SSRIs)
    • Tricyclic antidepressants (TCA)
  2. Anxiolytic Drugs
    • Benzodiazepines
    • Azapirone
    • Beta-blockers
  3. Anticonvulsant drugs
    • Valproate
    • Gabapentin
  4. Atypical antipsychotic drugs
    • Risperidone
    • Olanzapine
72
Q

Identify 6 non-pharmacological treatment options for anxiety.

A

Anxiety - Non-pharmacological Treatments

  1. Relaxation, Breathing Training, Mindfulness - deep breathing, progressive muscle relaxation, imagery, hyperventilation control, mindfulness
  2. Exposure Therapy - gradually exposing patients to identical or similar stimuli to what he/she fears, to habituate the patient to the stimulus
  3. Systematic Desensitisation - exposure therapy & relaxation training
  4. Cognitive‐Behavioural Therapy - focuses on information processing, learning and problem solving by identifying automatic thoughts and core beliefs associated with anxiety, then challenging and restructuring unhelpful thoughts and beliefs
    • What’s the worst thing that could happen? How likely is it that it will happen? What’s an alternative explanation?
  5. Social interventions - managing stress, friendships & supports, relaxing activities
  6. Diet - avoid alcohol, caffeine, illicit substances, foods with preservatives, medications with pseudoephedrine (where practical)
73
Q

Explain Gillick’s ratio.

A

Gillick’s Ratio

A minor can consent to medical treatment once s/he has achieved a “sufficient understanding and intelligence to enable him or her to understand fully what is proposed”.

74
Q

Give 4 aspects making up the profile of a resilient child.

A

Profile of a Resilient Child

  1. Social competence
    • Responsiveness o Flexibility
    • Empathy
    • Caring
    • Communication skills
    • Sense of humour
  2. Problem solving skills
    • Critical thinking
    • Generating alternatives
    • Planning
    • Producing change
  3. Autonomy
    • Self-esteem
    • Self-efficacy
    • Independence
    • Adaptive/healthy distancing
  4. Sense of Purpose and Future
    • Goal directedness
    • High motivation
    • Educational aspiration
    • Persistence
    • Hopefulness
    • Coherence