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FINALS > ONCOLOGY/ENDOCRINOLOGY > Flashcards

ONCOLOGY/ENDOCRINOLOGY Flashcards

1
Q

What are the clinical features of hypercalcaemia?

A

Bones, stones, groans + psychiatric moans

  • abdo pain, vomiting, constipation, polyuria, polydipsia, weight loss
  • depression, tiredness, weakness, confusion
  • pyrexia, renal stones/failure, cardiac arrest
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2
Q

What ECG changes can hypercalcaemia cause?

A

short QT interval

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3
Q

How do you manage hypercalcaemia?

A
  1. 0.9% NaCl

2. Zoledronic acid infusion

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4
Q

What are the markers to define neutropenic sepsis?

A

Neutrophil count <0.5x10^9 in patient having cancer treatment + one of:

  • temp over 38
  • other signs/symptoms consistent with sepsis
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5
Q

What abx are used to treat neutropenic sepsis?

A

Tazocin (piperacillin/tazobactam) plus vancomycin

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6
Q

When do you suspect tumour lysis syndrome?

A

Cancer pt recently started chemotherapy presenting with AKI in presence of high phosphate + uric acid level
- tends to have low calcium

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7
Q

What are the 3 types of NSCLC?

A
  1. adenocarcinoma
  2. squamous cell carcinoma
    - best survival due to potential operability
  3. large cell carcinoma
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8
Q

What are the stages of the ECOG performance scale?

A
  1. Fully active
  2. Restricted in physically strenuous activity
  3. Able to carry out all self-care - up 50% waking hours
  4. Only limited self-care - bed/chair for more than 50% waking hours
  5. Completely disabled/confined to bed/chair
  6. Deceased
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9
Q

What investigations should be performed in suspected SIADH? What will they show?

A
  1. Fluid status - euvolaemic or hypervolaemic
  2. Serum osmolality - LOW
  3. Urine osmolality - HIGH
  4. TSH - r/o hypothyroid
  5. Serum cortisol - r/o Addisons
  6. CXR - SCLC
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10
Q

What lung cancers can cause Cushing’s syndrome?

A

Small cell lung cancer

- secrete ACTH

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11
Q

What types of lung cancer can secrete PTH-rp?

A

Squamous cell - causing hypercalcaemia

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12
Q

What are the risk factors for breast cancer?

A

Prolonged oestrogen exposure:
- early menarche/late menopause, nulliparity or first child over 30y old, no breast feeding, COCP, HRT
Post-menopausal
Dense breasts
Lifestyle
- obesity, smoking, lack of exercise, alcohol, radiation
FHx
- 2x risk if 1st degree relative, more if they were under 50

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13
Q

Where do 50% of breast cancers appear? (anatomically)

A

upper outer quadrant

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14
Q

What are the 2ww criteria for pts with suspected breast cancer?

A

Aged over 30 with unexplained breast lump
OR
Aged over 50 with any of the following in ONE nipple only:
- discharge, retraction, any changes of concern

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15
Q

When is a mastectomy indicated for breast cancer?

A

Multifocal disease
Local recurrence
Invasion over 4cm

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16
Q

What are the clinical features of oesophageal cancer?

A
  • progressive worsening dysphagia
  • dysphagia for solids progressing to liquids
  • odynophagia
  • retrosternal chest pain
  • hoarseness/cough (rare)
  • weight loss
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17
Q

What is Peutz-Jeghers syndrome? What cancer(s) are they at increased risk of?

A

Multiple benign intestinal hamartomas, episodic obstruction + intussusception
- increased risk of GI, breast, ovarian, cervical, pancreatic, testicular cancers

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18
Q

What cancer are you at risk of with HNPCC (Lynch syndrome)?

A

Colorectal 30-70%
Endometrial 30-70%
Gastric 5-10%

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19
Q

What are the 2ww criteria for suspected bowel cancer?

A
  1. Over 40y with unexplained weight loss AND abdo pain
  2. Over 50y with unexplained rectal bleeding
  3. Over 60y with IDA OR changes in bowel habit
  4. FOB in faeces
  5. Rectal or abdominal mass
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20
Q

What is the classic triad for presentation of renal cancer?

