GP Flashcards
(318 cards)
1
Q
What is acne vulgaris?
A
chronic inflammatory dermatosis
obstruction of pilosebaceous follicles w/ keratin plugs which results in comedones, inflammation and pustules
2
Q
Acne vulgaris causes
A
genetics
hormones
age
environment - diet, stress, pollutant exposure
3
Q
What are the 4 key elements of acne pathophysiology?
A
increased sebum production
follicular hyperkeratinisation
propionibacterium acnes (P.acnes)
colonisation inflammation
4
Q
Acne pathophysiology - Sebum production
A
- increase in sebum production - primarily driven by hormonal changes (androgen eg testosterone increase). Stimulate sebaceous gland to produce more sebum
- increased sebum provides lipid-rich environment that favours proliferation of skin
5
Q
Acne pathophysiology - follicular hyperkeratinisation
A
- occlusion further exacerbated by abnormal keratinocyte proliferation and differentiation w/in pliosebaceous unit, leading to follicular hyperkeratinisation
- results in formation of keratinous plug - microcomedo - precursor lesion for all acne lesions
5
Q
Acne pathophysiology - colonisation w/ P.acnes
A
- lipid-rich environment created by increased sebum production also promotes overgrowth of anaerobic bacteria like P.acnes
- P.acnes metabolises sebum triglycerides into free fatty acids which act as chemotactic factors attracting neutrophils and monocytes, thereby initiating inflammatory response
P.acnes colonises skin, exacerbates acne
6
Q
Acne pathophysiology - inflammation
A
- immune system responds to P.acnes by releasing pro-inflammatory cytokines eg IL-1, IL-8 and TNF-a
- response leads to inflammation, erythema and formation of inflammatory lesions including papules, pustules, nodules and cysts
7
Q
Acne vulgaris - comedones
A
combo of hyperkeratinisation and increased sebum
closed = whiteheads, follicular opening completely obstructed
open = blackheads, partial obstruction w/ air exposure causing melanin or lipid oxidation
8
Q
Acne vulgaris - papule and pustule development
A
if inflammation persists around blocked follicle, evolves into papules - small raised bump indicating underlying inflammation w/out pus formation
- pustules = visible accumulation of pus due to intense infiltration by neutrophils responding to bacterial antigens and cellular debris w/in follicle
9
Q
Acne vulgaris - nodule and cyst formation
A
- severe inflammatory responses lead to deeper lesions
- characterised by significant infiltration by macrophages, lymphocytes, plasma cells, along w/ extensive tissue destruction resulting in fibrosis if not properly managed
- nodules = firm lumps beneath surface
- cysts = fluctuant due to necrotic material encapsulated w/in fibrous tissue
10
Q
Acne vulgaris presentation
A
comedones - whiteheads and blackheads
papules and pustules
nodules and cysts
ice-pick scars
hypertrophic scars
11
Q
What is acne fulminans?
A
v.severe acne
associated w/ systemic upset eg fever
often seen in male adolescents
hospital admission often required
usually responds to oral steroids
12
Q
Acne vulgaris differentials
A
rosacea
folliculitis
perioral dermatitis
13
Q
Mild to moderate acne management
A
12wk course of topical combo therapy:
- topical adapalene + topical benzoyl peroxide
- topical tretinoin + topical clindamycin
- topical benzoyl peroxide + topical clindamycin
14
Q
Moderate to severe acne management
A
12wk course of either:
- topical adapalene + topical benzoyl peroxide
- topical tretinoin + topical clindamycin
- topical adapalene + topical benzoyl peroxide + either oral lymecycline or oral doxycycline
- topical azelaic acid + either oral lymecycline or oral doxycycline
- combined oral contraceptives = oral abx alternative in women
15
Q
Oral antibiotic usage
A
- tetracyclines should be avoided in pregnant or breastfeeding women and in children <12
- only continue treatment that includes abx for >6m in exceptional circumstances
- topical retinoid or benzoyl peroxide should be co-prescribed w/ oral abx to reduce abx resistance
16
Q
What is a complication of long-term antibiotic use?
A
gram -ve folliculitis
use high-dose oral trimethoprim to treat
17
Q
To reduce risk of antibiotic resistance developing, what shouldn’t be used to treat acne?
A
montherapy w/ topical abx
monotherapy w/ oral abx
combo of topical and oral abxs
18
Q
Acne vulgaris complications
A
scarring
nodulocystic lesions
secondary infection
post-inflammatory erythema
post-inflammatory hyperpigmentation
anxiety, depression, social withdrawal
19
Q
Acne vulgaris treatment related complications
A
abx resistance
tetracycline staining of teeth
isotretinoin side effects - teratogenicity, hyperlipidaemia and hepatotoxicity
20
Q
What is acute bronchitis?
A
self limiting chest infection
inflammation of trachea and major bronchi - oedematous large airways and sputum production
usually resolves before 3 wks, but 25% still have cough beyond this
leading cause is viral
21
Q
Acute bronchitis symptoms
A
acute onset of:
cough
sore throat
rhinorrhoea
wheeze
low grade fever
22
Q
Acute bronchitis investigations
A
clinical diagnosis
CRP testing may be used to guide whether abx therapy is indicated
23
Q
Acute bronchitis v pneumonia
A
sputum, wheeze, breathlessness absent in acute bronchitis
no other focal chest signs in acute bronchitis other than wheeze
systemic features present in pneumonia
24
Acute bronchitis management
analgesia
good fluid intake
consider abx therapy if pts:
- systemically unwell
- have pre-existing co-morbidities
- have CRP of 20-100mg/L or >100mg/L
doxycycline first line (can't be used in pregnant women or children, alternative = amoxicillin)
25
What is an acute stress reaction?
psychological shock - manifests following exposure to severe stress or traumatic events
rapid onset of symptoms that may persist for up to a month
26
Acute stress reaction pathophysiology
acute disruption in homeostasis due to overwhelming amount of stress, leading to hyperarousal of sympathetic nervous system
results in release of adrenaline and cortisol, which cause the observable physical and psychological symptoms
27
Acute stress reaction causes
- Individual susceptibility factors = genetic predisposition, prior psych history, neurobiological factors
- Precipitating factors = traumatic incidents, sudden life changes
- Psychosocial factors = socioeconomic status, coping mechanisms, social support
28
Acute stress reaction symptoms
- Cognitive = confusion, disorientation, intrusive thoughts, derealisation, depersonalisation
- Behavioural = avoidance behaviour, hypervigilance
- Physiological = tachycardia, HTN, sweating, trembling
29
Acute stress reaction differentials
panic disorder
PTSD
adjustment disorder
30
Acute stress reaction management
immediate management - safety, stabilise injuries
CBT therapy, mindfulness-based interventions
follow up care - monitoring, refer to mental health specialist
cultural considerations
educational resources
31
Examples of allergic disorders
asthma
allergic rhinitis
food allergies
atopic dermatitis
32
Allergic disorder diagnosis
clinical history
skin prick tests
serum-specific IgE antibody testing
33
Allergic disorder pathophysiology
IgE antibodies, mast cells and eosinophils
exposure to an allergen leads to cross-linking of IgE on mast cells and basophils, triggering degranulation and release of mediators like histamine
34
Allergic disorder management
allergen avoidance
pharmacotherapy targeting inflammatory pathways - antihistamines nasal corticosteroids
immunotherapy
35
Microcytic anaemia red flag
new onset microcytic anaemia in elderly pts should be urgently investigated to exclude underlying malignancy
36
microcytic anaemia causes
Thalassemia
Anaemia of chronic disease
Iron deficiency
Lead poisoning,
Sideroblastic anemia
37
Normocytic anaemia causes
A – Acute blood loss
A – Anaemia of chronic disease
A – Aplastic anaemia
H – Haemolytic anaemia
H – Hypothyroidism
38
Megaloblastic macrocytic anaemia causes
B12 deficiency
folate deficiency
eg 2nd to methotrexate
39
Normoblastic macrocytic anaemia causes
alcohol
liver disease
hypothyroidism
pregnancy
reticulocytosis
myelodysplasia
drugs: cytotoxics
40
What is myelodysplastic syndrome?
