MRCP Part 1 Exam
Pregnancy and Thyroid Hormone - ANS Pregnancy increases the amount of TBG (thyroid binding
globulin) so increases the total thyroxin levels but not free thyroxine
Hyperthyroid in pregnancy - ANS Untreated - fetal loss, premature labour, maternal heart failure
Graves disease most common
HCG can activate TSH receptors - transient gestational hyperthyroid - these fall in trimester 2 & 3
treatment - propylthiouracil in first trimester
this can cause hepatic injury
carbimazole in 2nd trimester once lower risk of congenital abnormalities
Monitoring - free thyroxine levels should be kept upper third normal so to avoid fetal hypothyroid
- thyrotrophin receptor stimulating antibodies should be checked weeks 30-36
DO NOT - block and replace or use radioiodine.
Hypothyroid in pregnancy - ANS Thyroxine replacement is safe in pregnancy and breastfeeding
TSH measured each trimester and 6-8 weeks post partum
Women often require an increased dose - up to 50% by weeks 4-6
untreated - developmental abnormalities, miscarriage, still birth, low birth weight, pre-eclampsia,
anaemia
Gentamicin - ANS Aminoglycoside antibioitic
Given IV or topically
Ototoxic - irreversible due to auditory or vestibular nerve damage
Nephrotoxic - causes tubular necrosis, accumulates in renal failure requiring increased monitoring,
furosemide increases this risk
CI - Myasthenia Gravis
,Dosed via height and weight and renal function. Peak and trough levels monitored with dose
adjustments based on trough levels
CSF: Protein levels - ANS normal = 0.2-0.4 g/L
Causes of raised CSF protein
GBS
Froin's syndrome - a spinal canal blockage characterised by xanthochromia, raised protein and CSF
hypercoagulability
TB, bacterial or fungal meningitis
viral encephalitis
Vigabatrin - ANS Irreversibly inhibits GABA transaminase-->increased GABA levels in synapse
Uses = tx infantile spasms (Viga"Baby"trin)
Or used as adjunct therapy for adults with refractory complex partial seizures
SE = visual field constriction and even visual loss in 40% of patients- visual fields must be checked every
6 months as visual loss can be irreversible
Tricuspid regurgitation - ANS Signs: pansystolic murmer, parasternal heave, giant V waves, pulsatile
hepatomegaly
causes: IVDU endocarditis, rheumatic heart disease, right ventricle infarction, pulmonary hypertension,
carcinoid syndrome, epsteins anamoly (rare heart defect that causes tricuspid regurg)
Corticosteroid side effects - ANS COME IN PIGG
Cushings
,opthalmic - glaucoma, catterachts
M - musculoskeletal - OP, proximal myopathy, avascular necrosis
Endocrine- hyperglycaemia, weight gain, hirsuitism, high lipids
Immunosupression
Neutrophilia
Psychiatric - mania, psychosis, insomnia, depression
Intracranial hypertension
Gastric - pancreatitis, ulcers,
Growth suppression in kids
Acne - Systemic glucocorticoids can cause drug-induced acne. This is characterised as monomorphic
papular rash without comedones or cysts. This does not respond to acne treatment but improves on
drug discontinuation
Therapeutic Steroids - ANS Fludocortisone - mostly mineralocorticoid
hydrocortisone - some glucocorticoid, some mineralocoticoid
Dexamethsone - high glucocorticoid
Medication overuse headache - ANS Headache for over 15 days a month, whilst taking regular analgesia
triptans and opioids are highest risk
very common, can affect 1/50 people
management - stop simple analgesia and triptans, wean down any opioids
the headaches may initially worsen before getting better in severity and duration
other withdrawal symptoms - anxiety, vomiting, restlessness, sleep disturbance, tachycardia,
hypotension
, Multiple Myeloma - ANS malignant tumor of plasma cells in the bone marrow
Peak age 60-70s
Presentation: Signs of hypercalcaemia, including confusion, bone pain and fractures, renal failure,
lethargy, infections,
Ix - high calcium, low phosphate, high total protein, high Cr or low EGFR
Further Ix - Bence Jones proteins, whole body MRI, bone marrow biopsy
Dx- one major and one minor criteria OR 3 minor +signs and symptoms
major criteria are based on bone marrow: Plasmacytoma (as demonstrated on evaluation of biopsy
specimen)
30% plasma cells in a bone marrow sample
Elevated levels of M protein in the blood or urine
minor: 10% to 30% plasma cells in a bone marrow sample.
Minor elevations in the level of M protein in the blood or urine.
Osteolytic lesions (as demonstrated on imaging studies).
Low levels of antibodies (not produced by the cancer cells) in the blood.