A
  1. Haematuria
  2. Loin pain
  3. Abdominal mass
    Also: weight loss, fatigue, anorexia, night sweats, left varicocele
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21
Q

When would you consider a PSA test + DRE in men?

A
  • any lower UTI symptoms e.g. nocturia, frequency, hesitancy, urgency, retention
  • erectile dysfunction
  • visible haematuria
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22
Q

What are the 4 types of leukaemia? At what age do they tend to affect people?

A
  1. ALL - under 5s or over 45s
  2. AML - over 75s
  3. CLL - over 55s
  4. CML - over 65s
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23
Q

What is the gold standard investigation for leukaemia?

A

bone marrow biopsy

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24
Q

What are the features of ALL/AML?

A
  • bone/joint pain, trouble standing/walking
  • loss of appetite, continuous weight loss
  • painless lump in stomach, neck, armpit or groin
  • lethargy, weakness, pallor, dizzy
  • repeated frequent infections, fevers lasting several days
  • night sweats/irritable
  • prone to easy + frequent bruising, nose/gum bleeds
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25
Q

What will be seen on a blood film in ALL or AML? How do you differentiate?

A

Blast cells

- AML has Auer rods

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26
Q

What are the clinical features of CLL?

A

Often asymptomatic

  • symmetrical painless lymphadenopathy
  • infections, anaemia
  • B symptoms = night sweats, fever, weight loss
  • can cause warm AIHA
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27
Q

What is Richter’s transformation?

A

CLL can transform into high-grade lymphoma

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28
Q

What will a blood film show for CLL?

A

Smear or smudge cells

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29
Q

What are the 2 peaks of age in which Hodgkin’s lymphoma can develop?

A

20y + 75y

- twice as common in males

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30
Q

What do Reed-Sternberg cells on lymph biopsy indicate?

A

Hodgkin’s lymphoma

- multiple nuclei with nucleoli inside them

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31
Q

What are the clinical features in Hodgkin’s lymphoma?

A

Lymphadenopathy - painless, non-tender, asymmetrical

Systemic - weight loss, pruritus, night sweats, fever

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32
Q

Describe the components of the Ann-Arbour staging system?

A

I: single node/one region
II: more than one region but on same side of diaphragm
III: nodes on both sides of diaphragm
IV: spread beyond lymph (e.g. lungs + liver)

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33
Q

What, clinically, can help you to differentiate between Hodgkin’s + Non-Hodgkin’s lymphoma?

A
  • lymphadenopathy in Hodgkin’s can experience alcohol-induced pain in node
  • B symptoms tend to occur earlier in Hodgkin’s + later in non-Hodgkin’s
  • Extra nodal disease much more common in non-Hodgkin’s lymphoma
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34
Q

What is Addison’s disease? What is the most common cause?

A

Primary adrenal insufficiency

- most common cause is autoimmune (80%)

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35
Q

What are the signs + symptoms of Addison’s disease?

A
  • lethargy, weakness, anorexia, N+V, weight loss, ‘salt-craving’
  • hyperpigmentation (especially palmar creases) vitiligo, loss of pubic hair in women, hypotension, hypoglycaemia
    Addisonian crisis = collapse, shock, pyrexia
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36
Q

What investigations should be performed in suspected Addison’s disease?

A
  1. U+E - hyponatraemia, hyperkalaemia
    - urea may be high
  2. Hypoglycaemia
  3. ABG - metabolic acidosis
  4. Short synACTHen test
    - do plasma cortisol before AND 30mins after given synacthen: if cortisol over 500 then r/o Addisons
  5. Serum ACTH - inappropriately high at 9am
37
Q

How do you manage Addison’s disease?

A
  1. Hydrocortisone - usually in 2-3 doses
  2. Fludrocortisone

Warn against abruptly stopping steroids. Advice to double dose during intercurrent illness + to always wear bracelet/carry steroid card

38
Q

What causes secondary adrenal insufficiency?