grp of haematological disorders where bone marrow functions abnormally and there's abnormal growth of pluripotent stem cells in bone marrow
this causes insufficiency in no of mature blood cells, which may affect RBCs, WBCs and/or platelets
30% pts eventually progress to acute myeloid leukaemia
40
Anaemia differentials
coeliac
colorectal cancer
bleeding peptic ulcer
Crohn's
non-Hodgkin's lymphoma
colonic diverticular bleeding
myeloma
acute myeloid leukaemia
myelodysplastic syndrome
41
Iron deficiency anaemia presentation
fatigue
pallor
palpitations
pica
koilonychia
angular chelitis
42
Thalassaemia presentation
weakness
jaundice
bone deformities
hepatosplenomegaly
43
Sideroblastic anaemia presentation
fatigue
dyspnoea
bronze skin pigmentation (iron overload)
44
Haemolysis presentation
jaundice
dark urine
fatigue
splenomegaly
45
B12 or folate deficiency presentation
fatigue
pallor
glossitis
neuro symptoms -peripheral neuropathy, hyperactive reflexes or subacute combined degeneration of spinal cord
46
Myelodysplastic syndrome presentation
fatigue
recurrent infections
easy bruising
pallor
petechiae
47
Anaemia investigations
FBC
reticulocyte count
peripheral smear examination
serum ferritin and iron studies
B12 and folate
haptoglobin lvl and direct antiglobulin test (DAT)
48
B12 deficiency causes
pernicious anaemia - autoimmune condition leading to intrinsic factor deficiency and subsequent malabsorption of B12
49
Folate deficiency causes
poor dietary intake
malabsorption syndrome
medications - methotrexate
50
What is sideroblastic anaemia?
rare disorder
prevents bone marrow from incorporating iron into haemoglobin
can be hereditary or acquired
51
What are anal fissures?
longitudinal tears in anoderm - squamous epithelium lining distal anal canal
peak incidence = 30-40 yrs
52
Anal fissure causes
Primary (idiopathic):
- increased anal resting pressure
- trauma
- constipation and straining
Secondary:
- IBD
- infectious causes
- malignancy
- trauma
53
Anal fissure pathophysiology
Mechanical - trauma can cause micro-tears, initiating fissure formation. Repeated can exacerbate, and prevent healing
Ischaemic - increased resting pressure in internal anal sphincter reduces blood flow, impairing healing
Inflammatory - predispose individual to fissure formation and impair healing process
Chronic fissures - fibrosis and hypertrophy of papilla and sentinel pile formation
54
Anal fissure classification
acute = <6wks
chronic = >6wks
around 90% occur on posterior midline
55
Anal fissure presentaiton
Pain - sharp, severe, localised. Most intense during and after bowel movements (so pt may avoid going toilet)
Bleeding - bright red, on paper or in bowl after use
Pruritus ani
Discharge
Constipation
56
Anal fissure physical examination findings
erythema, oedema or discharge
linear tear in anoderm, may be associated w/ sentinel pile (hypertrophied skin tag) at distal end
gentle palpation of perianal area - localised tenderness or induration
sentinel pile may be a palpable, small, firm nodule
DRE w/ caution, as extremely painful for pt, but important to do
57
Acute anal fissure management
dietary advice - high fibre w/ high fluid intake
bulk-forming laxatives
lubricants before defecation
topical anesthetics
analgesia
58
Chronic anal fissure management
same as acute, but topical glyceryl trinitrate (GTN) = first line
if not effective, refer to consider for surgery or botox
59
Anaphylaxis definition
severe, life threatening, generalised or systemic hypersensitivity reaction
60
Anaphylaxis causes
foods - nuts, fish, milk, eggs
insect venom - bees, wasps, fire ants
medications - penicillin, NSAIDs, abxs
latex
idiopathic
61
Anaphylaxis pathophysiology - sensitisation phase
during initial exposure to an allergen, antigen-presenting cells (APCs) process and present allergen to naive T cells, which differentiate into allergen-specific T helper 2 (Th2) cells
Th2 cells release cytokines, eg IL-3 and IL-13, promoting production of allergen-specific IgE antibodies by B cells
IgE antibodies bind to high affinity receptors on mast cell and basophil surfaces, sensitising these cells for future allergen exposure
62
Anaphylaxis pathophysiology - effector phase
upon subsequent exposure to same allergen, the allergen cross-links the IgE molecules on the surface of mast cells and basophils, triggering release of preformed and newly synthesised inflammatory mediators
63
Anaphylaxis pathophysiology - preformed mediators
histamine, tryptase and chymase are stored in granules w/in mast cells and basophils, and are rapidly released on activation
mediators cause vasodilation, increased vasc permeability, smooth muscle contraction and mucus secretion
leads to clinical manifestations of anaphylaxis
64
Anaphylaxis pathophysiology - newly synthesised mediators
following activation, mast cells and basophils synthesise and release various cytokines, chemokines and lipid mediators (eg prostaglandins and leukotrienes)
mediators contribute to late-phase response, amplifying and prolonging inflammatory process
65
Non-IgE mediated anaphylaxis
less common, but still contribute to anaphylaxis
complement activation, direct mast cell activation by agents (eg radiocontrast media or opioids) and IgG- or IgA-mediated immune complex formation
66
Anaphylaxis presentation
sudden onset and rapid progression of Airway and/or Breathing and/or Circulation problems
throat and tongue swelling
resp wheeze
dyspnoea
htn
tachycardia
skin and mucosal changes - generalised pruritus, widespread erythematous or urticarial rash
67
Anaphylaxis management
IM adrenaline
<6m = 100-150 mg
6m - 6yrs = 150m
6-12yrs = 300mg
>12yrs = 500mg
repeat every 5mins if needed
anterolateral aspect of middle 1/4 thigh
68
Refractory anaphylaxis
resp and/or cv problems persist despite 2 doses of IM adrenaline
give IV fluids for shock
get expert help for consideration of IV adrenaline infusion
69
Anaphylaxis management following stabilisation
non-sedating oral antihistamines
new diagnoses refer to specialist and given adrenaline injector and training
risk-stratified approach to discharge
70
Risk-stratified approach to anaphylaxis discharge
- fast-track (after 2hrs) if good response to anaphylaxis and complete resolution of symptoms
- minimum 6hrs after symptom resolution if 2 doses of IM /needed or previous biphasic reaction
- minimum 12 hrs after symptom resolution if severe reaction needing >2 doses, pt has severe asthma, late night or area where access to emergency access care may be difficult
71
Atrial fibrillation risk factors
HTN
IHD
HF
cardiomyopathy
cardiothoracic surgery
DM
obesity
pneumonia
smoking
thyrotoxicosis
caffeine
alcohol excess
CKD
72
Atrial fibrillation pathophysiology - triggers
most common - rapid firing from pulmonary veins, but can be SVC, coronary sinus, vein of Marshall and atrial appendages
Automaticity - spontaneous depolarisation of myocardial cells i absence of external stimulus. Often due to enhanced automaticity where cells outside sinoatrial node begin firing at faster rate than node itself
Triggered activity - afterdepolarisations caused by influx of calcium ions during phase 4 of action potential. Can be early or delayed
Micro-reentry - small circuit allows for re-entry w/in anatomical or functional obstacle
73
Atrial fibrillation pathophysiology - substrate
structural and electrophysiological changes that facilitate maintenance of AF once its been initiated
Electrical remodelling - shortening of AP duration, decrease in wavelength and refractory period heterogeneity, leads to multiple wavelet re-entry circuits
Structural remodelling - changes in atrial size, shape and fibrosis. Disrupts normal myocardial architecture, leads to slow conduction and re-entry circuits
74
Atrial fibrillation pathophysiology - perpetuators
AF can lead to further remodelling, which continues the arrhythmia
Atrial dilatation - AF causes atrial stretch, increases dispersion of refractoriness and promotes re-entry. Upregulates angiotensin II, promoting fibroblast proliferation and fibrosis
Further Fibrosis due to AF, more heterogenous substrate to promote arrhythmia maintenance
Ionic remodelling - changes in ion channel expression can alter AP characteristics, further promoting AF
75
Atrial fibrillation classification
Paroxysmal - typically self-terminating w/in 48hrs, but can be up to 7days. May recur
Persistent - >7days, long-term episodes that require intervention
Long standing persistent - continuous AF >1yr
Permanent - presence accepted by pt and clinician, rhythm control strategies no longer persued
76
Atrial fibrillation presentation
asymptomatic - palpation of radial pulse is irregularly irreegular
palpitations
fatigue
complications - ischaemic stroke, mesenteric ischaemia, acute limb ischaemia, haemodynamic instability
77
Signs of haemodynamic compromise in atrial fibrillation
HR >150bpm
BP < 90 mmHg
syncope or severe dizziness
SOB
chest pain
78
Atrial fibrillation investigations
12-lead ECG - irregularly irregular rhythm, absence of P waves and variable ventricular response
Transthoracic echo
bloods
holter monitor - continuous ECG
TOE
79
Atrial fibrillation differentials
irregular pulse - 2nd or 3rd degree heart block
atrial flutter
ventricular ectopic beats
sinus tachycardia
anxiety and anxiety attacks
tyroid disease
endocarditis
80
Atrial fibrillation rate control
beta blockers (CI = asthma)
calcium channel blockers
digoxin
81
Atrial fibrillation rhythm control
beta blockers
dronedarone
amiodarone
catheter ablation
82
Catheter ablation outcomes
around 50% experience early recurrence that often resolves spontaneously
after 3yrs, 55% pts remain in sinus rhythm after 1 procedure
complications: cardiac tamponade, stroke, pulmonary vein stenosis
83
CHA2DS2-VASc
Congestive heart failure
HTN
Age >65 (1p) >75 (2p)
Diabetes
Stroke, TIA or thromboembolism (2p)
Vasc disease
Sex (female)
1p in males, consider anticoag.
