GP part 1 Flashcards
what is bronchitis
this is when the trachea and bronchi become inflamed, swell and fill with mucus causing a chough
what is acute bronchitis
this is usually caused by a viral infection and lasts a few weeks
- most people wont need treatment
what is chronic bronchitis
if someone has a cough with mucus for most days of the month, for three months out of the year. This goes on for at least two years
who is at higher risk of developing bronchitis
smokers
asthma, COPD or other breathing conditions
GORD
autoimmune disorders
around a high level of air pollutants
what are the symptoms of bronchitis
persistent cough that lasts one to three weeks
may bring up mucus
dyspnoea
fever
runny nose
fatigue
what causes bronchitis
Viruses - Influenza, respiratory syncytial virus, adenovirus, rhinovirus, coronavirus
bacteria- Bordetella pertussis, Mycoplasma pneumonia, chlarmydia pneumonia
pollution
smoke
how is bronchitis diagnosed
clinical diagnosis
respiratory examination
nasal swab
chest X ray of more chronic
bloods
sputum sample
pulmonary function tests
how is bronchitis treated
acute bronchitis treatment is managing the symptoms such as over the counter analgesics and rest. Humidifier may hlep
may be prescribed:
anti-viral
bronchodilators
anti-inflammatory - corticosteroids
cough suppressants - dextromethorphan and benzonatate
antibiotics if bacterial infection is suspected
what is anaemia
it is defined as a low concentration of haemoglobin in the blood
what are the normal ranges of haemaglobin in
1. women
2. men
- 120-165g/L
- 130-180g/L
what is the normal MCV range in
1. women
2. men
- 80-100 femtoliters
- 80-100 femtoliters
what are the three categories anaemia is divided into
- microcytic anaemia
- normocytic anaemia
- macrocytic anaemia
what are the causes of microcytic anaemia
TAILS
Thalassaemia
Anaemia of chronic disease
Iron deficiency anaemia
Lead poisoning
Sideroblastic anaemia
what is a common cause of anaemia of chronic disease
Chronic kidney disease - reduced production of erythropoietin by the kidneys, the hormone responsible for stimulating red blood cell production. Treatment is with erythropoietin.
what are the causes of normocytic anaemia
3 As and 2 Hs
Acute blood loss
Anaemia of chronic disease
Aplastic anaemia
Haemolytic anaemia
Hypothyroidism
what are the two types of macrocytic anaemia
Megaloblastic or normoblastic
what is the cause of megaloblastic macrocytic anaemia
it is due to impaired DNA synthesis which prevents cells from dividing normally. Rather than dividing the cells grow into large abnormal cells
what are the causes of megaloblastic anaemi
B12 deficiency
Folate deficiency
what are the causes of normoblastic macrocytic anaemia
Alcohol
Reticulocytosis (normally from haemolytic anaemia or blood loss)
hypothyroidism
liver disease
drugs such as azathioprine
what is reticulocytosis
increased concentration of reticulocytes (immature red blood cells). This happens when there is a rapid turnover of red blood cells, such as with haemolytic anaemia or blood loss.
