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Phase 2a - Systems > Miscellaneous > Flashcards

Miscellaneous Flashcards

1
Q

what 4 things must a patient demonstrate the ability to do, in order to consent a procedure/refuse treatment?

A

1) understand relevant info
2) retain that info for long enough to make the decision
3) use/weigh that info
4) communicate their decision

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2
Q

what are the key underpinning principles of the mental capacity act?

A

presume capacity unless proven otherwise.
encourage/enable them to make their own decision.
have the right to make unwise decisions.
proxy choices must consider best interests + what patient would have wanted.

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3
Q

what is valid consent?

A

1) given by a patient with capacity to make the decision
2) voluntary + free from undue pressure
3) sufficiently informed
4) continuing - patient may change their mind at any time

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4
Q

what must be included when informing a patient about a procedure?

A 
risks and benefits.
possible consequences of treatment and non-treatment.
explain other options.
disclose uncertainty.
encourage questions!
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5
Q

what causes typhoid/paratyphoid?

A

Salmonella typhi/paratyphi.
incubated 3-21d.
faecal-oral spread.

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6
Q

how would typhoid present?

A

malaise, headache, high fever with bradycardia, cough, constipation (then diarrhoea after 1wk).
rose spots on truk.

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7
Q

how would you diagnose typhoid/paratyphoid?

A

blood cultures of S typhi/paratyphi

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8
Q

how would you treat typhoid infection?

A

fluid replacement + good nutrition.

+ oral ciprofloxacin.

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9
Q

what causes poliomyelitis?

A

highly contagious picornavirus.

droplet or faecal-oral spread.

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10
Q

describe the signs of poliomyelitis. how is it treated?

A

flu prodrome.
pre-paralytic stage - fever, tachycardia, headache, vomiting, neck stiffness.
paralytic stage.

no drug treatment available :(

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11
Q

list 4 different ways HIV can be spread

A

sexual (vaginal and anal), blood products, vertical transmission (natural birth, breastfeeding), IVDU, needle stick injuries, organ donation

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12
Q

describe the brief immunology of how HIV infects the body

A

HIV binds to CD4 glycoprotein receptors (gp120) on T helper lymphocytes, monocytes, macrophages and neural cells.

CD+ve cells migrate to lymphoid tissue where the virus replicates producing countless new virions. These are released and infect more CD4 cells and as the infection progresses, the function of CD4 cells decreases and the actual number of cells depletes.

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13
Q

how does the viral load affect a patient clinically?

in HIV

A

as viral load increases, the CD4 count decreases making the disease more severe and the patient more ill.

CD4 initially increases dramatically as it tries to fight off the infection, but eventually decreases as the virus takes over.

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14
Q

when does HIV become AIDS?

A

CD4 count below 200.

presence of AIDS defining illness.

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15
Q

explain the stages of infection with HIV.

A

1) acute infection - asymptomatic, when the virus first enters the body.
2) serocoversion illness - transient illness 2-6wks after exposure - malaise, fever, myalgia, pharyngitis, maculopapular rash or meningoencephalitis.
3) asymptomatic infection - latent stage
4) persistent generalised lymphadenopathy - enlarged nodes for 3+ months, then fever, night sweats, diarrhoea, weight loss, minor opportunistic infections (AIDS-related complex - prodrome to AIDs itself).
5) AIDS - presence of AIDS defining illness and CD4 count of less than 200.

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16
Q

how would you confirm a diagnosis of AIDS?

A

serum/saliva ELISA test, must be at least 12 weeks after exposure.
rapid antibody tests - immunoassays used in primary care.

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17
Q

list 2 respiratory AIDS defining illnesses

A

pneumocystis jivoreci (PCP), TB, aspergillus, EBV, reticular nodules, strep pneumoniae

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18
Q

list 2 GI AIDS defining illnesses

A

oral candida, diarrhoea caused by shigella, salmonella, campylobacter, CMV, adenovirus, perianal warts and ulceration

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19
Q

name an eye AIDS defining illness

A

CMV retinits

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20
Q

give 3 CNS AIDS defining illnesses

A

cryptococcal meningitis, toxoplasmosis, cerebral lymphoma, encephalopathy.

