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Phase 2a > Miscellaneous > Flashcards

Miscellaneous Flashcards

1
Q

HIV/AIDS

What group is HIV part of and what does this mean?

A
  • Lentivirus group (retrovirus) meaning it encodes reverse transcriptase, allowing DNA copies to be produced from viral RNA – error prone, meaning a significant mutation rate contributing to treatment resistance.
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2
Q

HIV/AIDS

What is the initial response to HIV virus and how does it spread?

A
  • Local inflammation with a mucosal macrophage/dendritic cell established before spreading to other cells.
  • As these are antigen presenting cells, some migrate to local lymph nodes to present antigen to T cells where infection of T helper cells occurs.
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3
Q

HIV/AIDS

How does HIV bind to cells?

A
  • Via its GP120 envelope glycoprotein to CD4 receptors on T helper cells, monocytes + macrophages.
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4
Q

HIV/AIDS

What happens once HIV has bound to CD4 receptors?

A
  • CD4 cells migrate to lymphoid tissue where virus replicates with production of billions of new virions which are released + infect new CD4 cells.
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5
Q

HIV/AIDS

How does HIV replicate?

A
  • Viral capsid enters, enzymes + nucleic acid uncoated + released.
  • Reverse transcriptase makes single stranded RNA into double stranded DNA + viral DNA is integrated to host cell’s DNA via integrase.
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6
Q

HIV/AIDS

How does HIV lead to decreased immune function?

A
  • Depletion/impaired function due to viraemia causes uncontrolled activation of CD4 T cells + so apoptosis of CD4 cells.
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7
Q

HIV/AIDS

Why is HIV not stopped?

A
  • Able to avoid antibodies + CD8 cytotoxic T lymphocytes due to viral envelope glycoprotein being poorly immunogenic + mutations.
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8
Q

HIV/AIDS

What is the epidemiology of HIV?

A
  • Mostly HIV-1, less HIV-2.
  • Men > women as HIV spreads well by anal intercourse, very prevalent in male-male sexual activity.
  • Majority of new infections worldwide are 15–24y/o.
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9
Q

HIV/AIDS

What are high risk groups for HIV?

A
  • Homosexual men + heterosexual women.
  • IV drug users.
  • Commercial sex workers, truck drivers.
  • Uncircumcised men.
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10
Q

HIV/AIDS

What are the routes of acquisition of HIV?

A
  • Sexual intercourse (vaginal + anal), STIs enhance transmission.
  • Mother-to-child in utero.
  • Contaminated blood + organ donation (minimal in developed countries).
  • Contaminated needles.
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11
Q

HIV/AIDS

What is the first stage in the clinical presentation of HIV?

A

Acute primary infection (seroconversion, 2–6 weeks)…

  • Transient immunosuppression + fall in CD4 count followed by gradual rise.
  • Acute rise in viral load then fall to set point.
  • Transient, non-specific symptoms (fever, malaise, myalgia, rash).
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12
Q

HIV/AIDS

What is the second stage in the clinical presentation of HIV?

A 
Asymptomatic phase (years)...
- Clinical latency with progressive loss of CD4 T cells resulting in poor immunity but asymptomatic (spreads infection further).
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13
Q

HIV/AIDS

What is the third stage in the clinical presentation of HIV?

A

Early symptomatic HIV…

  • Associated with rise in viral load + fall in CD4 count.
  • Symptoms like fever, night sweats, diarrhoea.
  • Opportunistic infections (herpes zoster, recurrent herpes simplex).
  • Collection of symptoms is AIDS-related complex (ARC).
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14
Q

HIV/AIDS

What is the final stage in clinical presentation of HIV.

A

AIDS…

- Symptoms of immune deficiency with a CD4 <200uL.

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15
Q

HIV/AIDS

What is the natural time frame for HIV to AIDs development?

A

HIV>[8 years]>ARC>[2 years]>AIDS>[2 years]>death.

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16
Q

HIV/AIDS

What are AIDS defining conditions?