A

Long-term steroid therapy causes suppression of HPA axis
- withdrawal then causes this

Iatrogenic ^^

39
Q

How do you manage an Addisonian crisis?

A
  1. Bloods - cortisol, ACTH, U+E, cultures
  2. BMs - may need glucose
  3. Hydrocortisone 100mg IV 6-hrly
    - change to oral steroids after 24h + if stable , add fludrocortisone if adrenal disease when change to oral
    - change to maintenance over 3-4 days
  4. IV fluid bolus - 1L normal saline over 30-60 mins with dextrose if hypoglycaemic
  5. Septic screen
  6. Treat underlying cause
40
Q

What medications can cause hypothyroidism?

A
  • drugs to treat hyperthyroid (carbimazole, PTU)
  • lithium
  • amiodarone
41
Q

What investigations should be performed to diagnose hypothyroidism?

A
  1. TSH - raised if primary, low in secondary
  2. T4 - low
  3. FBC - mild normocytic anaemia
  4. Serum cholesterol - raised
    - often improves on treatment of thyroid
  5. Anti-TPO
42
Q

What dose adjustment is required for women who have hypothyroidism who are pregnant?

A

Increase dose by 25-50 mcg

- due to increased demands of pregnancy

43
Q

In what patients should you have the initial levothyroxine dose as lower than normal for hypothyroidism?

A 
Elderly patients (those over 50/60)
Those with IHD
44
Q

What are the diagnostic criteria for T2DM for GLUCOSE?

A

If pt is SYMPTOMATIC:

  • Fasting glucose 7mmol/L or more
  • Random glucose/OGTT 11.1 mmol/L or more

If pt is ASYMPTOMATIC, this criteria must be met on 2 occasions

45
Q

Does a HbA1c of less than 48 rule out diabetes mellitus?

A

NO

- misleading HbA1c results can be caused by increased red cell turnover

46
Q

If a pt is on lifestyle + metformin treatment for T2DM, at what HbA1c value would you consider adding another drug?

A

58mmol/mol

47
Q

What lifestyle advice should be given to T2DM?

A
  • high fibre, low glycaemic index sources of carbs
  • low-fat dairy products + oily fish
  • control intake of foods containing saturated fats + trans-fatty acids
  • discourage use of foods marketed at diabetics
  • if overweight, initial target weight loss of 5-10%
48
Q

What BP treatment + targets should be in place for T2DMs?

A

Target of less than 140/80 mmHg
- if end organ damage present then less than 130/80

ACEi first line!

49
Q

What tests are required in diabetics to screen for complications?

A
  1. Diabetic nephropathy = annual ACR monitoring
  2. Diabetic retinopathy = annual retinal screening from 12yrs
  3. Dyslipidaemia = annual lipid profile
  4. HTN = annual BP
  5. Ulcers/neuropathy = foot check annually
  • HbA1c checked 6-monthly
50
Q

What are the 2 categories of ‘pre-diabetics’?

A
  1. Impaired fasting glucose

2. Impaired glucose tolerance

51
Q

What are risk factors for developing GDM? If you have any of these risk factors what is done?

A
  • raised BMI over 30
  • previous GDM
  • Asian, black or middle eastern
  • previous macrosomic baby
  • 1st degree relative with DM

Screening using OGTT at booking + again at 26 weeks

52
Q

What should be done pre-conception for women with pre-existing DM?

A
  • avoid unplanned pregnancy as reduces risks
  • aim for BMI below 30
  • reduce alcohol, stop smoking, optimise diet
  • screen for end-organ dysfunction + treat pre-pregnancy
  • aim for HbA1c below 43
  • avoid pregnancy in HbA1c above 85
53
Q

What medication do diabetics require antenatally?

A

5mg folic acid pre-conception until 13weeks gestation
Aspirin 75mg from 12 wks to birth (pre-eclampsia)
Glycaemic control using only metformin and/or insulin
Stop ACEi + A2A, if needed use methyldopa or labetalol

54
Q

What complications can occur for (i) mum (ii) foetus during pregnancy if diabetic?

