Core conditions 1 Flashcards
1
Q
Hypertension causes
A
- 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
2
Q
Secondary hypertension causes 1
A
- 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
3
Q
Secondary hypertension causes 2
A
- 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)
4
Q
Red flags for malignant hypertension
A
Headache, Visual disturbances, Seizures, Nausea/vomiting, Chest pain
5
Q
History of hypertension (renal, vasculature)
A
- 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
6
Q
History of hypertension (endocrine and social)
A
- 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)
7
Q
Hypertension: checking BP
A
- 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
8
Q
ABPM
A
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
9
Q
Investigations to assess for end organ damage/secondary causes hypertension
A
- 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
10
Q
Hypertension: when to offer lifestyle advice first
A
If QRISK <10% and stage 1 hypertension
11
Q
ACE inhibitors: side effects and MoA
A
- 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
12
Q
ACE inhibitors: contraindications and cautions
A
- 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
13
Q
ARB
A
- 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
14
Q
Calcium channel blocker
A
- 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
15
Q
Thiazide diuretics
A
- 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
16
Q
Measuring frailty
A
- 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
17
Q
Rheumatoid arthritis: symptoms
A
- 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
18
Q
Rheumatoid arthritis: deformities
A
- 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
19
Q
Rheumatoid arthritis: investigations
A
- 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)
20
Q
Special tests in RA
A
- Blood tests – latent TB, Hep B, Hep C, HIV status (pending clinical context) – before starting immunosuppressives.
- Lung Function - helpful as a baseline (prior to starting methotrexate or other treatments)
- Synovial fluid assessment – joint aspiration is essential to exclude septic arthritis and crystal arthropathies
21
Q
Treatment of RA: pain relief
A
- Patients with suspected RA should be referred to rheumatologists as soon as possible
- Anti-inflammatory medication i.e. NSAID’s and systemic/intraarticular glucocorticoids= can temporarily control the disease in patients starting DMARD’s or during flares. They reduce inflammation but dont provide long term control or prevent joint injury. Dont use for long periods of time
22
Q
Treatment for RA: DMARD
A
- DMARD’s= nonbiological and biological, can reduce or prevent joint damage and preserve function, should be started ASAP.
- Nonbiological DMARD’s: Methotrexate, hydroxychloroquine and Sulfalazine
- Biological DMARD’s: TNF-alpha inhibitors e.g infliximab, adalimumab; IL-1 receptor antagonists e.g anakinra and IL-6 receptor antagonists e.g tocilizumab etc.
- Patients are normally started on methotrexate first line, alternative is hydroxychloroquine or sulfasalazine
- If resistant to initial DMARD therapy then use a combination i.e. methotrexate + TNF inhibitor
Contraindications to Methotrexate: pregnancy, hepatic impairement
23
Q
RA: principles for treatment
A
- DMARDS are first line (normally methotrexate) but take at least 6 weeks to work. Often in the short term whilst starting DMARD’s symptom relief can be with corticosteroids (often as an IM depot injection which lasts several weeks, +/- intra-articular corticosteroids, +/- systemic corticosteroids (IV or oral).
- Treatment is likely long term (at least 2 years) and DMARD’s are slow to work but effective
- If failure to respond may need biological treatment
24
Q
RA: Risks of treatment
A
- Methotrexate/Leflunamide: teratogenic for female and male patients, need to be on reliable contraception
- DMARDS cause immunosuppression. Live vaccines are contraindicated and advised to have the influenza and pneumococcal
25
Monitoring RA
- Disease severity is assessed clinically (history and examination), blood tests (acute phase reactants) and imaging of joints (US)
- Acute phase reactants: ferritin, CRP, fibrinogen, prothrombin
- Calculating DAS28 score
- Patient Reported outcomes measures (PROMS)
- Active RA: actively inflamed joints, fever, anaemia, elevated ESR and CRP
- Bloods: FBC, U&E, LFT, CRP, ESR
26
Non-pharmacological treatment for RA
*●*Patient education
●Psychosocial interventions
●Rest, exercise, and physical and occupational therapy
●Nutritional and dietary counselling
●Interventions to reduce risks of cardiovascular disease, including smoking cessation and lipid control
●Screening for and treatment of osteoporosis
●Immunizations to decrease risk of infectious complications of immunosuppressive therapies.
