Tuesday [15/09/2021]

Question 1

You are the FY1 in a busy geriatric service. You are tasked with writing the discharge summaries and prescriptions for a number of patients who are to be discharged this afternoon.

You are well supported by your team and your consultant has asked that you review the regular medications of each of the patients and contact her if you feel there are any changes that should be made prior to discharge.

One of the patients is a 78-year-old female who was admitted with a simple urinary tract infection (UTI) and hypoactive delirium, now resolved after treatment with a course of antibiotics.

Her past medical history includes hypertension, hypercholesterolaemia, depression, recurrent epistaxis and a provoked deep vein thrombosis (DVT) 2 years ago.

Based on the information provided, which of her regular medications should you consider stopping prior to discharge?

Answer 1

The STOPP tool identifies medications where the risk outweighs the therapeutic benefits in certain conditions

Question 2

What is the STOPP tool with regards to warfarin?

Answer 2

Warfarin is an anticoagulant and vitamin K antagonist that can be used to treat a number of conditions, including DVT. However, the STOPP criteria states that it has no proven added benefit when given for longer than 6 months for uncomplicated DVT. As this patient had a DVT 2 years ago and there is no other indication for anticoagulation, this should be stopped. Furthermore, there is mention in the history of recurrent epistaxis and this has quite possibly been caused by warfarin therapy

Question 3

Define multimorbidity?

Answer 3

The presence of two or more long-term health conditions, including: Defined physical or mental health conditions, learning disabilities, symptom complexes such as chronic pain, sensory impairments and alcohol or substance misuse.

Question 4

Mx of multimorbidity?

Answer 4

Reducing treatment burden and optimising care is the goal in managing comorbidity
Maximise the benefits of existing treatments
Offer alternative follow-up arrangements if they are struggling to meet them
Reduce the number of high risk medications being prescribed and consider the use of non-pharmacological treatments
Consider a ‘bisphosphonate holiday’ in those taking bisphosphonates for longer than three years as there is no consistent evidence of continued benefits after this point. Discuss stopping bisphosphonates after 3 years and include patient choice, fracture risk and life expectancy in the discussion.
Consider the use of screening tools such as STOPP/ START in older people to recognise medicine safety concerns: STOPP identifies medications where the risk outweighs the therapeutic benefits in certain conditions and START suggests medications that may provide additional benefits ie proton pump inhibitors for gastroprotection in patients on medications increasing bleeding risk
Especially consider stopping the use of medications such as NSAIDS, warfarin and aspirin in patients with peptic ulcer disease, and pay particular attention to the prescription of reno-toxic or renally cleared drugs in reduced renal function
Ask patients about the benefits and harms of their individual treatments, considering the overall prognostic benefit
Develop an individualised management plan: Record what actions will be taken, include goals, prioritise healthcare appointments, anticipate changes and explore other areas of importance to the patient
Promote self-management through education and engagement strategies
Support carers and families of patients
Use the action plan to follow up with the patient at agreed points: NHS England recommends a yearly review of all medications for people aged over 65, however, medications should be reviewed periodically to ensure that patients are being informed, given adequate laboratory tests and that treatments are optimised

Question 5

A 65-year-old man presents to the emergency department with inability to move his left arm and leg that started 40 mins ago. His past history includes well-controlled type 2 diabetes mellitus and atrial fibrillation for which he takes metformin and warfarin, respectively. He drinks 20 units of alcohol per week.

His heart rate is 130 beats/min and blood pressure is 150/90 mmHg. On examination, no neurological abnormalities were found and the patient reported that he is feeling well and ready to go home.

What is the most appropriate next step?

Answer 5

If a patient is on warfarin/a DOAC/ or has a bleeding disorder and they are suspected of having a TIA, they should be admitted immediately for imaging to exclude a haemorrhage.

First of all, we need to exclude haemorrhage by doing a head CT scan as this will determine further management whether it is an ischaemic event or a haemorrhagic event. Secondly, this patient is on warfarin which is a risk factor for having intracranial bleeds. Finally, he consumes alcohol regularly which is associated with subdural haemorrhage.

Question 6

When is amiodarone used?

Answer 6

Amiodarone is an antiarrhythmic used in treating atrial fibrillation (AF) through rhythm control. However, this is not the best next step. Moreover, this patient is elderly and consequently, rate control is a better approach in managing his AF.

Question 7

What is alteplase and when is it used?

Answer 7

Alteplase is a fibrinolytic that must not be given unless haemorrhage has been excluded. It is given if the onset of symptoms is within 4.5 hours and no contraindications are present.