Investigation of HTN - ANS clinic measurement >140/90 -> offer home BP monitoring or ambulatory
if >150/95 - stage 2 HTN - treat everyone
if >135/85 - stage 1 - treat if under 80 AND one of - renal disease, diabetes, cardiovascular disease, signs
end organ damage or 10 yr CV risk >10%
Management HTN - ANS lifestyle: low Na diet, less caffeine, exercise, weight loss, balanced diet, stop
smoking, reduce alcohol
Pharmocotherapy
If <55 or T2DM - A, then A+C or A+D, then A+C+D, then if K <4.5 add spiro, if >4.5 add alpha or beta
blocker
If >55 or black - C, then C+A or C+D, then A+C+D, then as above
Pregnancy and Thyroid Hormone - ANS Pregnancy increases the amount of TBG (thyroid binding
globulin) so increases the total thyroxin levels but not free thyroxine
Hyperthyroid in pregnancy - ANS Untreated - fetal loss, premature labour, maternal heart failure
Graves disease most common
HCG can activate TSH receptors - transient gestational hyperthyroid - these fall in trimester 2 & 3
treatment - propylthiouracil in first trimester
this can cause hepatic injury
carbimazole in 2nd trimester once lower risk of congenital abnormalities
Monitoring - free thyroxine levels should be kept upper third normal so to avoid fetal hypothyroid
- thyrotrophin receptor stimulating antibodies should be checked weeks 30-36
DO NOT - block and replace or use radioiodine.
Hypothyroid in pregnancy - ANS Thyroxine replacement is safe in pregnancy and breastfeeding
TSH measured each trimester and 6-8 weeks post partum
Women often require an increased dose - up to 50% by weeks 4-6
untreated - developmental abnormalities, miscarriage, still birth, low birth weight, pre-eclampsia,
anaemia
Gentamicin - ANS Aminoglycoside antibioitic
Given IV or topically
Ototoxic - irreversible due to auditory or vestibular nerve damage
Nephrotoxic - causes tubular necrosis, accumulates in renal failure requiring increased monitoring,
furosemide increases this risk
CI - Myasthenia Gravis
,Dosed via height and weight and renal function. Peak and trough levels monitored with dose
adjustments based on trough levels
CSF: Protein levels - ANS normal = 0.2-0.4 g/L
Causes of raised CSF protein
GBS
Froin's syndrome - a spinal canal blockage characterised by xanthochromia, raised protein and CSF
hypercoagulability
TB, bacterial or fungal meningitis
viral encephalitis
Vigabatrin - ANS Irreversibly inhibits GABA transaminase-->increased GABA levels in synapse
Uses = tx infantile spasms (Viga"Baby"trin)
Or used as adjunct therapy for adults with refractory complex partial seizures
SE = visual field constriction and even visual loss in 40% of patients- visual fields must be checked every
6 months as visual loss can be irreversible
Tricuspid regurgitation - ANS Signs: pansystolic murmer, parasternal heave, giant V waves, pulsatile
hepatomegaly
causes: IVDU endocarditis, rheumatic heart disease, right ventricle infarction, pulmonary hypertension,
carcinoid syndrome, epsteins anamoly (rare heart defect that causes tricuspid regurg)
Corticosteroid side effects - ANS COME IN PIGG
Cushings
,opthalmic - glaucoma, catterachts
M - musculoskeletal - OP, proximal myopathy, avascular necrosis
Endocrine- hyperglycaemia, weight gain, hirsuitism, high lipids
Immunosupression
Neutrophilia
Psychiatric - mania, psychosis, insomnia, depression
Intracranial hypertension
Gastric - pancreatitis, ulcers,
Growth suppression in kids
Acne - Systemic glucocorticoids can cause drug-induced acne. This is characterised as monomorphic
papular rash without comedones or cysts. This does not respond to acne treatment but improves on
drug discontinuation
Therapeutic Steroids - ANS Fludocortisone - mostly mineralocorticoid
hydrocortisone - some glucocorticoid, some mineralocoticoid
Dexamethsone - high glucocorticoid
Medication overuse headache - ANS Headache for over 15 days a month, whilst taking regular analgesia
triptans and opioids are highest risk
very common, can affect 1/50 people
management - stop simple analgesia and triptans, wean down any opioids
the headaches may initially worsen before getting better in severity and duration
other withdrawal symptoms - anxiety, vomiting, restlessness, sleep disturbance, tachycardia,
hypotension
, Multiple Myeloma - ANS malignant tumor of plasma cells in the bone marrow
Peak age 60-70s
Presentation: Signs of hypercalcaemia, including confusion, bone pain and fractures, renal failure,
lethargy, infections,
Ix - high calcium, low phosphate, high total protein, high Cr or low EGFR
Further Ix - Bence Jones proteins, whole body MRI, bone marrow biopsy
Dx- one major and one minor criteria OR 3 minor +signs and symptoms
major criteria are based on bone marrow: Plasmacytoma (as demonstrated on evaluation of biopsy
specimen)
30% plasma cells in a bone marrow sample
Elevated levels of M protein in the blood or urine
minor: 10% to 30% plasma cells in a bone marrow sample.
Minor elevations in the level of M protein in the blood or urine.
Osteolytic lesions (as demonstrated on imaging studies).
Low levels of antibodies (not produced by the cancer cells) in the blood.
Investigation of HTN - ANS clinic measurement >140/90 -> offer home BP monitoring or ambulatory
if >150/95 - stage 2 HTN - treat everyone
if >135/85 - stage 1 - treat if under 80 AND one of - renal disease, diabetes, cardiovascular disease, signs
end organ damage or 10 yr CV risk >10%
Management HTN - ANS lifestyle: low Na diet, less caffeine, exercise, weight loss, balanced diet, stop
smoking, reduce alcohol
Pharmocotherapy
If <55 or T2DM - A, then A+C or A+D, then A+C+D, then if K <4.5 add spiro, if >4.5 add alpha or beta
blocker
If >55 or black - C, then C+A or C+D, then A+C+D, then as above