what are generic symptoms of anaemia
Tiredness
Shortness of breath
Headaches
Dizziness
Palpitations
Worsening of other conditions, such as angina, heart failure or peripheral arterial disease
what are some specific symptoms of iron deficiency anaemia
Pica
hair loss
what are generic signs of anaemia
pale skin
conjunctival pallor
tachycardia
raised respiratory rate
what are specific signs of iron deficiency anaemia
Koilonychia - spoon shaped nails
angular cheilitis
atrophic glossitis - smooth tongue
brittle hair and nails
what are specific signs of haemolytic anaemia
jaundice
what are specific signs of thalassaemia
bone deformities
what signs can indicate chronic kidney disease
oedema
hypertension
excoriations on the skin
what investigations should be done in someone with symptoms of anaemia
Full blood count for haemoglobin and mean cell volume
Reticulocyte count (indicates red blood cell production)
Blood film for abnormal cells and inclusions
Renal profile for chronic kidney disease
Liver function tests for liver disease and bilirubin (raised in haemolysis)
Ferritin (iron)
B12 and folate
Intrinsic factor antibodies for pernicious anaemia
Thyroid function tests for hypothyroidism
Coeliac disease serology (e.g., anti-tissue transglutaminase antibodies)
Myeloma screening (e.g., serum protein electrophoresis)
Haemoglobin electrophoresis for thalassaemia and sickle cell disease
Direct Coombs test for autoimmune haemolytic anaemia
Colonoscopy and OGD in unexplained iron deficiency anaemia
Bone marrow biopsy
what are causes of iron deficiency anaemia
insufficient dietary iron
reduced iron absorption
increased iron requirements - pregnancy
loss of iron through bleeding - cancer/ulcer
what is the most common cause of iron deficiency in adults
blood loss
- menstruation
- cancer
- oesophagitis or gastritis
- peptic ulcers
- inflammatory bowel disease
- angiodysplasia
what is the most common cause of iron deficiency anaemia in children
dietary insufficiency
what medications can interferes with iron absorption
anything that reduces stomach acid
- PPIs
where is iron absorbed
duodenum and jejunum
what can cause raised ferritin
inflammation
liver disease
iron supplements
haemochromotosis
how does iron travel round the body
travels round the blood bound to the carrier protein transferrin. the total iron binding capacity is the space for the iron to attach to on all the transferring molecules combined and is therefore directly related to how much transferrin is in the blood.
what is the equation for working out transferrin saturation
serum iron/total iron binding capacity
what is ferritin
it is a protein that stores iron inside cells
it is an acute phase protein released with inflammation
what is the transferrin saturation
this indicates the total iron in the body
what can cause iron overload in the body
haemochromotosis
iron supplements
acute liver damage
what is the management for iron deficiency anaemia
new iron deficiency in adulthood without a clear cause should be investigated further: colonoscopy and OCD
- oral iron (ferrous sulphate or ferrous fumarate)
- iron infusion (IV CosmoFer)
- blood transfusion in severe anemia
what are common side effects of oral iron
black stools
constipation
what are risks that come with iron infusion
allergic reactions
anaphylaxis
should be avoided in infections as there is a potential for it to feed bacteria
what are key causes of B12 deficiency
pernicious anaemia
insufficient dietary B12
medications that reduce absorption (PPI and metformin )
what is pernicious anaemia
Pernicious anaemia is an autoimmune condition involving antibodies against the parietal cells or intrinsic factor.
what is the pathophysiology of pernicious anaemia
The parietal cells of the stomach produce a protein called intrinsic factor. Intrinsic factor is essential for the absorption of vitamin B12 in the distal ileum. In pernicious anaemia, autoantibodies target either the parietal cells or intrinsic factor, resulting in a lack of intrinsic factor and a lack of absorption of vitamin B12.
what neurological symptoms can Vitamin B12 deficiency lead to
Peripheral neuropathy, with numbness or paraesthesia (pins and needles)
Loss of vibration sense
Loss of proprioception
Visual changes
Mood and cognitive changes
what antibodies are used to diagnose pernicious anaemia
Intrinsic factor antibodies - first line
Gastric parietal cell antibodies
what is the management of pernicious anaemia
IM hydroxocobalamin injections are initially given to all patients with B12 deficiency, depending on symptoms