Question 8

A 39-year-old man presents with six months of polyuria and polydipsia. He has also been experiencing fleeting episodes of arthralgia and lethargy. Past medical history is unremarkable and he is not on any medications. When asked about family history, he states that his parents are okay but remembers his grandma had to have regular removal of her blood throughout her life. He is not sure why as she died from heart disease when he was a child.

Nothing abnormal is found on examination and blood glucose is within range. Blood tests are then performed and the results are given below.

Full blood count:
Hb 181 g/L Male: (135-180)
Female: (115 - 160)
Platelets 300 * 109/L (150 - 400)
WBC 5.1 * 109/L (4.0 - 11.0)

Urea & electrolytes:
Na+ 151 mmol/L (135 - 145)
K+ 3.6 mmol/L (3.5 - 5.0)
Urea 4.5 mmol/L (2.0 - 7.0)
Creatinine 99 µmol/L (55 - 120)
CRP 2 mg/L (< 5)

Liver function tests:
Bilirubin 14 µmol/L (3 - 17)
ALP 90 u/L (30 - 100)
ALT 42 u/L (3 - 40)
γGT 33 u/L (8 - 60)
Albumin 40 g/L (35 - 50)

Osmolality tests:
Serum osmolality 301 mOsmol/kg (285 - 295)
Urine osmolality 272 mOsmol/kg

After water deprivation:
Urine osmolality 241 mOsmol/kg

After desmopressin is given:
Urine osmolality 853 mOsmol/kg

Which test will confirm the diagnosis?

Answer 8

Hereditary haemochromatosis is a cause of cranial diabetes insipidus

Blood tests show hypernatraemia with high serum osmolality and low urine osmolality that only returns to normal upon administration of desmopressin. Together with the presented urinary symptoms, this is diagnostic of central diabetes insipidus

Question 9

Causes of central diabetes insipidus?

Answer 9

Lethargy and arthralgia are a common first presentation of hereditary haemochromatosis, which may cause central diabetes insipidus. The family history is also suggestive. This disease is autosomal recessive so skips generations (in this question, parents are unaffected but grandparent affected). The biggest clue is that regular removal of blood is the treatment of haemochromatosis, with the aim of preventing iron toxicity. Also, these patients often die of heart disease due to iron deposition, which can be seen on autopsy as grey pigmentation of the myocardium.
Even without this knowledge, the other choices do not fit the test results, so you may deduce that haemochromatosis is the most likely cause and that ferritin is therefore the correct answer.

Question 10

What is the short synacthen test used for?

Answer 10

The short synacthen test is for adrenocortical insufficiency, which is a cause of nephrogenic diabetes insipidus (i.e. urine osmolality does not return to normal with desmopressin). In addition, adrenal insufficiency causes hyponatraemia and hyperkalaemia due to a lack of aldosterone, which is the opposite of what is seen here.

Question 11

What is the anti-Ro and Anti-La test used for?

Answer 11

Anti-Ro and Anti-La are tested for Sjogren’s syndrome, which is also a cause of nephrogenic diabetes insipidus. Remember that nephrogenic diabetes insipidus does not respond to desmopression. The patient does not have any symptoms of Sjogren’s either e.g. xerostomia and xerophthalmia

Question 12

What is the Caeruloplasmin test used for?

Answer 12

Caeruloplasmin is the test for Wilson’s disease, which does not cause diabetes insipidus.

Question 13

Define DI?

Answer 13

Diabetes insipidus (DI) is a condition characterised by either a decreased secretion of antidiuretic hormone (ADH) from the pituitary (cranial DI) or an insensitivity to antidiuretic hormone (nephrogenic DI).

Question 14

Causes of cranial DI?

Answer 14

Causes of cranial DI
idiopathic
post head injury
pituitary surgery
craniopharyngiomas
histiocytosis X
DIDMOAD is the association of cranial Diabetes Insipidus, Diabetes Mellitus, Optic Atrophy and Deafness (also known as Wolfram’s syndrome)
haemochromatosis

Question 15

Causes of nephrogenic DI

Answer 15

genetic: the more common form affects the vasopression (ADH) receptor, the less common form results from a mutation in the gene that encodes the aquaporin 2 channel
electrolytes: hypercalcaemia, hypokalaemia
lithium
lithium desensitizes the kidney’s ability to respond to ADH in the collecting ducts
demeclocycline
tubulo-interstitial disease: obstruction, sickle-cell, pyelonephritis

Question 16

Features of DI

Answer 16

polyuria
polydipsia

Question 17

Ix for DI

Answer 17

high plasma osmolality, low urine osmolality
a urine osmolality of >700 mOsm/kg excludes diabetes insipidus
water deprivation test

Question 18

Mx for DI

Answer 18

nephrogenic diabetes insipidus: thiazides, low salt/protein diet
- central diabetes insipidus can be treated with desmopressin

Question 19

A 63-year-old man is admitted to the emergency department with acute abdominal pain. On examination he is tachycardic and pyrexial with a soft and non-distended abdomen which is very tender on palpation throughout, there are no abdominal masses or renal angle tenderness. He has a past medical history of hypertension and stable angina.

