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MRCP Part 1 > Pastest > Flashcards

Pastest Flashcards

Harder, slower, scarier

1
Q

How do you distinguish anteriolateral vs high lateral infarction?

A

Antero-lateral V4-6, I, and aVL.

High lateral V5-6, I, and aVL

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2
Q

How does metformin increase ovulation in PCOS?

A

Increases insulin sensitivity within the ovary to improve ovulation.

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3
Q

Explain the immunopathological process of SLE

A

Activation of the classical complement pathway occurs owing to the large number of double stranded DNA and other immune complexes that form and fix complement.

These immune complexes deposit in the kidneys and other organs where they attract other components of the immune system that cause tissue damage.

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4
Q

What does over warfarinization affect on the clotting screen?

A

INR - determined by PT (but can also increase APTT as well)

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5
Q

When do you consider prophylaxis in cluster headaches?

A

If headaches are frequent or last more than 3 weeks.

Normally verapamil or lithium is used

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6
Q

What are the benefits of Meptazinol as analgesia?

A

Meptazinol is a partial mu opioid receptor agonist; as such, it is an effective opioid analgesic associated with a lower risk of constipation.

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7
Q

What does an ABG demonstrate in Grave’s Disease?

A

Compared with normal subjects, hyperthyroid patients show significantly lower resting arterial CO2 tension, tidal volume and significantly higher mean inspiratory flow and PaO2. This can, of course, lead to misdiagnosis of patients with hyperthyroidism as having hyperventilation syndrome.

Patients with hyperthyroidism also show a greater ventilatory response to hypoxia than normal patients. These ventilatory changes are significantly correlated with T3 levels.

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8
Q

How does HIV enter cells?

A

Two envelope proteins on the surface of the HIV virus are involved in initial binding to human cells. GP120 binds to the primary receptor (the CD4 moleculre) and then to a co-receptor (CXCR4 (T cell) or CCR5 (macrophage)); GP41 then mediates movement through the cell membrane.

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9
Q

Damage to what structure causes hemiballism?

A

Subthalmic nucleus

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10
Q

What are the causes of protein losing enteropathy?

A 
Sarcoidosis
Inflammatory bowel disease
Pseudomembranous colitis
CMV colitis
Tuberculosis
Connective tissue diseases
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11
Q

What is the appropriate follow up for adenomatous colonic polyps?

A

5 year interval for low risk patients
-one to two adenomas both <1cm

3 year follow up for medium risk
-3-4 adenomas or 1-2 where one >/=1cm

1 year follow up high risk
-5 or more small adenomas or more than 3 with at least 1 at or above 1cm.

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12
Q

Which cranial nerves arise from the midbrain?

A

Midbrain – the trochlear nerve (IV) comes from the posterior side of the midbrain. It has the longest intracranial length of all the cranial nerves.

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13
Q

Which cranial nerves arise from the pons?

A

Trigeminal (V)

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14
Q

Which cranial nerves arise from the medulla?

A

Medulla oblongata – posterior to the olive: glossopharyngeal, vagus, accessory (IX-XI). Anterior to the olive: hypoglossal (XII).

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15
Q

Which cranial nerve arises from the midbrain-pontine junction?

A

Oculomotor (III)

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16
Q

Which cranial nerves arise from the pontine-medulla junction?

A

Pontine-medulla junction – abducens, facial, vestibulocochlear (VI-VIII).

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17
Q

How does glucose cause diabetic retinopathy?

A

Polyol pathway. Glucose converted to sorbitol which accumulates damaging retinal cells via osmotic effects.

Also increased thickness of capillary basement membrane, leukocyte stasis and adhesion to vascular endothelium.

Glucose also persistently activates protein kinase C ad MAPK causing programmed cell death

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18
Q

What conditions are associated with fragile X?

A

Epilepsy (25%), strabismus, otitis media, sinusitis, joint dislocation, orthopaedic problems, apnoea

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19
Q

Causes of clubbing?

A

Suppurative disease, long standings bronchiectasis, acute lung abscess, empyema, malignant disease (esp carcinoma bronchus and pleural malignancy), fibrosing alveolitis, asbestosis.

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20
Q

What is the mechanism of action of terlipressin in hepatorenal syndrome?

A

Terlipressin = synthetic ADH analogue
(non significant ADH effect (only 3% compared to real ADH))

Increases vascular and extravascular tone and therefore increased arterial vascular resistance. Decreases splanchnic hypervolaemia. This decreases renin activity due to decreased afferent and efferent flow.

Useful as a bridge to transplantation. May have mortality benefit.

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21
Q

What are the 3 cardinal features of lewy body dementia to help differentiate from alzheimers?

A

Fluctuating cognitive function
Varying alert level
Significant daytime somnolence

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22
Q

What is the worst antimalarial in G6PD?

A

Primiquine

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23
Q

What is the gold standard test for syphilis?

A

Swab and PCR is now the best

not serology

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24
Q

How does syphilis serology alter before and after treatement?

A

Non-treponeme specific (VDRL, RPR) +ve in active disease but -ve after treatment or in late disease
-Can be +ve in pregnancy, SLE, TB etc

Treponeme-specific (TPHA, FTA) +ve in active disease and remains +ve following treatment.
-Also +ve in other related treponeme disease (e.g. yaws)

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25
Q

What are the advantages and disadvantages of clindamycin use in cellulitis?

A

Used if patient is pen allergic

Switches off bacterial toxin production
Does increase risk of C. Diff so used second line

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26
Q

Why may CXR and sputum be -ve in TB reactivation post TNF-a initiation?

A

60% is extrapulmonary so you must have very high index of suspicion.

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27
Q

What are the 2 important causes of shock following an inferior MI and how do you differentiate?

A

RIGHT VENTRICULAR INFARCTION
1/3 of inferior wall MI. Acute loss of RV function causes pooling of blood in right ventricle with consequent decreased preload in left ventricle resulting in hypovolaemic shock. NO MURMURS OR PULM OEDEMA. On Swann Ganz catheter high right atrium pressure but low left. Aggressive IVF to increase venous return to RV and preload LV

PAPILLARY MUSCLE RUPTURE (particularly if circumflex involved)
Torrential acute mitral regurgitation causing rapid pulmonary oedema
LOUD PAN SYSTOLIC MURMUR AND CHEST CREPITATIONS

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28
Q

How can you differentiate Bartter and Gitlleman Syndrome?

A

Both hypokalaemic metabolic alkalosis with NORMAL BP

Gittleman = LOW urinary calcium (low calcium secretion) secondary to abnormal NaCl transporter

Bartter = NORMAL calcium.
-More likely to present in childhood with failure to thrive

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29
Q

What is the endemic typhus vector?

A

Endemic typhus = Rickettsia Prowazekii = Human body louse, pediculus humonis humonis

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30
Q

What is the scrub typhus vector?

A

Scrub typhus = Orientia tsutsugamushi = Trombiculid Mite

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31
Q

What are the clinical features of Carney Complex?