- with neurological sx: alternate days until there is no further improvement in the symptoms
- without neurological sx: 3 times weekly for two weeks
and then maintenance
what is the maintenance therapy for B12 deficiency
pernicious anaemia: 2-3 monthly injections for life
diet related - oral cyanocobalamin or twice yearly injections
what do you treat first if a patient has both B12 and folate deficiency
the B12 deficiency
why do you treat B12 deficiency before folate deficiency
giving patients folic acid when they have a B12 deficiency can lead to subacute combined degeneration of the cord, with demyelination in the spinal cord and severe neurological problems
what is haemolytic anaemia
this is anaemia caused by the destruction of red blood cells, resulting in a low haemoglobin concentration
what inherited conditions can cause chronic haemolytic anaemia
hereditary spherocytosis
hereditary elliptocytosis
thalassaemia
sickle cell anaemia
G6DP deficiency
what acquired conditions can lead to the destruction of red blood cells
autoimmune haemolytic anaemia
alloimmune haemolytic anaemia (transfusion reactions and haemolytic disease of the newborn)
paroxysmal nocturnal haemoglobinuria
microangiopathic haemolytic anaemia
prosthetic valve related haemolysis
what are features of haemolytic anaemia
anaemia
splenomegaly - filled with destroyed red blood cells
jaundice
what investigations should be done for someone with suspected haemolytic anaemia
full blood count - normocytic anaemia
blood film - schistocytes
direct coombs test is positive in autoimmune haemolytic anaemia
what is the most common inherited haemolytic anameia in northern europeans
hereditary spherocytosis
what is the inheritance pattern of hereditary spherocytosis
autosomal dominant
what is hereditary spherocytosis
a genetic condition which causes fragile, sphere shaped red blood cells that easily break down when passing through the spleen
what is the presentation of hereditary spherocytosis
anaemia
jaundice
gallstones
splenomegaly
aplastic crisis in the presence of parvovirus
what are key findings of herediraty spherocytosis
raised mean corpuscular haemoglobin concentration on a full blood count
raised reticulocyte count
spherocytes on a blood film
what is the treatment of hereditary spherocytosis
folate supplementation
blood transfusions when required
splenectomy
cholecystectomy if gallstones become a problem
what is G6DP deficiency
this is caused by a defect in the gene coding for glucose 6 phosphate dehydrogenase, which is responsible for protecting the cells from oxidative damage
how is G6PD deficiency inherited
in an X linked recessive pattern
in what groups of people is G6PD deficiency more common in
mediterranean, asian and african patients
how does G6PD deficiency cause haemolytic anaemia
causes acute episodes which is triggered by infections, drugs or fava beans. This is due to an increase in ROS
what are key medications that can cause acute episodes of haemolytic anaemia in G6PD deficiency
ciprofloxacin
sulfonylureas
sulfasalazine
how does G6PD deficiency present
jaundice
gallstones
anaemia
splenomegaly
what is seen on a blood film in someone with G6PD deficiency
Heinz bodies
what is autoimmune haemolytic anaemia
this is when there is antibodies created against the patients own red blood cells leading to red blood cell destruction
what are the two types of autoimmune haemolytic anaemia
warm and cool - based on what temperature at which the auto-antibodies destroy the red blood cells
what is warm autoimmune haemolytic anaemia
haemolysis occurs at normal or above normal temperatures - usually idiopathic
what is cold reactive autoimmune haemolytic anaemia
called cold agglutinin disease - at lower temperatures (less than 10 degrees) the antibodies attach to the red blood cells causing agglutination. The immune system is activated and the red blood cells are destroyed
what can cold autoimmune haemolytic anaemia be secondary to
lymphoma
leukaemia
SLE
infections - mycoplasma, EBV, CMV, HIV
what is the management of autoimmune haemolytic anaemia
blood transfusions
prednisolone
rituximab
splenectomy
what is alloimmune haemolytic anaemia
this occurs due to foreign red blood cells or foreign antibodies
what are the two scenarios where alloimmune haemolytic anaemia occurs
transfusions reactions
haemolytic disease of the newborn
what is paroxysmal nocturnal haemoglobinuria
caused by a specific genetic mutation in the haematopoietic stem cells in the bone marrow which occurs during the patients lifetime.