2p in females, no treatment yet
>2 offer anticoag
84
ORBIT score
bleeding risk, anticoagulation considerations
Older age
Renal impairment (GFR<60)
Bleeding history
Iron low
Taking antiplatelets
85
Medications to reduce stroke risk in AF
DOACs:
apixaban
dabigatran
edoxaban
rivaroxaban
warfarin 2nd line where DOAC contraindicated or not tolerated
86
Atrial fibrillation complications
result from cardiac emboli:
stroke
acute limb ischaemia
mesentery ischaemia
87
Electrical signals in heart
start in SAN, co-ordinated electrical conduction
Travels down surrounding atrial tissue to AV node, which delays signal to allow for atrial contraction first
signal travels through His-Purkinje system to send signal to left and right bundle branches, distributing signs to ventricles and allowing for contraction
88
Supraventricular tachycardia pathophysiology: re-entry
mostly in AVRT, AVNRT and some atrial tachycardia
- normal electrical conduction from atria to ventricles in normal pathway
- however, after this, retrograde conduction occurs via accessory pathway from ventricles back up to atria
- leads to repetitive impulse propagation and subsequent tachycardia
89
Supraventricular tachycardia pathophysiology: Increased automaticity
responsible for >70% of focal atrial tachycardia
- normally, SA node generates spontaneous APs to trigger myocardial contraction, but due to increased automaticity, a grp of cardiac cells gain ability to generate spontaneous AP which takes over from SA node functioning
- occurs due to pathological changes in cells' normal membrane resting potential
- leads to rapid and spontaneous depolarisation of cells, which become dominant rhythm and result in tachy episodes
- alternatively, SA node itself may exhibit enhanced automaticity, trigger APs more frequently, leading to tachyarrhythmias
90
Supraventricular tachycardia pathophysiology: triggered activity
largely responsible for AF and atrial flutter, and 30% of focal atrial tachycardias
- SVT occurs due to extra 'after-depolarisations' which occur immediately after cell re-polarisation
- if after-depolarisation reaches a sufficient amplitude to bring membrane to electrical threshold for depolarisation, spontaneous AP occurs, causes trigger response that causes extra-systoles
91
What is atrio-ventricular nodal re-entrant tachycardia?
most common paroxysmal SVT
originates from re-entrant retrograde electrical circuit involving AV node, results in initiation and propagation of a cardiac tachyarrhythmia
92
What is atrio-ventricular ren-entrant tachycardia?
2nd most common paroxysmal SVT
originates via re-entrant retrograde electrical circuit, but involves an accessory pathway between atria and ventricles rather than AV node
eg Wolff-Parkinson-White pattern - accessory pathway capable of anterograde conduction leads to ventricle pre-excitation
Delta wave on ECG
93
What is atrial tachycardia?
either focal or multi-focal
Focal = single focus of atrial tissue generating more rapid APs, leads to rapid tachyarrhythmia
Multi-focal = synonymous w/ atrial flutter, re-entrant electrical circuit in atria leading to rapid and recurrent de-polarisation w/out normal SA node functioning and conduction
94
Supraventricular tachycardia symptoms
palpitations
dizziness or light-headedness
dyspnoea
chest pain or tightness
progressive fatigue
pounding in head/neck
95
Supraventricular tachycardia investigatiosn
ECG - narrow complex tachycardia (<120ms)
Holter monitoring
echo - majority normal
exercise testing
96
Acute management of haemodynamic instability caused by tachyarrhythmia
cardioversion - direct current cardioversion performed under sedation or general anaesthesia
97
Supraventricular tachycardia differentials
sustained ventricular tachycardia
premature atrial or ventricular beats
long QT syndrome
hyperthyroidism
98
Acute management of regular narrow-complex tachycardia
vagal maneouvres - valsava, cold stimulus to face, carotid sinus massage
pharmacological treatment - adenosine rapid IV bolus
99
Acute management of irregular narrow-complex tachycardia
>48hrs AF, can't use cardioversion unless anti-coagulated for 3wks, if urgent, use heparin
<48hrs AF, chemical cardioversion using flecainide, propafenone or amiodarone can be considered
100
Long term management of supraventricular tachycardia
radio-frequency ablation
beta blockers
calcium channel blockers
flecainide and sotalol
101
What is ventricular tachycardia?
severe cardiac arrhythmia originating from ventricles. HR > 100bpm
102
Monomorphic vs polymorphic ventricular tachycardia
Monomorphic = exhibits uniform QRS complexes, typically resulting from re-entry circuits w/in ventricular scar tissue
Polymorphic = eg Torsades de Pointes, varying QRS morphologies. Usually stems from prolonged QT intervals due to ion channel abnormalities or certain medications
103
Ventricular tachycardia causes
IHD
cardiomyopathy
valvular heart disease
congenital long QT syndrome
catecholaminergic polymorphic VT
brugada syndrome
electrolyte abnormalities
drug toxicity
alcohol and substance misuse
104
Ventricular tachycardia pathophysiology simplified
abnormal automaticity
triggered activity
re-entry circuits
electrical instability
105
Ventricular tachycardia presentation
palpitations
chest pain
dyspnoea
syncope
haemodynamic instability - hyn, shock acute HF
106
Ventricular tachycardia investigations
ECG - wide QRS. complexes, AV dissociation, fusion or capture beats
blood tests
chest x-ray
echo - TTE
107
Ventricular tachycardia differentials
supraventricular tachycardia w/ Aberrancy
AF w/ rapid ventricular response
sinus tachycardia
108
Ventricular tachycardia management
assess and stabilise
If stable = antiarrhythmics eg amiodarone or lidocaine, then consider electrical cardioversion
If unstable = synchronised cardioversion
If polymorphic = treat underlying cause like electrolyte imbalance or withdraw medication. If QT normal, consider IV beta blockers or pacing
109
Torsades de Pointes treatment
slow IV magnesium sulfate
110
Long term management of ventricular tachycardia
implantable cardioverter defibrillator placement
antiarrhythmic drug therapy
catheter ablation
monitor and follow up
111
Ventricular tachycardia complications
cardiac arrest
pulseless electrical activity
syncope
myocardial ischaemia and infarction
congestive heart failure
tachycardia induced cardiomyopathy
112
Asthma definition
chronic resp condition characterised by recurrent episodes of airflow obstruction, bronchial responsiveness and underlying inflammation
113
Asthma causes
- genetic predisposition
- environment - allergens, resp infections, irritants, occupational exposures
- immunological factors - Th2 cell mediated response, produces IL-4, IL-5, IL-13 = hyperresponsiveness
114
Asthma risk factors
personal of FH of atopy
antenatal - maternal smoking, viral infection in pregnancy
low birth weight
not breastfed
exposure to allergens
air pollution
'hygiene hypothesis'
115
What is the hygiene hypothesis?