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21
Q

how is HIV treated?

A

highly active anti-retroviral therapy (HAART) - started early, at CD4 count 350 and below (starting to be given to all with HIV)

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22
Q

give some examples of HAART drugs

A 
nucleoside reverse transcriptase inhibitors (NRTI) - zidovudine, didanosine, lamivudine.
protease inhibitors (PI) - slow cell-to-cell spread, lengthening time to first clinical event.
non-nucleoside reverse transcriptase inhibitors.
integrase strand transferase inhibitors.
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23
Q

give some ways that HIV can be prevented?

A

blood screening, Caesarean birth for HIV+ve mothers, bottle feeding, condoms or abstinence, fewer sexual partners, regular testing, decrease alcohol intake, circumcision

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24
Q

give 3 risk factors for HIV

A 
men who have sex with men (MSM).
unsafe sex.
other STIs.
mother-to-child transmission.
multiple simultaneous partners.
IVDUs - sharing needles.
uncircumcised man.
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25
Q

amyloid deposition is a feature of which 2 diseases apart from amyloidosis?

A

Alzheimer’s and diabetes mellitus type 2.

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26
Q

what is happening in AL amyloidosis and what does it cause?

A

AL is primary clonal proliferation of plasma cells with production of monoclonal Ig - deposition causes nephrotic syndrome, proteinuria, angina, arrhythmias, neuropathies, carpal tunnel syndrome, malabsorption, periorbital purpura and macroglossia.

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27
Q

what is happening in AA amyloidosis and what does it cause?

A

AA is secondary to chronic inflammatory disorders, such as RhA, IBD and infections (e.g. TB, osteomyelitis) - presents wtih CKD and hepatosplenomegaly.

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28
Q

what is the amyloid in AA produced from?

A

serum A amyloid - acute phase protein

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29
Q

what features do you get in AL but NOT in AA?

A

cardiac involvement or macroglossia.

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30
Q

what is familial amyloidosis?

A

autosomal dominant mutation of a transport protein made in the liver causing sensory/autonomic neuropathy ± renal/cardiac involvement

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31
Q

what investigation would you perform to diagnose amyloidosis? what stain would you use?

A

biopsy affected tissue, stain with Congo red stain - used polarised light microscopy

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32
Q

how would you treat the different types of amyloidosis?

A

treat underlying disease in AA to slow progression.
AL - myeloma treatment, so melphalan + prednisolone.
liver transplant cures familial.

prognosis is 1-2yrs.

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33
Q

what is amyloidosis?

A

group of disorders characterised by extracellular deposits of a protein in an abnormal fibrillar form, resistant to degradation

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34
Q

what is AL amyloidosis associated with?

A

myeloma, Waldenstroms, lymphoma

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35
Q

give 4 causes of a breast lump, apart from cancers

A

fibroadenoma, breast cysts, intraductal papilloma, hamartoma, abscess, intra-mammary lymph node, breast implant, lipoma, fat necrosis

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36
Q

what is a fibroadenoma?

A

benign overgrowth of collagenous mesenchyme of one breast lobule

37
Q

how does a fibroadenoma present?

A

less than 30yrs.
firm, smooth, mobile lumps.
painless.
may be multiple.

38
Q

how do fibroadenomas progress? how should they be managed?

A

1/3rd regress, 1/3rd stay the same, 1/3rd get bigger.

observe and reassure, USS if in doubt.

39
Q

how do breast cysts present?

A

> 35yrs, esp perimenopausal.
benign, fluid-filled rounded lump.
not fixed to surrounding tissue, occasionally painful.

40
Q

how would you treat a breast cyst?

A

aspirate.

41
Q

what happens in duct ectasia?

A

ducts become blocked and secretions stagnate

42
Q

how does duct ectasia present?

A

typically around menopause.
present with nipple discharge (green/brown/bloody) ± nipple retraction ± lump.
no treatment needed.

43
Q

what is an intraductal papilloma?

A

benign tumours within breast ducts - growths of gland tissue, with fibrous tissue and blood vessels.

