01/11/2024

Question 1

Examples of GLP-1 mimetics?

Answer 1

Exanatide
Liraglutide
Lixisenatide
Gulaglutide

Question 2

What should you do after trialling triple therapy for T2DM?

Answer 2

Switch 1 of the drugs for a GLP-1 mimetic particuarly if high BMI

Question 3

Management of opioid misuse?

Answer 3

IV or IM naloxone

Question 4

Anaphylaxis management?

Answer 4

IM adrenaline 500 micrograms 1 in 1000 in anterolateral aspect of middle 1/3rd of the thigh
Every 5 minutes if necessary
Fluids for shock
Oxygen if required

If Sx persist despite 2 doses of IM adrenaline get expert help to consider IV adrenaline infusion

Following stabilisation:
Non sedating oral antihistamines
Measure serum tryptase levels in first 12 hours
Refer to specialist allergy clinic if its the first time
Give an Andrea line injector
Monitor for biphasic reaction

Question 5

In a non urgent scenario how long does it take to transfuse a pack of RBC?

Answer 5

90-120 minutes

Question 6

Serotonin syndrome vs NMS?

Answer 6

Serotonin syndrome: onset is hours. hyperreflexia, clonus, confusion, hyperthermia & sweating, dilated pupils, diarrhoea

NMS: onset is days. hyporeflexia, rigidity, normal pupils, fever, hypertension, tachycardia, tachypnoea, agitated delirium with confusion

Question 7

What could you measure to determine if it’s serotonin syndrome or NMS?

Answer 7

Measure CK. generally only raised in NMS

Question 8

Management of predominately voiding LUTS in men?

Answer 8

Reduce fluid intake at specific times to reduce urinary frequency
Pelvic floor muscle training & bladder training

Alpha blocker (e.g. doxazosin, tamsulosin) if mod/sev
And/or
5 alpha reductase inhibitor (e.g. finasterine or dutasteride) can be offered if prostate is enlarged and pt is high risk of progression
+/-
Antimuscarinic drugs (e.g. oxybutinin, tolterodine, darifenacin) if mixed Sx of voiding and storage not responding to alpha blocker

Question 9

Management of predominately overactive bladder LUTS in men?

Answer 9

Moderate fluid intake and give temporary containment products e.g. pads or collecting devices
Supervised bladder training

If Sx persist…
Antimuscarinics e.g. oxybutinin, tolterodine, darifenacin
If these all fail consider mirabegron

Question 10

How do we manage Nocturia in men?

Answer 10

Moderate fluid intake at night
Furosemide 40mg late afternoon can be considered
Oral Desmopressin can be considered too

Question 11

How do we determine the severity of LUTS on men?

Answer 11

Using the international prostate symptom score (IPSS)
This us a questionnaire about symptom severity and quality of life
Score 0 = asymptomatic
Score 1-7 = mildly symptomatic
Score 8-19 = moderately symptomatic
Score 20-35 = severely symptomatic

Question 12

Who is hereditary spherocytosis common in?

Answer 12

People of Northern European descent

Question 13

What causes hereditary spoherocytosis?

Answer 13

AD defect of RBC cytoskeleton - the normal biconcave disc shape is replaced by a sphere-shaped RBC = RBC survival is reduced and destroyed by the spleen

Question 14

Features of hereditary spherocytosis?

Answer 14

FTT
Neonatal jaundice
Gallstones
Splenomegaly
Aplastic crisis precipitated by parvovirus infection

Question 15

How is hereditary spherocytosis diagnosed?

Answer 15

‘patients with a family history of HS, typical clinical features and laboratory investigations (spherocytes, raised mean corpuscular haemoglobin concentration [MCHC], increase in reticulocytes) do not require any additional tests

if the diagnosis is equivocal= EMA binding test and the cryohaemolysis test

Question 16

Who is G6PD deficiency most common in?

