Core conditions 1 Flashcards
Hypertension causes
- Acute BP increase: pain/anxiety, white coat hypertension
- Primary/ essential hypertension
- Secondary hypertension: 5% of causes. ROPED= Renal disease, Obesity, Pregnancy induced, Endocrine, Drug induced
Secondary hypertension causes 1
- Renal disease: most common due to renal vascular disease (atherosclerosis, fibromuscular dysplasia) and intrinsic renal disease (CKD, AKI, glomerulonephritis, polycystic kidney disease)
- Obesity: causes by fat compressing the kidneys, activation of the renin-angiotensin-aldosterone system, increased sympathetic nervous system activity
- Pregnancy: includes gestational hypertension and pre-eclampsia
Secondary hypertension causes 2
- Endocrine: Primary hyperaldosteronism (Conn’s syndrome- mineralocorticoid excess), Crushing’s (glucocorticoid excess), Phaeochromocytoma (catecholamine excess), Acromegaly (growth hormone excess)
- Drug induced: Glucocorticoids, oral contraceptives, NSAID’s, SSRI’s, Sympathomimetic agents (EPO)
Red flags for malignant hypertension
Headache, Visual disturbances, Seizures, Nausea/vomiting, Chest pain
History of hypertension (renal, vasculature)
- Renal: pink urine (haematuria), frothy urine (proteinuria), flank tenderness/pain, weight loss, ankle/leg swelling
- Vasculature: headache, epistaxis, intermittent claudication, lower limb weakness, cold legs/feet
History of hypertension (endocrine and social)
- Endocrine: Cushings (weight gain), Phaeochromocytoma (headache, palpitations, sweating), Acromegaly (tall, swollen hands/feet), Conn’s (muscle spasm, paraesthesia), Hyper/hypothyroidism (heat/cold intolerance, weight gain/loss)
- Ask about gout and menstrual history. Ask about family situation and job (stress)
Hypertension: checking BP
- If blood pressure normal then check every 5 years
- If clinic BP >180/120 investigate for end organ damage, if no damage repeat clinic BP in 7 days
- Refer for same day specialist review if: retinal haemorrhage/papilloedema, life threatening symptoms, suspected phaeochromocytoma
- If BP between 140-180 assess CVD risk
- If <40 with hypertension consider referral for secondary cause and weigh up long term treatment
- If stage 2 hypertension consider specialist evaluation of secondary causes
ABPM
Takes multiple (14+) blood pressure recordings over a 24 hour period, you take two at the same time. Done automatically by a machine attached to your arm
Investigations to assess for end organ damage/secondary causes hypertension
- Bedside: carry out QRISK score, urine dipstick, 12 lead ECG /9left ventricular hypertrophy), Fundoscopy
- Bloods: serum electrolytes, creatine, protein: creatine ratio, eGFR, fasting glucose/lipids
- Imaging: ECHO, US/MRI of renal arteries
- Special tests (for secondary causes): 24 hour urinary metanephrines (phaeochromocytoma, Urinary free cortisol and/or dexamethasone suppression test (Cushing’s syndrome), Renin/aldosterone levels to exclude Conn’s syndrome
Hypertension: when to offer lifestyle advice first
If QRISK <10% and stage 1 hypertension
ACE inhibitors: side effects and MoA
- ACE converts angiotensin 1 to angiotensin 2. Angiotensin 2 causes vasoconstriction of blood vessels and increased aldosterone. Aldosterone retains sodium so fluid volume increases. Ace inhibitors stop this from happening
- Side effect: cough due to accumulation of bradykinin in the lungs (normally broken down by ACE)
- Rare side effect: Hyperkalaemia can cause arrhythmias. Postural hypotension, avoid by taking medication at bedtime. Angiodema can be life threatening
ACE inhibitors: contraindications and cautions
- Contraindications: Pregnancy, Hyperkalaemia, renal artery stenosis
- Caution: Acute illness that might dehydrate i.e. D and V (temporarily suspend) to avoid AKI and postural hypotension, dont use with ARB’s
- Check serum creatine and potassium before and after starting treatment
- ACE comes from the lungs
ARB
- Blocks Angiotensin 2 by blocking the AT1 receptor
- Does not affect Bradykinin so no cough or angiodema
- Side effects: Hyperkalaemia, orthostatic hypotension, dizziness, renal impairment
- Examples: Losartan
Calcium channel blocker
- Attach to L-type calcium channels and the smooth muscle of the coronary and peripheral arteriolar vasculature causing vascular smooth muscle to relax and dilate arterioles
- Examples: Verapamil, amlodipine
- Used in hypertensive patients with diabetes, angina, asthma and peripheral vascular disease (unlike beta blockers)
- Side effects: dizziness, headache, fatigue
- Verapamil and Diltiazem should be avoided in patients with heart failure or atrioventricular block
Amlodipine can cause ankle swelling
Thiazide diuretics
- Reduce sodium and water in the body, can be used in oedema as well
- Examples: Bendroflumethiazide, Indapamide
- Acts on distal tubule on the sodium chloride co-transporter, blocks reabsorption
- Side effects: dehydration → AKI, low chloride/sodium/potassium, postural hypotension
- Caution in diabetes, Hypercalcaemia and gout
- Can cause mild hyperglycaemia
- Loop diuretics i.e. Furosemide are preferred to thiazide diuretic when there is congestive heart failure
Measuring frailty
- An informal assessment of gait speed
- Self reported health status i.e. how would you rate your health on a scale from 0 to 10, scores of 6 or less indicate frailty
- Formal assessment of gait speed, more than 5 seconds to walk 4 meters indicates frailty
- The PRISMA-7 questionnaire, a score of 3 and above indicates frailty
Rheumatoid arthritis: symptoms
- Joint pain (small joints of the hands and feet which are symmetrical), joint swelling, morning stiffness, difficulty moving and ability to perform motor tasks.
- Its a chronic relapsing/remitting course
- Systemic symptoms: fatigue, loss of energy and weight loss
- Extra articular symptoms: Sicca, breathlessness and rashes
- Physical signs: joint tenderness on palpitation, reduced movement/function, joint swelling and joint deformity
Rheumatoid arthritis: deformities
- Boutonniere deformity: DIP hyperextension and PIP flexion (affects PIP)
- Swan neck deformity: DIP flexion and PIP hyperextension (affects DIP)
- Z thumb deformity: hyperextension of the interphalangeal join, fixed flexion and subluxation of the metacarpophalangeal joint
- Ulnar deviation
Rheumatoid arthritis: investigations
- Clinical diagnosis
- Bedside: urinalysis at baseline
- Bloods: FBC, ESR, CRP, U&E’s, LFT, autoantibodies (rheumatoid factor and anti-CCP), TFT. Anti-CCP is more specific then rheumatoid factor. Positive RG and anti-CCP indicate a more severe course of RA
- Imaging: US joints (most sensitive for synovitis), Joint radiographs at baseline (often normal in early RA), Chest XR (prior to starting methotrexate and to exclude TB)