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Year 4 revision > CCC revision > Flashcards

CCC revision Flashcards

1
Q

risk factors for breast cancer

A
  • uninterrupted oestrogen exposure e.g. nulliparity, not breastfeeding, early menarche, late menopause, HRT, prolonged use OCP, obesity (after menopause)
  • alcohol and smoking
  • chest and mediastinal radiotherapy
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2
Q

characteristics of inherited breast cancers (BRCA 1 and 2)

A
  • often younger presentation
  • cluster in family of young members, male and ovarian cancers
  • bilateral BC
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3
Q

between what ages are women screened for breast cancer

A

50-70 years - mammogram every 3 years

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4
Q

what are interval cancers

A

cancers occurring between each episode of screening

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5
Q

why is peau d’orange / breast inflammation an important sign to pick up on

A

can indicate inflammatory breast cancer - rapid onset, metastases quickly and has poorer cure rates and responses to treatment

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6
Q

breast cancer triple assessment

A
  • imaging: mammogram/USS/MRI, CT or bone scan for mets
  • clinical examination of breast and axilla
  • biopsy - core needle or FNA

= confident diagnosis in 95% cases

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7
Q

questions to ask in breast cancer history

A
  • how long
  • any skin/nipple changes
  • pain/discharge
  • related to menstrual cycle?
  • lumps under arm?
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8
Q

tumour markers for breast cancer

A

Ca15.3, CEA

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9
Q

what is a triple negative breast cancer

A

negative for oestrogen receptor (ER), progesterone receptor and HER2 receptor

difficult to treat with conventional therapy - most common subtype in BRCA1 carriers

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10
Q

poor prognostic factors for breast cancer

A
  • > 5cm
  • higher grade
  • ER negative
  • HER2 positive
  • LN involvement
  • triple negative
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11
Q

types of curative surgery for breast cancer

A

breast: wide local excision, mastectomy
axilla: sentinel node biopsy - axillary clearance if evidence of spread to LNs

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12
Q

3 main areas of metastatic spread in breast cancer

A

lung bones liver

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13
Q

which type of breast cancer responds best to chemo

A

ER negative/HER2 positive

50% of breast cancers are ER positive (oestrogen receptor positive)

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14
Q

during the menopause where is oestrogen produced

A 
adipose tissue
skin
liver
muscle
breast tissue
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15
Q

3 main types of hormonal treatments for breast cancer

A
  • oestrogen antagonists (tamoxifen)
  • oophorectomy (younger women)
  • aromatase inhibitors
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16
Q

what type of breast cancer does tamoxifen work on

A

ER positive - because blocks oestrogen receptors = reduced tumour growth

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17
Q

how do aromatase inhibitors (anastrozole, letrozole) work

A

aromatase = rate limiting enzyme in oestrogen synthesis = reduces oestrogen levels in body

used in post-menopausal women or in combination with something else in pre-menopausal

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18
Q

what are tamoxifen side effects similar to

A

menopause symptoms - because due to reduced oestrogen

NB: increases risk of VTE and PE

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19
Q

how effective is adjuvant radiotherapy for breast cancer

A

reduces risk of local relapse by 50-66%

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20
Q

how often are the chemotherapy cycles for breast cancers and how many cycles are given

A

cycle every 3 weeks

6-8 cycles

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21
Q

how does HER-2 receptor breast cancer function

A
  • HER2 receptors send signals to the cells to grow and divide
  • too many HER2 receptors can send too many growth signals = cells grow too quickly
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22
Q

what is used for the treatment of HER2 positive breast cancer

A

HERCEPTIN - trastuzumab

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23
Q

how does Herceptin work

A

monoclonal Ab - specific for HER2 - binds to HER2 = slows tumour growth

NOT chemotherapy
three weekly regimen
risk of allergic reaction

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24
Q

major side effect of herceptin

A

cardio toxicity - so must have good cardiac function and needs cardiac monitoring during treatment

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25
Q

most common type of lung cancer

A

NSCLC 85%

adenocarcinoma (35%)
SCC (30%)
large cell (10%)

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26
Q

types of pain common in lung cancer (especially late disease)

A

chest pain
bone pain (mets)
RUQ pain (liver pain)
headaches (brain mets)

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27
Q

when might haemoptysis be an early sign of lung cancer

A

very central cancer - T3/4

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28
Q

what syndrome might be associated with an apical tumour (Pancoast tumour)

A

Horner’s syndrome - ptosis, miosis, anhidrosis

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29
Q

main treatment of SCLC

A

chemotherapy - responsive but high relapse rate

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30
Q

why to give prophylactic brain radiotherapy in SCLC

A

often metastasise to brain

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31
Q

2 main mutations driving adenocarcinomas lung cancer

A

ALK

EGFR

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32
Q

which receptors are implicated in immunotherapy for lung cancer

A

PD-1

PDL

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33
Q

side effects of cancer immunotherapy

A

not as many as chemo

but can lead to autoimmune side effects e.g. lung fibrosis and destruction of thyroid gland