His admission bloods show the following:

Hb 136 g/l (135-180 g/l) Urea 4.2 mmol/l (2-7 mmol/l)
Platelets 442 x 109/l (150-400 x 109/l) Creatinine 86 µmol/l (55-120 µmol/l)
WBC 11.8 x 109/l (4-11 x 109/l) CRP 11.2 mg/l (<10 mg/l)
Amylase 73 u/l (70-300 u/l) Lactate 6.9 mmol/l (0.2-2 mmol/l)

Which of the following is the most likely diagnosis for the cause of his pain?

Answer 19

Mesenteric ischaemia: triad of CVD, high lactate and soft but tender abdomen

Question 20

What would be a sign of GI perforation on examintion of a patient?

Answer 20

The soft abdomen goes against there being any gastrointestinal perforations as this would cause peritoneal irritation and involuntary guarding on examination

Question 21

What blood test result would be raised in acute pacnreatitis?

Answer 21

Acute pancreatitis could also present with diffuse abdominal tenderness but the normal amylase rules this out.

Question 22

What does a very high lactate with history CVD suggest?

Answer 22

The very high lactate level with a history of cardiovascular disease suggests acute infarction of tissue somewhere in the body and coupled with the tenderness with lack of guarding in the abdomen would make the most likely cause of his pain a mesenteric infarct

Question 23

3 main ischaemic lower GI conditions

Answer 23

Ischaemia to the lower gastrointestinal tract can result in a variety of clinical conditions. Whilst there is no standard classification it can be useful to separate cases into 3 main conditions
acute mesenteric ischaemia
chronic mesenteric ischaemia
ischaemic colitis

Question 24

Common predisposing factors for bowel ischaemia?

Answer 24

increasing age
atrial fibrillation - particularly for mesenteric ischaemia
other causes of emboli: endocarditis, malignancy
cardiovascular disease risk factors: smoking, hypertension, diabetes
cocaine: ischaemic colitis is sometimes seen in young patients following cocaine use

Question 25

Common features bowel ischemia?

Answer 25

abdominal pain - in acute mesenteric ischaemia this is often of sudden onset, severe and out-of-keeping with physical exam findings
rectal bleeding
diarrhoea
fever
bloods typically show an elevated white blood cell count associated with a lactic acidosis

Question 26

Dx of bowel ischaemia

Answer 26

CT Ix of choice

Question 27

What is acute mesenteric ishcaemia? Presentation

Answer 27

Acute mesenteric ischaemia is typically caused by an embolism resulting in occlusion of an artery which supplies the small bowel, for example the superior mesenteric artery. Classically patients have a history of atrial fibrillation.

The abdominal pain is typically severe, of sudden onset and out-of-keeping with physical exam findings.

Question 28

Mx of acute mesenteric ischaemia

Answer 28

urgent surgery is usually required
poor prognosis, especially if surgery delayed

Question 29

When does chronic mesenteric ischaemia occur?

Answer 29

Chronic mesenteric ischaemia is a relatively rare clinical diagnosis due to it’s non-specific features and may be thought of as ‘intestinal angina’. Colickly, intermittent abdominal pain occurs.

Question 30

What is ischaemic colitis?

Answer 30

Ischaemic colitis describes an acute but transient compromise in the blood flow to the large bowel. This may lead to inflammation, ulceration and haemorrhage

Question 31

Where is ischaemic colitis likely to occur?

Answer 31

It is more likely to occur in ‘watershed’ areas such as the splenic flexure that are located at the borders of the territory supplied by the superior and inferior mesenteric arteries.

Question 32

Ix for ischaemic colitis?

Answer 32

‘thumbprinting’ may be seen on abdominal x-ray due to mucosal oedema/haemorrhage

Question 33

Mx for ischaemic colitis?

Answer 33

• usually supportive
• surgery may be required in a minority of cases if conservative measures fail. Indications would include generalised peritonitis, perforation or ongoing haemorrhage

Question 34

Which type of MND has worst progonosis?