A

(i) MATERNAL = hypo-unawareness, especially in 1st trimester
- increased rate of pre-eclampsia + infection
- higher rate of LSCS

(ii) FOETUS
- miscarriage, macrosomia, IUGR, polyhydramnios, malformations, pre-term labour, stillbirth

55
Q

What are the complications which can arise due to shoulder dystocia?

A
  1. PPH
  2. Perineal tears
  3. Brachial plexus injury = Erbs palsy
56
Q

What additional tests can be done to diagnose T1DM?

A

C-peptide

GAD antibodies

57
Q

What are the ACDC sick day rules?

A
  1. Never stop or omit insulin - just adapt
  2. Check BMs every 2h + at night
  3. Check blood ketones
  4. Give fast-acting if raised BM
  5. If ketones are high when BM low, drink sugary fluids
  6. Keep well hydrated
58
Q

What are the risk factors for DKA?

A
  • inadequate insulin therapy
  • infection
  • acute/recurrent illness
  • MI
59
Q

What investigations should be performed in suspected DKA?

A
  1. Plasma glucose - hyperglycaemia
  2. ABG - acidosis
    - if it is HHS, the pH is usually above 7.3 and bicarb above 15mmol/L
  3. Capillary/serum ketones over 3mmol/L
  4. U+E - raised urea + creatinine, low sodium, high K+
  5. Raised lactate
  6. FBC - leucocytosis
60
Q

How do you acutely manage DKA?

A
  1. Fluid replacement done over 48h. Avoid bolus as this risks cerebral oedema
    - calculate by adding deficit to maintenance
  2. Give fixed rate insulin 0.1units/kg/hr
    - once BM below 15mmol/L, start 5% dextrose infusion also
  3. Monitor K+, may need to correct hypokalaemia
  4. Monitor glucose, pH + ketones to assess progress + determine switch to SC insulin
  5. Continuous ECG monitoring for hypokalaemia
    - ST depression, prominent U waves
61
Q

What are the complications which can occur due to DKA?

A
  1. CEREBRAL OEDEMA
    - headache, agitation, irritability, unexpected fall in HR + rise in BP = ASSESS
    - falling GCS, breathing pattern abnormalities, occulomotor palsies, pupils unequal = TREAT
    - use mannitol 20%, hypertonic NaCl
  2. HYPOKALAEMIA
  3. VTE
62
Q

What investigations are performed in suspected Lyme’s disease?

A

Testing in early disease may be of little value as seroconversion happens after this

  1. ELISA
  2. ECG if signs of cardiac disease - AV block
63
Q

How do you manage Lyme’s disease?

A

Cefuroxime

Amoxicillin

64
Q

How does HIV tend to present?

A

Seroconversion is symptomatic in 60-80% + presents as glandular fever type illness usually 3-12 weeks after infection
- sore throat, lymphadenopathy, malaise, myalgia, arthralgia, diarrhoea, maculopapular rash, mouth ulcers

65
Q

What are the AIDS defining illnesses? When do they occur?

A

Occur when CD4 count less than 200

  1. Kaposi’s sarcoma
  2. PCP
  3. CMV
  4. Candidiasis - bronchial or oesophageal
  5. Lymphomas
  6. TB
66
Q

How is HIV diagnosed?

A
  1. Serum HIV ELISA
  2. Serum HIV rapid test
    - false negatives may occur in window period. Positives should be confirmed with 2nd test
  3. Serum p24 antigen test - present in periods of increased viral replication
  4. HIV RNA PCR (viral load) - assess baseline before treatment
  5. CD4 count - assists in severity
67
Q

When should testing be performed in asymptomatic patients who have had possible exposure?

A

4 weeks after exposure

68
Q

What is defined as a late diagnosis of HIV?

A

When CD4 count is less than 350 within 3 months of diagnosis
- pts likely to have had HIV for over 3y + at high risk of transmitting it

69
Q

When must post-exposure prophylaxis be commenced after HIV encounter? How long is it taken for?