Answer 16

People from the med and Africa

Question 17

How is G6PD inherited?

Answer 17

In an x-linked recessive fashion

Question 18

What can precipitate a crisis in a pt with G6PD deficiency?

Answer 18

Drugs - Antimalarial, ciprofloxacin, sulpha-group drugs
Infections
Broad beans

Question 19

Sx of G6PD deficiency?

Answer 19

neonatal jaundice
intravascular haemolysis
gallstones
splenomegaly

Question 20

How is G6PD deficiency diagnosed?

Answer 20

G6PD enzyme assay

Question 21

Blood film findings in G6PD deficiency?

Answer 21

Heinz bodies
Bite and blister cells can also be seen

Question 22

What antibiotic is used for legionella?

Answer 22

Macrolides: typically erythromycin/clarithromycin

Question 23

Causes of avascular necrosis of the hip?

Answer 23

long-term steroid use
chemotherapy
alcohol excess
trauma

Question 24

What investigations is diagnostic for avscular necrosis of the femoral head?

Answer 24

MRI

Question 25

What causes Lyme disease?

Answer 25

spirochaete Borrelia burgdorferi carried by ticks

Question 26

Symptoms of Lyme disease?

Answer 26

In the first 30 days: Erythema migrans Systemic: headache, lethargy, fever, arthralgia After 30 days: Cardiovascular - heart block, peri & myocarditis Neurological - facial nerve palsy, Radicular pain & meningitis

Question 27

What is erythema migrans?

Answer 27

A bulls eye rash at the site of the tick bite Painless >5cm and slowly grows in size

Question 28

How to diagnose Lyme disease?

Answer 28

Can be diagnosed clinically if erythema migrans is present Otherwise ELISA antibodies to borrelia burgdorferi. If negative but still suspected and test was done within 4weeks of Sx onset -> repeat test in 4-6 weeks

Question 29

Management of Lyme disease?

Answer 29

Doxycycline

Question 30

What is Jarisch-Herxheimer reaction?

Answer 30

After first dose of doxycycline in Lyme disease - fever, rash, tachycardia Seen in other spirochaetal diseases too e.g. syphilis

Question 31

MOA of acetazolamide for idiopathic intracranial hypertension?

Answer 31

It’s a carbonic anhydrase inhibitor = reduces CSF production

Question 32

What is familial hypercholesterolaemia?

Answer 32

An AD condition that results in high levels of LDL cholesterol which if left untreated may cause early cardiovascular disease

Question 33

Who should you suspect familial hypercholesterolaemia in?

Answer 33

adults with: a total cholesterol level greater than 7.5 mmol/l and/or a personal or family history of premature coronary heart disease (<60) children of affected parents: if one parent is affected by familial hypercholesterolaemia, arrange testing in children by age 10 if both parents are affected by familial hypercholesterolaemia, arrange testing in children by age 5

Question 34

What criteria is used to diagnose familial hypercholesterolaemia?

Answer 34

The Simon Broome criteria

Question 35

Outline the Simon broome criteria for familial hypercholesterolaemia?

Answer 35

in adults total cholesterol > 7.5 mmol/l and LDL-C > 4.9 mmol/l or children TC > 6.7 mmol/l and LDL-C > 4.0 mmol/l, plus: for definite FH: tendon xanthoma in patients or 1st or 2nd degree relatives or DNA-based evidence of FH for possible FH: FHx of MI in <50 years in 2nd degree relative, <60 in 1st degree relative, or a FHx of raised cholesterol levels

Question 36

Is CK raised in PMR?

Answer 36

No!1

Question 37

Long term adverse effects of lithium use?

Answer 37

Hyperparathyroidism & resultant hypercalcaemia Nephrotoxicity & Diabetes insipidus Hypothyroidism Idiopathic intracranial hypertension Weight gain

Question 38

Features of addisons disease?