A
  • Oesophageal candidiasis.
  • Mycobacterium TB.
  • Persistent herpes simplex.
  • Kaposi’s carcinoma.
  • Non-Hodgkin’s lymphoma.
  • HIV dementia.
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17
Q

HIV/AIDS

What are the investigations for HIV?

A

Enzyme-linked immunosorbent assay (ELISA)…
- Can take up to 3 months for HIV antibody/antigen detection.
- Confirmatory assay diagnostic.
Rapid point of care testing…
- Immunoassay kit provides rapid result from finger-prick/mouth swab, needs serological confirmation.
Nucleic acid testing/viral PCR…
- Qualitative test for presence of viral RNA, used to aid diagnosis of HIV in babies.

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18
Q

HIV/AIDS

What methods are used to monitor HIV infection?

A

Viral load…
- Quantification of HIV RNA.
CD4 count…
- Monitors immune system function.

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19
Q

HIV/AIDS

What are the treatment for HIV?

A

High active antiretroviral therapy (HAART)…
- Before CD4<200uL is ideal.
Nucleoside reverse transcriptase inhibitors (NRTI)…
- Inhibit synthesis of DNA by reverse transcription + also act as DNA chain terminators.
Non-nucleoside reverse transcriptase inhibitors (NNRTI).
- Bind directly to + inhibits reverse transcriptase.
Protease inhibitors…
- Act competitively on HIV enzyme involved in production of functional viral proteins + enzymes.
Integrase inhibitors…
- Inhibits insertion of HIV DNA into human genome.

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20
Q

HIV/AIDS

What is the prevention of HIV?

A
  • Education on transmission, contraception.
  • Give IV drug users clean needles.
  • Pre/post-exposure prophylaxis in high-risk individuals (antiretroviral therapy).
  • Male circumcision.
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21
Q

BREAST CANCER

What is the pathophysiology of breast cancer?

A
  • Can arise from epithelial lining of ducts (ductal) or epithelium of terminal ducts of lobules (lobular).
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22
Q

BREAST CANCER

What are the 4 types of breast cancer?

A 
Invasive ductal carcinoma...
- MOST common.
Lobular carcinoma...
- Accounts for 10–15%
Medullary cancers...
- Often younger patients.
Colloid/mucoid cancers...
- Often elderly patients.
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23
Q

BREAST CANCER

What is the epidemiology of breast cancer?

A
  • 1/8 women (most common cancer in women, second most common cause of death in UK).
  • Rare in men (1% of all breast cancers).
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24
Q

BREAST CANCER

What are the risk factors for breast cancer?

A
  • BRCA1/BRCA2 mutations.
  • Early menarche/late menopause.
  • Continuous combined HRT.
  • Increasing age, never having borne a child/first child after 30y/o.
  • Not breastfeeding.
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25
Q

BREAST CANCER

What are BRCA1/BRCA2 genes?

A
  • Tumour suppression genes that act as inhibitors of cellular growth.
26
Q

BREAST CANCER

What is the difference between BRCA1/BRCA2?

A 
BRCA1 (5–10% breast cancers)...
- Mutation of long arm of c17.
- 65% lifetime risk, stronger incidence.
BRCA2...
- Mutation of long arm of c13.
- 45% lifetime risk.
27
Q

BREAST CANCER

What is the clinical presentation of breast cancer?

A
  • Nipple discharge/retraction.
  • Dimpling of skin (peau d’orange) = sinister as caused by lymphatic invasion.
  • Oedema/erythema.
  • PAINLESS lump.
28
Q

BREAST CANCER

What are lumps of concern in breast cancer?

A
  • Hardness/irregularity/focal nodularity.
  • Asymmetry with other breast.
  • FIxation to skin/muscle.
29
Q

BREAST CANCER

What are the complications of breast cancer?

A
  • Spread to liver, lungs, bones, brain + nearby lymph nodes (axilla).
  • Lymphoedema after axillary surgery.
30
Q

BREAST CANCER

Name 4 differentials of breast cancer which are benign lesions.