studies show increased risk of asthma and other allergic conditions in developed countries
reduced exposure to infectious agents in childhood prevents normal development of immune system, results in Th2 predominant response
116
What are a number of asthma patients sensitive to?
aspirin
117
Asthma pathophysiology - airway inflammation
initiated by activation of immune cells (Th2 cells, mast cells, eosinophils) in response to triggers
releases pro-inflammatory mediators (cytokines, chemokines, histamine, leukotrienes) that cause airway oedema, mucus production, and bronchoconstriction
infiltration of inflammatory cells into airway wall further exacerbates inflammatory response, leads to persistent airway inflammation and damage
118
Asthma pathophysiology - bronchoconstriction
narrowing of airways and obstruction of airflow
caused by contraction of airway smooth muscle, triggered by release of inflammatory mediators eg histamine and leukotrienes
119
Asthma pathophysiology - mucus production and airway remodelling
chronic asthma can lead to airway remodelling, including subepithelial fibrosis, increased smooth muscle mass, mucus gland hypertrophy and angiogenesis
can result in irreversible airflow obstruction and progressive decline in lung function
extent is associated w/ disease severity and duration, may not be reversible
120
Intermittent asthma GINA classification
symptoms <1 a wk
brief episodes of symptoms
nocturnal symptoms not >2 a month
normal pulmonary function between episodes
121
Mild persistent asthma GINA classification
symptoms >1 a wk but <1 a day
episodes may effect activity
nocturnal symptoms >2 a month
pulmonary function test shows FEV1 and PEFR >80% predicted
122
Moderate persistent asthma GINA classification
daily symptoms occur w/ daily use of short acting beta2 agonists
nocturnal symptoms >1 wk
pulmonary function tests show FEV1 and PEFR between 60% to 80% predicted
123
Severe persistent asthma GINA classification
continuous daily symptoms w/ frequent exacerbations limiting physical acitivities
frequent nocturnal asthma symptoms
pulmonary function tests show FEV1 and PEFR <60% predicted or best possible w/ treatment
124
Asthma presentation
wheezing
cough
dyspnoea
chest tightness
125
Asthma first line investigations
measure eosinophil count OR fractional nitri oxide (FeNO)
asthma diagnosis if:
- eosinophil > reference range
- FeNO ≥ 50 ppb
126
Asthma investigations if not confirmed by eosinophil count or FeNO
measure bronchodilator reversibility (BDR) w/ spirometry. If:
- FEV1 increase ≥ 12% and 200 ml or more from pre-bronchodilator measurement
OR
FEV1 increase ≥ 10% of predicted normal FEV1
if spirometry not available or delayed, measure PEF x2 daily for 2wks. Diagnose asthma if PEF variability ≥ 20%
127
Asthma and eosinophils
- T2 inflammation
- play direct role in airway inflammation by releasing granules containing cytotoxic proteins (eosinophil peroxidase and major basic protein) which damage epithelial cells and perpetuate inflammation
- Activated by IL-5 and other cytokines in T2 pathway, distinguishing them from neutrophils and lymphocytes - which are more associated w/ other immune responses
128
Fractional exhaled nitric oxide (FeNO)
reflects lvl of nitric oxide produced by airway epithelial cells in response to eosinophilic inflammation, an asthma hallmark
measured by handheld device
129
Bronchodilator reversibility testing in asthma
measure FEV1 before and after bronchodilator administration, increase of ≥12% and ≥200 mL indicates significant improvement, shows its asthma and not a fixed airway obstruction
130
Asthma management of ≥ 12 years with newly diagnosed asthma
1: low dose inhaled corticosteroid / formoterol combo inhaler as symptom relief
- If highly symptomatic or a severe exacerbation, start w/ low-dose (MART) maintenance and reliever therapy, treat acute symptoms as appropriate
2: low dose MART - ICS / formoterol combo inhaler for daily maintenance and symptom relief as needed
3: moderate-dose MART
4: check FeNO lvl and blood eosinophil count. If either is raised = refer
if not, consider LTRA or LAMA trial
5: refer to specialist if still not controlled w/ moderate dose MART, and LTRA and LAMA trials
131
Asthma complications
status asthmaticus - severe and persistent asthma attack that doesn't repsond to bronchodilators
pneumonia
COPD
pneumothorax
airway remodelling
osteoporosis
anxiety and depression
132
Acute exacerbation of asthma management
- hospital admission
- supplemental oxygen therapy - 15L via non-rebreathe mask
- high-dose inhaled SABA eg salbutamol, terbutaline, given by nebulizer
- 40-50mg prednisolone orally daily, for at least 5 days or until pt recovers
- if not responded, nebulised ipratropium bromide (SAMA)
133
Eczema causes
genetics - FLG gene, GSTs, cytokine genes
environmental - allergens, irritants, climate, stress
smoking
alcohol
134
What is filaggrin?
crucial for maintaining skin's barrier and hydration
deficiency leads to increased susceptibility to infection and further barrier impairment
filaggrin breakdown products help maintain hydration in low humidity conditions
135
Eczema pathophysiology
epidermal barrier dysfunction
filaggrin deficiency
genetic factors
immune dysregulation and inflammation
neuroimmune interactions
alteration of cutaneous microbiome
136
Factors contributing to epidermal barrier dysfunction
reduced filaggrin production
skin enzyme imbalance
tight junction abnormalities
microbial colonisation
release of inflammatory signals
137
Eczema alteration of cutaneous microbiome
pts often exhibit reduced microbial diversity and increased staphylococcus aureus colonisation
superantigens from S.aureus contribute to pathogenesis by triggering excessive immune responses and promoting chronic inflammation
138
Eczema symptoms
pruritus
erythema
skin lesions - acute, subacute or chronic depending on stage and location
distribution pattern - flexural areas
xerosis
lichen simplex chronicus - 2nd to dcratching or rubbing
prurigo nodularis
2ndry infections
139
Acute, subacute and chronic lesions
- Acute = erythematous papules or vesicles that may coalesce into larger plaques w/ serious exudate
- Subacute = intermediate stage where acute lesions begin to resolve, characterised by erythematous scaling plaques w/ possible crusting
- Chronic = long standing inflammation and repeated scratching, lichenification, hyperpigmentation or hypopigmentation, fissures and excoriations
140
Atopic eczema diagnosis
itchy skin condition in last 12 months + 3 or more of:
- onset <2yrs
- hx of flexural involvement
- hx of generally dry skin
- personal hx of other atopic disease
- visible flexural dermatitis
141
Eczema differentials
psoriasis
tinea corporis (ringworm)
contact dermatitis
142
Eczema management
pt education
emollients
topical corticosteroids
topical calcineurin inhibitors
antimicrobials
phototherapy
systemic therapies - immunosuppresive agents
biologic therapy - dupilumab
itch management - sedating antihistamines
143
Eczema complications
skin infections - staph aureus colonisations, viral and fungal
eye complications
psychosocial impact
systemic complications - asthma, allergic rhinitis, CV disease
144
What is atrophic vaginitis?