44
Q

describe the 2 types of intraductal papilloma

A

central type - develops near nipple, usually solitary, arise in the run up to menopause.
peripheral type - usually multiple, found in younger women, higher risk of malignancy

45
Q

how would you investigate intraductal papilloma?

A

galactogram - too small to be palpated/seen on mammogram.

± biopsy

46
Q

how would you treat an intraductal papilloma?

A

micrododechtomy - duct excision

47
Q

give 4 risk factors for breast carcinoma

A

nulliparity.
1st pregnancy >30yo.
early menarche, late menopause, HRT, obesity, BRCA genes, not breastfeeding, past breast cancer.

48
Q

what are the 2 genes associated with breast carcinoma?

A

BRCA1 and BRCA2 - tumour suppressor genes, so mutations lead to tumours.

49
Q

what is the most common type of breast carcinoma? list the other types.

A

**invasive ductal carcinoma (epithelial cells of milk ducts)
non-invasive ductal carcinoma in situ (DCIS) = premalignant.
invasive lobular carcinoma.
medullary cancers, mucoid cancers.

50
Q

what receptors might breast carcinomas over express?

A

60-70% are oestrogen receptor +ve. some are progesterone receptor +ve.
30% over-express HER2 (growth factor receptor gene)

51
Q

is a breast carcinoma being HER2+ve a sign of a disease with good prognosis, or an aggressive disease?

A

HER2+ve cancers are very aggressive and have a poorer prognosis.

52
Q

list 4 clinical features of breast carcinoma

A

painless increasing mass, nipple discharge/inversion, orange peel skin, ulceration, oedema and erythema, skin tethering

53
Q

what is the triple assessment used to investigate a breast malignancy?

A

physical examination.
radiology (US and mammography).
histology/cytology - fine needle aspiration (FNA) and core biopsy.

54
Q

describe the staging system of breast carcinoma

A

I - confined to breast, mobile
II - confined to breast, mobile, lymph nodes in ipsilateral axilla
III - tumour fixed to muscle but not wall, ipsilateral lymph and skin involvement
IV - complete fixation of tumour to chest wall, distant mets.
also TNM

55
Q

how would you manage the different stages of breast carcinoma?

A

I-II - surgery, wide local excision, mastectomy ± breast reconstruction and axillary node clearance - adjuvant radiotherapy, possible neo-adjuvant chemo.
chemo - CMF regimen, tamoxifen/aromatase inhibitors (if ER+ve), herceptin if HER2+ve.
III-IV - bisphosphonates for bony lesions, tamoxifen, radiotherapy.

56
Q

give a cause of primary and secondary lymphatic insufficiency

A

primary - inherited deficiency of lymphatic vessels (Milroy disease)
secondary - obstruction by malignancy, filarial infection, post-irradiation therapy.

57
Q

how do you treat lymphoedema?

A

compression stockings and physical massage

58
Q

what is filariasis caused by?

A

mosquito infection causing lymphatic insufficiency

59
Q

what does an acute filariasis infection cause?

A

fever, lymphadenitis, chyluria

- elephantitis.

60
Q

how would you treat filariasis and what complication could occur?

A

diethlycarbamazine.

immune hyperreactivity - cough, wheeze, lung fibrosis

61
Q

what is lymphoedema?

A

chronic non-pitting oedema due to lymphatic insufficiency, most commonly affecting legs.
can cause cobblestone thickening of the skin.

62
Q

what is Milroy disease?

A

autosomal dominant disease causing congenital lymphoedema.

lower leg swelling from birth.

63
Q

give 3 symptoms of opiate poisoning

A

coma, pinpoint pupils, depressed respiratory rate, convulsions, hypotension, cyanosis and apnoea

64
Q

how would you treat opiate poisoning and how does the antidote work?

A

IV naloxone - competitive antagonist causes a rapid blockade, therefore rapid reversal of symptoms - short half life so need repeated doses, causes diarrhoea and cramps

65
Q

how does paracetamol overdose present?

A

asymptomatic, then vomiting and RUQ pain and then jaundice/encephalopathy from liver damage

66
Q

how would you treat a patient presenting with paracetamol overdose, both half an hour after taking it, and 4h later?