A

Autosomal dominant inactivation of Protein Kinase A on Chromosome 17

Criteria (2 of the following or 1 feature and affected first degree relative):

  • Spotty skin pigmentation
  • Myxoma
  • Endocrine tumours
  • Psammomatous melanocytic schwannoma (PMS)
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32
Q

What are the CYP450 Inhibitors?

A

STICKFACES.COM

Sodium valproate
Ticlodipine
Isoniasid
Cimetidine
Ketoconazole
Fluconazole
Alcohol binge
Ciprofloxacin/ Chloramphenicol
Erythromycin
Sulphonamides
Cranberry juice/ Grapefruit juice
Omeprazole
Metronidazole
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33
Q

What are the CYP450 inducers?

A

BS CRAP GPS (“BS CRAP GPS induce rage”)

Barbituates
St John's Wort
Carbamazepine
Rifampicin
Alcohol (chronic)
Phenytoin
Griseofulvin
Phenobarbital
Sulphonylureas
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34
Q

What is the mechanism of action of aminophylline?

A

Phosphodiesterase inhibitor

Phosphodiesterase catalyses conversion of cAMP to 5’ adenosine monophosphate. Blockage increases cAMP intracellularly causing bronchodilatation.

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35
Q

Pain and temperature is carried via which spinal tract?

A

Spinothalamic tract near anterior horn on OPPOSITE side to dorsal root (desicates early)

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36
Q

Proprioception is carried via which spinal tract?

A

Dorsal column

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37
Q

What spinal tract carries motor signals?

A

corticospinal tract

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38
Q

The femoral nerve supplies which muscles?

A

Iliacus, Iliopsoas, Quadriceps

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39
Q

The obturator nerve supplies which muscles?

A

Adductor longus, adductor magnus, gracillus

Weakness of adduction and sensory loss of medial thigh
Damage common during childbirth

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40
Q

What are the 2 divisions of the sciatic nerve?

A

Common peroneal nerve

Tibial nerve

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41
Q

What are the muscles supplied by the common peroneal nerve?

A 
Tibialis anterior (dorsiflexion)
Extensor Hallucis Longus (flexion toe)
Peronei longus and brevis (eversion of foot)
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42
Q

What are the muscles supplied by the tibial nerve?

A

Gastrocnemius (plantarflexion)
Soleus
Tibialis Posterior (inversion)

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43
Q

How do you differentiate lambert eaton vs myasthenia beyond the onset of weakness?

A

Lambert eaton -> hyporeflexia is classic
-Autonomic involvement (Light-headedness, dry mouth etc)

Myasthenia you DONT get autonomic features
-You do get ocular features

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44
Q

How do you differentiate multifocal motor neuropathy?

A

Sounds like MND but nerve conduction studies will show demyelination and conduction block.
MND will have normal nerve conduction studies

PURE MOTOR SYNDROMES NO SENSORY

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45
Q

What are the pure motor syndromes?

A

NMJ disorders (myasthenia and lambert eaton)

Myopathies

Multifocal motor neuropathy (demyelination and conduction block on NCS)

Motor neurone disease (both upper and lower signs)

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46
Q

What does prolonged F-wave latency on nerve conduction studies indicate?

A

Strictly it means demyelination but very classic of early GBS

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47
Q

Fasciculation potential or active and chronic denervation on nerve conduction studies indicates what?

A

motor neurone disease

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48
Q

How do you differentiate familial hypocalciuric hypercalcaemia and hyperparathyroidism?

A

Hypercalcaemia with commonly high PTH (therefore often misdiagnosed as hyperparathyroidism)

In familial hypocalciuric hypercalcaemia urinary calcium excretion is LOW.

This is an autosomal dominant condition which usually presents with renal stones (rarely acute pancreatitis)

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49
Q

What are the radiological changes seen in ank spond?

A 
Blurred joint margins
Subchondral erosions
Sclerosis or fusion of sacroiliac joints
Loss of lumbar lordosis
Bamboo spine (tramtrack appearance)
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50
Q

What are the T stages for lung cancer?

A

T1 = <3cm

T2 = 3-7cm (T2a = 3-5cm; T2b = 5-7cm)

  • Atelectasis (part of lung)
  • Invasion: visceral pleura, main bronchus >2cm from carina

T3 = >7cm

  • Atelectasis (whole lung)
  • Invasion: phrenic N, Diaphragm, Chest wall, Mediastinal pleura, Main bronchus <2cm, parietal pericardium

T4
-Invasion: Mediastinal organs, vertebral bodies, carina, tumour nodules in different ipsilateral lobe

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51
Q

What are the lymph node stages in lung cancer?

A

N1 = Ipsilateral bronchopulmonary/ Hilar

N2 = Ipsilateral mediastinal/ subcarinal

N3 = Contralateral side

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52
Q

What is the difference between FAP and Gardener syndrome?

A

Both are APC gene mutations

FAP:

  • Multiple small and large bowel adenomas
  • Colorectal Ca risk 90-100% (Colectomy at 16)
  • 5% risk of duodenal Ca (endoscopic surveillance mandatory, 2nd commonest cause of death)

Gardener is FAP phenotype PLUS osteomas jaw, skull and long bone

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53
Q

What is enteric hyperoxaluria?

A

Oxalate stone risk in small bowel surgery/ Crohns

Treatment with calcium to bind oxalate and decrease absorption.
Should also decrease oxalate intake (Beetroot and Rhubarb)

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54
Q

What clinical signs should you look for prior to starting activated charcoal?

A

Decreased bowel sounds

Paralytic ileus common after overdose.
Associated with increased risk of charcoal aspiration and pneumonitis

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55
Q

How do you treat gout in HIV?

A

Colchicine is best

Allopurinol increases plasma levels of didanosine >100%

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56
Q

What is the best lipid lowering drug when on warfarin?

A

Atorvastatin and pravastatin (don’t interfere)

Rosuvastatin increases effects along with bezafibrate and simvastatin

Cholestyramine decreases effects of warfarin

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57
Q

What are the adverse effects of carbimazole?

A

Nausea, rash, pruritis, arthralgia, alopecia, agranulocytosis, jaundice

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58
Q

How do you diagnose visceral leishmaniasis?

A

Serological usually used

Microscopy and culture is gold standard
-Either a lymph node aspirate, splenic biopsy (commonly done in 3rd world) or bone marrow

Skin biopsy can be used in cutaneous but not visceral leishmaniasis

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59
Q

What are the types of autoimmune hepatitis and their respective antibodies?

A

Type 1
-ANA and/or SMA (affects both adults and children)

Type 2
-LKM1 (children only)

Type 3
-Soluble liver kidney antigen (adults in middle age)

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60
Q

What are the autoimmune hepatitis associations?

A

Ammenorrhoea common

Associations:

  • Hypergammaglobulinaemia
  • HLA B8, DR3
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61
Q

What factors affect MDRD eGFR?

A

Pregnancy
Muscle mass
Eating red meat 12hrs before

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62
Q

What are the types of melanoma?