falling lvls of circulating oestrogen, frequently seen in post-menopausal women
causes thinning and drying of vaginal mucosa, leading to both urinary and sexual problems
145
Atrophic vaginitis causes
reduction in oestrogen lvls
premature ovarian failure
ovarian failure following chemo and radiotherapy
anti-oestrogenic medications eg tamoxifen and danazol
postpartum changes in hormones
146
Atrophic vaginitis pathophysiology
related to changes in vaginal tissues and local pH
vaginal mucosa becomes drier, thinner and more easily broken, leading to epithelial irritation and inflammation
glycogen production lvls in vagina fall, decreases lactobacilli which normally maintain acidic environment of vagina
absence allows increasingly alkaline environment in which infection is more likely to develop
147
Atrophic vaginitis symptoms
vagina dryness
local irritation - pruritus, pressure and burning pain of vagina
painful intercourse
vaginal bleeding
urinary symptoms
vaginal discharge
148
Atrophic vaginitis signs
external:
- reduced pubic hair
- loss of labial fat pad
- narrowing of vaginal introitus
- thinning of labia minora
internal:
- smooth, shiny vaginal mucosa w/ loss of skin folds
- mucosa drynesss
- loss of vaginal muscle tone
- erythema or bleeding
149
Atrophic vaginitis differentials
endometrial cancer
GU infections - candidiasis, bacterial vaginosis or trichomonas
skin conditions - lichen sclerosus or lichen planus
reaction to irritants - soap, clothing or washing powder
150
Atrophic vaginitis management
topical oestrogens - creams, rings, pessaries
systemic HRT if other post-menopausal symptoms
151
What is blepharitis?
inflammation of eyelid margins
either due to meibomian gland dysfunction (common, post. blepharitis) or seborrhoeic dermatitis / staphylococcal infection (less common, anterior blepharitis)
more common in pts w/ rosacea
152
Blepharitis pathophysiology
meibomian glands secrete oil on to eye surface to prevent evaporation of tear film
any problem affecting meibomian glands (blepharitis) can hence cause drying of eyes which in turn leads to irritation
153
Blepharitis presentation
usually bilateral
grittiness and discomfort, particularly around eyelid margins
sticky eyes in the morning
red eyelid margins
swollen eyes in staphylococcal blepharitis
154
Blepharitis complications
2ndry conjunctivitis
styes
chalazions
155
Blepharitis management
soften lid margin using hot compress twice a day
lid hygiene - remove debris, mix cooled boiling water and baby shampoo
artificial tears for symptom relief in ppl w/ dry eyes or abnormal tear film
156
What is a chalazion?
retention cyst of meibomian gland
firm painless lump in eyelid
most resolve spontaneously but some require surgical drainage
157
Chalazion (meibomian cyst) presentation
palpable nodule
eyelid erythema
induration
absence of pain
eyelid oedema
ptosis
158
Chalazion (meibomian cyst) differentials
hordeolum (stye)
dacrocystitis (inflammation of lacrimal gland)
blepharitis
dermoid cyst
sebaceous gland carcinoma
basal cell carcinoma
159
Chalazion (meibomian cyst) complications
superimposed infection
eyelid cellulitis
spontaneous rupture
scarring
160
What is benign paroxysmal positional vertigo?
most common causes of vertigo
sudden onset dizziness and vertigo triggered by head position
average = 55yrs
less common in younger pts
161
Benign prostatic positional vertigo presentation
vertigo triggered by head position change (eg rolling over in bed or gazing upwards)
may be associated w/ nausea
10-20s episode
+ve Dix-Hallpike manoeuvre
162
What is the Dix-Hallpike manoeuvre?
used to test for benign paroxysmal positional vertigo
1. pt sits upright with head turned 45 degrees to one side
2. pt quickly lowered to supine position with head hanging, extended 20-30 degrees below horizontal plane.
3. observes pt's eyes for 30-60s, looking for nystagmus
4. repeat w/ head 45 degrees in opposite direction
163
Benign paroxysmal positional vertigo management
good prognosis, usually resolves spontaneously after few wks - months
symptomatic relief:
Epley manoeuvre (sit and turn head, lie back so head hangs, turn head other way while lying, then turn head and body further round, so lying into bed, sit up)
exercises at home - termed vestibular rehabilitation
Betahistine
164
Benign paroxysmal positional vertigo prognosis
1/2 w/ BPPV have recurrence 3-5yrs after diagnosis
165
What is benign prostatic hyperplasia?
proliferation of different prostate layers, usually more focussed on inner prostate
results in urinary system compression
commonly from 40 onwards but symptoms may not be apparent until decades later
166
Benign prostatic hyperplasia causes
- androgens (testosterones and dihydrotestosterone)
- inflammation
- age (>80% of 80+yrs)
- race (black men more likely to need treatment younger)
- genetics
167
Benign prostatic hyperplasia pathophysiology
2 prostate growth phases:
1 = puberty, prostate doubles
2 = 25+, continues to grow, when BPH tends to occur
As inner prostate layers propagate, urethra will be compressed and bladder wall may thicken. Processes result in LUTS
168
Benign prostatic hyperplasia presentation
Storage:
- frequency
- nocturia
- urge incontinence
Voiding:
- hesitancy
- poor stream
- dribbling
incomplete emptying, urinary retention, UTIs, bladder stones, haematuria
169
Benign prostatic hyperplasia DRE
enlarged, smooth, firm and non-tender prostate
170
Benign prostatic hyperplasia investigations
urine dipstick - blood, glucose, protein and infection
frequency-volume chart
PSA - raised
urine microscopy, culture and sensitivity
post-void residual urine measurement
US
171
Benign prostatic hyperplasia differentials
prostate cancer
prostatitis
172
Benign prostatic hyperplasia v prostatitis
both cause LUTS, but prostatitis may also present w/ perineal, penile or testicular pain, ejaculatory pain, dysuria or systemic systems
check for infection
173
Benign prostatic hyperplasia lifestyle changes
avoid fluids before bed
reduce consumption of diuretic fluids eg alcohol and coffee
'double voiding' - emptying twice at toilet
174
Benign prostatic hyperplasia medical treatment
a-blockers eg tamsulosin - reduce smooth muscle tone to improve urine flow
5a-reductase inhibitor eg finasteride - converts testosterone to DHT
referral
surgery
175
Surgery options for benign prostatic hyperplasia
TURP - transurethral resection of prostate - remove tissue
TUIP - transurethral incision of prostate - widen urethra
176
Alpha blockers side effects
dizziness
postural hypotension
dry mouth
depression
drowsiness
177
5a-reductase inhibitors side effects
impotence and reduced interest in sex
178
TURP side effects
impotence
179
Benign prostatic hyperplasia complications
UTIs
acute urinary retention
bladder stones
bladder damage
kidney damage
180
What is bursitis?
inflammation of a joint, most commonly the olecranon, trochanters, shoulders and knees
181
Bursitis causes
repetitive trauma
direct trauma
infection
gout
rheumatoid arthritis
idiopathic
182
Olecranon bursitis presentation
non-septic = subacute onset of swelling over olecranon process, tenderness and erythema
septic = tenderness, fever
movement should be painless until swollen bursa is compressed in full flexion
183
Bursitis investigations
clinical, rule out septic concern
aspiration of fluid for microscopy and culture if septic bursitis is considered
184
In bursitis, what does infected fluid look like?
purulent
straw-coloured suggests non-infective cause
185
Bursitis management
activity modification
ice application
compression
elevation
analgesics and anti-inflammatories
aspiration - significant fluid accumulation
corticosteroid injections
186
What is oral candidiasis?
