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Likely to come up Flashcards

1
Q

What is atherosclerosis

A

The accumulation of lipids, macrophages and smooth muscle in the intima of arterial walls

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2
Q

Which arteries is atherosclerosis most common ?

A

LAD
Circumflex
RCA

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3
Q

What is the triad of factors that can lead to atherosclerosis ?

A

Vascular endothelial injury e.g. by smoking
Increased coagulation of blood cells e.g. DM
Reduced blood flow e.g. Obesity/lack of exercise

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4
Q

What occurs when the endothelium of the blood vessel becomes damaged ?

A

It secrets chemoattractants which lead to leukocytes accumulating in the intma

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5
Q

What is a foam cell ?

A

A macrophage that has tried to phagocytose low-density lipoproteins

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6
Q

What make up the atherosclortic plaques

A

Foam cells
LDLs
SMCs

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7
Q

What are the criteria for hypertension diagnosis

A

140/90 in clinical setting

135/85 with ambulatory or home reading

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8
Q

What the types of hypertension ?

A

Essential/primary (95%) cases where cause is unknown

Unessential/secondary where cause is known

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9
Q

What are 4 big causes of hypertension ?

A 
ROPE 
Renal disease 
Obesity 
Pregnancy  
Endocrine: primary aldosteronism
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10
Q

What are the clinical stages of hypertension ?

A

Stage 1 140/90
Stage 2 >160/100
Stage 3 >180/120

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11
Q

What are the ambulatory stages of hypertension ?

A

Stage 1 135/85

Stage 2 150/95

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12
Q

When should people be screened for hypertension ?

A

Every 5 years

Every year in DM

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13
Q

Name complications of HTN

A 
IHD 
Cerebrovascular accident i.e. stroke or haemorrhage 
Hypertensive retinopathy 
Hypertensive nephropathy 
HF
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14
Q

What is 1st line management for all patients with stage 1 hypertension

A

Lifestyle change

Reduce alcohol, caffeine and salt intake

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15
Q

What requires pharmacological intervention for hypertension ?

A

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

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16
Q

First line HTN under 55 caucasian

A

ACE-I e.g. ramipril

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17
Q

First line HTN over 55 and Afro-Caribbean

A

CCB e.g. amlodipine

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18
Q

2nd line HTN under 55 caucasian

A

ACE-I +
CCB or
Thiazide like diuretic e.g. indapamide

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19
Q

2nd line HTN Afro-Caribbean

A

CCB +
Angiotensin 2 receptor blocker e.g. candesartan
or
Thiazide LD e.g. indapamide

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20
Q

3rd line HTN

A

ACE-I + CCB + TLD

Ramipril + Amlodipine + indapamide

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21
Q

Things to consider when treating HTN 3rd line

A

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

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22
Q

HTN treatment targets

A

<80yo then <140/90

>80yo then <150/90

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23
Q

Name types of heart failure

A

Systolic HF: inability of the ventricle to contract properly
Diastolic HF: inability of the ventricle to relax and fill

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24
Q

What is the epidemiology of HF ?

A

Affects 1-3% of the general population

10% of the elderly affected

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25
Q

Name causes of heart disease ?

A 
ISH - main cause 
Cardiomyopathy 
Valvular disease 
Cor pulmonale 
Hypertension 
Alcohol excess
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26
Q

3 cardinal symptoms of HF

A

SOB
Fatigue
Ankle swelling

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27
Q

How will HF appear on a X-ray

A 
ABCDE 
Alveolar oedema 
Kerley B lines 
Cardiomegaly 
Dilated upper lobes vessels
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28
Q

How will a blood test of someone with HF appear ?

A

Brain natriuretic peptide (BNP) is the key marker

Troponin I, Troponin T and creatine kinase will be both raised

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29
Q

How can an echocardiogram be useful in HF

A

Assesses the dimensions of the cardiac chambers and assess for valvular disease

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30
Q

Differentials of HF

A

Pneumonia
COPD/pulmonary fibrosis
Ageing/physical inactivity

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31
Q

First line management HF

A

ACE-I e.g. ramipril
BB e.g. bisoprolol
Loop diuretic: furosemide
Plus: Revascularisation e.g. PCI appropriate

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32
Q

2nd line management HF

A

Add aldosterone receptor antagonist e.g. spironolactone

GTN spray

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33
Q

What can be used if ACE-I is not tolerated ?