A

Superficial spreading
-Most common, irregularly pigmented macule or plaque, May have irregular edge and colour variation

Nodular
-Pigmented nodule, often rapidly growing and aggressive, usually on legs or trunk

Lentigo maligna melanoma

  • Older patients with long standing lentigo maligna
  • Slowly expanding, irregular pigmented macule

Acral lentiginous melanoma

  • Palms, SOLES, and toenails
  • Flat and discoloured
  • Most common type in chinese and japanese
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63
Q

How does ileostomy cause hypocalcaemia?

A

Lose large amounts of magnesium.
Hypomagnesaemia impairs PTH secretion. This causes hypocalcaemia which is resistant to increased provision of calcium. Must replace Mg2+

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64
Q

What are the 2 pathways for triggering apoptosis?

A

Extrinsic - initiated by death receptors on the cell surface of the target cell

Intrinsic - pathway triggered at the mitochondrial level

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65
Q

What are the causes of fixed splitting of the second heart sound?

A

Atrial septal defect
Right heart failure
Pulmonary hypertension

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66
Q

What do B2 adrenoreceptors do?

A

Arteriolar dilatation, Bronchodilatation, decreased bronchial secretion, decreased gut motility, relaxation of pregnant uterus

Metabolic effects: lipolysis, glycogenolysis and gluconeogenesis

(B blockers do the opposite)

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67
Q

Explain the current mechanisms underlying the treatment of pulmonary oedema

A

High catecholamine levels and activation of RAAS drive peripheral vasoconstriction, which increases myocardial O2 demand.

Conventionally treatment has been with diuretics (no evidence of mortality benefit) and effects probably due to vasodilatory action.

More powerful vasodilators (IV diamorphine and GTN) are more attractive now

ACEi and B-blockers early have morbidity and mortality benefit.

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68
Q

What is the mechanism of metthaemoglobinuria?

A

Iron in Haem is Fe2+

Oxidising agents convert to Fe3+ (inactive ferric form)

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69
Q

What are the antibodies involved in paraneoplastic pemphigus?

A

Envoplakin, periplakin, bullous pemphigoid antigen I, desmoplakin, desmoplakin II, plectin and alpha 2- macroglobulin-like-1

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70
Q

Where are chancroid ulcers usually found?

A

Prepuce and frenulum in men

Treatment is single dose azithromycin, IM ceftriazone or 7 days erythromycin.

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71
Q

How does liver cirrhosis result in metabolic alkalosis?

A

Low albumin associated with severe disease drives relative intravascular volume depletion.
-Aldosterone release increases as a result.

Steroid hormone metabolism decreased by liver impairment.

Additionally albumin behaves as a weak acid therefore hypoalbuminaemia itself adds to metabolic alkalosis.

Production of urea (would be one way to compensate) is also impaired.

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72
Q

What is Tolosa-Hunt Syndrome?

A

Granulomatous inflammatory process that involves the anterior cavernous sinus/ superior orbital fissure region.

This causes progressive syndrome over several weeks vs quicker like cavernous sinus thrombosis.

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73
Q

What parkinsons drug causes haematuria?

A

L-dopa

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74
Q

Describe the nomenclature of pacemaker

A

First letter = chamber to be paced (A = atrium, V = ventricle, D = Duel

Second letter = chamber that is sensed ( A, V or D)

Third letter = response to a sensed beat beat by pacemaker (I = inhibits, T = trigger, D = both)

VOO = Fixed output setting

Fourth letter refers to whether or not the pacemaker has rate-adaptive properties (R)

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75
Q

What is MacLeod Syndrome?

A

Unilateral emphysema following childhood bronchiolytis

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76
Q

What is the mechanism of action of LMWH?

A

Binds antithrombin III

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77
Q

What part of Vitamin A contributes to vision?

A

Vitamin A is a collective term for several related biologically active molecules.

Retinaldehyde is a form of vitamin a derived from oxidation of retinol (also vit a). The cis form is found in the opsin proteins in the rods (rhodopsin) of the retina.

Exposure to light results in change to trans isomer and resulting changes in membrane potentials. This causes signals to brain.

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78
Q

What are the 3 features that demonstrate a “true” koebner phenomenon?

A

Lichen planus
Psoriasis
Vitiligo

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79
Q

Vigatriban is a treatment for epilepsy. What is its classic side effect?

A

Visual field defects.

Onset from 1 month to several years
In most cases it persists despite stopping treatment

Visual field assessment should be carried out before treatment and at 6 monthly intervals.

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80
Q

What are the risk factors for gastric cancer?

A 
H. Pylori
Low dietary vitamin C
Family history
High salt diet
Race (Japan> UK > Sweden)
Gastric surgery
Pernicious anaemia
Smoking
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81
Q

What food items interfere with warfarin?

A

Cranberry juice and pomegranate juice - Inhibitors of 2C9 (main P450 responsible for warfarin metabolism)

Brussel sprouts and liver - Contain large amounts of vitamin K and so decrease effects.

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82
Q

What food should be avoided in statin therapy?

A

Grapefruit juice
Powerful inhibition of 3A4
May cause toxicity to simvastatin, ciclosporin and other drugs.

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83
Q

What is Alkaptonuria and what HLA is it associated with?

A

Homogentisic acid oxidase deficiency that leads to a defect in tyrosine metabolism (amino acid metabolism) and accumulation of homogentisic acid.

Increased incidence in those who are HLA-DR7 positive

Treatment involves dietary reduction in tyrosine and phenylalanine

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84
Q

What lab test is used to evaluate the genetics of trinucleotide repeat disorders?

A

TP-PCR

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85
Q

What is ornithine aminotransferase deficiency?

A

Causes atrophy of choroid and retina.

Begins as small yellowish spot and increasing to a circular lesion edged with pigment.
Children present with myopia and decreased night vision which progresses from tunnel vision to blindness in middle life. Cataracts also develop.
Some patients have proximal muscle weakness

Deficiency results in massive rise in plasma ornithine with particularly high concentration in CSF and aqueous humour.

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86
Q

What is Darier’s disease?

A

Autosomal with classic cutaneous features

Warty papules and plaques in seborrhoeic areas (central chest and back, scalp, flexures), palmar pits and nail dystrophy.

Secondary infection of the lesions can lead to crusting and malodour.

Retinoid acitretin used to treat symptomatic cases.

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87
Q

Anaemia and gallstones can indicate what disease?

A

Hereditary spherocytosis.

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88
Q

What is the mechanism of action of nucleoside reverse transcriptase inhibitors?

A

These are a nucleoside which lack a 3’- hydroxyl group.
Insert into reverse transcriptase and prevents formation of 3’-5’ phosphodiester bond.

NRTIs are pro-drugs taken into host cell and phosphorylated to active form (i.e. have to be phosphorylated to work)

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89
Q

What are the adverse effects common to nucleoside reverse transcriptase inhibitors?

A

Peripheral neuropathy
Bone marrow suppression (Tx with GCSF)
Lactic acidosis

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90
Q

What adverse effect is most associated with didanosine?

A

Pancreatitis

“PancreaDIDis = DIDanosine”

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91
Q

What adverse effect is most associated with zidovudine?

