16/10/2024 Flashcards

1
Q

Antibiotic choice for bacterial meningitis?

A

IV cefotaxime
If <3 months or >50 then amoxillicin should be given too

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Antibiotic choice for managing bacterial meningitis contacts?

A

Oral ciprofloxacin
(Or rifampicin)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Interpretation of AAA screening?

A

<3.0 Cm is normal
3-4.4 = rescan every 12 months
4.5-5.4 = rescan every 3 months
>=5.5cm OR expanding >1cm a year = 2 week referral to vascular surgery for EVAR or open repair

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

pathophysiology of acoustic neuroma

A

Benign, slow growing tumours that form along the branches of the vestibulocichlear nerve

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Features of acoustic neuroma and relate them to the cranial nerve?

A

CN 5 - absent corneal reflex
CN 7 - facial palsy (palsy of forehead too as LMN lesion)
CN 8 - vertigo, U/L sensorineural hearing loss, U/L tinnitus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Investigations for acoustic neuroma?

A

Audiometry to show sensorineural hearing loss
MRI with gadolinium contrast

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Features of neurofibromatoiss type 2?

A

B/L acoustic neuromas
Multiple intracranial schwannomas, meningiomas and ependymomas

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Management of eclampsia?

A

Once a decision to deliver baby has been made give IV bolus of 4g magnesium sulphate over 5-10 minutes followed by an infusion of 1g/hour
Continue Tx for 24 hours after last seizure or after delivery

Remember if considering delivery <34/40 give corticosteroids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Causes of gingival hyperplasia

A

Drugs - phenytoin, Ciclosporin, CCB
AML

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

When should you consider medical/surgical management of miscarriage rather than expectatnt management?

A
  1. If increased risk of haemorrhage e.g. late first trimester or coagulopathy
  2. Previous adverse/traumatic experience associated with pregnancy
  3. Infection
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Management of missed miscarriage?

A

Oral mifepristone -> 48 hours give misoprostol (oral, vaginal, sublingual)

If bleeding has not started within 48 hours of misoprostol advise pt to contact HCP
Offer antiemetics and analgesia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Tx of incomplete miscarriage?

A

Single dose of misoprostol (vaginal, oral, sublingual)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

When should a pregnancy test be performed after medical miscarriage?

A

3 weeks

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Tx of thyrotoxicosis?

A

Propanolol to control Sx
Carbimazole - high doses for 6 weeks until pt is euthyroid and then reduced
Radioiodine Tx

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Why is Carbimazole used first line for thyrotoxicosis ahead of propothyluracil?

A

Due to its risk of liver damage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

MOA of Carbimazole?

A

blocks thyroid peroxidase from coupling and iodinating the tyrosine residues on thyroglobulin → reducing thyroid hormone production

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Rules for breastfeeding with HIV?

A

Never advised

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Which antibodies should you test for in suspected T1DM?

A

Anti-glutamic acid decarboxylase (anti-GAD)
Insulin autoantibodies (IAA)
Islet cell antibodies (ICA)

Note they are present in up to 70% of people at time of diagnosis but titre declines with time!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

When should you test c-peptide and autoantibodies in suspected diabetes?

A

Not routinely to confirm T1DM but if some atypical features e.g. high GMI, >=50
Basically when you are unsure between T1 and T2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Why can mitral stenosis cause haemoptysis?

A

Mitral valve will become thicker, obstructing blood flow across the mitral valve from the left atrium to the left ventricle, leading to an increase in pressure within the left atrium, pulmonary vasculature and right side of the heart.
This might cause increased pressure in the pulmonary circulation causing rupture of pulmonary vessels, leading to haemoptysis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Outline acute asthma Tx?