common fungal infection infecting oral cavity
caused by candida albicans, yeast-like fungus normally present in mouth
more common in infants, elderly and immunosuppressed
187
188
Pseudomembranous candidiasis
white or yellowish/white plaques adhering to oral mucosa
curdled milk-like appearance
plaque can be easily wiped, revealing underlying erythematous base that may bleed upon removal
189
Erythematous (atrophic) candidiasis
diffuse erythema involving oral mucosa
varying degrees of severity
burning sensations, dysgeusia or xerostomia
angular chelitis may accompany
190
Hyperplastic (chronic) candidiasis
less common
persistent white plaques that can't be easily wiped away
lesions typically on buccal mucosa or lateral borders of tongue
increased risk for malignant transformation
191
Median rhomboid glossitis
central papillary atrophy on dorsum of tongue in rhomboid shape extending from circumvallate papillae to tip of tongue
area may appear smooth, depapillated and erythematous
192
Angular chelitis
can accompany other forms or present as isolates
erythema, fissuring, crusting and maceration at corners of mouth
193
Candida-associated denture stomatitis
common in pts w/ ill-fitting or poorly maintained dentures
diffuse erythema beneath denture-bearing areas
discomfort or burning sensation under their prostheses
194
Oral candidiasis risk factor modification
diabetes - ensure optimal glycaemic control
denture use - proper hygiene
inhaled corticosteroids - advise pts to rinse mouth after
immunocompromised - investigate cause and treat
194
Oral candidiasis management
risk factor modification
topical antifungals - nystatin suspension, miconazole gel
systemic antifungals - oral fluconazole
195
What is vaginal candidiasis?
thrush
80% = candida albicans
20% = other species
196
Vaginal candidiasis predisposing factors
diabetes mellitus
drugs - abx, steroids
pregnancy
immunosuppression - HIV, iatrogenic
197
Vaginal candidiasis presentaiton
'cottage cheese', non-offensive discharge
vulvitis - superficial dyspareunia, dysuria
itch
vulval erythema, fissuring, satellite lesions
198
Vaginal candidiasis investigations
high vaginal swab not routinely indicated if clinical features are consistent
199
Vaginal candidiasis management
local - clotrimazole pessary
oral - itraconazole 200mg bd for 1 day or fluconazole 150mg stat
if pregnant, only local may be used
200
Recurrent vaginal candidiasis management
recurrent = >4 eps a yr
check compliance
confirm diagnosis, exclude differentials
induction-maintenance regime:
induction - oral fluconazole x3days for 3 doses
maintenance - oral fluconazole wkly x 6ms
201
Chronic fatigue syndrome presentation
- Immune: recurrent sore throat, tender lymph nodes, myalgia, joint pain
- Neuro: headaches, photophobia, phonophobia, blurred vision
- Autonomic: dysfunction, NHH, POTS, palpitations, GI disturbances
- Cognitive: concentration, memory, attention issues
- Sleep disturbances
- Psychiatric: anxiety, depression
- Pain
202
Chronic fatigue syndrome diagnosis
IOM criteria:
1. substantial reduction or impairment in ability to engage in pre-illness lvls of occupational, educational, social or personal activities that persists >6m, accompanied by fatigue
2. Post-exertional malaise
3. unrefreshing sleep despite adequate hrs
Additionally, at least one of:
4. cognitive impairment
5. orthostatic intolerance - lightheadedness, dizziness or fainting upon standing up
203
Chronic fatigue syndrome management
refer if criteria met and symptoms persist for 3m
- energy management
- physical activity and exercise
- cognitive behavioural therapy
204
Chronic kidney disease causes
diabetic nephropathy
chronic glomerulonephritis
chronic pyelonephritis
HTN
adult polcystic kidney disease
205
Presentation of early chronic kidney disease
fatigue
polyuria or nocturia
HTN
puffiness or swelling
206
Presentation of severe chronic kidney disease
decreased urine output
fluid overload symptoms
uraemic symptoms - nausea, vomiting, anorexia, hiccups
neuro symptoms - difficulty focusing, fatigue
CV - chest pain, SOB
anaemia
bone and mineral disease
metabolic acidosis - rapid breathing, confusion, lethargy
207
Chronic kidney disease definiton
>3m of either:
eGFR <60mL/min/1.73m2
urine albumin : creatinine ratio (ACR) >3mg/mmol
208
Chronic kidney disease classification
G1= eGFR >90
G2 = eGFR 60-89
G3a = eGFR 45-59
G3b = eGFR 30-44
G4 = eGFR 15-29
G5 = eGFR <15
A1= A:C <3mg/mmol
A2= A:C 3-30mg/mmol
A3= A:C >30mg/mmol
209
What is accelerated progression in chronic kidney disease?
sustained decline in eGFR w/in 1yr of either 25% or 15mL/min/1.73m2
210
Chronic kidney disease investigations
proteinuria - Albumin creatinine ratio
eGFR monitored regularly throughout yr
211
Modification of Diet in Renal Disease equation variables
serum creatinine
age
gender
ethnicity
211
Factors that can affect GFR result
pregnancy
muscle mass eg amputees, body-builders
eating red meat 12hrs prior to sample being taken
212
Causes of anaemia in renal failure
reduced erythropoietin lvls
reduced erythropoiesis due to toxic effects of uraemia on bone marrow
reduced absorption of iron
anorexia/nausea due to uraemia
reduced red cell survival
blood loss due to capillary fragility and poor platelet funcrion
stress ulceration leading to chronic blood loss
212
Chronic kidney disease complications
anaemia
mineral bone disease
HTN
213
Management of anaemia in renal failure
target haemoglobin 10-12 g/dl
many require IV iron
214
Management of mineral bone disease secondary to CKD
reduce dietary intake of phosphate
phosphate binders
vitD - alfacalcidol, calcitriol
parathyroidectomy
215
Management of HTN secondary to CKD
most require >2 drugs to treat
ACE inhibitors
furosemide
drugs tend to reduce filtration pressure so changes in eGFR and creatinine expected
216
COPD environmental exposures
cigarette smoking
other tobacco products
pollution and occupational exposures
217
COPD genetic and molecular influences
genetic susceptibility - FH of severe early-onset
gene polymorphisms
antioxidant enzymes
metalloproteinase dysregulation (MMPs and TIMPs)
excess elastase
218
COPD other clinical factors
airway responsiveness and atopy
asthma
abnormal lung development
infections
females appear more susceptible
219
COPD risk reduction
smoking cessation
exposure avoidance
physical activity
anti-inflammatory and antioxidant therapy
220
COPD pathophysiology - inflammation
inhalation of noxious particles or gases (cigarette smoke, occupational irritants) triggers an inflammatory response in airways and luck parenchyma
infiltration of neutrophils, macrophages and lymphocytes, leads to release of pro-inflammatory cytokines and chemokines
221
COPD pathophysiology - protease-antiprotease imbalance
associated w/ imbalance between proteases (eg neutrophil elastase, matrix metalloproteinases) and antiproteases (eg alpha-1 antitrypsin, tissue inhibitors of metalloproteinases)
excess protease activity degrades extracellular matrix components, leading to destruction of lung parenchyma and emphysema development
222
COPD pathophysiology - oxidative stress
inhaled pollutants can induce production of reactive oxygen species in lung, resulting in oxidative stress
can cause direct cellular damage, impair protease activity and promote inflammation, contributing to pathogenesis of COPD
223
COPD pathophysiology - airway remodelling
chronic inflammation can lead to structural changes in airways, including thickening of airway wall, increased mucus production and goblet cell hyperplasia
changes result in airflow obstruction and reduced lung function
224
COPD pathophysiology - alveolar destruction
emphysematous changes involve: alveolar wall destruction, leading to formation of larger, less efficient airspaces and a reduction in SA available for gas exchange
225
COPD features
cough - often productive
dyspnoea
wheeze
in severe cases, RHF may develop, results in peripheral oedema
226
COPD investigations
spirometry
CXR- hyperinflation, bullae, alt. diagnoses
bloods - polycythaemia (chronic hypoxaemia)
BMI
226
What confirms a COPD diagnosis?
post-bronchodilator FEV1:FVC <0.7
227
How is COPD categorised?