A

Anaemia

“Zidovudine gets ZID of the haemoglobin”

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92
Q

Give some examples of nucleoside reverse transcriptase inhibitors

A 
Abacavir
Didanosine
Emtricitabine
Lamivudine
Stavudine
Tenofovir (Nucleotide not nucleoside)
Zidavudine
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93
Q

What is the mechanism of action of non-nucleoside reverse transcriptase inhibitors?

A

Binds to different site of reverse transcriptase to NRTIs and creates a hydrophobic pocket which slows DNA synthesis.

Unlike NRTIs they do not require phosphorylation to be active.

NOT effective against HIV-2-reverse transcriptase as non competitive

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94
Q

What are the universal adverse effects of non-nucleoside reverse transcriptase inhibitors?

A

Hepatotoxicity and skin rash

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95
Q

What adverse effect is most associated with Efavirenz?

A

Vivid dreams

“EfaVIVIDs = VIVID dreams”

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96
Q

Give some examples of NNRTIs

A

Delaviridine
Efavirenz
Nevirapine

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97
Q

What is the mechanism of action of protease inhibitors?

A

Block HIV-1 protease ability to cleave protein precursors effectively blocking viral maturation

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98
Q

What are the generic adverse effects of protease inhibitors?

A

Hyperglycaemia
GI effects
Lipodystrophy

(liPROdystrophy, hyPROglycaemia, PROfuse diarrhoea)

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99
Q

What adverse effect is most associated with indinavir?

A

Nephropathy

“Indinavir = IN DA KIDNEY”

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100
Q

What adverse effect is ritonavir most associated with?

A

P450 inhibition

“ritONavir turns ON drugs by inhibiting P450”

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101
Q

What are some examples of protease inhibitors?

A

Atazanavir
Indincavir
Ritonavir

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102
Q

What is the mechanism of action of integrase inhibitors?

A

Blocks ability to incorporate into host genome

103
Q

What are the adverse effects of integrase inhbitors?

A

Elevated creatine kinase

104
Q

Give some examples of integrase inhibitors

A

Dolutegravir
Elvitegravir
Raltegravir

105
Q

What are the two types of fusion inhibitors?

A

Enfuviritide
-Binds GP41 to prevent penetration (GP41 on envelope)

Miraviroc

  • Binds CCR5 preventing attachment
  • CCR5 is on T cells/ monocytes
106
Q

What are the steps in Crohn’s exacerbation management?

A

Corticosteroids used to induce remission

Immunosuppressant drugs

  • Examples: Thiopurines (azathioprine, mercaptopurine) or methotrexate
  • Used as adjunct in acute exacerbations, also used to maintain remission
  • Can be used post “macroscopic resection” to maintain remission (unlike biologics)

Biologics

  • Induce remission in severe disease not responding.
  • Also effective at maintaining remission (not post surgery)
107
Q

What are the steps in UC exacerbation management?

A

Steroids
Ciclosporin
Infliximab if not tolerating above

108
Q

How can you systematically localise heart blocks?

A

Autonomic manoeuvres (carotid/ valsalva) worsen AV nodal block but not infranodal.

Atropine improves AV node block (increases HR) but worsens block in His-Perkinje system.

109
Q

What is the trinucleotide repeat for Huntington’s disease?

A

CAG

110
Q

What is the trinucleotide repeat for myotonic Dystrophy?

A

CTG

myoTonic = cTg

111
Q

What is the trinucleotide repeat in Fragile X syndrome?

A

CGG

fraGile = cGG

112
Q

What is the trinucleotide repeat in oculopharyngeal muscular dystrophy?

A

GCG

C to SEE

113
Q

What is the trinucleotide repeat in Freidreich’s ataxia?

A

GAA

AAAtaxia

114
Q

What are the most to least common valve sites for infective endocarditis?

A 
Mitral valve
Aortic valve
Both aortic and mitral
Tricuspid
Rarely pulmonary
115
Q

In hepatitis endemic areas what is the most common cause of acute viral liver failure?

A

In endemic areas, virtually everyone is infected with Hep A in childhood and immune as adults.

This means outbreaks are usually Hep E.

116
Q

How should you test for Hep C in immunocompromised?

A

In the immunocompromised or those on dialysis may have Hep C but -ve Hep C antibodies

Requires virology testing by PCR

117
Q

What are the CKD stages G and A?

A 
G1 >90
G2 89-60
G3a 59-45
G3b 45-30
G4 29-15
G5 <15

A1 ACR <3 mg/mmol
A2 3-30 mg/mmol
A3 >30 mg/mmol

118
Q

How should you manage HIV in pregnancy?

A

Oral zidovudine from 28 weeks gestation decreases risk of transmission

Optimal regimen is to commence zidovudine as an IV infusion at onset of labour AND continue treatment in neonate up to 6 weeks of age.

119
Q

How do you diagnose CJD?

A

LP and perform RT-Qu1C peptide assay

-Has a 95-98% diagnostic sensitivity and 100% specificity for sporadic CJD.

120
Q

How do you determine prognosis in myeloma?

A

International scoring system (ISS) uses combination of serum B2 microglobulin and albumin

121
Q

Neurofibromatosis type 1 diagnostic criteria?

A

At least 6 cafe au lait spots (5mm diameter in prepubertal patients and 1.5cm in post pubertal patients) typically on trunk.

Axillary freckling and/or inguinal freckling

At least 2 Lisch nodules (iris hamartomas)

Neurofibromas (more than one cutaneous neurofibroma or one plexiform neurofibroma)

Characteristic bone abnormalities

Optic nerve glioma

Diagnosis of NF1 in a first degree relative

122
Q

What is the Truelove and Witt’s criteria for a severe attack of acute collitis?

A 
At least 6 stools per day
Visible blood and at least 1 feature of systemic upset:
1. Temp above 37.8
2. Pulse >90
Anaemia
ESR >30mm/1st hour
123
Q

What are the features of a rheumatoid pleural effusion?

A

Up to 5% of patients with RA develop pleural effusion at some stage.

Exudates
Typically pH <7.2
High LDH
Low glucose level

RA is unlikely to be the cause of the effusion if glucose fluid level is over 1.6mmol/l.

Large amounts of cholesterol can accumulate in long standing rheumatoid pleural effusions

124
Q

How does tetanus toxin interferre with acetylcholine-mediated transmission at the motor endplate?

A

The specific fusion complex is made up of synaptobrevin, syntaxin and synaptosome associated protein (SNAP-25). The fusion complex serves to join the membranes of an acetylcholine vesicle and a nerve cell.

Botulinum toxin types BoNT/B, D, F, G and tetanus toxin (TeNT) cleave specific sites of synaptobrevin (VAMP)

125
Q

How does bolutinum toxin type C affect acetylcholine mediated transmission at the motor endplate?

A

This is different to tetanus and the other botulinum toxins which cleave specific sites of synaptobrevin (VAMP)

126
Q

When are patients most at risk of getting Kaposi sarcoma in HIV nowadays?

A

In general incidence has fallen due to HIV treatment. However there is a high incidence in the immediate 6 months after starting ART.

2 theories:

  • IRIS activates dormant HHV-8
  • Second is just that you are most immunosuppressed prior to starting treatment so likely to develop kaposi around this time and less likely later.
127
Q

What is the escalation of treatments for acne?