The mutation results in a loss of the proteins on the surface of red blood cells than inhibit the complement cascade, allowing the activation of the complement cascade on red blood cells and their destruction
what is the characteristic presenting feature of paroxysmal nocturnal haemoglobinuria
red urine in the morning - contains haemoglobin and haemosiderin
anaemia
thrombosis
smooth muscle dystonia
what is the management of paroxysmal nocturnal haemoglobinuria
eculizumab - monoclonal antibody which targets complement component C5
bone marrow transplant
what is microangiopathic haemolytic anaemia
it involves destruction of red blood cells as they travel through the circulation
this most often is caused by abnormal activation of the clotting system, with thrombi partially obstructing small vessels
these obstructions churn the red blood cells causing haemolysis
what causes microangiopathic haemolytic anaemia
it is normally secondary to an underlying condition such as:
haemolytic uraemic syndrome
disseminated intravascular coagulation
thrombotic thrombocytopenic purpura
SLE
cancer
what is a key blood film finding of someone with microangiopathic haemolytic anaemia
schistocytes
what is prosthetic valve haemolysis
it is a key complication of prosthetic hear valves, which can occur in both bioprosthetic and metallic valve replacement
what causes prosthetic valve haemolysis
caused by turbulent flow around the valve and the shearing of the red blood cells, the valve churns up the cells and they break down
what is the management of prosthetic valve haemolysis
monitoring
oral iron and folic acid supplementation
blood transfusions if severe
revision surgery may be required in severe cases
what is the pathophysiology of sickle cell anaemia
During fetal development, at around 32-36 weeks gestation, fetal haemoglobin (HbF) production decreases, and adult haemoglobin (HbA) increases. There is a gradual transition from HbF to HbA. At birth, around half the haemoglobin is HbF, and half is HbA. By six months of age, very little HbF is produced, and red blood cells contain almost entirely HbA.
Patients with sickle-cell disease have an abnormal variant called haemoglobin S (HbS). HbS results in sickle-shaped red blood cells
what is the inheritance pattern on sickle cell anaemia
autosomal recessive
what chromosome is affected in sickle cell anaemia
chromosome 11
when is sickle cell anaemia screened for in the UK
it is tested as part of the newborn blood spot screening test at around 5 days of age
what are complications of sickle cell anaemia
Anaemia
Increased risk of infection
Chronic kidney disease
Sickle cell crises
Acute chest syndrome
Stroke
Avascular necrosis in large joints such as the hip
Pulmonary hypertension
Gallstones
Priapism (painful and persistent penile erections)
what is a sickle cell crisis
it refers to a spectrum of acute exacerbations caused by sickle cell disease
what can trigger a sickle cell crisis
dehydration
infection
stress
cold weather
how is sickle cell crisis managed
low threshold for hospital admission
treating infections that may have triggered the crisis
keeping them warm
good hydration with IV fluids
analgesia (avoid NDAIDs where there is renal involvement)
what is a vaso-occlusive crisis
this is also known as a painful crisis and is caused by sickle shaped red blood cells clogging capillaries causing distal ischaemia
how does vaso-occlusive crisis present
pain and swelling in the hands or feet
can affect the chest, back
associated with a fever
can cause priapism in men - urological emergency
what is a splenic sequestration crisis
this is caused by red blood cells blocking blood flow within the spleen and causes an acutely enlarged and painful spleen, which can lead to aaemia and hypovolaemic shock due to blood pooling in the spleen
what is the management of splenic crisis
emergency - ABCDE
blood transfusions
fluid resuscitation
what is aplastic crisis
this is a temporary absence in the creation of new red blood cells and it is normally triggered by infection with parvovirus B19
what is acute chest syndrome
this occurs when the vessels supplying the lungs become clogged with red blood cells
can be triggered by fat embolism or infection
how does acute chest syndrome present
fever
shortness of breath
chest pain
cough
hypoxia
what will a chest X ray show in acute chest syndrome
pulmonary infiltrates
what is the management of acute chest syndrome
medical emergency - treatment of underlying cause
Analgesia
Good hydration (IV fluids may be required)
Antibiotics or antivirals for infection
Blood transfusions for anaemia
Incentive spirometry using a machine that encourages effective and deep breathing
Respiratory support with oxygen, non-invasive ventilation or mechanical ventilation
what are the general management principals for sickle cell disease
Avoid triggers for crises, such as dehydration
Up-to-date vaccinations
Antibiotic prophylaxis to protect against infection, typically with penicillin V (phenoxymethylpenicillin)
Hydroxycarbamide (stimulates HbF)
Crizanlizumab
Blood transfusions for severe anaemia
Bone marrow transplant can be curative
what is hydroxycarbamide
it is a drug which works by stimulating the production of fetal haemoglobin which doesnt lead to the sickling of red blood cells unline HbS
what is crizanlizumab
it is a monoclonal antibody that targets P selectin, which is an adhesion molecule found on endothelial cells on the inside walls of blood vessels and platelets
it prevents red blood cells from sticking to blood vessel walls and reduces the frequency of vaso-occlusive crisis
what is acute stress reaction/disorder
this is a stress response that can happen within a month of experiencing a traumatic event
what are symptoms of an acute stress reaction
Anxiety.
