Graves’ Extrathyroidal features
The severity of Grave’s eye disease can be graded using the mnemonic NOSPECS
No signs / symptoms
Only signs (e.g: upper lid retraction)
Signs & symptoms (including soft-tissue involvement)
Extra-ocular muscle involvement
Sight loss due to optic nerve involvement
Management of Grave’s Eye disease
Thyrotoxicosis isn’t causing the eye symptoms its the antibodies. Therefore need to treat both simultaneously. Control thyroxtocosis using agents such as carbimazole and allow the thyroid to recover with RadioI or surgery. RadioI can worsen thyroid disease in some patients
C: Manage risk factors (Smoking)
Mild -> Eye lubricants
Moderate/Severe -> Steroids
Early referral to opthalmology (they might give steroids and in emergency they might do orbital decompression)
Type I - anaphylactic
Type II - cytotoxic, autoantibody mediated (bind to csf and destruct cells) e.g. HDN, transfusion reaction, ITP
Type III - Immune complex mediated
Type IV - Sensitised T cell mediated (delayed), contact dermatitis
Type V - Stimulatory antireceptor antibody, Graves, MG
MEN 1 and MEN 2 are the main types
MEN 1 - 3Ps parathyroid hyperplasia, pituitary tumours and pancreatic islet cell tumours
MEN 2 - Hyperparathyroidism + 2Cs Carcinoid producing tumour Phaeo, calcitonin producing tumour (Meduallary thyroid producing tumour)
Causes of acute HTN
- Phaeo - serum catecholamines
- Conn’s Syndrome - High aldosterone: renin ratio (renin lowers to compensate) (HTN, Low K+, met alk)
- Thyrotoxicosis - TSH Receptor antibody test
- Cushing Syndrome - dexamethasone suppression test
- Stress/Anxiety - holter BP
4. Renal Artery Stenosis - dipstick, renal ultraouns
- Rx underlying condition
- ↓ pulmonary vascular resistance
CCB: e.g. nifedipine
Sildenafil (PDE-5 inhibitor)
Bosentan (endothelin receptor antagonist)
- Cardiac failure (ACEi + β-B (caution if asthma) Diuretics)
- Heart-Lung Tx
Allergic bronchopulmonary aspergillosis is a hypersensitivity reaction to bronchial colonisation by Aspergillus fumigatus mould, typically affecting patients with asthma or cystic fibrosis or atopy. Exposure of fungus causes IgG and IgE antibodies.
- bronchoconstriction: wheeze, cough, dyspnoea. Patients may have a previous label of asthma
- bronchiectasis (proximal)
- eosinophilia, RAST, Raised IgE
itraconazole is sometimes introduced as a second-line agent
Stroke pt presenting within 4 hours.
Urgent CT head and CT angiography were organized, which excluded intracranial haemorrhage and confirmed occlusion of the proximal anterior circulation
Thrombolysis + Thrombectomy
Recent NICE guidance states that thrombectomy should be offered as soon as possible and within 6 hours of symptom onset, together with intravenous thrombolysis (if within 4.5 hours), to people who have an acute ischaemic stroke and confirmed occlusion of the proximal anterior circulation demonstrated by computed tomographic angiography (CTA) or magnetic resonance angiography (MRA). This patient meets these criteria and should be offered both thrombolysis and clot retrieval.
A 45-year-old woman presents to the GP with a new rash on her face. On examination, there is a raised purple lesion covering the nose, cheeks and lips. At first, this was diagnosed as rosacea however it has rapidly progressed. The GP also notes axillary and inguinal lymphadenopathy. On further questioning, she notes some fatigue as well as some dyspnoea over the last 6 months. She has smoked 10 cigarettes a day for the last 8 months and drinks 10 units of alcohol a week.
Given the most likely diagnosis, which of the following is associated with her condition?
This question is asking about a woman presenting with facial rash, lymphadenopathy, dyspnoea and fatigue. If we presume from the description the facial rash is fitting with lupus pernio, this presentation typically matches sarcoidosis.
A 70-year-old gentleman a past medical history of ischemic heart disease and hypertension, presents with progressive facial and upper limb swelling. Visibly distended veins can be observed on his chest and neck. This has been ongoing for the past three weeks and he also complains of increased breathlessness, particularly on exertion. He is an ex-smoker and drinks 13 units of alcohol per week.
What is the most likely cause of this presentation?
svc syndrome secondary to lung ca
Small bowel bacterial overgrowth syndrome (SBBOS) is a disorder characterised by excessive amounts of bacteria in the small bowel resulting in gastrointestinal symptoms.
Risk factors for SBBOS
neonates with congenital gastrointestinal abnormalities
Hydrogen breath test
antibiotic therapy: rifaximin is now the treatment of choice due to relatively low resistance. Co-amoxiclav or metronidazole are also effective in the majority of patients.
Painful RUQ with signs of reduced synthetic liver function
glucocorticoids (e.g. prednisolone) are often used during acute episodes of alcoholic hepatitis
pentoxyphylline is also sometimes used
UC Management induction
mild: < 4 stools/day, only a small amount of blood
moderate: 4-6 stools/day, varying amounts of blood, no systemic upset
severe: >6 bloody stools per day + features of systemic upset (pyrexia, tachycardia, anaemia, raised inflammatory markers)
Mild to moderate:
- proctitis > topical (rectal) aminosalicylate, after 4 weeks, add an oral aminosalicylate,
- proctosigmoiditis and L-sided ulcerative colitis >
topical (rectal) aminosalicylate, after 4 weeks, add a high-dose oral aminosalicylate +- topical corticosteroid
- extensive disease - topical (rectal) aminosalicylate and a high-dose oral aminosalicylate:
if remission still not achieved add oral/ topical treatments aminosalicylate / corticosteroid
Severe: Treat as inpt with IV steroids
SBP mx and prophylaxis
Caused by ecoli Managed by IV Cef Give proph ciprofloxacin: - people with cirrhosis and ascites with an ascitic protein of 15 g/litre or less until the ascites has resolved - prev SBP
PSC Ix and Mx
(MRCP) is now the standard procedure to diagnosis primary sclerosing cholangitis as it is sensitive as ERCP and non-invasive. Beaded appearance. Limited role for liver biopsy which would show onion skin obliterative cholangitis, not routinely done.
pANCA might be positive.