A

Topical treatments like antibiotics

Oral antibiotic trial for 3 months

Further antibiotic trial for 3 months with different agent

Referral to dermatology for oral isotretinoin.

128
Q

How do you grow Nocardia spp?

A

Nocardia use paraffin as a source of carbon for growth.

In this technique, a paraffin wax-coated glass rod is placed in the inoculated carbon-free broth

Nocardia grow on the rod at the air-liquid interface.

129
Q

Mouse foot-pad inoculation is used to cultivate which bacterium?

A

Mycobacterium leprae.

130
Q

What are the 3 predominant ketones seen in DKA?

Which can linger the longest still contributing to mild acidosis at 36hrs?

A

A range of ketoacids are formed in DKA.

  • Acetone (responsible for pear drop breath)
  • Beta-hydroxybutyrate
  • Acetoacetic acid

Acetoacetate forms acetone and beta hydroxybutyrate.
Both acetoacetate and acetone fall before the 36hr mark but beta hydroxybutyrate can linger for some time.

131
Q

UTI relapse is defined as what?

What are the most common causes?

A

Recurrence of bacteriuria with the same organism within 7 days of completing antibacterial treatment.

Usually occurs in conditions in which it is difficult to eradicate the bacteria:

  • Stones
  • Scarred kidneys
  • Polycystic kidneys
  • Bacterial prostatitis.
132
Q

How do you decide on the appropriate treatment in SLE?

A

Simple arthralgia and fatigue respond well to hydroxychloroquine.

Methotrexate is used if there is arthritis (synovitis) but not for arthralgia (joint pain without swelling)

Prednisolone/ azathioprine or cyclophosphamide would be more for serious internal organ involvement (renal, neurological, eye or lung)

133
Q

How does hypocalcaemia occur in ethylene glycol poisoning?

A

The principle end product of metabolism of ethylene glycol that causes significant toxicity is oxalic acid. This then combines with calcium to form insoluble calcium oxalate and drives presentation with acidosis and kidney disease

134
Q

How do you differentiate Type 1 and Type 2 Amiodarone induced thyrotoxicosis and how does the treatment differ?

A

Type-1 = positive antibodies and uptake on radioisotope scan
-Treated with Propylthiouracil

Type 2 = Destructive

  • Absent uptake and negative antibodies
  • Treated with steroids
135
Q

What urinary troubles is risperidone associated with?

A

Increased daytime frequency (pollakiuria)

Enuresis

Urinary retention

Urinary incontinence

Dysuria

136
Q

Safest anti-depressent while breastfeeding?

A

Sertraline

Much lower levels in breast milk

137
Q

What peak expiratory flow is typical for a 70kg man?

A

520-700 l/min

138
Q

What total lung capacity is typical for a 70 kg man?

A

5-6.5 litres

139
Q

What functional residual capacity is typical for a 70 kg man?

A

2-3 litres

140
Q

What tidal volume is typical for a 70 kg man?

A

500-700ml

141
Q

What inspiratory reserve volume is typical for a 70kg man?

A

3300ml

142
Q

What are the laboratory findings seen in Wilson’s disease?

A 
Raised AST
Low caeruloplasmin
Low serum copper
Raised urinary copper excretion
Low serum uric acid (increased excretion)

Aminoaciduria, glycosuria and calciuria also occur with poor acidification of urine

143
Q

What indicates drug induced immune haemolytic anaemis Vs. auto-immune haemolytic anaemia or transfusion reaction?

A

All 3 will have positive direct coombs

Drug induced haemolytic anaemia will have no antibodies on antibody screen

144
Q

A posterior gastric ulcer is most likely to involve which artery?

A

Splenic artery

Runs along the upper border of the pancreas and results in a severe haemorrhage

145
Q

A lesser curve gastric ulcer may involve which artery?

A

Left gastric artery

146
Q

A greater curve gastric ulcer may involve which vessels?

A

Gastroepiploic vessels

147
Q

Why does the hypothalamic-pituitary axis get activated during an immune response?

A

IL-1 and TNF-a stimulate release of corticotrophin releasing hormone from the hypothalamus. This HPA activation is integral to the stress response. Results in release of cortisol; at high levels cortisol suppresses the immune response and therefore prevents a lethal overactivation of immune processes.

148
Q

What is birch apple syndrome?

A

Throat and mouth may become itchy after eating apples in between 50-75% of individuals who have allergic rhinitis related to birch tree pollen.

Celery is another food known to cause mouth irritation.

149
Q

What is the treatment of epididimo-orchitis based on age?

A

Under 35 more likely STI and treat as such

Over 35 more likely gram negative enteric bacteria
Ofloxacin first line

150
Q

What is the most commonly affected channel in congenital long QT syndrome?

A

Long QT syndrome type 1 is the most common (30-35% all cases)

LQT1 gene is KCNQ1 which has been isolated to chromosome 11.

Codes for volted gated potassium channel KvLQT1 that is highly expressed in the heart.

This is a slow delayed rectifier potassium channel mutation

151
Q

What is the mechanism of action of vancomycin?

A

Binds to D-alanyl-D-alanine residues preventing the synthesis of polymers essential to the formation of the bacterial cell wall.

Where polymers do form, vancomycin also prevents their crosslinking to form the cell wall.

152
Q

What is the mechanism of action of adenosine?

A

Purine nucleoside which acts as a G protein coupled receptor agonist of the adenosine A1 receptor.

This leads to inhibition of adenylate cyclase and hence a reduction in cyclic AMP.

153
Q

Parinaud syndrome is a failure of vertical gaze usually associated with convergent nystagmus, as well as mydriasis and impaired pupillary reflexes. Where in the brain does it occur?

A

Dorsal midbrain

154
Q

3rd cranial nerve arises from where?

A

Ventral midbrain

155
Q

What is the only absolute contraindication to electroconvulsive therapy?

A

Raised intracranial pressure.

156
Q

Terlipressin is a prodrug of what?

A

Terlipressin can be regarded as a circulating depot of lysine vasopressin. Following IV injection 3 glycyl moieties are cleaved from the N-terminus to release lysine vasopressin which then reduced blood flow in the splanchnic circulation and reduce portal hypertension

157
Q

What’s the difference between a type 1 and type 2 error?

A

Type 1 (alpha) is the incorrect rejection of a true null hypothesis (i.e. false positive)

Type 2 (beta) is when the null hypothesis is incorrectly accepted (i.e. false negative)

158
Q

How is the bleeding time affected in haemophilia A and B?

A

Bleeding time is NORMAL.
-This is because there is normal adhesion of platelets to the endothelium, which is the predominant factor when assessing the bleeding time.

This is vitally important for differentiating from Von Willebrands disease. Particularly type III which can present severely with haemarrthrosis and look like haemophilia. APTT will also be raised as there is a relative deficiency of factor VIII. The only clue will be that bleeding time is prolonged.

159
Q

What is the appearance of hairy leukoplakia?

A

May be very similar to candida forming irregular white patches on the tongue (most commonly on the sides of the tongue), and oral mucosa.