Answer 34

Progressive bulbar palsy

Question 35

Define MND

Answer 35

Motor neuron disease is a neurological condition of unknown cause which can present with both upper and lower motor neuron signs. It rarely presents before 40 years and various patterns of disease are recognised including amyotrophic lateral sclerosis, primary lateral sclerosis, progressive muscular atrophy and progressive bulbar palsy. In some patients however, there is a combination of clinical patterns

Question 36

Most common type of MND? Presentation

Answer 36

Amyotrophic lateral sclerosis (50% of patients)
typically LMN signs in arms and UMN signs in legs
in familial cases the gene responsible lies on chromosome 21 and codes for superoxide dismutase

Question 37

Presentation of primary lateral sclerosis

Answer 37

UMN sigsn only

Question 38

Progressive muscular atrophy presentation

Answer 38

LMN signs only
affects distal muscles before proximal
carries best prognosis

Question 39

Progressive bulbar palsy presentation

Answer 39

palsy of the tongue, muscles of chewing/swallowing and facial muscles due to loss of function of brainstem motor nuclei
carries worst prognosis

Question 40

Summarise common types of MND

Answer 40

Amyotrophic lateral sclerosis (50% of patients)
typically LMN signs in arms and UMN signs in legs
in familial cases the gene responsible lies on chromosome 21 and codes for superoxide dismutase

Primary lateral sclerosis
UMN signs only

Progressive muscular atrophy
LMN signs only
affects distal muscles before proximal
carries best prognosis

Progressive bulbar palsy
palsy of the tongue, muscles of chewing/swallowing and facial muscles due to loss of function of brainstem motor nuclei
carries worst prognosis

Question 41

A 26-year-old woman is asked to attend the emergency department by her GP following the results of some blood tests she had taken the day before. The results of these and her previous results are shown below:

Test Previous results Yesterday’s results Reference range
Na+ 137 mmol/L 142 mmol/L (135 - 145)
K+ 4.7 mmol/L 4.3 mmol/L (3.5 - 5.0)
Bicarbonate 25 mmol/L 24 mmol/L (22 - 29)
Urea 6.4 mmol/L 15.3 mmol/L (2.0 - 7.0)
Creatinine 87 µmol/L 183 µmol/L (55 - 120)

She was started on ramipril two weeks ago due to a raised blood pressure. She feels slightly nauseous but otherwise has not been aware of any symptoms.

Which of the following is likely to be responsible for her blood results?

Answer 41

Bilateral renal artery stenosis

After starting an ACE inhibitor, significant renal impairment may occur if the patient has undiagnosed bilateral renal artery stenosis

Question 42

What can bilateral renal stenosis potentially cuase?

Answer 42

Hypertension

Question 43

how would patients present with glomerulonephritis?

Answer 43

Glomerulonephritis can be a renal cause of acute kidney injury. However, patients would typically present with features of either nephrotic or nephritic syndrome depending on the exact subtype.

Question 44

Sx of nephrotic syndrome

Answer 44

Nephrotic syndrome is a group of symptoms that indicate your kidneys are not working properly. These symptoms include

too much protein in your urine, called proteinuria
low levels of a protein called albumin in your blood, called hypoalbuminemia
swelling in parts of your body, called edema
high levels of cholesterol and other lipids (fats) in your blood, called hyperlipidemia

Question 45

Does lower UTI cause renal impairment?

Answer 45

No, but pyelonephritis can

Question 46

can renal calculi cause renal impiarment and what signs would appear?

Answer 46

Renal calculi can cause renal impairment via obstruction. However, this is unlikely as she is not experiencing any symptoms suggestive of this, such as pain or haematuria.

Question 47

Patient group are ACE-inihibotrs not so good at treating?

Answer 47

Angiotensin-converting enzyme (ACE) inhibitors are now the established first-line treatment in younger patients with hypertension and are also extensively used to treat heart failure. They are known to be less effective in treating hypertensive Afro-Caribbean patients.

Question 48

Which patient group can ACE-inhiibtors also treat?

Answer 48

ACE inhibitors are also used to treat diabetic nephropathy and have a role in the secondary prevention of ischaemic heart disease.

Question 49

How do ACE-inhibotrs work?

Answer 49

inhibit the conversion angiotensin I to angiotensin II
ACE inhibitors are activated by phase 1 metabolism in the liver

Question 50

SE of ACE-inhibitors?

Answer 50

cough
occurs in around 15% of patients and may occur up to a year after starting treatment
thought to be due to increased bradykinin levels
angioedema: may occur up to a year after starting treatment
hyperkalaemia
first-dose hypotension: more common in patients taking diuretics

Question 51

CI to taking ACE0inhibitors?