A

1h - activated charcoal

4h - N-acetylcysteine, which replenishes glutathione stores

67
Q

what is the mechanism of benzodiazepine overdose and therefore what symptoms does it cause?

A

increases GABA so exerts an excessive inhibitor effect on neurons.
symptoms - drowsiness, dizziness, ataxia, coma, respiratory depression.

68
Q

how do you reverse the symptoms of benzodiazepine overdose?

A

IV flumazenil - competitive inhibitor of GABA receptor

69
Q

what changes in the heartbeat can digoxin overdose cause and how do you treat that?

A

bradycardia, prolonged QRS and PR, AV block.

can be corrected with atropine.

70
Q

how does cyanide cause death with overdose?

A

binds to iron and inhibits cytochrome oxidase so no ATP produced - reduced aerobic respiration

71
Q

if a patient has inhaled cyanide, how long will they survive?

A

death within minutes

72
Q

if a patient ingests cyanide, what are the stages of overdose?

A

1st phase - anxiety and confusion.
2nd phase - pulse changes
3rd phase - fits and shock and coma

73
Q

how do you treat cyanide overdose?

A

100% oxygen, GI decontamination.

if GCS decreasing - IV dicobalt EDTA or sodium nitrite with sodium thiosulphate.

74
Q

what are 5 clinical features of organophosphate overdose?

A

SLUDGEM - salivation, lacrimation, urination, defecation, GI motility, emesis (vomiting), miosis (pupil constriction)

75
Q

how does the treatment for organophosphate overdose work?

A

atropine blocks ACh receptors.

pralidoxime regenerates acetylcholinesterase.

76
Q

how does carbon monoxide cause problems?

A

combines with haemoglobin to reduce oxygen carrying capacity of blood, can inhibit cytochrome oxidase

77
Q

what are 3 symptoms of CO poisoning?

A

headache, mild exertional drowsiness, vomiting, stomach pains, anorexia, fits, coma, chest pain, metabolic acidosis

78
Q

how do you treat CO poisioning?

A

100% oxygen.

hyperbaric chamber.

79
Q

give 4 reasons why you might suspect a soft tissue sarcoma in a patient with a swelling

A

> 5cm diameter, enlarging, painful, deep to fascia, solid mass (not cystic), recurrence at site of previous excision

80
Q

how would you investigate a sarcoma?

A

MR scan of primary, incisional biopsy, CXR, CT scan of thorax

81
Q

name 3 familial sarcoma syndromes

A

neurofibromatosis-1/-2, retinoblastoma, Gardner’s syndrome, Werner’s syndrome, Gorlin’s syndrome

82
Q

how would you treat a sarcoma?

A

primary - wide excisional surgery, adjuvant radiotherapy.

metastatic - palliative surgery, radiotherapy or chemo.

83
Q

what are the commonest primary bone tumours/sarcomas in adolescence/early adulthood?

A

osteosarcoma and Ewing’s sarcoma

84
Q

what sarcomas are secondary to radiation damage?

A

chondrosarcomas and osteosarcomas

85
Q

when would you suspect bone sarcoma?

A

night pain, non-mechanical and swelling not associated with the joint

86
Q

what class of drug is tamoxifen and what is it used to treat?

A

selective oestrogen receptor modulator.

early and metastatic ER+ve breast cancer.

87
Q

describe the mechanism of action of tamoxifen

A

it’s a prodrug metabolised by the liver and its active metabolites compete with oestrogen in the body to bind to oestrogen receptors.
ER+ve cancers rely on oestrogen to grow, so as oestrogen cannot bind to receptors on cancer cells, the tumour growth is reduced/stopped.

88
Q

how would you treat organophosphate overdose?

A

wear gloves, remove soiled clothes, wash patient.

atropine + pralidoxime

89
Q

give 3 “other” AIDS defining illnesses

A

Kaposi’s sarcoma, Leishmaniasis, Burkitt’s lymphoma, cervical carcinoma, herpes simplex, wasting syndrome, shingles.

Phase 2a - Systems (18 decks)

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