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34
Q

T1-T4 staging for colorectal cancer

A
  • T1 = tumour invades submucosa only
  • T2 = tumour also invades muscularis propria (muscle)
  • T3 = tumour invades peri-colonic tissues
  • T4a = tumour invades local peritoneum
  • T4b = tumour invades local organs
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35
Q

M1a-M1c staging for colorectal cancer

A 
M1a = 1 organ 
M1b = >1 organ 
M1c = peritoneal surface
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36
Q

5 year survival of stage 1-4 CRC

A 
1 = 95%
2 = 80-90%
3 = 65%
4 = 5-10%
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37
Q

red flag bowel cancer symptoms

A 
PR bleeding
weight loss
change in bowel habits
PR mucous
anorexia
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38
Q

2 main referral options for urgent suspected CRC

A
  • straight to test if are fit - colonoscopy or flexible sigmoidoscopy
    OR
  • colorectal surgeon/gastro review within 14 days if significant comorbidities or frail
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39
Q

another method of bowel cancer screening (apart from the FIT test age 60-74)

A

bowel screening scope (sigmoidoscopy) at 55 - one off test to detect left sided polyps) - if normal then go to normal bowel screening at 60 years

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40
Q

how is CRC treated

A

neoadjuvant chemo (usually)

before surgery

might have radiotherapy alone for rectal cancer

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41
Q

why is rectal cancer treated more aggressively (neoadjuvant therapy) than colon cancer

A

more local recurrence

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42
Q

what are patients tested for before receiving 5FU/capecitabine therapy

A

DPD enzyme deficiency - results in an inability to metabolise 5FU = toxicity and much more severe side effects to the chemo

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43
Q

follow up investigations for CRC

A

CEA 6-monthly
CT 18 months, 3 years and 5 yearly
colonoscopy within 12 months if not completed at diagnosis and 3 years post last colonoscopy

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44
Q

at what age can men request a PSA test from their GP

A

over 50

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45
Q

urinary symptoms which might merit a PSA test

A

reduced flow
increased frequency
nocturia
hesitancy

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46
Q

metastatic symptoms of prostate cancer

A

anaemia
bone pain
fatigue

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47
Q

what would be the pathway after an elevated PSA

A
  1. urology clinic on 2-week wait (urinary symptoms, sexual and bowel functions, other comorbidities, DRE)
  2. referral for pre-biopsy MRI scan
  3. TRUS biopsy
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48
Q

histological grading system for prostate adenocarcinoma

A

Gleason grading (being replaced with ISUP score)

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49
Q

T1-T4 staging of prostate cancer

A

T1. No palpable/visible cancer

T2. Cancer WITHIN the prostate

T3. Cancer breaching prostate capsule

T4. T4 is cancer growing into rectum/bladder

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50
Q

what would constitute a low risk prostate cancer

A

T1c/T2a, GS<=6, PSA<=10

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51
Q

what would constitute an intermediate risk prostate cancer

A

T2b/c or GS 7 or PSA 10-20

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52
Q

what would constitute a high risk prostate cancer

A

GS>=8 or PSA>=20

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53
Q

main treatment options for prostate cancer

A
  • surgery - in men <70 with no comorbidities (long term incontinence and impotence risks)
  • radiotherapy including brachytherapy
  • hormonal treatment
  • active surveillance
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54
Q

when might radiotherapy be used for prostate cancer instead of surgery

A

older men or with comorbidities - long term bowel problems risk

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55
Q

when might brachytherapy be used for prostate cancer and who should it be avoided in

A

fit men with no comorbidities

avoid in men with larger prostates/significant urinary symptoms

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56
Q

options for advanced prostate cancer

A

chemo, palliative radio

androgen deprivation therapy (ADT) - side effects such as hot flushes, shrinkage of penis, loss of muscle, weight gain, higher risk DM, osteoporosis, hyperlipidaemia, mood changes