Answer 38

Lethargy Weakness Anorexia N&V Weight loss Salt craving Hyperpigmentation in primary Vitiligo Loss of pubic hair in women Hypotension - often postural Hypoglycaemia Hyponatraemia nd hyperkalaemia

Question 39

Why is hyperpigmentation only associated with primary adrenal insufficiency and not secondary?

Answer 39

As in primary there is high ACTH whereas in secondary (when lesi0ns in pituitary) there is no ACTH The more ACTH, the more melanocyte stimulating hormones produced = melanocytes stimulated =more melanin

Question 40

Where does the hyperpigmentation that occurs in addisons most commonly occur?

Answer 40

In sunexposed areas, recent scars, pressure points, areas of friction, palmar creases, mucous membranes

Question 41

Investigations for addisons?

Answer 41

9am cortisol & then if this indicates likely diagnosis refer to endocrinology for syncathen test U&Es for Na and k Blood glucose Other investigations in secondary cate: ACTh level, plasma renin and aldosterone, TFTs, autoantibodies, CT/MRI of adrenals or pituitary

Question 42

Management of addisons?

Answer 42

Hydrocortisone - given as 3 divided doses throughout the day Fludrocortisone Androgen replacement with DHEA may be used in certain circumstances decided by endocrinology e.g. pt may ahve low libido

Question 43

How should you advise pts with addisons to adjust corticosteroids during periods of increased stress to prevent adrenal crisis?

Answer 43

A moderate intercurrent illness (e.g. flu) they should double their usual dose of hydrocortisone until recovered. Severe nausea they should take 20 mg hydrocortisone orally and sip oral rehydration solution Severe intercurrent illness (such as vomiting, persistent diarrhoea or other severe illness i.e. not absorbing drug) they should use their emergency injection (100 mg hydrocortisone) and seek immediate medical advice, emphasizing that it is an Addison's disease emergency. Had an injury they should take 20 mg hydrocortisone orally immediately to avoid shock — serious trauma will require administration of their emergency injection (100 mg hydrocortisone) and admission. If doing strenuous exercise e.g. a marathon they will need to double their meds.

Question 44

Steroids and WCC?

Answer 44

Glucocorticoids can increase WCC upon initiation - it’s predominantly neutrophils

Question 45

What are risk factors for euglycaemic DKA?

Answer 45

Fasting Use of SGLT2i Insulin use prior to hospital admission Pregnancy

Question 46

Outline typical fluid replacement regime for a DKA pt with systolic bp on admission of 90mmHg or over?

Answer 46

1L of 0.9% Sodium chloride in the first hour 1L of 0.9% Sodium chloride with potassium chloride in the next 2 hours 1L of 0.9% Sodium chloride with potassium chloride in the next 2 hours 1L of 0.9% Sodium chloride with potassium chloride in the next 4 hours 1L of 0.9% Sodium chloride with potassium chloride in the next 4 hours 1L of 0.9% Sodium chloride with potassium chloride in the next 6 hours Note potassium chloride is only given if K+ level in the first 24 hours is between 3.5-5.5mmol/L

Question 47

Which pts may need a slower infusion in the e fluid resuscitation of a DKA pt?

Answer 47

Young adults (18-25) as they are at much higher risk of cerebral oedema

Question 48

What is whipple's triad? What does it indicate?

Answer 48

Symptoms and signs of hypoglycemia Plasma glucose < 2.5 mmol/L Reversibility of symptoms on the administration of glucose This is the clinical presentation of pancreatic Insulinoma

Question 49

What is an inuslinoma?

Answer 49

The most common pancreatic endocrine tumour. It’s a neuroendocrine tumour deriving mainly from pancreatic Islets of Langerhans It causes high insulin, rapid weight gain, features of hypoglycaemia, high C-peptide

Question 50

What is Sheehan’s syndrome?

