Likely to come up Flashcards
What is atherosclerosis
The accumulation of lipids, macrophages and smooth muscle in the intima of arterial walls
Which arteries is atherosclerosis most common ?
LAD
Circumflex
RCA
What is the triad of factors that can lead to atherosclerosis ?
Vascular endothelial injury e.g. by smoking
Increased coagulation of blood cells e.g. DM
Reduced blood flow e.g. Obesity/lack of exercise
What occurs when the endothelium of the blood vessel becomes damaged ?
It secrets chemoattractants which lead to leukocytes accumulating in the intma
What is a foam cell ?
A macrophage that has tried to phagocytose low-density lipoproteins
What make up the atherosclortic plaques
Foam cells
LDLs
SMCs
What are the criteria for hypertension diagnosis
140/90 in clinical setting
135/85 with ambulatory or home reading
What the types of hypertension ?
Essential/primary (95%) cases where cause is unknown
Unessential/secondary where cause is known
What are 4 big causes of hypertension ?
ROPE Renal disease Obesity Pregnancy Endocrine: primary aldosteronism
What are the clinical stages of hypertension ?
Stage 1 140/90
Stage 2 >160/100
Stage 3 >180/120
What are the ambulatory stages of hypertension ?
Stage 1 135/85
Stage 2 150/95
When should people be screened for hypertension ?
Every 5 years
Every year in DM
Name complications of HTN
IHD Cerebrovascular accident i.e. stroke or haemorrhage Hypertensive retinopathy Hypertensive nephropathy HF
What is 1st line management for all patients with stage 1 hypertension
Lifestyle change
Reduce alcohol, caffeine and salt intake
What requires pharmacological intervention for hypertension ?
All patients with stage 2 or above hypertension
All patients over 80 with stage 1 hypertension that have a Q-risk score of more than 10%, DM, renal disease, CVD or end organ damage
First line HTN under 55 caucasian
ACE-I e.g. ramipril
First line HTN over 55 and Afro-Caribbean
CCB e.g. amlodipine
2nd line HTN under 55 caucasian
ACE-I +
CCB or
Thiazide like diuretic e.g. indapamide
2nd line HTN Afro-Caribbean
CCB +
Angiotensin 2 receptor blocker e.g. candesartan
or
Thiazide LD e.g. indapamide
3rd line HTN
ACE-I + CCB + TLD
Ramipril + Amlodipine + indapamide
Things to consider when treating HTN 3rd line
TLD e.g. indapamide can cause hypokalemia
If K < 4.5 then K sparing diuretic e.g. spironolactone
If K > 4.5 then alpha blocker or beta blocker
HTN treatment targets
<80yo then <140/90
>80yo then <150/90
Name types of heart failure
Systolic HF: inability of the ventricle to contract properly
Diastolic HF: inability of the ventricle to relax and fill
What is the epidemiology of HF ?
Affects 1-3% of the general population
10% of the elderly affected
Name causes of heart disease ?
ISH - main cause Cardiomyopathy Valvular disease Cor pulmonale Hypertension Alcohol excess
3 cardinal symptoms of HF
SOB
Fatigue
Ankle swelling
How will HF appear on a X-ray
ABCDE Alveolar oedema Kerley B lines Cardiomegaly Dilated upper lobes vessels
How will a blood test of someone with HF appear ?
Brain natriuretic peptide (BNP) is the key marker
Troponin I, Troponin T and creatine kinase will be both raised
How can an echocardiogram be useful in HF
Assesses the dimensions of the cardiac chambers and assess for valvular disease
Differentials of HF
Pneumonia
COPD/pulmonary fibrosis
Ageing/physical inactivity
First line management HF
ACE-I e.g. ramipril
BB e.g. bisoprolol
Loop diuretic: furosemide
Plus: Revascularisation e.g. PCI appropriate
2nd line management HF
Add aldosterone receptor antagonist e.g. spironolactone
GTN spray
What can be used if ACE-I is not tolerated ?
Angiotensin receptor blockers e.g. spironolactone
3rd line management HF
Cardiac resynchronisation
Digoxin
What are some compensatory mechanisms for HF
Venous return
Outflow resistance
Sympathetic system activation
Renin-Angiotensin System
What is Cor Pulmonale
Right sided heart failure due to respiratory disease
What can cause cor pulmonale ?