FEV1:
>80% = S1,mild
50-79% = S2, moderate
30-49% = S3, severe
<30% = S4, v. severe
228
COPD general management
smoking cessation advice
annual influenza vaccination
one-off pneumococcal vaccination
pulmonary rehab to those functionally disabled by COPD
229
NICE criteria to determine if pt has asthmatic / steroid responsive features
- any previous diagnosis of asthma or atopy
- higher eosinophil count
- substantial (>400ml) variation in FEV1 over time
- substantial (>20%) diurnal variation in peak expiratory flow
230
COPD bronchodilator therapy
SABA or SAMA
for pts who remain breathless or have exacerbations despite SA bronchodilators, decide if pt has 'asthmatic features/features suggesting steroid responsiveness'
231
COPD management if no asthmatic features
+ LABA and LAMA
232
COPD management if asthmatic features
LABA + ICS
if pt remains breathless or have exacerbations - triple therapy eg LAMA + LABA + ICS
use combined inhalers where possible
233
COPD oral theophylline
only recommended after trials of long and short-acting bronchodilators or ppl who can't use inhaled therapy
234
COPD prophylactic abx therapy
azithromycin prophylaxis
shouldn't smoke, have optimised standard treatment and continue to have exacerbations
235
What should be considered in pts w/ chronic productive cough in COPD?
mucolytics
- N-acetylcysteine, carbocysteine
236
Phosphodiesterase-4 inhibitors in COPD
eg roflumilast
reduce risk of COPD exacerbations in pts w/ severe COPD and hx of frequent exacerbations
237
What is cor pulmonale?
RV enlargement / failure due to lung disease
peripheral oedema, raised jugular venous pressure, systolic parasternal heave, loud P2
use loop diuretic for oedema, consider long-term O2 therapy
238
Signs pt should be offered long term oxygen therapy
pO2 <7.3 kPa or pO2 7.3 - 8 kPa +...
- secondary polycythaemia
- peripheral oedema
pulmonary HTN
239
What is long term oxygen therapy?
pt breathes supplementary oxygen for at least 15hrs a day
oxygen concentrators used to provide fixed supply
240
COPD respiratory complications
pneumonia
acute exacerbations
hypoxia
hypercapnia
241
COPD CV complications
pulmonary HTN
cor pulmonale
IHD and arrhythmias
242
COPD MSK and metabolic complications
osteoporosis
weight loss and malnutrition
243
COPD mental health complications
anxiety and depression
244
Causes of COPD exacerbation
- bacterial infection (streptococcus pneumoniae, H.influenzae)
- viral infection (rhinovirus, influenza, parainfluenza, covid)
- air pollution
- allergens
- medication non-compliance
- pulmonary embolism
245
COPD exacerbation pathophysiology
Increased inflammation, mucosal oedema and bronchospasm further limit expiratory flow
Gas trapping worsens, increasing ventilation-perfusion mismatch
Resulting hypoxia and hypercapnia trigger neural drive, increasing ventilation
Resp muscles fatigue, leads to 'neuromechanical decoupling' that reduces ventilatory drive
Existing cardiac dysfunction worsens due to increasing pulmonary vasc resistance
246
Signs of COPD exacerbation on physical exam
- increased resp effort - tachpnoea, nasal flaring, use of accessory muscles, paradoxical chest wall movement
- tachycardia
- reduced breath sounds
- prolonged expiratory phase w/ wheezing
- crackles - could indicate infective component
247
COPD exacerbation investigations
pulse oximetry - sats
CXR - exclude causes
ABG
FBC
sputum culture
248
COPD exacerbation differentials
pneumonia
pulmonary embolism
pulmonary oedema
249
COPD exacerbation
1. resp support
2. pharmacological management: bronchodilation (SABA or SAMA via inhaler or nebs), corticosteroids (oral pred x5d), abx
3. optimise pt for discharge
4. prevention of exacerbations
250
What is conjunctivitis?
infective (pink eye) or allergic
inflammation of conjunctiva, thin transparent membrane that covers sclera and lines inner surface of eyelids
251
Conjunctivitis bacterial causes
staphylococcus aureus
streptococcus pneumoniae
haemophilus influenzae
moraxella catarrhalis
252
Conjunctivitis common causative viruses
adenovirus
herpes simplex
varicella zoster
enterovirus
253
Fungal and parasitic conjunctivitis causes
candida spp
aspergillus spp
fusarium spp
parasitic = acanthamoeba spp.
254
Bacterial v viral conjunctivitis
bacterial = purulent discharge, eyes may be 'stuck together' in the morning
viral = serous discharge, recent URTI, preauricular lymph nodes
255
Infective conjunctivitis Hx
acute onset of symptoms, typically unilateral but may become bilateral w/in 24-48hrs
recent exposure to infected individual, swimming in contaminated water, or contact lens use
presence of comorbidities eg URTI or atopy
256
Infective conjunctivitis symptoms
ocular discomfort, itching, burning sensation
foreign body sensation or grittiness in affected eye
photophobia (viral)
discharge
257
Infective conjunctivitis signs
conjunctival infection and chemosis
eyelid swelling and erythema
palpable preauricular lymphadenopathy
subconjunctival haemorrhage (adenoviral)
258
Infective conjunctivitis management
normally self-limiting - resolves w/in 1-2wks
topical abx therapy offered eg chloramphenicol (2-3drops hrs, or ointment qds)
topical fusidic acid for pregnant women
no contact lens during
don't share towels
don't need to stay off school
259
Allergic conjunctivitis pathophysiology
T1 hypersensitivity reaction
initial exposure = sensitisation of mast cells, which upon re-exposure, release inflammatory mediators (histamine, prostaglandins, leukotrines)
cause vasodilation, increased vasc permeability, and recruitment of eosinophils, results in manifestation
260
Allergic conjunctivitis presentation
bilateral ocular itching and redness
watery or stringy, muscoid discharge
conjunctival chemosis and hyperemia
eyelid oedema and erythema
tearing and photophobia
261
Allergic conjunctivitis management
allergen avoidance
basic eye care - avoid rubbing eyes, cool compress
Pharmacotherapy:
- topical antihistamines eg olopatadine, ketotifen
- topical mast cell stabilisers eg sodium cromoglicate
- topical corticosteroids (severe cases)
allergen specific immunotherapy considered in cases that are unresponsive to conventional treatment
262
Constipation definition
defecation that is unsatisfactory because of infrequent stools (<3 times wkly), difficult stool passage (straining or discomfort) or seemingly incomplete defecation
263
Causes of constipation
functional
medication-induced
IBS-C
colorectal cancer
hypothyroidism
264
Constipation complications
overflow diarrhoea
acute urinary retention
haemorrhoids
265
Constipation differential
IBS
constipation
hypothyroidism
paralytic ileus
small bowel obstruction
primary hyperparathyroidism
large bowel obstruction
urogenital prolapse
cow's milk protein intolerance / allergy
266
Symptoms associated w/ constipation
infrequent bowel movements
hard or lumpy stools
difficulty passing stools
sensation or incomplete evacuation after bowel movement
bloating or abdo discomfort
267
Constipation clinical examination
thorough abdo examination - distension, tenderness, palpable masses, percussion
DRE - tone of anal sphincter, rectal masses, stool consistency and volume
anorectal manometry - if defecatory disorders are suspected
268
Constipation further investigations
bloods - anaemia, coeliac, TFT
stool tests - faecal calprotectin
imaging - masses
269
Constipation differentials
IBS
scleroderma
amyloidosis
parkinson's
multiple sclerosis
Hirschsprung's
anal fissure
rectal prolapse
hypothyroidism
opioid use
269
Constipation management
lifestyle modifications - regular activity, proper toilet habits
diet - high fibre, adequate fluid
pharmacological - bulk forming laxatives, osmotic laxatives, stimulant laxatives
follow up
270
Irritant contact dermatitis
results from exposure to substances that cause direct damage to skin. Irritants strip skin of natural oils, leading to dryness, itching and inflammation
commonly detergents, soaps, cleaning products, solvents
low humidity can exacerbate
271
Allergic contact dermatitis
allergic response ensues following sensitisation to allergen. Upon re-exposure, a delayed-type hypersensitivity reaction occurs
RF = previous sensitisation to allergen and genetic predisposition
commonly: nickel, fragrances, rubber accelerators, preservatives in personal care products
272
Mixed contact dermatitis
features of both ICD and ACD
occurs when pt w/ pre-existing ACD are exposed to irritants
273
Irritant contact dermatitis pathophysiology
- irritant breaches stratum corneum (outermost skin layer). Disruption leads to keratinocyte damage, triggering cascade of inflammatory responses
- keratinocytes, upon damage, release pro-inflammatory cytokines (IL-1a), TNF-a and IL18. These recruit neutrophils and monocytes to inflammation site
- simultaneously, damaged keratinocytes also produce chemokines eg IL-8 and MIP-3a to enhance leukocyte infiltration
- additional mediators = MMPs, AMPs and NGF
273
Allergic contact dermatitis pathophysiology
- T4 hypersensitivity reaction, sensitisation essential initially. Haptens penetrate through skin barrier and conjugate w/ proteins to form complete antigens
- Langerhans cells or dendritic cells capture these haptens, migrate to regional lymph nodes, where they present them to naive T cells. Clonal expansion of hapten-specific T cells
- upon re-exposure, memory T cells recognise antigen and release cytokines (IFN-γ, TNF-α, IL-2)
- simultaneously, chemokines released by activated by T cells recruit more inflammatory cells to inflammation site
274
Contact dermatitis subtypes
Phototoxic and photoallergic- skin in contact w/ certain substances, then exposed to sunlight
Systemic - person already sensitised to allergen then comes into systemic contact (ingestion or inhalation)
Pigmented - substance exposure causes hyperpigmentation of skin
275
Contact dermatitis presentation
Acute Phase:
- erythema
- vesicles and bullae
- oedema
- pruritus
Chronic Phase:
- lichenification
- fissuring
- hypopigmentation / hyperpigmentation
276
Contact dermatitis investigations
patch testing
skin biopsy
lab tests
referral
277
Contact dermatitis differentials
atopic dermatitis
psoriasis
seborrheic dermatitis
278
Contact dermatitis management
ID and avoidance of offending agent
symptomatic treatment - topical corticosteroids, emolients
patient education
refer to derm
follow up
279
What is gout?