However, oral hairy leukoplakia lesions cannot be dislodged, whereas candida can easily be scraped away.

160
Q

How do B-cells become plasma cells?

A

B-cells have surface IgG and MHC class II. When a B-cell meets an antigen these receptors recognise then the B-cell can undergo somatic hypermutation (where an enzyme makes random mutations in the antibody variable region genes) and isotype switching (i.e. switching through the immunoglobulin classes).

If these processes result in an antibody that more strongly binds to their targets then these B-cells will survive and differentiate into plasma cells with the new specificity.
-They now lack IgG and MHC class II and cannot undergo somatic hypermutation or isotype switching again
161
Q

What are the 3 types of nephropathy seen in ankylosing spondylitis?

A

AA amyloidosis: when disease has been going on for many years. (apple-green birefringence seen)

NSAID induced nephropathy

IgA nephropathy: also common among young men in the absence of ank spond

162
Q

What is the mechanism of action of sotalol?

A

Risk of Torsades, should have ECG 2-3 days after initiation to look for prolonged QT.

163
Q

How is paracetamol metabolised?

A

Conjugation to glucuronic acid

-Requires glutatione which forms conjugates with NAPQI metabolite

164
Q

What is the pathophysiology of Hyper-IgM syndrome?

A

X linked condition where levels of IgG, IgA and IgE are undetectable but there are high levels IgM and IgI.

This is due to role of CD40 in B-cell maturation and isotype switching (also called CD40 ligand deficiency).

B-cell defect which presents with recurrent sinopulmonary infections and particularly susceptible to PJP. Patients can develop cryptosporidial infection, leading to sclerosing cholangitis, liver failure, and also increased risk of malignancy predominantly abdo cancers.

165
Q

What is the narcolepsy tetrad?

A

Chronic daytime sleepiness,
Cataplexy
Hyperagogic/ hypopompic hallucinations
Sleep paralysis

166
Q

How do you differentiate between hepatic adenoma and hepatic angioma?

A

Hepatic adenoma occur in women of childbearing age. Associated with COCP. Mainly asymptomatic

Usually right lobe of liver and can be hypervascular (look like angioma)

167
Q

What is the most common cause of lithium induced nephrotic syndrome?

A

Minimal change disease

Less commonly FSGS

168
Q

What drugs do you use for PEP and PEPSE after exposure to HIV?

A

Truvada (Tenofovir and emtricitabine) + Raltegravir for 28 days.

169
Q

What is the calculation for confidence interval?

A

For exam 1.96 is just 2

170
Q

What is the genetics of Prader-Willi?

A

Non-mendelian

  • 70% due to deletion or disruption of genes on proximal arm of paternal copy chromosome 15 (15q11-13).
  • 28% due to maternal disomy
171
Q

How does ciclosporin cause renal impairment?

A

Chronic interstitial nephritis

172
Q

What bone disease is associated with diabetes mellitus and peritoneal dialysis?

A

Adynamic bone disease

  • Increased incidence of hip fractures.
  • Tendency towards hypercalcaemia as bone loses capacity to buffer serum calcium
173
Q

What is the pathophysiology of liver fibrosis?

A

Stellate cells have similar morphology to fibroblasts but with additional fat droplets. These are located in Disse space. Essential to hepatic fibrogenesis responding to mediators released by parenchymal and Kupffer cells, and mediating their transformation to myofibroblasts.

Transforming growth factor beta (TGF-B) initiates process.

Transformed stellate cell then stimulates production of extracellular matrix products in addition to products for matrix degradation.

174
Q

GLP-1 analogues are contraindicated in which complication of diabetes?

A

Suspected gastroparesis

175
Q

How do you differentiate vitiligo and pityriasis?

A

Vitiligo characteristically symmetrical

Pityriasis usually confined to trunk with fine scale.

176
Q

What are the ECG changes during the course of pericarditis?

A

ST elevation with concavity upward in all leads facing the epicardial surface (i.e. anterior, inferior and lateral)

Only “cavity” leads aVR, V1 and rarely V2 show ST depression

This is followed by return of ST segments to baseline and flat or inverted T waves.

THERE CAN BE NO LOSS OF R WAVES OR DEVELOPMENT OF Q WAVES

177
Q

What are the two main locations for respiratory drive?

A

Peripheral chemoreceptors -> carotid bodies (and a lesser extent aortic arch).
-These detect plasma pH for metabolic changes in acid base

Central chemoreceptors -> response to plasma CO2 tension
-Control of normal respiration

178
Q

Insulin regulates which enzymes?

A

Down regulation of pyruvate carboxylase (key step in gluconeogenesis)

Upregulation of pyruvate dehydrogenase, glucokinase, glycogen synthetase, G6PD

179
Q

What antibiotic is used in meningitis prophylaxis?

A

Ciprofloxacin

180
Q

What genetic mutation is most associated with pancreatic cancer?

A

KRAS

  • Codes for GTPase
  • 80-90% pancreatic adenocarcinomas have mutations in the KRAS2 gene
181
Q

What is the most common side effect of imatinib?

A

Nausea

182
Q

What are the antibody mediated antibodies?

A

IL-4, IL-5, IL-6, IL-10

183
Q

What are the cell mediated cytokines?

A

IL-2, Interferron Gamma

184
Q

What are the acute phase response cytokines?

A

IL-1, IL-6, TNF-a

185
Q

How does adenosine interact with dipyridamole?

A

Adenosines effect prolonged by dipyridamole

  • Effects may last for up to several minutes

Adenosine contraindicated in 2nd or 3rd degree heart block, sick sinus syndrome or verapamil use.

186
Q

Goodpasture’s is associated with which HLA?

A

HLA DRB1*15:01

187
Q

Psoriasis is associated with which HLA?

A

HLA Cw6

188
Q

Why does digoxin have a slow onset of action and require a loading dose?

A

High degree of protein binding

Half life around 30-40 hours

189
Q

What are the 4 dyslipidaemia syndromes and their basic pathophysiology?

A

“1LP, 2LD, b adds V, 3 is E, 4 gets more”

Type 1 = LPL deficiency

Type 2 = LDL receptor deficiency

Type 2b = LDL receptor deficiency and VLDL

Type 3 = ApoE deficiency

Type 4 = Overproduction of VLDL

190
Q

What are the features of type 1 dyslipidaemia?

A

Autosomal recessive. (very rare)

  • Caused by LPL deficiency which results in triglyceride accumulation (can result in pancreatitis)
  • May also be caused by ApoC2
  • Chylomicrons, triglycerides and cholesterol are increased
191
Q

What are the features of type 2 dyslipidaemia?

A

Familial hypercholesterolaemia

Type 2 (Autosomal dominant)

  • LDL receptor deficiency causes LDL build up
  • This results in classic tendon xanthoma
  • May also be caused by ApoB100
  • Also causes corneal arcus
  • High cholesterol but triglycerides and HDL may be normal
Type 2b (autosomal dominant)
-All of the above but VLDL also elevated
192
Q

What are the features of type 3 dyslipidaemia?