A

Angiotensin receptor blockers e.g. spironolactone

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34
Q

3rd line management HF

A

Cardiac resynchronisation

Digoxin

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35
Q

What are some compensatory mechanisms for HF

A

Venous return
Outflow resistance
Sympathetic system activation
Renin-Angiotensin System

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36
Q

What is Cor Pulmonale

A

Right sided heart failure due to respiratory disease

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37
Q

What can cause cor pulmonale ?

A

COPD - most common cause of chronic symptoms
PE - most common cause of acute symptoms
Chronic bronchitis
Pulmonary fibrosis
Cystic fibrosis

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38
Q

What is the pathology of cor pulmonale ?

A

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

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39
Q

What are specific symptoms of cor pulmonale ?

A 
Hypoxia 
Cyanosis 
Raised JVP (due to backlog) 
Peripheral oedema 
Third heart sound
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40
Q

What is the NICE criteria for AKI

A

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

41
Q

What are pre-renal causes of AKI ?

A

Dehydration
Hypotension
HF

42
Q

What are the renal causes of AKI ?

A

Glomerulonephritis
Interstitial nephritis
Acute tubular necrosis

43
Q

Post-renal causes

A

Kidney stones
Malignancy
Ureter or urethral strictures
Enlarged prostate or prostate cancer

44
Q

What investigations can be used to try and determine a cause ?

A 
FBC 
U&Es 
LFT 
Urinalysis 
Urinary tract ultrasound 
Abdominal CT or MRI
45
Q

DD for AKI

A

Chronic kidney disease
Increased muscle mass
Drug side effects

46
Q

What are potential complications of AKI ?

A 
Hyperkalaemia 
Fluid overload 
Heart failure 
Metabolic acidosis 
Uremia → can lead to encephalopathy or pericarditis
47
Q

Name RFs for AKI

A 
CKD 
HF 
DM 
Liver disease 
Age > 65 
Cognitive impairment 
Nephrotoxic medications such as NSAIDs and ACE-I
Contrast mediums
48
Q

What are the stages of renal failure by eGFR ?

A 
Stage 1 100-90
Stage 2 89-60
Stage 3a  59-45
Stage 3b 44-30
Stage 4 29-15
Stage 5 <15
49
Q

Concerning AKI from creatinine and urine what are the levels of stage 1 (risk) AKI ?

A

Creatinine- increased serum level >0.3mg/dl or 150-200% from baseline
Urine - production <0.5ml/kg/hour for >6 horus

50
Q

Concerning AKI from creatinine and urine, what are the levels of stage 2 (injury) AKI ?

A

Increased serum creatinine level >200-300%

Urine production <0.5ml/kg/hour for > 12 hours

51
Q

Concerning AKI from creatinine and urine what are the levels of stage 3 (failure) AKI ?

A

Increased serum level from baseline >0.5ml/dl

Urine production <0.3ml/kghour x24 hours

52
Q

What is RA

A

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

53
Q

What is the epidemiology of RA

A

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

54
Q

Which genes are associated with RA ?

A

HLA DR4 - often present

HLA DR1 - sometimes present

55
Q

What is the cellular pathology of RA ?

A

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

56
Q

What is the classical RF presentation

A

Symmetrical distal polyarthropathy
Pain
Swelling
Stiffness which improves as the day progresses

57
Q

What joints are typically affected in RA ?

A 
Metacarpal phalangeal (MCP) 
Proximal interphalangeal (PIP) 
Metatarsophalangeal joints 
Can also affect the larger joints such as knees, shoulders and elbows
58
Q

What is a surgical emergency at can occur with RA ?

A

Atlantoaxial subluxation
Caused by damage to the ligaments and bursa around the odontoid peg
Subluxation can lead to spinal cord compression

59
Q

What are the classical signs of RA in the hands ?

A

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

60
Q

What is swan neck deformity ?

A

Hyperextended PIP with flexed DIP

61
Q

Boutonniere’s deformity

A

Hyperextended DIP with flexed PIP

62
Q

Name some key extra-articular manifestations of RA

A 
Pulmonary fibrosis 
Bronchiolitis obliterans 
Felty's syndrome 
Anaemia of chronic disease 
CTS 
Amyloidosis
63
Q

What investigations would be ordered for a patient with RA ?