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57
Q

major risk of ADT

A

increase in CV mortality in those with pre-existing CVD

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58
Q

2 gene mutations increasing risk of prostate cancer

A

BRCA II

pTEN

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59
Q

most common metastatic spread from prostate cancer

A

bones - especially lumbar spine (MSCC) and pelvis

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60
Q

where does BPH vs prostate cancer occur

A

BPH = centre of gland

adenocarcinomas = posterior/peripheral parts of gland

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61
Q

why is prostate cancer often asymptomatic

A

1st affected area is peripheral/posterior zone = far from urethra = no symptoms

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62
Q

investigations for prostate cancer apart from DRE

A

TRUS biopsy
MRI scan
isotope radio nucleotide bone scan - bone mets

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63
Q

TNM staging for prostate cancer

A

TX: Primary tumour cannot be assessed
T0: No evidence of primary tumour
T1: Clinically unapparent tumour not palpable nor visible by imaging
T2: Tumour confined within prostate
T3: Tumour extends through the prostate capsule
T3a: Extracapsular extension (unilateral or bilateral)
T3b: Tumour invades seminal vesicle(s)
T4: Tumour is fixed or invades adjacent structures other than seminal vesicles: bladder neck, external sphincter, rectum, levator muscles, and/or pelvic wall

N0 No regional lymph node involvement.
N1 Regional lymph node involvement

M0: No distant metastasis
M1: Distant metastasis
M1a: Non-regional lymph node(s)
M1b: Bone(s)
M1c: Other or multiple site(s) with or without bone disease
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64
Q

LFT which might suggest bone mets in prostate cancer

A

raised ALP

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65
Q

4 main types of hormonal treatment for prostate cancer (advanced disease or in conjunction with radiotherapy)

chemical castration

A
  • LHRH agonists: leuprorelin, goserelin
  • GNrH antagonist: degarelix
  • oestrogen therapy
  • anti-androgens: bicalutamide, enzalutamide
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66
Q

side effects of LHRH agonists

A
  • loss of libido
  • tumour flare on initiation of treatment
  • long term = increased cardiac risk, osteoporosis
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67
Q

benefit of GNrH antagonists

A

no risk of tumour flare

given monthly via SC injection when tumour flare can lead to significant symptoms e.g. with MSCC

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68
Q

how might chemotherapy be used in prostate cancer

A

cytotoxic treatment with docetaxel and prednisolone + carbazitaxel with metastatic disease

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69
Q

prognosis of prostate cancer

A
  • low risk = 99% at 10 years
  • all patients = 84% at 10 years
  • metastatic disease = median survival 3.5 years
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70
Q

what is raised in hepatocellular carcinoma

A

alpha fetoprotein

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71
Q

how is oxycodone metabolised and when should it be avoided

A

metabolised and excreted hepatically

so should be avoided in liver injury - use morphine instead

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72
Q

most common sites of metastases for lung cancer

A

BRAIN
liver
bones
adrenals

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73
Q

another name for herceptin

A

trastuzumab

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74
Q

what should be monitored during Herceptin treatment

A

left ventricular function due to risk of cardiomyopathy = frequent ECHOs

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75
Q

what can venlafaxine be used to treat in context of breast cancer

A

hot flushes due to medical/surgical menopause

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76
Q

what is the CHAD2DS2-VASc score

A 
CHF/LVEF <40% 
Hypertension 
Age >75 years = 2
Diabetes
Stroke/TIA/Thromboembolism = 2

Vascular disease
Age 64-75 years
Sex category (female)

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77
Q

what is the HAS BLED score

A

Hypertension (>160mmHg)
Abnormal liver/renal function
Stroke

Bleeding Hx/predisposition
Labile INR
Elderly >65 years
Drug/alcohol use

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78
Q

normal HbA1c levels

A

20-42

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79
Q

main antibiotic used for prophylaxis of neutropenic sepsis

A

levofloxacin

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80
Q

what is extrinsic vs intrinsic asthma

A
  • extrinsic - more commonly starts in childhood, common in atopic people
  • intrinsic - tends to develop in adulthood = ‘non-allergic’ asthma
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81
Q

what is FeNO and when is it offered to diagnose asthma

A

fractional exhaled nitrous oxide

measures amount of fractional exhaled NO which is increased by eosinophil activity

should be offered to adults aged 17+ AND if there is diagnostic uncertainty in under 17s, OR normal/obstructive spirometry with negative BD reversibility

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82
Q

asthma spirometry

A

FEV1/FVC <70% - obstructive

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83
Q

how is the bronchodilator test carried out

A
  1. Patients are asked to stop their SABA 6 hours beforehand, and LABA 12 hours beforehand
  2. Carry out the initial spirometry if not already done so
  3. Patient given 400 micrograms of Salbutamol and must wait for 15 minutes
  4. Carry out spirometry:
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84
Q

what would indicate a positive bronchodilator reversibility result

A

increase in FEV1 of 12% or more and 200ml or more increase in volume

negative test result = COPD??? v mild increase could be COPD on a background of asthma???