A

Remnant hyperlipidaemia (aka familial dysbetalipoproteinaemia, broad base disease)

ApoE deficiency. Important for the uptake of remnants (chylomicrons and VLDL) and so these build up.

Causes palmer xanthoma
Treated with fibrate

193
Q

What are the features of type 4 dyslipidaemia?

A

Familial hypertryglyceridaemia

Overproduction of VLDL -> triglycerides -> pancreatitis

194
Q

What are the features of abetalipoproteinaemia?

A

Deficiency of ApoB48 and ApoB100
No VLDL, LDL or chylomicrons and so cannot process fats

Results in steatorrhoea and decreased vitamins ADEK

  • Vit E deficiency -> retinitis pigmentosa and spinocerebellar degeneration
  • Acanthocytes on bloods film
  • Vitamin K deficiency causing increased PT
195
Q

What area of the brain is involved in regulation of satiety?

A

Ventromedial nucleus (along with arcuate nucleus of hypothalamus)

196
Q

What area of the brain is involved in regulation of blood pressure and heart rate?

A

Dorsomedial hypothalamic nucleus = blood pressure and heart rate

Posterior nucleus = blood pressure, shivering response and release of vasopressin

197
Q

CYP-2D6 is involved with metabolism of which drugs?

A

B-blockers (esp. metoprolol)
Dihydrocodeine (metabolised to morphine via CYP-2D6
MDMA
Certain SSRIs

198
Q

CYP-2C8 is involved with metabolism of which drugs?

A 
Omeprazole
Diazepam
Barbituates
Dapsone
Pioglitazone
199
Q

CYP-2C19/19 is involved with metabolism of which drugs?

A

Omeprazole
Diazepam
TCAs
Proguanil

200
Q

Oncholysis (separation of nail from bed) is associated with what?

A

Trauma
Infection
Drugs: Tetracyclines (esp. doxy), psoralens

201
Q

In hypoglossal (XII) nerve paralysis the tongue deviates to which side?

A

Affected side

202
Q

Why is giving buprenorphine and morphine together stupid?

A

Buprenorphine = partial agonist at opioid receptors

-Antagonises action of full agonist such as morphine reducing effect of both

203
Q

What is the best treatment for rate control SVT in pregancy?

A

Metoprolol

204
Q

What features of intestinal polyps are most associated with malignancy?

A 
Sesile (flat) higher risk than pedunculated (stalked)
Higher number = higher risk
Polyps more than 1.5cm
Histology showing:
-Villous architecture
-Severe dysplasia
-Squamous metaplasia
205
Q

What is the management of Kallman Syndrome?

A

Depends on the patients desires:

  • If you dont want kids then no need to stimulate spermatogenesis with GnRH or gonadotrophin
  • Testosterone injections, inplants or patches are more reliable than oral preparation
  • If at a later stage they want kids then pulsed therapy with GnRH analogues are required
206
Q

Which HLA is associated with Felty’s syndrome?

A

HLA DRW4 found in 95% of patients with Felty’s syndrome and 70% of patients with RA alone

HLA DR4 is in 50-75% patients with RA and correlates with poor prognosis. More likely to be found in Felty’s but not as specific as DRW4

207
Q

HLA-B8DR3 is associated with which condition?

A

Sjogrens

208
Q

What are the features of a C5 nerve root palsy?

A

Altered sensation upper arm and shoulder
Weakness of biceps and shoulder abduction
Reduced biceps reflex

209
Q

What are the features of a C6 nerve root palsy?

A

Weakness of biceps and shoulder (like C5)

Sensory loss forearm and hand

210
Q

What are the features of a C7 nerve root palsy?

A

Radial nerve supplied muscles (triceps, extensor carpi radialis)
Diminished triceps reflex but preserved biceps and bracheoradialis

211
Q

What are the features of a C8 nerve root palsy?

A

Weakness of intrinsic hand muscles and sensory loss hand and forearm

212
Q

What are the features of a T1 nerve root palsy?

A

Intrinsic hand muscles and sensory loss proximal forearm.

DOES NOT affect hand unlike C8

213
Q

What are the side effects of Bosentan?

A

Flushing, hypotension, dyspepsia, fatigue.

Most serious:
-Hepatotoxicity (contraindicated in moderate to severe liver disease.

Contraindicated in pregnancy

214
Q

By what process are solutes removed from the blood during haemodialysis?

A

Convection

215
Q

What degree of IQ corresponds to degree of mental disability?

A 
69-50 = mild
49-35 = moderate
34-20 = severe
<20 = profound
216
Q

What monoclonal antibody can be used in HUS?

A

Eculizumab is a monoclonal antibody to complement factor C5 which blocks complement activation.

Evidence suggests Shiga toxin associated HUS is associated with complement activation, particularly C3 and C9.

Earlier intervention with eculizumab is most effective, and small studies suggest its use is associated with improved neurological outcomes.

217
Q

Which antibiotic is classically associated with worsening of muscle weakness associated with GBS?

A

Ciprofloxacin

218
Q

How do you determine B-cells on immunochemistry?

A

Presence of CD19

219
Q

What is the treatment for molluscum contagiosum?

A

Cryotherapy is best

Podophyllotoxin also demonstrated efficacy but causes local inflammatory reaction which limits use.

Rash spontaneously resolved over the course of 18 months.

220
Q

What cytochrome is responsible for pioglitazone metabolism?

A

CYP2C8

221
Q

Rituximab puts you at risk of which particular reactivation infection?

A

Hep B

Pts should be screened for previous exposure to hepatitis B prior to starting rituximab.

222
Q

What is the modified valsalva maneouvre?

A

It is highly successful at converting paroxysmal SVT (rates of around 40% cardioversion, vs. 17% for the standard Valsalva)

223
Q

What is the gold standard treatment of SVC obstruction?

A

Stenting

224
Q

What is riboflavin used for in the body?

A

Dietary sources include liver, milk, cheese, eggs, some green vegetables, beer, marmite and bovril

225
Q

In a wide split fixed S2 with ejection systolic murmur how can you differentiate between ostium primum and secondum ASD?

A

LBBB in ostium primum

RBBB in ostium secundum

226
Q

What is the treatment for gastroparesis?

A

Domperidone now first line
Erythromycin second line
—————————
Due to long term neurological side effects metoclopramide is no longer recommended

227
Q

What is a common cause of stridor in patients with rheumatoid arthritis?

A

Seen in studies in up to 75% of patients with RA. It can cause sore throat, hoarse voice and stridor but is often asymptomatic. However, symptoms can rapidly worsen in the post-operative period. It is unrelated to any lung fibrosis.

Diagnosis can be with flow-volume loop, direct laryngoscopy and HRCT of the larynx.

Patients can need urgent tracheostomy and steroids, both orally and via joint injection

228
Q

Where in the kidney is EPO produced?

A

The main extra-renal site of production is in the perisinusoidal cells in the liver where production occurs in the fetal and perinatal period.

229
Q

What drugs inhibit the tubular secretion of digoxin?

A 
Verapamil
Nifedipine,
Quinine,
Quinidine
----------------------

Dose of digoxin should be decreased if co-administering

230
Q

What is the treatment for Behcet’s disease?