A

Stepwise progression:

Oxygen 15L NRB
Inhaled salbutamol
Nebulised Salbutamol (if severe or life threatening)
40-50mg prednisolone orally (at least 5 days)
Add nebulised ipratropium bromide 0.5mg 4-6 hourly
Consider IV magnesium sulphate 1.2-2g over 20 minutes

Consult with senior medical start -> consider IV aminophylline
Treat in ITU/HDU - consider intubation & ventilation or ECMO

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

When should you give further Tx after metformin monotherapy in T2DM?

A

If already on 1 drug and HbA1c has risen to 58mmol/mol\

(Note SGLT2 inhibitors may be added on at any point if any risk of or established CVD/heart failure)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

HbA1c target if T2DM treated with metformin?

A

48

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

HbA1c target if T2DM treated with any diabetic drug which can cause hypoglycaemia?

A

53

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

HbA1c target if T2DM is already being treated with 1 drug but HbA1c previously rose to 58?

A

53

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What are typical carboxyhaemoglobin levels in smokers and non-smokers?

A

Non-smoker = <3%
Smoker = <10%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What should you think if a pt has cabroxyhaemoglobin levels of >10%?

A

CO poisoning

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Features of carbon monoxide toxicity?

A

headache: 90% of cases
nausea and vomiting: 50%
vertigo: 50%
confusion: 30%
subjective weakness: 20%
severe toxicity: ‘pink’ skin and mucosae, hyperpyrexia, arrhythmias, extrapyramidal features, coma, death

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

How long do cephalohaematomas take to resolve?

A

Up to 3 months

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What type of murmur does tricuspid regurgitation produce?

A

Pan-systolic

31
Q

Which antibiotics are used as prophylaxis in oesophageal variceal haemorrhage?

A

Quinolones

32
Q

What should you do if you have an uncontrolled varicella haemorrhage?

A

Insert a Sengstaken-Blakemore tube

If this fails then consider TIPSS

33
Q

Prophylaxis of variceal haemorrhage?

A

Propanolol
Endoscopic variceal band ligation at 2-weekly intervals until all varices have been eradicated. Use PPI cover

If not successful in preventing further episodes consider TIPSS

34
Q

What is Pseudocholinesterase deficiency?

A

Autosomal dominant condition
Causes a defective form of the enzyme which is unable to metabolize succinylcholine leading to prolonged neuromuscular paralysis

35
Q

Peripheral blood smear findings in AML?

A

Myeloblast cells
Auer rods

36
Q

Peripheral blood smear findings in ALL?

A

Lymphoblast cells

37
Q

Peripheral blood smear findings in CML?

A

Immature granulocytes
Eosinophilia and basophilia
Usually few blast cells

38
Q

Peripheral blood smear findings in CLL?

A

Small lymphocytes with scant cytoplasm
Smudge cells

39
Q

Management of a breast abscess as a complication of mastitis?

A

Incision and drainage

40
Q

What are precipitating factors for hyperosmolar hyperglycaemic states?

A

Inter current illnes
Dementia
Sedative drugs

41
Q

BG level in HHS?

A

> 30mmol/L

42
Q

Management of HHS?

A

IV 0.9% sodium chloride 0.5-1L
(Monitor K+ levels!!)

Insulin should only be given if BG stops falling whilst giving IV fluids
VTE prophylaxis
Catheter to monitor urine output
Tx underlying cause

43
Q

Complications of HHS?

A

Usually hyperviscocity -> MI or stroke

44
Q

What are metabolic consequences of refeeding syndrome?

A

Low phosphate - hallmark feature!
Low K+
Low magnesium
Abnormal fluid balance

45
Q

Pathophysiology of low phosphate in refeeding syndrome?

A

Reintroduction of carbs causes a shift from fat to carbohydrate metabolism which activates insulin secretion = increases cellular uptake of glucose
This also stimulates intracellular movement of phosphate as its used in synthesis of ATP and 2,3-diphosphoglycerate levels in erythrocytes = reduces serum phosphate levels
So chronic malnutrition = depleted phosphate stores and when refeeding starts the sudden demands for phosphate in anabolic processes exceeds supplies = hypophosphataemia

46
Q

Clinical consequences of hypophosphataemia seen in refeeding syndrome?