Answer 51

pregnancy and breastfeeding - avoid
renovascular disease - may result in renal impairment
aortic stenosis - may result in hypotension
hereditary of idiopathic angioedema
specialist advice should be sought before starting ACE inhibitors in patients with a potassium >= 5.0 mmol/L

Question 52

Interactions ACE-inhibitors

Answer 52

patients receiving high-dose diuretic therapy (more than 80 mg of furosemide a day)
significantly increases the risk of hypotension

Question 53

Monitoring ACE-inhibitors?

Answer 53

urea and electrolytes should be checked before treatment is initiated and after increasing the dose
a rise in the creatinine and potassium may be expected after starting ACE inhibitors
acceptable changes are an increase in serum creatinine, up to 30% from baseline and an increase in potassium up to 5.5 mmol/l.
significant renal impairment may occur in patients who have undiagnosed bilateral renal artery stenosis

Question 54

A 78-year-old man is admitted to a medical ward with community-acquired pneumonia (CAP). Blood tests during the third day as an inpatient finds he has developed an acute kidney injury (AKI), with eGFR dropping from 58 to 26ml/min/1.73 m2 and creatinine rising from 122 to 196umol/L.

Which of the following of his regular medications should be stopped?

Answer 54

ACE inhibitors should be stopped in AKI as may worsen renal function

Question 55

What does AKI refer to?

Answer 55

An acute kidney injury (AKI) refers to a rapid decrease in renal function and is often defined as a rise from baseline serum creatinine of >26umol/L in 48 hours, or a >1.5 fold increase in serum creatinine within 1 week. A 25% or greater decline in eGFR within 7 days is also used to define AKI in children and young people. AKI is generally associated with low urine outputs of < 0.5 ml/kg/hour.

Question 56

Causes of AKI categorisation?

Answer 56

Causes of AKI can be categorised as either prerenal (for example hypovolaemia), renal (examples include nephropathies, glomerulonephritis, and nephrotoxic drugs), and postrenal (or obstructive) causes such as renal calculi and prostatic enlargement. The elderly are especially vulnerable, and the patient in this question has likely developed his AKI from decreased renal blood flow (i.e. a prerenal cause) that often results from severe infections.

Question 57

Which drugs should you stop if patient has AKI?

Answer 57

If a patient suffers from an acute kidney injury (AKI), ACE inhibitors should be stopped as they can worsen renal function and provoke hyperkalaemia. Other drugs to temporarily discontinue include angiotensin II receptor antagonists (A2RBs), NSAIDs (except low-dose aspirin), diuretics, and aminoglycosides. Although less likely to directly worsen renal function, metformin and lithium should also be stopped in the event of an AKI. This is due to an increased risk of drug toxicity when excretion by the kidneys is impaired.

Question 58

How does atorvastatin work?

Answer 58

Atorvastatin is a statin, which lowers cholesterol by inhibiting HMG-CoA reductase. Atorvastatin can be safely prescribed in renal disease patients for the primary and secondary prevention of cardiovascular events.

Question 59

MoA for bisoprolol? Is it nephrotixoic?

Answer 59

Bisoprolol is a β-blocker that is selective for heart β1 adrenoreceptors. It has negative inotropic effects and is commonly prescribed for hypertension, angina, secondary prevention of myocardial infarction, and to improve survival in heart failure. It is not nephrotoxic and can be prescribed in patients with kidney disease.

Question 60

Which drug is finasteride and when is it Rx?

Answer 60

Finasteride is a 5α-reductase inhibitor and treats benign prostatic hyperplasia (BPH) by blocking dihydrotestosterone synthesis. It can be prescribed for patients with poor renal function. The α1-receptor blocker tamsulosin is another commonly prescribed drug for BPH, improving urinary flow by promoting smooth muscle relaxation at the bladder neck

Question 61

Which patients should you be wary of giving finateride to?

Answer 61

It is generally safe to take in kidney disease, although should be used with caution in patients with an eGFR of < 10 mL/minute/1.73 m2.

Question 62

While working on a paediatrics ward as a junior doctor you are looking after 2-year-old boy with X-linked nephrogenic diabetes insipidus. He was recently diagnosed after his parents noticed that he was experiencing excessive polydipsia and polyuria. What is the pharmacological treatment of choice in this condition from the list below?

Answer 62

Chlorothiazide.
The aim of this question is to make sure you don’t get caught out by the differing mechanism of nephrogenic compared to cranial diabetes insipidus (DI). As the treatment for each is very different.

Question 63

Why does desmopressin work in cranial DI as a Tx?

Answer 63

Cranial diabetes insipidus essentially means the body is unable to produce sufficient amounts of vasopressin a.k.a antidiuretic hormone (ADH). This is can be treated with synthetic forms of vasopressin such as desmopressin.

Question 64

Why does desmopressin not work for cranial DI?