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85
Q

when might PEFR be used for asthma

A

Should be carried out over 2-4 weeks weeks in adults if there is diagnostic uncertainty after initial assessment and FeNO test with normal spirometry OR obstructive with normal FeNO

VERY COMMONLY USED IN CHILDREN

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86
Q

when are asthma symptoms usually worst

A

evenings - lowest cortisol levels

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87
Q

normal PEFR of adults

A

80-100% of their normal means asthma is well controlled

400-700ml for an adult

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88
Q

absolute gold standard for diagnosing asthma

A

direct bronchial challenge test with histamine/metacholine

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89
Q

what allergens to avoid in asthma

A

high levels pollution
smoke
NSAIDs
beta blockers

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90
Q

how much can CO be reduced by in AF

A

20% - ventricles not fully filled by atria

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91
Q

characteristics of:

a. initial episode
b. paroxysmal AF

A

a) . Initial episode:
- AF > 30 seconds diagnosed on an ECG

b). Paroxysmal AF
- > 2 Self-terminating, recurrent episodes lasting 30 seconds to 7 days
OR
- <48 hours terminated with cardioversion

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92
Q

characteristics of

a. persistent AF
b. long-standing AF

A

a) . Persistent:
- Episodes lasting more than 7 days CONTINUOSLY
- OR AF >48 hours which needs cardioversion

After 48 hours, spontaneous termination unlikely after this length of time

b). Continuous AF >12 months

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93
Q

what is permanent AF

A

This is characterised by joint decision by patient and doctor to cease further attempts at sinus rhythm

  1. AF that doesn’t stop DESPITE cardioversion
  2. AF that stops but then reoccurs within 24 hours OR
  3. AF that lasts >1 years when cardioversion is not attempted
94
Q

PIRATES mnemonic for causes of AF

A 
PE, pneumonia
Infection
Rheumatic or valvular disease
Anaemia, alcohol and caffeine
Thyroid (hyperthyroidism)
Elevated BP 
Sleep apnoea/obesity
95
Q

4 big risk factors for AF

A

AGE - over 65
hypertension
COPD
hyperthyroidism

96
Q

what causes dyspnoea in AF

A

pulmonary back pressure to the lungs and congestion

97
Q

what is apical-pulse deficit

A

in AF - when apical pulse at the apex of the heart is > than radial pulse in the wrist

98
Q

investigations into AF

A
  1. 1st line: ECG
  2. 24 hour ambulatory ECG if suspected paroxysmal AF
  3. Exercise Tolerance test if exacerbated by exercise
  4. Bloods: cardiac enzymes. eGFR, TFT’s, FBC’s, blood pressure
  5. CXR: for heart failure
99
Q

how can atrial flutter be cured

A

radio frequency catheter ablation

100
Q

what should be done before cardioversion (in AF)

A

heparinisation

101
Q

1st line treatment for AF

A 
rate control: 
most commonly a Beta-Blocker such as: 
- Atenolol (cardioselective) 
- Bisoprolol 
- NOT sotalol

OR a CCB

  • Verapamil
  • Diltiazem
102
Q

when might digoxin or amiodarone be used for rate control

A
  1. Digoxin: only for elderly, sedentary people with NON-paroxysmal AF
  2. Amiodarone: short term
103
Q

then might rhythm control be considered for AF

A
  1. Patients with REVERSIBLE cause of AF: chest infection
  2. Chronic heart failure
  3. new onset AF
  4. Atrial flutter

OR when clinical judgment dictates rhythm control as 1st line in under 65’s

104
Q

main method of rhythm control for AF

A

electrical/DC cardio version if AF has been happening for LESS than 48 hours

105
Q

what must be done if the AF has been happening for more than 48 hours and cardio version is still 1st line

A

period of therapeutic anticoagulation - minimum of 3 weeks prior and 4 weeks afterwards with INR>2 OR on a NOAC

106
Q

1st line medical drug for paroxysmal AF

A

beta-blockers

107
Q

drug used in AF if there is an underlying heart disease

A

amiodarone

108
Q

why must stall be initiated by a specialist if used for AF

A

side effect of life-threatening arrhythmias and QTc interval

109
Q

other rhythmic control drugs which can be used if there is no underlying heart disease

A

sotalol
flecainide
propafenone

110
Q

when might flecainide only be used in reality for AF

A

life-threatening SVTs or when symptoms can’t be managed with other antiarrhythmics

111
Q

CHAD2DS2-VASc scores for men and women which would normally require anticoagulation

A 
men = 1+
women = 2+
112
Q

how much does AF increase the risk of stroke

113
Q

management of a patient with 2+ on chadvasc score

A

vit K antagonist - warfarin
DOAC

consider also if score of 1

114
Q

what type of operation relieves the need for anticoagulation (in AF) and what is it

A

left atrial appendage occlusion - last resort for those with very high HASBLED score
- in 90% of thrombus formation are in left atrium