27
Prognosis of RA without treatment
- 70% of joint erosion in the first two years
- At 20 years over 60% of patients with RA belong to functional class III or IV and require significant support
- Increased incidence of: infections, cardiovascular disease, Lymphomas
- Life expectancy of RA less than population due to: polyarticular disease, systemic extra-articular disease, persistent disease activity (high ESR, CRP), Positive rheumatoid factor and circulating immune complex, HLA-DR beta chain
28
RA: joint failure
- Can progress to secondary osteoarthritis even with medication, can have disabling joint disease
- Mechanical symptoms with pain on weight bearing and walking and knee or ankle involvement with locking and giving away. Treated different to inflammation of RA
- Osteoporosis can cause avascular necrosis of the hip and secondary osteoarthritis
- Aims of therapy in end stage disease: Pain relief, protection of remaining articular structures, maintenance of function, relief from fatigue and weakness
- May progress to surgery
29
RA and pregnancy
- Often improves or completely remits
- Will need a wash out period from methotrexate and leflunomide before conception
- Pre-conception councelling from rheumatologist and obstetrician
- Ideally pregnancy should be planned for when their disease is under good control on non teratogenic medication e.g TNF inhibitors, sulfasalazine
- Commence folic acid prior to pregnancy
- If RA becomes active in pregnancy, NSAIDs can be used until the 3rd trimester or low dose prednisolone. Or the patient can be commenced on a safe DMARD.
30
RA: serious infections and hepatitis B
- Serious infection: during serious infection DMARDS, biologics and tofacitinib should be held whilst on antibiotics. If history of serious infection, recommend DMARD’s over biological agents, medications administered more frequently are preferred as it can be stopped quickly
- Hepatitis B: in patients with natural immunity treatment for RA can be continued but viral load monitored for 6-12 months for reactivation. If active antiviral therapy should be obtained and RA treatment may proceed on advice from hepatologist
31
Rheumatoid arthritis: Hepatitis C, Tuberculosis, lung disease, diabetes
- Hepatitis C: patients with active HCV and normal liver function should continue with normal treatment. If liver disease present non hepatotoxic DMARDS (sulfasalazine or Hydroxychlorine) are preferred. Managed with hepatologist
- Tuberculosis: prior to treatment, patients with risk factors for TB should be screened for TB. In latent TB, one month of treatment should be given before immunosuppressive treatment starts
- Lung disease: adverse effects of methotrexate can cause pneumonitis
- Diabetes: glucocorticoids used with caution as can worsen diabetes
32
Malignancy and RA
- Non melanoma skin cancer: conventional DMARD’s preferred over biologics or tofacitinib but not contraindicated. Routine skin cancer surveillance
- Melanoma skin cancer: conventional DMARDS’s preferred. Avoid abatacept if history of melanoma. Skin cancer surveillance indicated
- History of lymphoproliferative disorder: prefer conventional DMARD’s, if biological agent needed use rituximab
- Solid organ malignancy: preferred conventional DMARD’s, if biological agent use rituximab. If 5 years from cancer can give normal treatment
33
Mortality in RA
Increased mortality, main cause of death is cardiovascular disease. Chronic inflammation can cause atherosclerosis, steroids and NSAID’s can increase risk of CVD. QRISK score includes RA as a risk factor. Import to control lifestyle factors
34
Alcoholic liver disease: overview
- Overconsumption of alcohol causes scarring of liver tissue due to destruction and regeneration of liver parenchyma
- Types: alcohol fatty liver disease, alcoholic hepatitis and cirrhosis
35
Cirrhosis
It comprises interconnecting fibrous tissue within which trapped hepatocytes regenerate, causing nodules. This disrupts the vascular architecture which may lead to portal hypertension. Cirrhosis is irreversible
36
Alcoholic liver disease: risk factors
- Alcohol consumption
- Genetics: can affect alcohol metabolicm enzymes like alcohol dehydrogenase and aldehyde dehydrogenase
- Malnutrition
- Co-existing lung condition: chronic viral hepatitis including hepatitis C
37
Alcoholic liver disease: symptoms
- Non-specific: fatigue, malaise, abdominal pain (not normally pain), anorexia, weakness, nausea and/or vomiting