A

Cardiac Dysfunction: Hypophosphatemia can impair myocardial contractility, leading to heart failure. It may also cause arrhythmias due to its role in maintaining normal cellular electrophysiology.
Respiratory Failure: Phosphate is essential for ATP production, necessary for respiratory muscle function. Severe hypophosphatemia can lead to muscle weakness, including the diaphragm and intercostal muscles, potentially resulting in acute respiratory failure.
Neurological Complications: These can range from confusion and seizures to coma, attributable to disturbed ATP metabolism in the central nervous system.
Haematological Effects: Reduced 2,3-diphosphoglycerate levels in erythrocytes affect oxygen release from haemoglobin, leading to tissue hypoxia. Hypophosphatemia can also result in hemolysis.
Rhabdomyolysis: Phosphate depletion impairs ATP production in muscles, which can lead to muscle breakdown and rhabdomyolysis.

47
Q

How to prevent refeeding syndrome?

A

Try to correct electrolytes before starting nutrition support
if a patient hasn’t eaten for > 5 days or is at risk, aim to re-feed at no more than 50% of requirements for the first 2 days.

48
Q

Investigation for phaeochromocytoma?

A

24 hour urinary collection of metanphrines

Tumour localisation with MRI or CT abdo

49
Q

Management of phaeochromocytoma?

A

Surgery is definitive
But pt must be stabilised with medical Tx first. Give alpha blockers before beta blockers

50
Q

Sx of trichomonas vaginalis?

A

vaginal discharge: offensive, yellow/green, frothy
vulvovaginitis
strawberry cervix
pH > 4.5
in men is usually asymptomatic but may cause urethritis

51
Q

Investigation of trichomonas vaginalis?

A

microscopy of a wet mount shows motile trophozoites

52
Q

Tx of trichomonas?

A

oral metronidazole for 5-7 days, although the BNF also supports the use of a one-off dose of 2g metronidazole

53
Q

Differences between BV and trochomonas?

A

BV has thin white discharge. Trichomonas has frothy, yellow-green
Trichomonas causes vulvovaginitis and strawberr crevices
BV on microscopy: clue cells
Trochomonas wet mount: motile trophozoites

Both cause pH >4.5 and you treat both with metronidazole

54
Q

Tx of hypercalcaemia?

A

Rehydration with normal saline - usually 3-4L a day
Following rehydration - bisphosphanates

55
Q

Most common type of breast cancer?

A

Invasive ductal carcinoma

56
Q

What scoring tool is used to estimate prognosis in breast cancer?

A

Nottingham prognostic index

57
Q

Breast cancer referral guidelines

A

2WW:
>=30 and any new breast lump
>=50 and any symptoms in 1 nipple e.g. discharge or retraction

Consider
If any skin Sx suggestive of breast cancer
If >=30 and unexplained lump in axilla
Non-urgent referral for unexplained breast lump in women <30

58
Q

Pathophysiology of haemochromatoiss?

A

Autosomal recessive - inheritance of both mutations on copies of HFE gene on chromosome 6
Causes a disorder or iron absorption and metabolism = iron accumulation

59
Q

Symptoms of haemochromatoiss?

A

Early = fatigue, ED and arthralgia often in hands

Later = bronzing of skin, hypogonadism e.g. amenorrhoea, diabetes, chronic liver disease, cardiac failure and arthritis

60
Q

Investigations for haemochromatoiss?

A

Liver studies - transferrin saturation >55% in men and >50% in women, raised ferritin, raised iron, low TIBC
LFTs for liver accumulation (can consider a liver biopsy for cirrhosis)
MRI to quantify liver and cardiac iron

Test family members using genetic testing for HFE mutation

61
Q

Investigations for haemochromatoiss?