115
Q

1st line drug for rate control of AF

A

beta blocker OTHER THAN SOTALOL

can also use rate limiting CCB (diltiazem) or combination therapy of BB, diltiazem and digoxin

116
Q

when is digoxin used for AF

A

non-paroxysmal AF for sedentary patients OR in HF

117
Q

what are the screenings for CKD

A
  • bloods: eGFR, serum urea, serum creatinine
  • BP
  • urine dip: proteinuria/albuminuria
118
Q

what can cause a disproportionately high serum urea

A

low protein intake

liver failure

119
Q

what is eGFR multiplied by if patient is afro-caribbean or black

120
Q

over how long is proteinuria measured for CKD

how is it actually measured in practice

A

traditionally = 24 hour urine collection

in practice = spot urine sample (preferably morning for P:Cr ratio OR albumin/creatinine radio

121
Q

some investigations into CKD

A
  • clinical history
  • biochemistry/haematology
  • urine: dipstick, microscopy (cells and casts)
  • immunology screen: SLE, vasculitis, myeloma
  • renal USS: obstruction/cystic disease, renovascular, small kidneys
  • +/- renal biopsy
  • angiogram in some cases
122
Q

metabolic complications of CKD

A
  • anaemia (normocytic) due to reduced EPO production
  • bone mineral disorder: low serum Ca2+, high PO4, high PTH
  • metabolic acidosis: low serum bicarbonate on VBG
  • hyperkalaemia
123
Q

renal features of CKD

A
  • fluid retention
  • polyuria
  • nocturia
124
Q

cardiovascular features of CKD

A
  • HTN
  • pulmonary oedema
  • LVH/dysfunction
  • vascular disease
  • dyslipidaemia
  • vascular calcification
125
Q

GI features of CKD

A
  • anorexia
  • N+V
  • malnutrition
  • peptic ulceration
126
Q

neurological features of CKD

A
  • peripheral neuropathy

- restless legs

127
Q

dermatological features of CKD

A
  • pigmentation

- pruritis

128
Q

endocrine features of CKD

A
  • erectile dysfunction
  • oligmenorrhoea
  • reduced fertility
129
Q

MSK features f CKD

A
  • bone pain
  • fractures
  • arthropathy
130
Q

at what eGFR does CKD need specialist referral

A

<30, stage 4

131
Q

management of CKD

A
  1. Treatment of underlying cause if possible
  2. Lifestyle changes
  3. Blood pressure control
  4. CVS risk reduction
  5. Dietary changes
  6. Anaemia management (EPO given)
  7. Bone disease: treated with Vitamin D analogues, reduced phosphate diet, phosphate binders
  8. Bicarbonate supplements for acidosis
  9. Education, planning, preparation for end-stage renal disease
  10. Survival and QofL
132
Q

which antiemetic should be avoided in Parkinson’s and why

A

metoclopramide and prochlorperazine

dopamine antagonists - make Parkinson’s worse

133
Q

possible infectious trigger of T1DM

A

autoimmune response to Coxsackie or rubella infection

134
Q

how is gestational DM diagnosed

A
  • fasting venous blood glucose of >5.6mmol/L OR

- 2 hour plasma glucose level 7.8mmol/L or above

135
Q

why does GDM increase risk of perinatal death

A

poor placental perfusion due to vascular impairment

136
Q

what is MODY

A

maturity onset diabetes of the young

B cell dysfunction due to genetic mutations in transcription factors etc

mutation in a single gene - if one parent has the gene mutation then child has 50% chance of inheriting it

usually develops <25 years old

137
Q

what mutation is in MODY 70% of the time and how would it be treated

A

HNF1-alpha mutation

lowers the amount of insulin produced in pancreas - don’t need to take insulin, just small doses of a sulphonylurea

138
Q

random plasma glucose cut off for diagnosing diabetes

139
Q

2 fasting blood glucose values needed to diagnose diabetes

140
Q

value needed from OGTT for diabeters

141
Q

what should be done if the 2nd HbA1c is less than 48

A

treated as high risk for developing diabetes - should be tested again at 6 months or sooner if symptoms develop

142
Q

when is HbA1c NOT appropriate

A
  • ALL children and young people
  • Patients of any age suspected of TD1M
  • Patients with sx of diabetes for LESS than 2 months
  • Patients at high risk who are acutely unwell
  • Patients taking meds that can cause rapid glucose rise
  • Patients with acute pancreatic damage, including pancreatic surgery
  • Pregnancy
  • Presence of genetic, haematological or illness factors that influence HbA1c
143
Q

what states can cause a raised HbA1c

A
  • Iron deficiency
  • Vitamin B12 deficiency
  • Decreased RBC production
  • Alcoholism
  • Chronic renal failure
  • Decreased intra-erhtyhrocyte pH
144
Q

what is a DAFNE course

A

course for T1DM

dose adjustment for normal eating course: 5 days plus follow up 8 weeks later 6-12 months after diagnosis