Answer 64

Nephrogenic diabetes insipidus on the other hand is caused by the kidneys inability to respond to vasopressin. This means giving a patient synthetic vasopressin will be ineffective. It may seem paradoxical that a thiazide diuretic would be a treatment for this condition as polyuria is a symptom of the disorder.

In simple terms DI leads to the production of vast amounts of dilute urine which is dehydrating and raises the plasma osmolarity, stimulating thirst. The effect of the thiazide causes more sodium to be released into the urine. This lowers the serum osmolarity which helps to break the polyuria-polydipsia cycle.

Question 65

A 20-month-old boy is brought to the GP by his father who is concerned that his son has gone off his food and is constipated.

The boy was born at term and is meeting all of his developmental milestones, and has had all of his vaccinations.

On examination, the boy is pale and has a large left-sided abdominal mass.

What is the most appropriate action?

Answer 65

For a child with a palpable abdominal mass or unexplained enlarged abdominal organ: refer very urgently (<48hr) for specialist assessment for neuroblastoma and Wilms’ tumour.

A palpable abdominal mass can indicate a neuroblastoma or Wilm’s tumour, which needs very urgent assessment by a paediatrician, a referral to be seen within a week would not be fast enough.

An abdominal X-ray would give clues towards the cause of the mass, however, many investigations need to be done and the paediatrician is best placed to do this.

Urinary vanillylmandelic acid and homovanillic acids are raised in neuroblastoma, but referral to the paediatrician would be more appropriate as they can do many investigations quickly.

The boy is not unstable, so does not need emergency treatment

Question 66

Where does a neuroblastoma arise from?

Answer 66

Neuroblastoma is one of the top five causes of cancer in children, accounting for around 7-8% of childhood malignancies. The tumour arises from neural crest tissue of the adrenal medulla (the most common site) and sympathetic nervous system.

Question 67

Median age onset neuroblastoma?

Answer 67

Median age of onset is around 20 months

Question 68

Features of a neuroblastoma?

Answer 68

abdominal mass
pallor, weight loss
bone pain, limp
hepatomegaly
paraplegia
proptosis

Question 69

Ix for neuroblastoma

Answer 69

raised urinary vanillylmandelic acid (VMA) and homovanillic acid (HVA) levels
calcification may be seen on abdominal x-ray
biopsy

Question 70

A 73-year-old patient attends the respiratory clinic. He has a three year history of COPD, with frequent exacerbations over the past year. He is an ex-smoker, having quit 2 years previously. He has required 5 courses of oral amoxicillin and prednisolone for infective exacerbations within the past 12 months. His most recent FEV1 was 47% of predicted. He is on a combination inhaler containing beclomethasone, glycopyrronium and formoterol.

Which is the best intervention to reduce his exacerbation frequency?

Answer 70

Azithromycin prophylaxis is recommended in COPD patients who meet certain criteria and who continue to have exacerbations

Question 71

Why are long-term antibiotics considered for COPD patients?

Answer 71

Patients with COPD who have frequent exacerbations, may be suitable for regular antibiotic therapy. One study found a reduced frequency of exacerbations in COPD patients with FEV1 <70% who had an exacerbation requiring steroids in the past 12 months, when given azithromycin for a year. Patients should have inhaled therapy optimised first with combination LABA/LAMA and ICS if appropriate. This patient is on a combination inhaler containing beclomethasone (steroid), glycopyrronium (LAMA) and formoterol (LABA).

Prescribing 250mg azithromycin daily or 500mg three times per week may reduce exacerbations in this type of patient.

Question 72

When is long-term oxygen considered in aptietns with COPD?

Answer 72

Long-term oxygen therapy is recommended in COPD patients with chronic hypoxia, polycythaemia, pulmonary hypertension or peripheral oedema but is not a treatment for reducing frequency of exacerbations.

Question 73

What should you do if patient has no beenfit from inhaled COC after 3m?

Answer 73

NICE guidelines state that if there is no evidence of benefit from inhaled corticosteroid after 3 months, patients should be switched to LABA/LAMA only. This is to reduce side-effects and would not reduce exacerbation frequency.

Question 74

General Mx of COPD

Answer 74

General management
>smoking cessation advice: including offering nicotine replacement therapy, varenicline or bupropion
annual influenza vaccination
one-off pneumococcal vaccination
pulmonary rehabilitation to all people who view themselves as functionally disabled by COPD (usually Medical Research Council [MRC] grade 3 and above)

Question 75

Bronchodilator therapy in COPD?