COPD - most common cause of chronic symptoms
PE - most common cause of acute symptoms
Chronic bronchitis
Pulmonary fibrosis
Cystic fibrosis
What is the pathology of cor pulmonale ?
Increased resistance in the pulmonary arteries results in the right ventricle being unable to effectively pump blood out of the ventricle and into the PA
This leads to a back pressure of blood in the right side of the heart which then has to pump harder to maintain pulmonary circulation eventually leading to hypertrophy and dilation
What are specific symptoms of cor pulmonale ?
Hypoxia Cyanosis Raised JVP (due to backlog) Peripheral oedema Third heart sound
What is the NICE criteria for AKI
Rise in creatinine > 25 micromol/L in 48 hours
Rise in creatinine > 50% in 7 day s
Urine output of <0.5ml/kg/hour for >6 hours
What are pre-renal causes of AKI ?
Dehydration
Hypotension
HF
What are the renal causes of AKI ?
Glomerulonephritis
Interstitial nephritis
Acute tubular necrosis
Post-renal causes
Kidney stones
Malignancy
Ureter or urethral strictures
Enlarged prostate or prostate cancer
What investigations can be used to try and determine a cause ?
FBC U&Es LFT Urinalysis Urinary tract ultrasound Abdominal CT or MRI
DD for AKI
Chronic kidney disease
Increased muscle mass
Drug side effects
What are potential complications of AKI ?
Hyperkalaemia Fluid overload Heart failure Metabolic acidosis Uremia → can lead to encephalopathy or pericarditis
Name RFs for AKI
CKD HF DM Liver disease Age > 65 Cognitive impairment Nephrotoxic medications such as NSAIDs and ACE-I Contrast mediums
What are the stages of renal failure by eGFR ?
Stage 1 100-90 Stage 2 89-60 Stage 3a 59-45 Stage 3b 44-30 Stage 4 29-15 Stage 5 <15
Concerning AKI from creatinine and urine what are the levels of stage 1 (risk) AKI ?
Creatinine- increased serum level >0.3mg/dl or 150-200% from baseline
Urine - production <0.5ml/kg/hour for >6 horus
Concerning AKI from creatinine and urine, what are the levels of stage 2 (injury) AKI ?
Increased serum creatinine level >200-300%
Urine production <0.5ml/kg/hour for > 12 hours
Concerning AKI from creatinine and urine what are the levels of stage 3 (failure) AKI ?
Increased serum level from baseline >0.5ml/dl
Urine production <0.3ml/kghour x24 hours
What is RA
A chronic and severe inflammatory autoimmune disorder of the synovial lining of the joints, tendons sheaths and bursa
Typically presents symmetrically and affects multiple joints
What is the epidemiology of RA
Affects ~1% of the population
2-3 times more common in women
Most often develops in middle age
Hands and feet are impacted in >80% of cases
Which genes are associated with RA ?
HLA DR4 - often present
HLA DR1 - sometimes present
What is the cellular pathology of RA ?
RF is an autoantibody that targets the Fc portion of the IgG antibody causing activation of the immune system against patients own IgG causing systemic inflammation
What is the classical RF presentation
Symmetrical distal polyarthropathy
Pain
Swelling
Stiffness which improves as the day progresses
What joints are typically affected in RA ?
Metacarpal phalangeal (MCP) Proximal interphalangeal (PIP) Metatarsophalangeal joints Can also affect the larger joints such as knees, shoulders and elbows
What is a surgical emergency at can occur with RA ?
Atlantoaxial subluxation
Caused by damage to the ligaments and bursa around the odontoid peg
Subluxation can lead to spinal cord compression
What are the classical signs of RA in the hands ?
Z shaped deformity of the thumb (sometimes called hitchhikers deformity)
Swan neck deformity
Boutonniere’s deformity
Ulnar deviation of the fingers at the MCP (knuckle) joints
What is swan neck deformity ?
Hyperextended PIP with flexed DIP
Boutonniere’s deformity
Hyperextended DIP with flexed PIP
Name some key extra-articular manifestations of RA
Pulmonary fibrosis Bronchiolitis obliterans Felty's syndrome Anaemia of chronic disease CTS Amyloidosis
What investigations would be ordered for a patient with RA ?