145
Q

what is a DESMOND course

A

diabetes education self management for newly diagnosed

course for T2DM

146
Q

most common cause of end stage renal disease

A

diabetic nephropathy - damage to small blood vessels = nephrosclerosis and less efficient filtration (takes about 20 years)

147
Q

what type of skin lesion can affect diabetics

A

necrobiosis lipodica

mostly affects female patients

148
Q

what examinations should be carried out of diabetic feet

A

temp
cap refill
pulses including doppler
ABPI

149
Q

ABPI values

A
  • ABPI 1.0 - <1.3 Normal - symptom free
  • ABPI < 0.99 - > 0.5 indicates some arterial disease and can be associated with intermittent claudication and if symptoms warrant it the patient should be referred for a vascular opinion.
  • ABPI < 0.5 indicates severe arterial disease symptoms include rest pain, gangrene and ulceration and requires urgent referral to vascular team.
150
Q

what is accelerated hypertension

A

clinic BP >180/110 PLUS signs of:

  • papilloedema
  • retinal haemorrhage
151
Q

immediate management of accelerated hypertension

A

same-day referral to secondary care: phaeochromocytoma

152
Q

what percentage of heart attacks and stroke are related to HTN

153
Q

in stage 1 HTN can the COCP be used

154
Q

main side effect of CCBs

A

peripheral oedema

  • abdo pain
  • nausea
  • tiredness
155
Q

when must drug treatment be offered for HTN

A

if stage 2 or higher

156
Q

when should an ACEi be taken at first and why

A

at night because brings down BP v quickly so can get more side effects standing up in the day

157
Q

can you combine ACEi and ARB

158
Q

who with stage 1 HTN should be offered an antihypertensive

A

anyone UNDER 80 years with any of the following:

  • organ damage
  • established CBD
  • renal disease
  • diabetes
  • 10 year CVD risk 20%+
159
Q

what antibiotics would be used in addition to tazocin for neutropenic sepsis if there are:

a. signs and symptoms of respiratory tract infection
b. suspicion of catheter related infection OR history of MRSA

A

a. clarithromycin

b. teicoplanin

160
Q

how long to give antibiotics for neutropenic sepsis

A
  • until patient is no longer febrile and neutropenic
  • if blood cultures negative and no source identified can stop antibiotics once patient has been apyrexial for at least 48 hours
161
Q

antibiotic given for neutropenic sepsis if patient has a mild allergic reaction to penicillin

162
Q

antibiotic given for neutropenic sepsis if patient has a severe allergic reaction to penicillin

A

teicoplanin + aztreonam/ciprofloxacin

163
Q

2 drugs patients undergoing myelosuppressive chemotherapy might be given

A
  • levofloxacin (to prevent neutropenic sepsis)

- co-trimoxazole (prophylaxis against pneumocystis jiroveci (PJP))

164
Q

potential fungal cause of pneumonia in patients on chemotherapy (immunosuppressed)

A

pneumocystitis jiroveci (PJP) - bilateral interstitial ground glass appearance on lung CT

165
Q

how is PJP diagnosed

A
  • PCR respiratory specimen

- beta-D-glucan

166
Q

treatment of PJP

A

high dose IV co-trimoxazole

14-21 days that can be switched to oral when patient shows clinical improvement

167
Q

most common causative agent of infected indwelling catheters and lines (in chemotherapy)

A

coagulase negative staph

e.g. Staph epidermidis

also staph aureus v common

168
Q

what are endogenous vs exogenous catheter infections

A
  • endogenous: flora from patient’s own skin/newly acquired flora leading to infection
  • exogenous: operator’s flora
169
Q

where is the concentration of organisms at its greatest and lowest in an intravascular catheter infection

A
  • highest = at biofilm INSIDE the catheter lumen

- lowest = peripheral blood

170
Q

what is time to positivity (TTP)

A

time taken from receiving and testing blood cultures to the time the blood culture flags up positively for bacterial colonisation

determined by the number of organisms put into the blood culture bottle

171
Q

what TTP time is strongly indicative of a line infection

A

if the line cultures become positive MORE than 2 hours before the peripheral cultures do (paired blood cultures)

172
Q

how is a line infection managed

A
  • remove line

- TEICOPLANIN (due to high prevalence of MRSA)

173
Q

typical Abx regime for a line infection in those

a. under 65 years
b. over 65 years

A

a. IV teicoplanin +/- ceftazidime

b. IV taxocin

174
Q

what is VAP

A

pneumonia developing 48 hours after intubation/mechanical ventilation

early onset VAP = within 4 days admission

late onset VAP = after 4 days admission

175
Q

good empirical Abx regime for VAP

A

IV tazocin (particularly in late infections in which pseudomonas cover is necessary)

OR meropenem

176
Q

neutropenic sepsis - what to ask in history

A

how long ago their chemo was - usually 7-14 days post chemo

  • line and access (IV vs oral)
  • localising symptoms: infection source? e.g. mucositis, SOB, chest pain, abdo pain, diarrhoea, headaches/neck stiffness
  • allergies!!