rapid onset crystal induced arthritis
most common inflammatory arthritis
typically affects MTP of toe
279
Contact dermatitis complications
2ndry infections: cellulitis, impetigo
lichenification
hypo/hyperpigmentation
anxiety and depression
allergic contact dermatitis
280
Gout causes
genetic predisposition
diet - purine-rich and high-fructose beverages
metabolic syndrome
renal function
medications - thiazide diuretics, low-dose aspirin, certain anti-tuberculosis meds
281
Gout pathophysiology
hyperuricaemia - when uric acid lvls exceed solubility limit in plasma, monosodium urate crystals may form
MSU formation - in joints and soft tissues, particularly cooler peripheral joints eg 1st MTP
Inflammatory response - crystals trigger, neutrophils recruited and phagocytose crystals. Leads to mediators release (IL-1β, TNF-a) and reactive oxygen species, causing symptoms
282
Chronic gout pathophysiology
repeated acute episodes can lead to chronic gouty arthritis, characterised by tophi formation, joint damage and chronic pain
tophi = nodules of MSU crystals surrounded by chronic inflammatory reaction, can develop in soft tissues, cartilage and bones
283
Gout presentation
acute monoarthritis - most commonly first MTPJ
typically abrupt, occurring over few hrs - severe pain, redness, swelling and tenderness
asymptomatic hyperuricaemia
acute polyarticular gout
tophaceous gout
gouty nephropathy
284
Gout investigations
clinical features and pt hx
synovial fluid fine needle aspiration
285
Gout synovial fluid analysis
-vely birefringent
needle shaped
monosodium urate crystals
286
Gout differentials
psuedogout
septic arthritis
287
Gout management
NSAIDs or colchicine (if CE: prednisolone)
lifestyle advice
serum urate-lowering therapy - allopurinol, delayed until inflammation has settled
288
When is urate lowering therapy advised for gout?
>= 2 attacks in 12m
tophi
renal disease
uric acid renal stones
prophylaxis if on cytotoxics or diuretics
289
How does colchicine treat gout?
inhibits microtubule polymerisation by binding to tubulin, interfering w/ mitosis. Inhibits neutrophil motility and activity
slower action onset
used w/ caution in renal impairment
SE: diarrhoea
290
Gout lifestyle modifications
reduce alcohol intake and avoid during acute attack
lose weight if obese
avoid foods high in purines eg liver, kidneys, seafood, oily fish and yeast products
consideration to stopping precipitating drugs (eg thiazides)
increase vitC intake
291
Gout complications
tophi - chronic gout
degenerative arthritis, osteoporosis
kidney stones (RF and complication)
mental health conditions
292
What is pseudogout?
form of microcrystal synovitis
caused by calcium pyrophosphate dihydrate crystals deposition in synovium
also known as calcium pyrophosphate crystal deposition disease (CPPD)
293
Pseudogout risk factors
haemochromastosis
hyperparathyroidism
acromegaly
low magnesium, low phosphate
Wilson's disease
294
Where does pseudogout usually effect?
knee, wrist and shoulder most commonly
295
Pseudogout joint aspiration
weakly +vely birefringent rhomboid-shaped crystals
296
Pseudogout x-ray
chrondrocalcinosis
seen in knee as linear calcifications of meniscus and articular cartilage
297
Pseudogout management
aspiration of joint fluid (exclude septic arthritis)
NSAIDs or intra-articular, IM or oral steroids as for gout
298
What are cutaneous warts?
verrucae
benign epithelial proliferations caused by HPV infection
299
Cutaneous warts risk factors
age - children and young adults
immune status - impaired
skin integrity
contact w/ infected individuals
environmental factors - pools, communal showers
300
What virus is associated with cutaneous warts?
HPV 1, 2, 4, 27 and 57
301
Cutaneous warts pathophyisology
- HPV enters keratinocytes
- virus replication, viral proteins bind and degrade tumour suppressor proteins, leads to unchecked cellular proliferation and survival - results in epithelial hyperplasia
- HPV can establish latency w/in basal cells at low copy number, minimal gene expression and allows evasion from host immune response
- HPVs can evade immune detections through lack or viraemia, absence of cell death and minimal inflammation, but once effective cell-mediated response is mounted, warts may regress
- physical wart forms due to HPV-induced hyperproliferation and aberrant differentiation of keratinocytes leading to acanthosis, papillomatosis and hyperkeratosis
302
Cutaneous warts classification
Common warts - firm, hyperkeratotic papules or nodules w/ roughened surface
Flat warts - small, smooth, flat-topped paplues
Filiform - thread-like or finger-like, around lips and eyelids
Plantar - soles of feet or weight-bearing, flat appearance w/ central black specks
Mosaic - plantar coalesce together
Anogenital - range from small, smooth papules to large cauliflower-like masses
303
Cutaneous warts presentation
small, firm bumps on skin w/ rough surface resembling cauliflower
most commonly hands, feet and face
Review:
location, morphology, symptoms, number and distribution
304
Cutaneous warts investigations
dermoscopy
biopsy
viral typing
305
Dermoscopic features suggestive of viral warts
- blackish dots or globules - thrombosed capillaries
- white halo surrounding wart - hyperkeratosis and acanthosis
- papillary strutures w/ red or pink seen in plane warts
306
Cutaneous warts differentials
molluscum contagiosum
corns and calluses
squamous cell carcinoma
306
307
Cutaneous warts management
tend to resolve spontaneously
topical treatments - salicylic acid
cryotherapy, surgical excision or laser therapy
immunotherapy
treatment review
308
Cutaneous warts complications
2ndry bacterial infections
spread of virus
autoinoculation
malignant transformation
pain and discomfort
cosmetic concerns and psych distress