Bloods Check RF If RF negative then check anti-CCP Other markers e.g. ESR and CRP X-ray Ultrasound
X-ray changes seen in RA
Joint destruction and deformity
Soft tissue swelling
Periarticular osteopenia
Bony erosions
1st line management in RA
Disease modifying anti-rheumatic drugs (DMARDs)
Methotrexate, hydroxychloroquine, leflunomide
Adjunct: NSAIDs, corticosteroids at first presentation
2nd line RA
2 DMARDs used in combination
3rd line RA
Methotrexate +
Biological therapy -usually a TNF-I e.g. adalimumab
4th line RA
Methotrexate +
Rituximab (CD20 MCAB)
Complications of RA
Extra-articular eye Extra-articular neurological Extra-articular haematological Extra-articular lungs Extra-articular kidneys
Haematological complications of RA
Anaemia of chronic disease
Fealty’s syndrome
Lung complications of RA
Pleural effusion
Diffuse fibrosing alveolitis
Rheumatoid nodules
Extra-articular kidneys
Amyloidosis - in advance RA - responsible for 10% of RA deaths
What is OA ?
An age related dynamic reaction pattern of the synovial joints in response to insult and injury
Often described as wear and tear
Symptoms of OA
Pain and stiffness which tends to get worse as the day goes on
X-ray signs for OA
LOSS
Loss of joint space
Osteophytes - bone spurs
Subchondral sclerosis - increased density of the bone along the joint line
Subchondral cysts - fluid filled holes in the bone
Signs in the hands OA
Heberden's nodes Bouchard's nodes Squaring at the base of the thumb at the carpometacarpal joints Weak grip Reduced range of motion
What are Herberden’s nodes ?
Small bony growths which affect the distal interphalangeal (DIP) joints
What are Bouchard’s nodes ?
Small bony growths that affect the proximal interphalangeal (PIP) joints
What investigations would you order for a patient with suspected OA ?
1st: X-ray affected joints
Serum C-reactive protein (CRP)
Serum erythrocyte sedimentation rate (ESR)
DDs for OA
Gout/Pseudogout
Buritis
Management of OA non-pharmacological
Weight loss
Physiotherapy
Occupational therapy
Orthotics
Management of OA 1st line
Topical analgesia
Plus: non-pharmacological management
Adjunct: intra-articular CS injections
Management of OA 2nd line
1st line + paracetamol
Management of OA 3rd line
2nd line + NSAIDs
Consider PPI
Management of OA 4th line
3rd line + opioid
RF for OA
Age
Female sex
Genetic predisposition
Obesity
Complications of NSAIDs
GI -gastric and peptic ulcers
Renal - AKI e.g. tubular necrosis or progressive kidney disease
Cardiovascular e.g. hypertension, HF , MI and stroke
Respiratory - exacerbate asthma
What type of respiratory condition is asthma ?
Obstructive
Triggers for asthma attack
Infection Exercise Animals Cold/damp Dust Strong emotion Night time and early morning
Features of a Hx that may suggest asthma
Episodic symptoms
Typically worse at night
Dry cough with wheeze and shortness of breath
Hx of atopic conditions such as eczema, hayfever and food allergies
FHx
Bilateral ‘‘polyphonic wheeze’’
NICE recommended diagnosis
1st line investigations
Fractional exhaled nitric oxide
Spirometry with bronchodilator reversibility
Long term management in order
Short acting beta 2 adrenergic receptor agonists Inhaled corticosteroids Long acting beta 2 agonists Long-acting muscarinic antagonists Leukotriene receptor antagonists Maintenance and reliever therapy
Give an example of a SABA
E.g. Salbutamol
Give an example of a low dose inhaled corticosteroid
Ipratropium bromide or beclometasone
Give an example of an oral leukotriene receptor antagonist
Montelukast
Give an example of an LABA
Salmeterol
What kind of therapy is considered if SABA, LDICS, OLRA and LABA are not working ?
Maintenance and reliever therapy (MART)
What is MART ?
Using a combination inhaler containing a LDCS and a fast acting LABA
E.g. ipratropium bromide and salmeterol