Intense fear or helplessness.
Experiencing flashbacks or nightmares.
Feeling numb or detached from one’s body.
Avoiding situations, places or other reminders related to the traumatic event.
what are examples of events which may lead to an acute stress reaction
Natural disasters, such as a tornado, fire or flood.
Sexual assault.
Physical assault.
Verbal abuse.
Witnessing bodily harm or death.
Serious accidents, such as a car accident.
Experiencing a severe injury or sudden illness.
War.
what is the difference between acute stress reaction and PTSD
the main difference is the length of the symptoms
- acute stress reaction involves stress reactions that happen three days - 4 weeks after a traumatic event
- stress reactions lasting longer than four weeks may meet the criteria for PTSD
what is adjustment disorder
this is a mental health condition that happens in response to a stressful life event. the emotional and behavioural symptoms are generally considered more intense that what would be expected for the type of event that occurred
what is the difference between an acute stress reaction and adjustment disorder
the stressful event that happens in adjustment disorder is typically less traumatic than an event that causes acute stress reaction
what are the symptoms of acute stress reaction
Recurring, uncontrollable and distressing memories of the event.
Recurring nightmares.
Flashbacks of the traumatic event.
Intense psychologic or physical distress when you’re reminded of the event.
Persistent difficulty feeling positive emotions, such as happiness, contentment or loving feelings.
An altered sense of reality, like feeling you’re in a daze or as if time is passing in slow motion.
Memory loss regarding important aspects of the traumatic event.
Efforts to avoid distressing memories, thoughts or feelings associated with the event.
Efforts to avoid external reminders associated with the event (people, places or things).
Disturbed sleep.
Irritability or anger outbursts.
Excessive attention to the possibility of danger (hypervigilance).
Difficulty concentrating.
An exaggerated response to loud noises, sudden movements or other stimuli (startle reflex).
what are risk factors for acute stress reaction
history of prior mental health conditions
catastrophic worry
avoidant coping style
minimal support system
how is acute stress reaction diagnosed
clinical diagnosis = DSM-5
how is acute stress reaction treated
psychotherapy - CBT
exposure therapy
may offer SSRI/SNRI
what is an anal fissure
it is a crack or tear in the lining of your anal canal
what are causes of anal fissure
chronic constipation and straining
obstructed defecation syndrome
infant dyschezia
chronic diarrhoea
childbirth
penetration
what are symptoms of an anal fissure
sharp pain when defecating
burning or itching with defecating
fresh blood in stool
anal muscle spasms
lump on the skin near the tear
rectal itching
what are possible contributing factors to the development of anal fissures
prior surgery
STIs
IBD
anal cancer
TB
diaper rash
what are possible complications of anal fissures
occur when they dont heal properly - chronic anal fissures
if they continue to go unhealed they can lead to fecal impaction, anal stenosis due to narrowing of anal canal, and anal fistula
how are anal fissures diagnosed
clinical diagnosis plus examination
DRE
how are anal fissures treated
most go away on their own - self help such as increasing fibre, avoiding dehydration, soaking
cream - lidocaine
glyceryl trinitrate ointment - cream which can help to restore blood flow and relax the anal sphincter
calcium channel blockers
botox - last resort
laxatives - bulk forming to help soften stool
surgery with chronic anal fissures that dont respond to medications - internal sphincterotomy
how would a patient with anaphylaxis present
urticaria
itching
angio-oedema with swelling of the eyes and lips
abdominal pain
shortness of breath
wheeze
swelling of the larynx
tachycardia
lightheadedness
collapse
what are the principals of airway management
ABCDE
IM adrenaline - repeated after 5 minutes if necessary
antihistamines can be given
steroids can be given
what blood test can be used to confirm anaphylaxis
it can be confirmed by measuring the serum mast cell tryptase within 6 hours of the event
what are indications that someone may need an adrenaline auto-injector