A
  • Fibroadenoma (most common).
  • Breast cysts.
  • Breast abscess.
  • Intraductal papilloma.
31
Q

BREAST CANCER

What is a fibroadenoma? How does it present and develop?

A
  • Benign overgrowth of collagenous mesenchyme of one breast lobule.
  • Usually <30y/o, firm, non-tender, highly mobile lump.
  • 1/3 regress, stay same + grow.
32
Q

BREAST CANCER

What is the investigation + treatment of fibroadenoma?

A
  • Observation + reassurance, ultrasound ± fine needle aspiration.
  • Surgical excision if large.
33
Q

BREAST CANCER

What is a breast cyst? How does it present? What are the investigations?

A
  • Palpable, fluid-filled rounded lump, not fixed to surrounding tissue, occasionally painful.
  • Common >35y/o, especially around menopause.
  • Diagnosis via aspiration.
34
Q

BREAST CANCER

What is a breast abscess? How does it present and what is the treatment?

A
  • Infection of mammary duct.
  • Warm, painful swelling.
  • Abx + drainage.
35
Q

BREAST CANCER

What is an intraductal papilloma? How does it present?

A
  • Benign, warty lesion usually located just behind areola.
  • Presents as small lump, sticky, possibly blood-stained discharge possible.
  • Women in 40s more likely to have one, younger = multiple.
36
Q

BREAST CANCER

What is the investigation of intraductal papilloma?

A

Triple assessment required in specialist breast clinic…

  • Examination.
  • Radiology.
  • Biopsy.
37
Q

BREAST CANCER

What is the prevention of breast cancer?

A
  • Promote awareness by public health campaigns.

- Breast cancer screening programme involving biplanar digital mammography every 3 years in women aged 50–70y/o.

38
Q

BREAST CANCER

What are the investigations for breast cancer?

A

Triple assessment…
- Clinical examination.
- Radiology (USS<35/yo, + mammography if >35y/o).
- Fine needle aspiration/core biospy for histology/cytology.
Check oestrogen receptor (ER), progresterone receptor (PR) + human epidermal growth factor 2 (HER2) status.

39
Q

BREAST CANCER

What is the surgical treatment for breast cancer?

A
  • Removal of tumour by wide local excision (WLE)/lumpectomy.
  • Mastectomy ± breast reconstruction.
  • Axillary node sampling/surgical clearance.
40
Q

BREAST CANCER

What is the medical treatment for breast cancer?

A

Radiotherapy…
- Recommended for all patients with invasive cancer after WLE.
- Given to bone metastases (give bisphoshonates).
- Side effects = pericarditis, rib fracture.
Chemotherapy.

41
Q

BREAST CANCER

What is the aim of endocrine therapy in breast cancer? What does expression of HER2 indicate?

A
  • Reduce oestrogen activity to reduce tumour growth, used in ER + PR +ve disease.
  • Adverse factor as tumour more likely to grow + divide.
42
Q 
BREAST CANCER
What is the endocrine therapy in...
i) post-menopausal women?
ii) pre-menopausal women?
iii) HER2+ve women?
A

i) Oestrogen receptor block (tamoxifen), aromatase inhibitors (anastrozole).
ii) Ovarian ablation via surgery/radiotherapy, GnRH analogues (goserelin).
iii) Trastuzumab.

43
Q

OVERDOSE

What is the effect of excessive opioid drug exposure? What is the clinical presentation? What is the treatment?

A
  • Diamorphine/codeine produce physical dependence such that acute withdrawal syndrome develops w/ profuse sweating, tachycardia, vomiting, diarrhoea.
  • Pinpoint pupils, reduced RR, coma, convulsions.
  • IV naloxone 400mg/2min until breathing adequate.
44
Q

AMYLOIDOSIS

What is amyloidosis?

A
  • Group of disorders characterised by extracellular deposits of protein in abnormal fibrillar form, resistant to degradation?
45
Q

AMYLOIDOSIS

What are the three types of amyloidosis?