A

Liver studies - transferrin saturation >55% in men and >50% in women, raised ferritin, raised iron, low TIBC
LFTs for liver accumulation (can consider a liver biopsy for cirrhosis)
MRI to quantify liver and cardiac iron

Test family members using genetic testing for HFE mutation

62
Q

Tx of haemochromatoiss?

A

Venesections - aim to keep transferrin saturation <50% and ferritin concentration <50

Second line - desferioxamine (iron chelation)

63
Q

Complications of haemochromatoiss?

A

Diabetes
Liver disease or cirrhosis or hepatocellular carcinoma
Sexual and endocrine dysfunction
Seconday cardiomyopathy
Hypothyroidism - iron can cause oxidative damage to the thyroid
Pseudogout due to chondrocalcinosis

64
Q

Interpretations ABPI?

A

> 1.4 suggests calcification e.g, in diabetes
1-1.4 normal
0.6-0.9 - claudication
Anything <0.5 suggests chronic limb-threatening ischaemia (used to be called critical limb ischaemia)
0.3-0.6 indicates rest pain
<0.3 is impending

65
Q

Statin and antiplatelet for peripheral arterial disease?

A

Atorvastatin 80mg ON
Clopidogrel 75mg OD

66
Q

What drug can sometimes be used for PAD when pts are not responding to exercise therapy and lifestyle modifications?

A

naftidrofuryl oxalate: vasodilator, sometimes used for patients with a poor quality of life

67
Q

What classification is used to grade chronic limb ischaemia?

A

Rutherford classification

68
Q

First line investigations for peripheral arterial disease?

A

Duplex USS
CT angiogram can guide revascularisation treatment

69
Q

Management of intermittent claudication?

A

offer a supervised exercise programme (~2 hours a week for 3 months - should be exercising to the point of maximal pain) if not available consider suggesting unsupervised exercise.
Offer referral for consideration of angioplasty or bypass surgery if this has not lef to Sx improvement alongside modifying RF
Consider offering naftidrofuryl oxalate only when exercise hasn’t helped and pt does not want referral. Review at 3-6 months. This is a vasodilator!
Offer information of cause, risk of limb loss and CVD risk, key modifiable risk factors, how to manage pain. Offer advice on foot care e.g. daily checking of feet, good shoes, not walking bare feet etc.

70
Q

Management of acute limb ischaemia?

A

emergency assessment by vascular specialist -> endovascular therapies or surgical interventions e.g. bypass surgery, amputation, percutaneous mechanical thrombus extraction etc
Pts are usually given IV opioids and IV UFH to prevent thrombus propagation.
All these pts need follow up with managing CVD risk… smoking cessation, diet, weight management, exercise, statin therapy with 80mg atorvastatin, prevention/Tx of diabetes, Tx of hypertension and clopidogrel 75mg daily.

71
Q

Management of chronic limb-threatening ischaemia?

A

refer urgently to a vascular MDT. Anage pain with paracetamol or opioids (+/- laxative)
All these pts need follow up with managing CVD risk… smoking cessation, diet, weight management, exercise, statin therapy with 80mg atorvastatin, prevention/Tx of diabetes, Tx of hypertension and clopidogrel 75mg daily.
Counsel them on risk of limb loss or cardiovascular events associated with PAD

72
Q

Chronic limb-threatening ischaemia vs acute limb ischaemia?

A

Chronic limb-threatening ischaemia — characterised by chronic, inadequate tissue perfusion in combination with ischaemic rest pain, with or without tissue loss (for example ulcers, gangrene) or infection. It represents the end stage of peripheral arterial disease

cute limb ischaemia is a sudden decrease in limb perfusion that threatens limb viability — decreased perfusion and symptoms and signs develop over less than 2 weeks. It is a medical emergency.

73
Q

Most common cause of death in diffuse cutaneous systemic sclerosis?

A

the most common cause of death is now respiratory involvement, which is seen in around 80%: interstitial lung disease (ILD) and pulmonary arterial hypertension (PAH)