- Estrogenic effects: gynaecomastia and testicular atrophy, loss of body hair, Amenorrhoea, loss of libido
- Portal hypertension: ascites, dilates veins (caput medusae), variceal bleeding and haemorrhage, Splenomegaly
38
Signs of alcoholic hepatitis
- Jaundice (common)
- Right upper quadrant pain (common)
- [Hepatomegaly] (common, present in 70% of patients with ALD): enlarged and smooth edge, not tender to palpitation
- Palmar erythema
- Peripheral oedema
- Clubbing
- Dupuytren's contracture
- Pruritis: If there is cholestasis leading to bile salt deposition in skin
- Xanthomas, Spider angiomas
39
Signs that occur in chronic but not acute liver disease
Portal hypertension, Spider naevi, Splenomegaly, Clubbing, Caput medusae
40
Alcoholic liver disease: investigations/bloods
- An AST:ALT ratio of >3 indicates alcoholic hepatitis
- ALP and GGT there may be a small rise
- Bilirubin: rise in conjugated bilirubin
- Albumin: reduced
- Elevated prothrombin time/INR
- Liver ultrasound
- Liver biopsy: gold standard but not often used because invasive
- Gastroscopy: Endoscopic variceal litigation (EVL) is hazardous. Emergency endoscopy and EVL is even more dangerous
41
Alcoholic liver disease: conservative management
- Alcohol abstinence
- Weight loss: if obese
- Vaccinations: hepatitis A and B
- Nutrition: high protein diet, consider enteral feeding tube if altered mental state
- Nutrition: lots of alcoholics dont eat enough, high protein diet of 1-1.5g of protein per kg of body weight each day
- Elf management: Alcoholics Anonymous 12 step programme (doesnt work for everyone)
42
Alcohol withdrawal
- The standard for treating acute alcohol withdrawal is benzodiazepines (e.g. diazepam)
- Quick-acting benzodiazepine (e.g. lorazepam) for alcohol withdrawal seizures
- Oral lorazepam is the first-line treatment for delirium tremens in alcohol withdrawal
43
Acute alcoholic hepatitis treatment
- Glucocorticoids i.e. prednisolone. Improves short term survival but has no long term benefits
- Maddrey's discriminant function (DF) can identify patients with severe acute alcoholic hepatitis: DF of >32 predicts a high mortality within 90 days, and means a liver biopsy should be considered, with corticosteroid treatment initiation
- Pentoxifylline can be used as an alternative to glucocorticoids if they are contraindicated (e.g. hepatitis B viral infection, tuberculosis, other serious infection)
44
End stage ALD
- In patients with end-stage ALD (cirrhosis with decompensation), liver transplantation can be considered
- Usually must be alcohol free for >6 months
45
ALD complications: hepatic encephalopathy and portal hypertension
- Hepatic encephalopathy: confusion, Drowsiness, Hyperventilation, Asterixis, Fetor hepaticus. Supportive care and laatives (lactulose)
- Portal hypertension: after cirrhosis causes large varices in the oesophagus, stomach, rectum and umbilicum. Can cause variceal haemorrhage, ascites and splenomegaly. Ascites can be complicated by spontaneous bacterial peritonitis. Portal hypertension can be managed by trans jugular intrahepatic portal systemic shunt (TIPSS)
46
ALD: Hepato-renal syndrome and Hepatocellular carcinoma
- Hepato-renal syndrome: portal hypertension causes vasodilation reducing blood flow to the kidneys and causing an AKI
- Hepatocellular carcinoma: hepatic ultrasound should occur every 6 months to 1 year
47
ALD: other complications
- Ascites and oedema: due to secondary hyperaldosteronism and low albumin
- Nutrition often declines: poor intake and catabolic effect of disease
- Osteoporosis: can cause fractures
- Sarcopenia: due to hypogonadism, treat with testosterone replacement
48
Treatment for ALD complications
- Ascites and oedema: Spironolactone titrate up to achieve weight loss of 500-1000g/day. Tightrope between fluid overload and dehydration. Too much diuretic can cause hyponatraemia, dehydration leading to hepatic encephalopathy, AKI or hepato-renal syndrome
- To prevent Wernicke-Korsakoff syndrome: high dose IV vitamin B and C and oral thiamine long term
- Oesophageal varicies: beta blockers to reduce hepatic portal pressure gradient
- Past spontaneous bacterial peritonitis: Rifaximin
- Chronic encephalopathy: rifaximin
49
Social effects of alcoholism
- Separation, divorce, estrangement, loss of employment and homelessness
- Domestic violence
- Road safety: drunk driving
- Child protection: negligence