NB: 60-70% of all febrile neutropenic patients have no identifiable aetiology of the fevers

177
Q

3 cancers most prone to developing neutropenic sepsis

A
  • haematological malignancies
  • germ cell cancers
  • breast cancers
178
Q

how many blood cultures should be taken and where

A

X2 for anaerobes and aerobes

lines (all ports) and peripheral or 2X peripheral if no line

179
Q

3 common gram +ves causing neutropenic sepsis (70% +ve)

A

staph aureus
coagulase negative staph
alpha and beta haemolytic strep

180
Q

common gram -ves causing neutropenic sepsis

A

E. coli
klebsiella pneumoniae
pseudomonas aeruginosa

181
Q

what is sometimes given in addition to Abx in neutropenic sepsis

A

G-CSF: colony stimulating factor such as:

  • filgrastim
  • lenograstim

haematopoietic growth factors that promote stem cell proliferation and shorten the duration of neutropenia

given when low neutrophils, predicted neutropenia >10 days, severe sepsis, multi organ failure, co-morbidities

182
Q

1st and 2nd most common causes of hypercalcaemia

A

1st = primary hyperparathyroidism

2nd = cancer

183
Q

2 main pathophysiologies of hypercalcaemia in cancer

A
  • TGF-alpha = polypeptide stimulator of cell growth and replication produced by tumour cells, very powerful stimulator of bone reabsorption
  • PTHrP - produced by some tumours which mimic PTH but doesn’t need low calcium levels to work
184
Q

most common malignancies which cause hypercalcaemia

A
  • Non-small cell lung cancer (squamous cell)
  • Breast cancer
  • Prostate cancer
  • Renal cell carcinoma
  • Multiple myeloma & lymphoma
  • Head & neck cancers
185
Q

CNS S&S of hypercalaemia

A
  • confusion
  • seizures
  • proximal myopathy
  • hyporeflexia
  • coma
  • depression and anxiety
186
Q

general S&S of hypercalcaemia

A
  • fatigue
  • weakness
  • bone pain
  • dehydration
187
Q

GI S&S of hypercalcaemia

A
  • Constipation
  • Weight loss/anorexia
  • N&V
  • Abdominal pain
  • Constipation
  • Ileus
  • Dyspepsia
  • Ileus
  • Pancreatitis
188
Q

cardiac S&S of hypercalcaemia

A
  • Bradycardia
  • Short QT interval
  • Wide T-wave
  • Prolonged PR interval
  • BBB
  • Arrhythmia
  • Cardiac arrest
189
Q

genitourinary S&S of hypercalcaemia

A
  • stones

- polyuria

190
Q

treatment for hypercalcaemia if level <3.0mm/L

A

rehydration with IV fluids - saline 1L every 4 hours for 24 hours then 6 hourly for 48-72 hours with adequate K+

191
Q

treatment for hypercalcaemia if level >3.0/symptomatic

A

at least 3L of saline in 24 hours and consider furosemide

PLUS consider bisphosphonate

192
Q

bisphosphonates to use in hypercalcaemia

A
  • IV zolendronic acid

- IV pamidronate (if renal function is poor)

193
Q

what is also added in hypercalcaemia if calcium is very high

A

calcitonin + corticosteroids

194
Q

presentation of MSCC if the compression is ABOVE L1

A

UMN symptoms - hypertonia, hyperreflexia, spasticity, positive babinski sign

195
Q

presentation of MSCC if lesion is BELOW L1

A

cauda equina:

  • sciatica in both legs
  • weakness of legs
  • saddle anaesthesia
  • faecal incontinence
  • urinary retention
196
Q

which MSCC patients are considered for neurosurgery

A
  • single area of MSCC
  • good performance status
  • predicted survival >3 months
  • not paraplegic for >48 hours (poor prognostic sign)

otherwise radiotherapy

197
Q

what percentage of patients treated within 24 hours will walk again

198
Q

S&S of SVCO

A
  • Breathlessness
  • Headache (worse on coughing)
  • Facial/neck/arm swelling
  • Distended neck & chest veins
  • Cyanosis
  • Visual disturbance
199
Q