A

Start within 72h exposure

  • take for 28 days
  • abstain from sex for 3 months until -ve result confirmed
70
Q

How is PCP managed?

A

High dose co-trimoxazole IV

Prednisolone if severe hypoxaemia

71
Q

What glucose level is defined as hypoglycaemia?

A

Less than 4mmol/L

72
Q

How do you manage hypoglycaemia if patients is (i) conscious (ii) confused (iii) unconscious ?

A

(i) CONSCIOUS
- glucojuice
(ii) CONFUSED
- glucogel - 2 tubes between gyms + cheeks
(iii) UNCONSCIOUS
- IV 50ml 20% glucose
OR
- 1mg SC/IM glucagon

73
Q

How is DKA diagnosed?

A
  1. pH under 7.3
  2. Glucose over 11mmol/L
  3. Ketones over 3 mmol/L or ++ in urine
74
Q

What causes low TSH, low T3, low T4?

A

Sick euthyroid or pituitary disease

75
Q

In what patients should you screen for thyroid abnormalities?

A
  • pts with AF
  • pts with hyperlipidaemia
  • diabetics (screen annually)
  • women with T1DM during 1st trimester + post-delivery
  • pts on amiodarone or lithium (check 2x/year)
  • pts with DS, Turner’s or Addison’s
76
Q

What are some complications of untreated thyrotoxicosis?

A
  • heart failure
  • angina
  • AF
  • osteoporosis
  • gynaecomastia
  • ophthalmopathy
  • thyroid storm
77
Q

What will TFTs show in sub-clinical hypothyroidism?

A

Normal T3 + 4

Minimally raised TSH

78
Q

What is the most common cause of primary hyperparathyroidism?

A

solitary adenoma

- associated with HTN + MEN 1+2

79
Q

How do you manage primary hyperparathyroidism?

A
  1. Total parathyroidectomy = definitive management
  2. Increased fluid intake + avoid thiazides
  3. Calcium mimetics such as cinacalet are used in pts unsuitable for surgery
80
Q

What are some causes of Cushing’s syndrome?

A
  1. Exogenous steroids
  2. Cushing’s disease (pituitary adenoma)
  3. Adrenal adenoma
  4. Paraneoplastic Cushing’s - from SCLC
81
Q

What is the most common cause of acromegaly?

A

Pituitary adenoma

- growth hormone is secreted from anterior pituitary

82
Q

What tests are required to diagnose acromegaly?

A

Random GH not helpful as it fluctuates

  1. IGF-1 = initial screening (raised)
  2. OGTT whilst measuring growth hormone
    - high glucose normally suppresses growth hormone
  3. MRI brain (pituitary tumour)
  4. Ophthalmology referral for visual field testing
83
Q

How is acromegaly treated?

A
  1. Trans-sphenoidal surgery to remove pituitary adenoma
  2. If caused by pancreatic or lung cancer - then remove said cancer
  3. Medications to block GH:
    - pegvisomant
    - ocretide (somatostatin analogue)
    - bromocriptine (dopamine agonist)
84
Q

What is primary polydipsia?

A

Pt has normally functioning ADH system but are drinking excess water leading to excess urine production
- they do not have DI

85
Q

Why is HHS a medical emergency?

A

Has a high mortality
Can be complicated by vascular problems
- MI, stroke, peripheral arterial thrombosis

86
Q

What is required to diagnose HHS?

A
  1. Hypovolaemia
  2. Marked hyperglycaemia (above 30mmol/L)
    - without significant ketonaemia or acidosis
  3. Significantly raised serum osmolality (above 320mosmol/kg)
87
Q

How do you calculate the serum osmolality?

A

(2xNa) + glucose + urea

88
Q

How do you manage HHS?

A
  1. Admit to HDU
  2. IV 0.9% NaCl
    - aim for +ve balance of 3-6L by 12h + remaining replacement w/in next 12h
    - aim for BMs between 10-15mmol/L
  3. Low-dose insulin if ketonaemia present (mixed DKA/HHS picture)
  4. Potassium chloride if K+ below 5.3

FINALS (14 decks)

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