Answer 75

a short-acting beta2-agonist (SABA) or short-acting muscarinic antagonist (SAMA) is first-line treatment
for patients who remain breathless or have exacerbations despite using short-acting bronchodilators the next step is determined by whether the patient has ‘asthmatic features/features suggesting steroid responsiveness’

Question 76

Criterai to determine whether patient has ashtmatic/steroid responve features in COPD

Answer 76

any previous, secure diagnosis of asthma or of atopy
a higher blood eosinophil count - note that NICE recommend a full blood count for all patients as part of the work-up
substantial variation in FEV1 over time (at least 400 ml)
substantial diurnal variation in peak expiratory flow (at least 20%)

Question 77

If no asthmatic features, how should you Tx COPD?

Answer 77

add a long-acting beta2-agonist (LABA) + long-acting muscarinic antagonist (LAMA)
if already taking a SAMA, discontinue and switch to a SABA

Question 78

Oral theophylline Tx

Answer 78

NICE only recommends theophylline after trials of short and long-acting bronchodilators or to people who cannot used inhaled therapy
the dose should be reduced if macrolide or fluoroquinolone antibiotics are co-prescribed

Question 79

Oral prophylactic antiobiotic therapy

Answer 79

azithromycin prophylaxis is recommended in select patients
patients should not smoke, have optimised standard treatments and continue to have exacerbations
other prerequisites include a CT thorax (to exclude bronchiectasis) and sputum culture (to exclude atypical infections and tuberculosis)
LFTs and an ECG to exclude QT prolongation should also be done as azithromycin can prolong the QT interval

Question 80

SWhen should mucolytics be given patient with COPD?

Answer 80

should be ‘considered’ in patients with a chronic productive cough and continued if symptoms improve

Question 81

Features of cor pulmonale

Answer 81

features include peripheral oedema, raised jugular venous pressure, systolic parasternal heave, loud P2

Question 82

Tx of cor pulmonale?

Answer 82

use a loop diuretic for oedema, consider long-term oxygen therapy
ACE-inhibitors, calcium channel blockers and alpha blockers are not recommended by NICE

Question 83

Factors which may improve survival in patients with stable COPD?

Answer 83

smoking cessation - the single most important intervention in patients who are still smoking
long term oxygen therapy in patients who fit criteria
lung volume reduction surgery in selected patients

Question 84

A 67-year-old male presents to his general practitioner with enlargement of his breast tissue. He is very embarrassed by the situation and it is preventing him from living his daily life. He has a complex past medical history comprising benign prostatic hyperplasia, severe hypertension and high cholesterol.

Which one of the following medications is most likely to cause the symptoms?

Answer 84

Spironolactone may cause gynaecomastia

Question 85

How does spironolactone work?

Answer 85

The correct answer is spironolactone. This drug is an aldosterone antagonist which acts in the cortical collecting duct.It is usually prescribed for ascites, drug-resistant hypertension, Conn’s syndrome and nephrotic syndrome.

Question 86

How can spinrolactone cause gynaecomastia?

Answer 86

It can cause gynaecomastia (enlargement of breast tissue) by decreasing testosterone production, increasing peripheral conversion of testosterone to estradiol, and displacing estradiol from sex hormone-binding globulin

Question 87

What to do if patient has gynaecomastia from spirinolactone?

Answer 87

If this happens, you can try and switch it to eplerenone to reduce the side effects.

Question 88

Type of drug is amlodipine? Common SE

Answer 88

Amlodipine is a calcium-channel blocker used to treat hypertension. It does not cause gynaecomastia. Its most common side effect is peripheral oedema.

Question 89

Tx of atorvastatin and what SE can it cause?

Answer 89

Atorvastatin is a statin used to control high cholesterol. It does not cause gynaecomastia but it can cause headaches, nausea, diarrhoea and cold-like symptoms.

Question 90

What is eplerenone? How does it work? And what SE?

Answer 90

Eplerenone is an aldosterone antagonist that is used as a second-line when spironolactone causes side effects. It seems to have a lower incidence than spironolactone of sexual side effects such as feminisation, gynaecomastia, impotence, low sex drive and reduction of the size of male genitalia.

Question 91

How does tamsulosin work? SE?

Answer 91

Tamsulosin is an alpha-1 antagonist used to treat benign prostatic hyperplasia. This drug can cause postural hypotension, drowsiness, dyspnoea and cough but it has not been shown to cause gynaecomastia.

Question 92

Adverse effects sprinolactone

Answer 92

hyperkalaemia
gynaecomastia: less common with eplerenone

Question 93

You review a 51-year-old hypertensive patient who you started on 2.5mg of ramipril one month ago. He is complaining of a tickly cough since starting the medication which is keeping him awake at night. However, is blood pressure is now within normal limits.

What should you advise him?

