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MLA content map > MLA: GP and Primary Healthcare > Flashcards

MLA: GP and Primary Healthcare Flashcards

1
Q

what are the features of allergic rhinitis?

A

sneezing, bilateral nasal obstruction, clear nasal discharge, post-nasal drip and nasal pruritus

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2
Q

what is the management of moderate to severe persistent symptoms/ineffective initial drug treatment of allergic rhinitis?

A

intranasal corticosteroids

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3
Q

what are the general features of haemolytic anaemia on bloods?

A

anaemia, reticulocytosis, low haptoglobin, raised LDH and indirect bilirubinw

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4
Q

what is seen on blood film in autoimmune haemolytic anaemia?

A

spherocytes and reticulocytes

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5
Q

what is warm AIHA?

A

most common type.- in warm AIHA the antibody (IgG) causes haemolytic best at body temperature and tends to occur in extravascular sites

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6
Q

what are the causes of warm AIHA?

A

idiopathic, autoimmune (SLE), neoplasia (lymphoma, CLL), drugs: methyldopa

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7
Q

what is the management of warm AIHA?

A
  1. treatment of any underlying disorder
  2. steroids (+/- rituximab)
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8
Q

which antibody is common in cold AIHA?

A

IgM - causes haemolytic best at 4 degrees

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9
Q

which type of AIHA involves haemolysis mediated by complement and is therefore more commonly intravascular?

A

cold AIHA

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10
Q

in which AIHA, do patients respond less well to steroids?

A

in cold AIHA

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11
Q

what are the causes of cold AIHA?

A
  1. neoplasia e.g. lymphoma
  2. infections e.g mycoplasma, EBV
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12
Q

which patient group have the highest prevalence of iron deficiency anaemia?

A

preschool-age children

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13
Q

what type of bleeding is the most common cause of iron deficiency anaemia in certain groups?

A

blood loss due to menorrhagia is the most common in pre-menopausal women, whereas GI bleeding is the most common in men and post-menopausal women

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14
Q

what are the features of iron deficiency anaemia?

A

fatigue, SOB on exertion, palpitations, pallor, nails changes (koilonychia - spoon shaped nails), hair loss, atrophic glossitis, post-cricoid webs, angular stomatitis

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15
Q

what does the FBC of an iron deficiency anaemia demonstrate?

A

hypochromic microcytic anaemia

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16
Q

what is important to remember about ferritin levels and iron deficiency anaemia?

A

serum ferritin is likely to be low as it correlates with iron stores. However, ferritin can be raised in stages of inflammation, so it is important to note that if ferritin is high, it does not rule out iron deficiency anaemia

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17
Q

what will happen to the level of TIBC in iron deficiency anaemia?

A

it will be high as a high level reflects low iron stores - transferrin saturation will be low

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18
Q

what is seen on blood film in IDA?

A

anisopoikilocytosis (RBCs of different shapes and sizes), target cells, ‘pencil’ poikilocytes

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19
Q

what is the difference between iron deficiency anaemia and anaemia of chronic disease on iron studies?

A

TIBC is high in IDA and low in AOCD, ferritin is low in IDA and high in AOCD

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20
Q

at are the megaloblastic causes of macrocytic anaemia?

A
  1. vitamin B12 deficiency
  2. folate deficiency
  3. secondary to MTX therapy
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21
Q

what are the normoblastic causes of macrocytic anaemia?

A

alcohol, liver disease, hypothyroidism, pregnancy, reticulocytosis, myelodysplasia, drugs: cytotoxic

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22
Q

what are the causes of microcytic anaemia?

A

iron-deficiency anaemia, thalassemia, congenital sideroblastic anaemia, anaemia of chronic disease, lead poisoning

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23
Q

what are anal fissures?

A

longitudinal or elliptical tears of the squamous lining of the distal anal canal

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24
Q

what are the risk factors for anal fissures?