2 main investigations into SVCO

A
  • CXR

- contrast CT thorax

200
Q

benign causes of SVCO

A
  • Non-malignant tumours (goiter)
  • Mediastinal fibrosis (idiopathic/post-RT)
  • Infection: TB
  • Aortic Aneurysm
  • Thrombus asx with indwelling catheter
201
Q

maximum number of oromorph doses in 24 hours

202
Q

adjunctive analgesics outside of the WHO pain ladder

A
  • Tricyclics: amitriptyline
  • Gabapentin
  • Pregabalin
  • NSAIDs
  • Steroids
  • Radiotherapy
  • TENS

most effective at treating neuropathic pain

203
Q

side effects of opiates

A
  • CONSTIPATION
  • 30% N+V - settles within 3-4 days
  • drowsiness - settles within 3 days
  • itchiness
  • addiction??
204
Q

2 methods of titrating a patient’s MST morphine

A
  • PRN oromorph

- 30-50% increase

205
Q

when would vomiting not usually help the nausea

A

chemotherapy patients

206
Q

management for nausea induced by raised ICP

A
  • dexamethasone 16mg

- cyclizine - 1st line antiemetic for raised ICP

207
Q

causes of cerebral N&V

A
  • raised ICP
  • emotions
  • radiotherapy
208
Q

features of toxic-induced nausea

A
  • frequent vomits
  • small volumes: ‘possets’
  • constant nausea
  • vomiting doesn’t relieve nausea
209
Q

1st and 2nd line managements of toxic causes of N&V

A

1st = haloperidol 1.5-5mg PO/SC nocte

2nd = levopromazine

210
Q

2 main treatments for vestibular causes of N&V

A
  • cyclizine

- hyoscine

211
Q

features of gastric-induced N&V

A
  • 1/2 vomits daily
  • satiety
  • nausea relieved by vomiting
  • MINIMAL NAUSEA BETWEEN VOMITING
  • hiccups
  • heartburn
212
Q

1st line treatment of gastric vomiting

A

Metaclopramide (pro-kinetic so moves contents through digestive system faster)

10-20mg PO/SC 30 minutes before food
OR
30-60mg SC over 24 hours

213
Q

treatments of anxiety/anticipatory related vomiting

A
  • CBT
  • benzos
  • complementary therapies
214
Q

what is used to treat indeterminate vomiting

A

levomapromazine 6.25-12.5mg nocte PO/SC

215
Q

what is used to treat chemotherapy-induced N&V

A

ondansetron (very constipating!!)

216
Q

1st line laxative used in opioid constipation

A

co-dansthrusate/co-danthramer OR Movicol

217
Q

3 medications to stop at the end of life

A
  • corticosteroids
  • antiepileptics
  • hypoglycaemics
218
Q

what to do when taking patients off steroids at the end of lie

A

if have been on them for a while - adrenals might have stopped producing corticosteroids (hypoadrenalism) = wean off slowly

219
Q

up to how many medications can be delivered in a syringe driver

220
Q

normal starting dose of midazolam in a syringe driver

A

10mg over 24 hour period in water for injection

221
Q

what substance for syringe drivers can NOT be added with sodium chloride

222
Q

main treatments for bone pain in cancer

A
  • NSAIDs
  • radiotherapy
  • bisphosphonates - pamidronate
223
Q

how can neuropathic pain be treated

A
  • TCAs
  • anticonvulsants: gabapentin, pregabalin
  • corticosteroids if there is nerve compression
224
Q

most common cause of SVCO

A

SCLC (65%)

225
Q

3 main treatments of SVCO

A
  • elevation of head and bed
  • diuretics
  • dexamethasone 16mg + PPI cover
226
Q

when to give dexamethasone for MSCC

A

BEFORE MRI

227
Q

4 electrolyte disturbances in tumour lysis syndrome

A
  • hyperkalaemia
  • hyperphosphataemia
  • hyperuricaemia
  • hypocalcaemia
228
Q

pathological SR sign for osteosarcoma (most common primary malignant tumour in paediatrics)

A

sunburst lesion

229
Q

max dose of co-codamol REGARDLESS of codeine strength

A

2 tablets 4 times a day - this is due to the paracetamol levels limiting the amount you can give (500mg paracetamol per tablet)

230
Q

what is Oramorph

A

liquid form of MST - but is used for breakthrough pain

takes 20-30 mins to work and works for 4 hours

max 6 doses in 24 hours

should be prescribed as 1/6 of the total daily morphine dose

231
Q

good starting dose for modified release morphine when going from weak opioids or going from non-opioids

A

weak opioids = around 15mg BD MST (30mg/24hr)

non-opioids = around 10mg BD MST (20mg/24hr)

Year 4 revision (5 decks)

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