Answer 93

Stop ramipril and Rx candesartan
Angiotensin-receptor blockers should be used where ACE inhibitors are not tolerated.
ACE inhibitors are commonly associated with a dry, persistent cough. A cough is unlikely to settle without stopping the ACE-inhibitor and prescribing a different class of drug. For a patient under 55 who is intolerant to an ACE-inhibitor the next step would be to offer an angiotensin 2 receptor blocker (ARB), eg candesartan.

Question 94

Lifestyle advace for treating hypertesnion

Answer 94

a low salt diet is recommended, aiming for less than 6g/day, ideally 3g/day. The average adult in the UK consumes around 8-12g/day of salt. A recent BMJ paper* showed that lowering salt intake can have a significant effect on blood pressure. For example, reducing salt intake by 6g/day can lower systolic blood pressure by 10mmHg
caffeine intake should be reduced
the other general bits of advice remain: stop smoking, drink less alcohol, eat a balanced diet rich in fruit and vegetables, exercise more, lose weight

Question 95

Tx for stage 1 hypertension

Answer 95

treat if < 80 years of age AND any of the following apply; target organ damage, established cardiovascular disease, renal disease, diabetes or a 10-year cardiovascular risk equivalent to 10% or greater
in 2019, NICE made a further recommendation, suggesting that we should ‘consider antihypertensive drug treatment in addition to lifestyle advice for adults aged under 60 with stage 1 hypertension and an estimated 10-year risk below 10%. ‘. This seems to be due to evidence that QRISK may underestimate the lifetime probability of developing cardiovascular disease

Question 96

Tx stage 2 hypertension

Answer 96

ABPM/HBPM >= 150/95 mmHg (i.e. stage 2 hypertension)
offer drug treatment regardless of age

For patients < 40 years consider specialist referral to exclude secondary causes.

Question 97

Step 1 to 4 Tx for hypertension

Answer 97

Step 1 treatment
patients < 55-years-old or a background of type 2 diabetes mellitus: ACE inhibitor or a Angiotensin receptor blocker (ACE-i or ARB): (A)
angiotensin receptor blockers should be used where ACE inhibitors are not tolerated (e.g. due to a cough)
patients >= 55-years-old or of black African or African–Caribbean origin: Calcium channel blocker (C)
ACE inhibitors have reduced efficacy in patients of black African or African–Caribbean origin are therefore not used first-line

Step 2 treatment
if already taking an ACE-i or ARB add a Calcium channel blocker or a thiazide-like Diuretic
if already taking a Calcium channel blocker add an ACE-i or ARB or a thiazide-like Diuretic
for patients of black African or African–Caribbean origin taking a calcium channel blocker for hypertension, if they require a second agent consider an angiotensin receptor blocker in preference to an ACE inhibitor
(A + C) or (A + D) or (C + A) or (C + D)

Step 3 treatment
add a third drug to make, i.e.:
if already taking an (A + C) then add a D
if already (A + D) then add a C
(A + C + D)

Step 4 treatment
NICE define step 4 as resistant hypertension and suggest either adding a 4th drug (as below) or seeking specialist advice
first, check for:
confirm elevated clinic BP with ABPM or HBPM
assess for postural hypotension.
discuss adherence
if potassium < 4.5 mmol/l add low-dose spironolactone
if potassium > 4.5 mmol/l add an alpha- or beta-blocker

Question 98

When and why should spironolactone be given to patients

Answer 98

Step 4 treatment
NICE define step 4 as resistant hypertension and suggest either adding a 4th drug (as below) or seeking specialist advice
first, check for:
confirm elevated clinic BP with ABPM or HBPM
assess for postural hypotension.
discuss adherence
if potassium < 4.5 mmol/l add low-dose spironolactone
if potassium > 4.5 mmol/l add an alpha- or beta-blocker

Question 99

If step 4 fails what to do?

Answer 99

Should be referred to a specialist

Question 100

new drugs direct renin inhibitors

Answer 100

Direct renin inhibitors
e.g. Aliskiren (branded as Rasilez)
by inhibiting renin blocks the conversion of angiotensinogen to angiotensin I
no trials have looked at mortality data yet. Trials have only investigated fall in blood pressure. Initial trials suggest aliskiren reduces blood pressure to a similar extent as angiotensin converting enzyme (ACE) inhibitors or angiotensin-II receptor antagonists
adverse effects were uncommon in trials although diarrhoea was occasionally seen
only current role would seem to be in patients who are intolerant of more established antihypertensive drugs

Question 101

Mx of hypertension

Answer 101

Question 102

Stages of hypertension

Answer 102

Question 103

Drug Mx of hypertesnion

Answer 103

Question 104

Tx for COPD flowchart

Answer 104