A

constipation, IBD, STIs

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25
Q

what are the features of anal fissures?

A
  1. painful, bright red, rectal bleeding
  2. around 90% of them occur on the posterior midline
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26
Q

if anal fissures are not on the posterior midline, what needs to be considered?

A

other underlying causes, e.g. Crohn’s

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27
Q

what is the management of acute anal fissures (<1 week)?

A
  1. soften stool -> dietary advice = high fibre diet with high fluid intake
    + bulk-forming laxatives are first line
  2. lubricants may be tried before defecation
  3. topical anaesthetics
  4. analgesia
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28
Q

what is the management of a chronic anal fissure?

A
  1. GTN is first-line
  2. if GTN is not effective after 8 week then secondary care referral should be considered for surgery (sphincterotomy) or botulinum toxin
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29
Q

what defines recurrent AF episodes?

A

when a patient has 2 or more episodes of AF

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30
Q

what is it called when episodes of AF terminate spontaneously?

A

paroxysmal AF - such episodes last less than 7 days (typically <24 hours)

31
Q

what defines persistent AF?

A

when the arrhythmia is not self-terminating - such episodes usually last greater than 7 days

32
Q

what is permanent AF?

A

continuous AF which cannot be cardioverted or attempts to do so are deemed inappropriate. Treatment goals are therefore rate control and anticoagulation where appropriate

33
Q

what are the two key parts of managing patients with AF?

A
  1. rate/rhythm control
  2. reducing stroke risk
34
Q

what is used first line to rate control a patient with AF?

A

beta-blocker or rate-limiting CCB (diltiazem)

35
Q

what is the management of attempting to rate control AF if one drug does not control the rate adequately?

A

combination therapy of any of the two:
1. beta blocker
2. diltiazem
3. digoxin

36
Q

with managing AF, when is the most likely time for a patient to suffer from an embolism?

A

when a patient switches from AF to sinus rhythm presents the highest risk for embolism leading to stroke

37
Q

what are the two scenarios in which cardioversion may be used in AF?

A
  1. electrical cardioversion as an emergency if the patient is haemodynamically unstable
  2. electrical/pharmacological CV as an elective procedure where a rhythm control strategy is preferred
38
Q

electrical cardioversion in AF is synchronised to which cardiac wave?

A

the R wave - to prevent the delivery of a shock during the vulnerable period of cardiac repolarisation when VF can be induced

39
Q

what are the options for cardioversion in patients who present with AF for less than 24 hours?

A
  1. electrical - ‘DC cardioversion’
  2. pharmacology - amiodarone if structural heart disease - flecainide/amiodarone in those without structural heart disease
40
Q

what is the management of someone with paroxysmal AF of onset >48 hours?

A

anticoagulation should be given for at least 3 weeks prior to cardioversion

41
Q

what is the alternative to 3 weeks of anticoagulation and then electrical CV in a patient presenting with AF >48 hours?

A

TOE to exclude a left atrial appendage thrombus - if excluded, patients may be heparinised and cardioverted immediately

42
Q

following a TIA, when should anticoagulation commence?

A

immediately once imaging has excluded haemorrhage

43
Q

what is the management of haemodynamically unstable AF patient?

A

electrical cardioversion immediately, as per the peri-arrest tachycardia guidelines

44
Q

what are the notable complications of electrical cardioversion in AF?

A

cardiac tamponade, stroke, pulmonary vein stenosis

45
Q

what is atrial flutter?

A

form of supraventricular tachycardia characterised by a succession of rapid atrial depolarisation

46
Q

what is the first line drug for bradycardia with haemodynamic compromise?

A

Atropine (500mcg IV)

47
Q

what is the management of bradycardia with haemodynamic compromise that has failed to respond to atropine?

A
  1. increase atropine, up to maximum of 3mg
  2. transcutaneous pacing
  3. isoprenaline/adrenaline infusion titrated to response
48
Q

what is the management of narrow-complex tachycardias demonstrating no sign of haemodynamic compromise?