given to all children and adolescents with anaphylactic reactions
may be given to children with generalised allergic reactions with certain risk factors:
asthma requiring inhaled corticosteroids
poor access to medical treatment
nut or insect sting allergies
significant co-morbidities
how do you use an adrenaline auto-injector
- prepare the devise - remove the safety cap on the non needle end
- grip the device with needle end pointing down
- administer the injection by firmly jabbing the device into the outer portion of the mid thigh until the device clicks
- remove the device and gently massage the area for 10 seconds
- phone an ambulance
what is narrow complex tachycardia
tis refers to a fast hear rate with a QRS complex duration of less than 0.12 seconds (three small squares on ECG)
what are the four main differentials for a narrow complex tachycardia
sinus tachycardia
supraventricular tachycardia
atrial fibrillation
atrial flutter
what does supraventricular tachycardia look like on ECG
looks like QRS immediately followed by a T wave, then a QRS, then a T wave etc
- there are P waves but they are buried in the T waves
- no saw tooth pattern
how is supraventricular tachycardia treated
vagal manoeuvers
adenosine
what does atrial fibrillation look like on ECG
absent P waves
irregularly irregular ventricular rhythm
how is atrial fibrillation treated
rate control/rhythm control
what does atrial flutter look like on ECG
atrial rate is normally around 300 bpm
saw tooth pattern
QRS at regular intervals
what is broad complex tachycardia
this refers to a fast heart rate with a QRS complex duration or more than 0.12 seconds/3 small squares on an ECG
what are the types of broad complex tachycardia
ventricular tachycardia/unclear cause
polymorphic ventricular tachycardia such as torsades de pointes
atrial fibrillation with bundle branch block
supraventricular tachycardia with bundle branch block
how is ventricular tachycardia treated
IV amiodarone
how is polymorphic ventricular tachycardia treated
IV magnesium
what causes atrial flutter
a re-entrant rhythm in either atrium, causing the electrical signal to re-circulate in a self perpetuating loop due to an extra electrical pathway in the atria
what can offer a permanent solution to atrial flutter
radiofrequency ablation
when is a QT interval considered prolonged
when its more than 440 milliseconds in men
more than 460 milliseconds in women
what does a prolonged QT interval represent
prolonged repolarisation of the heart muscle cells after contraction
what is at risk of developing when there is prolonged repolarisation
waiting for a long time for repolarisation can result in spontaneous depolarisation in some muscle cells. These abnormal spontaneous depolarisations before repolarisation are known as afterdepolarisations.
These spread throughout the ventricles causing a contraction before proper repolarisation, which is also known as torsades de pointes
what are causes of prolonged QT
long QT syndrome
medications such as antipsychotics, citalopram, flecainide, sotalol, amiodarone and macrolide antibiotics
electrolytic imbalances such as hypokalaemia, hypomagsesaemia and hypocalcaemia
what is the management of a prolonged QT interval
stopping and avoiding medications that prolong the QT interval
correcting electrolyte imbalances
beta blockers (NOT SOTALOL)
pacemakers or implantable defibs
what is acute management of torsades de pointes
correcting the underlying issue
magnesium infusion
defibrillation
what are ventricular ectopics
these are premature ventricular beats caused by random electrical discharges outside the atria
how do you manage ventricular ectopics
reassurance and no treatment in otherwise healthy people with infrequent ectopics
specialist advice in those with underlying heart disease, frequent or concerning symptoms
beta blockers are sometimes used
what is first degree heart block
this is when there is a delay in conduction through the atrioventricular node
despite this every atrial impulse leads to a ventricular contraction - every P wave is followed by a QRS
on ECG how does first degree heart block present
PR interval greater than 0.2 seconds (5 small or 1 big)
what is second degree heart block
some atrial impulses done make it through the atrioventricular node to the ventricles