Increased risk of CRC and cholangiocarcinoma
reducing dietary sodium
fluid restriction is sometimes recommended if the sodium is < 125 mmol/L
aldosterone antagonists: e.g. spironolactone ± loop diuretics are often added
drainage if tense ascites (therapeutic abdominal paracentesis)
prophylactic antibiotics to reduce the risk of spontaneous bacterial peritonitis. (>15g protein)
Dyspepsia -how do we manage?
If referral not needed:
- Give lifestyle advice and manage any causes
- Review meds
- Trial of full-dose PPI for one month OR a ‘test and treat’ approach for H. pylori
if symptoms persist after either of the above approaches then the alternative approach should be tried
- If still persist, test H pylori with breath test
First consider whether you need to refer or not.
Urgent: dysphagia or upper abdo mass or wt loss and >55 and reflux/abdopain/dyspepsia
Non-urgent referral: haematemesis or >55 and treatment resistant dyspepsia or upper abdo pain and low Hb or (other criteria)
- metformin is still first-line and should be offered if the HbA1c rises to 48 mmol/mol (6.5%)* on lifestyle interventions
- Whilst on metformin, target if 48 still, so increase dose if >48
- Any hypoglycaemics, target is <53
- if the HbA1c has risen to 58 mmol/mol (7.5%) then a second drug should be added. (aim for 48 but only add 2nd drug if 58)
- if despite this the HbA1c rises to, or remains above 58 mmol/mol (7.5%) then triple therapy
Causes of high sodium and low potassium (only)
In suspected primary aldosteronism -> aldosterone/renin ratio is the first-line investigation
Primary hyperaldosteronism is caused by bilateral adrenal hyperplasia (70%) or adrenal adenoma (30%). It commonly presents with hypertension, hypokalaemia (muscle weakness) and polyuria
following this HRCT abdomen and adrenal vein sampling is used to differentiate between unilateral and bilateral sources of aldosterone excess
adrenal adenoma: surgery
bilateral adrenocortical hyperplasia: aldosterone antagonist e.g. spironolactone
Causes of nephrogenic DI
Concurrent lithium use is relevant for nephrogenic diabetes insipidus.
Primary hyperparathyroidism with subsequent hypercalcaemia is another well-documented cause for nephrogenic diabetes insipidus.
Thyrotoxic storm is treated with beta blockers, propylthiouracil and hydrocortisone
beta-1-selective beta-blocker e.g. metoprolol (not propan)
propylthiouracil (an anti-thyroid drug) - faster onset than carbimazole and has peripheral conversion effects too
hydrocortisone (a steroid) e.g. dex (stops conversion of t4 to t3)
Causes of hypothyroidism
Hashimotos - non-painful, firm goitre, typically associated with hypothyroidism although there may be a transient thyrotoxicosis in the acute phase, other AI conditions
De Quervain’s - painful goitre,
How does gliclazide?
Gliclazide functions by releasing vesicles stored within the pancreas containing insulin and C-peptide. This happens because insulin is derived from proinsulin and C-peptide is formed as a byproduct.
CI in ketoacidosis
Can cause weight gain and hypos
Gliclazide overdose causes hyperinsulinemia and high C-peptide levels
Subclinical Hypothyroidism Management
I.e. Raised TSH, in range T4 ± symptoms
TSH is between 4 - 10mU/L and the free thyroxine level is within the normal range
if < 65 years with symptoms suggestive of hypothyroidism, give a trial of levothyroxine. If there is no improvement in symptoms, stop levothyroxine
‘in older people (especially those aged over 80 years) follow a ‘watch and wait’ strategy, generally avoiding hormonal treatment’
if asymptomatic people, observe and repeat thyroid function in 6 months
TSH is > 10mU/L and the free thyroxine level is within the normal range start treatment (even if asymptomatic) with levothyroxine if <= 70 years 'in older people (especially those aged over 80 years) follow a 'watch and wait' strategy, generally avoiding hormonal treatment
A 72-year-old woman presents with polyuria and polydipsia.
Investigations reveal the following:
Fasting glucose 4.5 mmol/l
Calcium 2.88 mmol/l (2.1-2.6)
Phosphate 0.75 mmol/l (0.8-1.4)
Parathyroid hormone 6 pmol/L (normal range = 0.8 - 8.5)
What is the management?
Despite a raised calcium level the parathyroid hormone level is inappropriately normal. This points towards a diagnosis of primary hyperparathyroidism. In other scenarios can be raised too. Typical exams q: elderly women with polydipsia. Raised Ca, Low Phosphate.
Causes of primary hyperparathyroidism 80%: solitary adenoma 15%: hyperplasia 4%: multiple adenoma 1%: carcinoma
the definitive management is total parathyroidectomy
conservative management may be offered if the calcium level is less than 0.25 mmol/L above the upper limit of normal AND the patient is > 50 years AND there is no evidence of end-organ damage
Salt restriction, fluid restriction if sodium is low
Spiro (MR anatagnoists) (furosemide is used as adjunct only)
Drain if tense ascites (if large drainage -> needs albumin cover)
If protein <15g/l then offer cipro prophylaxis