A

Corticosteroids first line

Second line: cyclophosphamide, azathioprine, etanercept

231
Q

Calcium channel blockers mainly act on which part of the conduction system?

A

Class IV agents mainly act on the sinoatrial and atrioventricular nodes, as these structures almost exclusively depolarise by slow calcium channels.

232
Q

What are the characteristic findings in eosinophilic fasciitis?

A

Swelling and tenderness of the forearms, with induction of the skin (peau d’orange)

Carpal tunnel syndrome

Flexion contractions of the fingers

Peripheral blood eosinophilia

Diagnosis is confirmed by deep biopsy

233
Q

How does the progesterone only pill prevent conception?

A

Thickens cervical mucus, preventing the entry of sperm

234
Q

What is the most important prognostic marker in AML?

A

Bone marrow karyotype.

This essentially is cytogenetic analysis of the blast cells.

Patients with certain genetic changes have a low risk of relapse, for example t(8:21) or chromosome 16 inversion. Conversely, patients with multiple cytogenetic abnormalities or changes in chromosome 5 or 7 have a higher risk of relapse.

235
Q

What is the treatment for rate control in long QT syndrome?

A

B-blockers

Decrease conduction through the AV node and have negatively ionotropic and chronotropic effects.

If patients continue to have rate disturbances on B-blocker, cervical sympathectomy or ICD is persued.

Lifestyle changes, such as avoiding competitive or particularly intensive sporting activity, may also be recommended.

236
Q

Which cancer is most associated with pemphigus?

A

Non-hodgkin’s lymphoma makes up the majority of cases of paraneoplastic pemphigus at around 39%.

237
Q

What are the adverse effects of Ribavirin?

A

Haemolytic anaemia
Nausea and vomiting
Dry mouth
Stomatitis

Cautions and contraindications:
-Should avoid during pregnancy and for 6 months after delivery. Counsel men to use barrier contraception.

  • Cardiac disease
  • Haemoglobinopathies
  • Severe liver dysfunction
  • Autoimmune disease
  • Previous psych history
238
Q

What pathological process is responsible for increased clot risk in protein C deficiency?

A

Protein C acts to inactivate the active forms of the procoagulant co-factors factors Va and VIIIa.

239
Q

What is the first virological marker detectable in the serum following Hep B infection?

A

HBsAg.

First becomes detectable approximately 4 weeks after exposure to the virus.

240
Q

Describe the locations of the following glucose transporters:

GLUT-1
GLUT-2
GLUT-3
GLUT4
GLUT-14
A

GLUT-1:

  • Erythrocytes and endothelial barrier cells (e.g. blood brain barrier)
  • Low level of glucose transport to facilitate respiration

GLUT-2
-Absorption of glucose, galactose and fructose from intestinal cells into portal circulation. Also expressed by hepatocytes, renal tubular cells and pancreatic beta cells.

GLUT-3:
-High affinity transporter in neurones and placenta

GLUT-4
-Insulin mediated glucose uptake in striated muscle and adipose tissue

GLUT-14

  • Testes
  • GLUT-14 expression associated with poor prognosis in gastric adenocarcinoma.
241
Q

What is the mechanism of action of nicorandil?

A

Activator of ATP-dependent potassium channels. Relaxes smooth muscle in veins and increased venous capacitance, which leads to reduced ventricular filling pressures and dilatation of the coronary arterioles

242
Q

What is the treatment for Strongyloides infection?

A

Albendazole or ivermectin

243
Q

Weber syndrome is caused by which vessels?

A
244
Q

What drugs cause Torsades and long QT syndrome?

A

Antiarrhythmic drugs
-Sotalol, quinidine, disopyramine, procainamide, flecainide

Certain non-sedating antihistamines
-Terfenadine and astemizole

Antibiotics
-Erythromycin, clarithromycin, azithromycin, levofloxacin, moxifloxacin, gatifloxacin, Co-trim, clindamycin, pentamidine, chloroquine

Antifungals
-Ketoconazole, itraconazole

Certain psychotropic medications
-risperidone, haloperidol, phenothiazines, thioridazine, trifluoperazine, sertindole, zimeldine, ziprasidone

TCA and tetracyclic antidepressants

Certain gastric motility agents
-cisapride

Lithium

245
Q

What is the treatment for syphilis?

A

Benzylpenicillin first line

Doxycycline or cephalosporins (e.g. ceftrixone 500mg IM for 10 days) second line

246
Q

Tertiary syphilis presentations can be split into which 3 groups?

A

Gummatous
-Granulomatous lesions typically involving skin and bone, though can occur anywhere

Cardiovascular
-Typically involving the ascending aorta and potentially leading to aneurysmal changes and aortic regurgitation

Neurological

  • Either general paresis presenting with dementia-like symptoms, or tabes dorsalis

30% of untreated patients will go onto develop tertiary disease

247
Q

What is the most common symptom seen in patients with Waldenstrom’s macroglobulinaemia?

A

Generalised muscle weakness

248
Q

What is the mechanism of action of thiazolidinediones?

A

Bind to specific receptors in the nucleus, “peroxisome proliferator activating receptor -y” (PPAR-y). This causes increased insulin sensitivity.

They do not cause hypoglycaemia when used alone, but can exagerate the hypoglycaemic effects of insulin or sulphonylureas.

Adverse effects include weight gain, fluid retention, and decreased bone mineral density.

249
Q

What is the mechanism of action of quinolones such as ciprofloxacin?

A

Inhibit DNA gyrase which prevents DNA replication and transcription, inducing cell death and preventing cell replication.

Bactericidal antibiotics

250
Q

What is the treatment for Clostridium tetani?

A

Administration of intravenous tetanus immunoglobulin, followed by debridement of the wound.

Antibiotic therapy involves the use of either penicillin or metronidazole, and is important particularly when there are generalised symptoms as seen here.

251
Q

What acid base disorder commonly occurs in drowning?

A

Inhalation of fluid leads to disordered gas exchange in patients with significant fluid aspiration, precipitating respiratory acidosis. Metabolic acid results from intravascular volume depletion, hypotension and consequent tissue hypoxia.

252
Q

What is the treatment for disseminated gonorrhea infection?

A

Ceftriaxone

253
Q

What are the features of Polyglandular syndrome type 1?

A 
Hypoparathyroidism (in around 90%)
Musculocutaneous candidiasis
Adrenal insufficiency (in around 60%)
Primary gonadal failure
Primary hypothyroidism
Hypopituitarism/diabetes insipidus (rarely)
----------------------------------

There might be associated malabsorption, pernicious anaemia, chronic active hepatitis or vitiligo.

254
Q

What are the features of Polyglandular syndrome type 2?

A 
Adrenal insufficiency (in all patients)
Hypothyroidism
Type 1 diabetes
Gonadal failure
Diabetes insipidus (rare)
---------------------------------

Associated conditions include vitiligo, myasthenia gravis, alopecia, immune thrombocytopenic purpura and pernicious anaemia.

MRCP Part 1 (11 decks)

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