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A. REVISION FROM QBANKS > 01/11/2024 > Flashcards

01/11/2024 Flashcards

1
Q

Examples of GLP-1 mimetics?

A

Exanatide
Liraglutide
Lixisenatide
Gulaglutide

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2
Q

What should you do after trialling triple therapy for T2DM?

A

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

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3
Q

Management of opioid misuse?

A

IV or IM naloxone

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4
Q

Anaphylaxis management?

A

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

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5
Q

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

A

90-120 minutes

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6
Q

Serotonin syndrome vs NMS?

A

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

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7
Q

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

A

Measure CK. generally only raised in NMS

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8
Q

Management of predominately voiding LUTS in men?

A

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

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9
Q

Management of predominately overactive bladder LUTS in men?

A

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

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10
Q

How do we manage Nocturia in men?

A

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

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11
Q

How do we determine the severity of LUTS on men?

A

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

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12
Q

Who is hereditary spherocytosis common in?

A

People of Northern European descent

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13
Q

What causes hereditary spoherocytosis?

A

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

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14
Q

Features of hereditary spherocytosis?

A

FTT
Neonatal jaundice
Gallstones
Splenomegaly
Aplastic crisis precipitated by parvovirus infection

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15
Q

How is hereditary spherocytosis diagnosed?

A

‘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

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16
Q

Who is G6PD deficiency most common in?

A

People from the med and Africa

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17
Q

How is G6PD inherited?

A

In an x-linked recessive fashion

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18
Q

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

A

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

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19
Q

Sx of G6PD deficiency?

A

neonatal jaundice
intravascular haemolysis
gallstones
splenomegaly

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20
Q

How is G6PD deficiency diagnosed?

A

G6PD enzyme assay

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21
Q

Blood film findings in G6PD deficiency?

A

Heinz bodies
Bite and blister cells can also be seen

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22
Q

What antibiotic is used for legionella?

A

Macrolides: typically erythromycin/clarithromycin

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23
Q

Causes of avascular necrosis of the hip?

A

long-term steroid use
chemotherapy
alcohol excess
trauma

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24
Q

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

A

MRI

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25
Q

What causes Lyme disease?

A

spirochaete Borrelia burgdorferi carried by ticks

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26
Q

Symptoms of Lyme disease?

A

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

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27
Q

What is erythema migrans?

A

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

28
Q

How to diagnose Lyme disease?

A

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

29
Q

Management of Lyme disease?

A

Doxycycline

30
Q

What is Jarisch-Herxheimer reaction?

A

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

31
Q

MOA of acetazolamide for idiopathic intracranial hypertension?

A

It’s a carbonic anhydrase inhibitor = reduces CSF production

32
Q

What is familial hypercholesterolaemia?

A

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

33
Q

Who should you suspect familial hypercholesterolaemia in?

A

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

34
Q

What criteria is used to diagnose familial hypercholesterolaemia?

A

The Simon Broome criteria

35
Q

Outline the Simon broome criteria for familial hypercholesterolaemia?

A

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

36
Q

Is CK raised in PMR?

A

No!1

37
Q

Long term adverse effects of lithium use?

A

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

38
Q

Features of addisons disease?

A

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

39
Q

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

A

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

40
Q

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

A

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

41
Q

Investigations for addisons?

A

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

42
Q

Management of addisons?

A

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

43
Q

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

A

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.

44
Q

Steroids and WCC?

A

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

45
Q

What are risk factors for euglycaemic DKA?

A

Fasting
Use of SGLT2i
Insulin use prior to hospital admission
Pregnancy

46
Q

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

A

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

47
Q

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

A

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

48
Q

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

A

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

49
Q

What is an inuslinoma?

A

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

50
Q

What is Sheehan’s syndrome?

A

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

51
Q

What is samters triad?

A

asthma, aspirin sensitivity and nasal polyposis

52
Q

What is the most common cause of puerperal pyrexia?

A

Endometritis

53
Q

What is endometritis?

A

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

54
Q

Presentation of endometritis?

A

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

55
Q

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

A

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

56
Q

What is conns syndrome?

A

Primary hyperaldosteronism caused by an adrenal adenoma

57
Q

Features of primary hyperaldosteronism?

A

Hypertension
Hypokalaemia - may cause muscle weakness
Metabolic alkalosis

58
Q

Risk factors for gestational diabetes?

A

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)

59
Q

What is the test of choice for gestational diabetes?

A

OGTT

60
Q

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

A

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

61
Q

When should women be tested for gestational diabetes with OGTT?

A

At 24-28 weeks

62
Q

Management of gestational diabetes?

A

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

63
Q

Problems with gestational diabetes?

A

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

64
Q

What is torsades de pointes?

A

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

65
Q

Causes of long QT interval?

A

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

66
Q

Management of torsades de pointes?

A

IV magnesium sulphate

67
Q

Pathophysiology of torsades de pointes?

A

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

A. REVISION FROM QBANKS (11 decks)

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