Answer 50

Aka pituitary apoplexy This occurs because post partum haemorrhage leads to avascular necrosis of the pituitary gland = ischaemic and cell death. In pregnancy the pitouyray gland can increase in size by up to 200% in women without adenomas Note it only affects the anterior pituitary gland as posterior pituitary gets a good blood supply from various arteries so is not susceptible to ischaemia when there is a drop in bp

Question 51

What is samters triad?

Answer 51

asthma, aspirin sensitivity and nasal polyposis

Question 52

What is the most common cause of puerperal pyrexia?

Answer 52

Endometritis

Question 53

What is endometritis?

Answer 53

Inflammation of the endometrium caused by an infection that is introduced during or after labour/delivery More common after a c-section which is why prophylactic antibiotics are given

Question 54

Presentation of endometritis?

Answer 54

Any time from the birth - several weeks postpartum Foul-smelling discharge or lochia Bleeding that gets heavier or does not improve with time Lower abdominal or pelvic pain Fever Sepsis

Question 55

What should you do if you are suspecting ovarian cancer and there is ascites or an abdominal or pelvic mass on examination?

Answer 55

You can bypass CA125 and pelvic USS and instead refer directly to gynaecology Ca service under 2 week wait

Question 56

What is conns syndrome?

Answer 56

Primary hyperaldosteronism caused by an adrenal adenoma

Question 57

Features of primary hyperaldosteronism?

Answer 57

Hypertension Hypokalaemia - may cause muscle weakness Metabolic alkalosis

Question 58

Risk factors for gestational diabetes?

Answer 58

BMI of > 30 kg/m² previous macrosomic baby weighing 4.5 kg or above previous gestational diabetes first-degree relative with diabetes family origin with a high prevalence of diabetes (South Asian, black Caribbean and Middle Eastern)

Question 59

What is the test of choice for gestational diabetes?

Answer 59

OGTT

Question 60

If a woman has previously had gestational diabetes, when should they be tested for it again in future pregnancies?

Answer 60

ASAP after booking and then again at 24-28 weeks if first test is normal

Question 61

When should women be tested for gestational diabetes with OGTT?

Answer 61

At 24-28 weeks

Question 62

Management of gestational diabetes?

Answer 62

newly diagnosed women should be seen in a joint diabetes and antenatal clinic within a week & women should be taught about self-monitoring of blood glucose advice about diet and exercise should be given if the fasting plasma glucose level is < 7 mmol/l a trial of diet and exercise should be offered if glucose targets are not met within 1-2 weeks of altering diet/exercise metformin should be started if glucose targets are still not met short-acting insulin should be added to diet/exercise/metformin if at the time of diagnosis the fasting glucose level is >= 7 mmol/l insulin should be started immediately if the plasma glucose level is between 6-6.9 mmol/l, and there is evidence of complications such as macrosomia or hydramnios, insulin should be offered

Question 63

Problems with gestational diabetes?

Answer 63

Macrosomia Shoulder dystocia Miscarriage, preterm, stillbirth or perinatal death Greater risk of developing obesity and T2DM later in life Postnatal adaptation problems e.g. hypoglycaemia

Question 64

What is torsades de pointes?

Answer 64

A form of polymorphic VT associated with a long QT interval It can deteriorate into V fib and hence lead to sudden death

Question 65

Causes of long QT interval?

Answer 65

Congenital antiarrhythmics: amiodarone, sotalol, class 1a drugs TCAs and SSRIs particuarly citalopram antipsychotics chloroquine terfenadine erythromycin electrolyte: hypocalcaemia, hypokalaemia, hypomagnesaemia myocarditis/MI hypothermia subarachnoid haemorrhage

Question 66

Management of torsades de pointes?

Answer 66

IV magnesium sulphate

Question 67

Pathophysiology of torsades de pointes?

Answer 67

A prolonged QT reflects prolonged myocyte repolarisation due to ion channel malfunction This prolonged repolarisation period also gives rise to early after-depolarisations