A 
Bloods 
Check RF 
If RF negative then check anti-CCP 
Other markers e.g. ESR and CRP 
X-ray 
Ultrasound
64
Q

X-ray changes seen in RA

A

Joint destruction and deformity
Soft tissue swelling
Periarticular osteopenia
Bony erosions

65
Q

1st line management in RA

A

Disease modifying anti-rheumatic drugs (DMARDs)
Methotrexate, hydroxychloroquine, leflunomide
Adjunct: NSAIDs, corticosteroids at first presentation

66
Q

2nd line RA

A

2 DMARDs used in combination

67
Q

3rd line RA

A

Methotrexate +

Biological therapy -usually a TNF-I e.g. adalimumab

68
Q

4th line RA

A

Methotrexate +

Rituximab (CD20 MCAB)

69
Q

Complications of RA

A 
Extra-articular eye 
Extra-articular neurological 
Extra-articular haematological 
Extra-articular lungs 
Extra-articular kidneys
70
Q

Haematological complications of RA

A

Anaemia of chronic disease

Fealty’s syndrome

71
Q

Lung complications of RA

A

Pleural effusion
Diffuse fibrosing alveolitis
Rheumatoid nodules

72
Q

Extra-articular kidneys

A

Amyloidosis - in advance RA - responsible for 10% of RA deaths

73
Q

What is OA ?

A

An age related dynamic reaction pattern of the synovial joints in response to insult and injury
Often described as wear and tear

74
Q

Symptoms of OA

A

Pain and stiffness which tends to get worse as the day goes on

75
Q

X-ray signs for OA

A

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

76
Q

Signs in the hands OA

A 
Heberden's nodes 
Bouchard's nodes 
Squaring at the base of the thumb at the carpometacarpal joints
Weak grip 
Reduced range of motion
77
Q

What are Herberden’s nodes ?

A

Small bony growths which affect the distal interphalangeal (DIP) joints

78
Q

What are Bouchard’s nodes ?

A

Small bony growths that affect the proximal interphalangeal (PIP) joints

79
Q

What investigations would you order for a patient with suspected OA ?

A

1st: X-ray affected joints
Serum C-reactive protein (CRP)
Serum erythrocyte sedimentation rate (ESR)

80
Q

DDs for OA

A

Gout/Pseudogout

Buritis

81
Q

Management of OA non-pharmacological

A

Weight loss
Physiotherapy
Occupational therapy
Orthotics

82
Q

Management of OA 1st line

A

Topical analgesia
Plus: non-pharmacological management
Adjunct: intra-articular CS injections

83
Q

Management of OA 2nd line

A

1st line + paracetamol

84
Q

Management of OA 3rd line

A

2nd line + NSAIDs

Consider PPI

85
Q

Management of OA 4th line

A

3rd line + opioid

86
Q

RF for OA

A

Age
Female sex
Genetic predisposition
Obesity

87
Q

Complications of NSAIDs

A

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

88
Q

What type of respiratory condition is asthma ?

A

Obstructive

89
Q

Triggers for asthma attack

A 
Infection 
Exercise 
Animals 
Cold/damp 
Dust 
Strong emotion 
Night time and early morning
90
Q

Features of a Hx that may suggest asthma

A

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’’

91
Q

NICE recommended diagnosis

A

1st line investigations
Fractional exhaled nitric oxide
Spirometry with bronchodilator reversibility

92
Q

Long term management in order

A 
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
93
Q

Give an example of a SABA

A

E.g. Salbutamol

94
Q

Give an example of a low dose inhaled corticosteroid

A

Ipratropium bromide or beclometasone

95
Q

Give an example of an oral leukotriene receptor antagonist

A

Montelukast

96
Q

Give an example of an LABA

A

Salmeterol

97
Q

What kind of therapy is considered if SABA, LDICS, OLRA and LABA are not working ?

A

Maintenance and reliever therapy (MART)

98
Q

What is MART ?

A

Using a combination inhaler containing a LDCS and a fast acting LABA
E.g. ipratropium bromide and salmeterol

Flash Cards From Mocks (5 decks)

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