A
  • AL amyloid (primary).
  • AA amyloid (secondary).
  • Familial amyloidosis.
46
Q

AMYLOIDOSIS

What is the pathophysiology of AL amyloid?

A

Proliferation of plasma cell clone leads to amyoidogenic monoclonal immunoglobulins which cause fibrillar light chain protein deposition, organ failure + death.

47
Q

AMYLOIDOSIS

What is the pathophysiology of AA amyloid?

A

Amyloid derived from serum amyloid A, acute phase protein, reflecting chronic inflammation in RA, Crohn’s etc.

48
Q

AMYLOIDOSIS

What is the pathophysiology of familial amyloidosis?

A
  • AD inheritance, results from mutations in transthyretin (transport protein produced by liver).
49
Q

AMYLOIDOSIS

What is the clinical presentation of AL amyloid?

A
  • Kidneys = glomerular lesions = proteinuria + nephrotic syndrome.
  • Heart = restrictive cardiomyopathy, arrhythmias.
  • Nerves = peripheral neuropathy, carpal tunnel.
  • GI = macroglossia, malabsorption.
  • Vascular = purpura.
50
Q

AMYLOIDOSIS

What is the clinical presentation of AA amyloid?

A
  • Proteinuria, nephrotic syndrome or hepatosplenomegaly.
51
Q

AMYLOIDOSIS

What is the clinical presentation of familial amyloidosis?

A
  • Sensory/autonomic neuropathy ± renal/cardiac involvement.
52
Q

AMYLOIDOSIS

What are the investigations for familial amyloidosis?

A
  • Rectum/subcutaneous fat used for biopsy.

- Biopsy +ve if congo red staining with apple-green birefringence under polarised microscopy.

53
Q

AMYLOIDOSIS

What is the treatment of amyloidosis?

A 
AL = optimise nutrition, prednisolone.
AA = treat underlying cause.
FA = liver transplant can cure.
54
Q

LYMPHOEDEMA

What is the pathophysiology of lymphoedema?

A
  • Chronic, non-pitting oedema caused by lymphatic insufficiency (like failure of lymphatic drainage).
55
Q

LYMPHOEDEMA

What is the aetiology of lymphoedema?

A
  • Primary = presents in early life due to inherited deficiency of lymphatics.
    Secondary = due to obstruction of lymphatic vessels from trauma, radiotherapy, surgery, malignant disease.
56
Q

LYMPHOEDEMA

What is the clinical presentation of lymphoedema?

A
  • Most commonly affects legs + tends to progress w/ age.
  • Legs can become enormous + prevent normal shoes.
  • Chronic disease may cause secondary ‘cobblestone’ thickening of skin.
57
Q

LYMPHOEDEMA

What is the treatment of lymphoedema?

A
  • Compression stocking.
  • Physical massage.
  • If recurrent cellulitis then prophylaxis with low-dose phenoxymethylpenicillin.
58
Q

SARCOMA

What is the pathophysiology of sarcoma?

A
  • Group of rare solid tumours of connective tissues.

- Soft tissue sarcomas (80%) are more common than bone sarcomas.

59
Q

SARCOMA

Give an example of some soft tissue sarcomas.

A 
Liposarcoma = malignant neoplasm of adipose tissue.
Leiomyosarcoma = malignant neoplasm of smooth muscle
Rhabdomyosarcoma = malignant neoplasm of skeletal muscle.
60
Q

SARCOMA

What is the clinical presentation of sarcoma?

A
  • Lump that’s painless at first.
  • Pain + soreness as lump grows + presses against nerves + muscles.
  • Metastases to lung initially giving respiratory symptoms.
61
Q

SARCOMA

What are the investigations + treatment of sarcoma?

A
  • MRI + core needle biopsy, CT chest for lung metastases.

- Surgical resection (if possible) + chemotherapy ± radiotherapy.

Phase 2a (12 decks)

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