A
  1. vagal manoeuvres followed by IV adenosine
  2. if the above is unsuccessful, consider a diagnosis of atrial flutter and then rate control (beta-blocker)
49
Q

what is the acute management of SVT

A
  1. vagal manoeuvres/carotid sinus massage
  2. IV adenosine -> 6, 12, 18
    (contraindicated in asthmatics, so they are given Verapamil)
  3. electrical CV
50
Q

what is Torsades?

A

form of polymorphic VT associated with long QT interval -> can deteriorate into VF and be a cause of sudden death

51
Q

which type of haemorrhage can cause a prolonged QT interval, and therefore risk Torsades?

A

SAH

52
Q

which drug is used in Torsades?

A

IV magnesium sulphate

53
Q

what are the two main types of VT

A
  1. monomorphic: myocardial infarction
  2. polymorphic VT: subtype is Torsades
54
Q

what are the features of life-threatening asthma attack in children?

A
  1. SpO2 <92%
  2. PEF <33%
  3. silent chest
  4. poor respiratory effort
  5. agitation
  6. altered consciousness
  7. cyanosis
55
Q

what is fibromyalgia?

A

syndrome characterised by widespread pain throughout the body with tender points at specific anatomical sites - the cause is unknown

56
Q

what underlies the management of fibromyalgia?

A
  1. explanation
  2. aerobic exercise - strongest evidence base
  3. CBT
  4. medication: pregabalin, duloxetine, amitriptyline
57
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A
57
Q
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58
Q

what are the sick day rules for T1DM?

A

if the patient is on insulin, they must not stop it due to the risk of DKA. They should continue their normal insulin regime but ensure that they are checking their sugars frequently

59
Q

what are the sick day rules for T2DM?

A

advise the patient to temporarily stop some oral hypoglycaemics during acute illness

60
Q

what does a T-score of -1.0 to -2.5 indicate

A

osteopenia

61
Q

what does a T-score of -2.5 or lower indicate?

A

osteoporosis

62
Q

what are the characteristics of a thromboses haemorrhoid?

A

anorectal pain and tender, tense blue-black swelling at the anal margin

63
Q

what is the management of a thrombosed haemorrhoid?

A

> if patient presents within 72 hours, then referral should be considered for excision
otherwise patients are managed with stool softeners, ice packs and analgesia

64
Q

how long does it usually take the symptoms of a thrombosed haemorrhoid to settle?

A

within 10 days

65
Q

which muscle is best for IM adrenaline?

A

vastus lateralis = large area devoid of major blood vessels and nerves, which reduces the risk of injury during the injection

66
Q

what is the classical presentation of primary hyperaldosteronism?

A

lethargy, headache, HTN, hypokalaemia, hypernatremia and high serum bicarbonate (metabolic alkalosis)

67
Q

what is the most common cause of anaemia in CKD?

A

due to reduced erythropoietin levels - normally a normochromic normocytic anaemia and becomes apparent when the eGFR is less than 35

68
Q

what is the pathophysiology of CKD causing mineral bone disease?

A
  1. 1-alpha hydroxylation normally occurs in the kidneys -> CKD leads to low vitamin D
  2. the kidneys normally excrete phosphate -> CKD leads to high phosphate
  3. the high phosphate levels drags calcium from the bones = osteomalacia
    + low calcium due to lack of vitamin D and high phosphate
69
Q

what are the main adverse effects of thyroxine therapy?

A

hyperthyroidism, reduced bone mineral density, worsening angina and atrial fibrillation

70
Q

which antibiotic is used as prophylaxis in COPD patients who fit a certain criteria and continue to have exacerbations?

A

Azithromycin

71
Q

what is a rare, but important, side effect of DPP4-inhibitors e.g. Sitagliptin?

A

Pancreatitis

72
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73
Q
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