what are the types of second degree heart block
mobitz type 1
mobitz type 2
what is mobitz type 1 heart block
this is where condution through the atrioventricular node takes progressively longer until it finally fails after which is resets and the cycle restarts
what is mobitz type 2 heart block
this is where there is intermittent failure of conduction throuhg the atrioventricular node, with an absence of QRS complexes following P waves
the PR interval remains normal
what is third degree heart block
this is a complete heart block where there is no observable relationship between P waves and the QRS complexes
there is significant risk or asystole
what is bradycardia
slow heart rate typically less than 60 bpm
what can cause bradycardia
medications - beta blockers
heart block
sick sinus syndrome
what is sick sinus syndrome
it encompasses many conditions that causes dysfunction in the sinoatrial node
what is sick sinus syndrome caused by
often caused by idiopathic degenerative fibrosis of the sinoatrial node and can result in bradycardia, arrhythmia and prolonged pauses
what is asystole
it is the absence of electrical activity in the heart
who is at risk of asystole
those with:
mobitz type 2 heart block
third degree heart block
previous asystole
ventricular pauses longer than 3 seconds
what is the management of unstable patients and those at risk of asystole
intravenous atropine (1st)
inotropes (isoprenaline or adrenaline)
temporary cardiac pacing
permanent implantable pacemaker)
what are options for temporary cardiac pacing
transcutaneous pacing - pads on patients chest
transvenous pacing - catheter fed through venous system to stimulate the heart
what is atropine
it is an antimuscarinic medication that works by inhibiting the parasympathetic nervous system
what are side effects of atropine
pupil dilation
dry mouth
urinary retention
constipation
what is atopic dermatitis
it is a long lasting skin condition leading to dry, itchy and inflamed skin
what are symptoms of atopic dermatitis
dry, cracked skin
itchiness
rash on swollen skin that varies in colour depending on skin colour
small, raised bumps on brown or black skin
oozing and crusting
thickened skin
darkening of the skin around the eyes
raw, sensitive skin from scratching
what age does atopic dermatitis begin at
before the age of 5 and may continue into teen and adult years
what are the different types of dermatitis
atopic dermatitis - eczema
contact dermatitis
seborrheic dermatitis - dandruff
what are risk factors for atopic dermatitis
having had eczema, allergies, hay fever or asthma in the past
family history
what are complications of atopic dermatitis
asthma and hay fever
food allergies
chronic itchy, scaly skin (neurodermatitis/lichen simplex chronicus)
patches of skin that is darker/lighter than surrounding skin due to post inflammatory hyperpigmentation/hypopigmentation
skin infections
irritant hand dermatitis
allergic contact dermatitis
mental health conditions
how can you prevent eczema flares
moisturise skin regularly
take a daily bath or shower
use gentle, non soap cleansers
pat dry after bathing
identify and avoid irritants
what are common triggers of atopic dermatitis
Rough wool fabric
Dry skin
Skin infection
Heat and sweat
Stress
Cleaning products
Dust mites and pet dander
Mold
Pollen
Smoke from tobacco
Cold and dry air
Fragrances
Other irritating chemicals
how is atopic dermatitis diagnosed
clinical history and examination of the skin
patch testing
what is the treatment for atopic dermatitis
emollients
topical steroids
‘wet wraps’
treating any complications such as bacterial or viral infection
what are specialised treatments used in severe eczema
zinc impregnated bandages
topical tacrolimus
phototherapy
systemic immunosuppressants - corticosteroids, methotrexate and azathioprine
what are examples of thin emollient creams
E45
Diprobase cream
Oilatum cream
Aveeno cream
Cetraben cream
Epaderm cream
what are examples of thick emollient creams
50:50 ointment (50% liquid paraffin)
Hydromol ointment
Diprobase ointment
Cetraben ointment
Epaderm ointment
what is the steroid ladder used for patients with atopic dermatitis
Mild: Hydrocortisone 0.5%, 1% and 2.5%
Moderate: Eumovate (clobetasone butyrate 0.05%)
Potent: Betnovate (betamethasone 0.1%)
Very potent: Dermovate (clobetasol propionate 0.05%)
what are the different types of eczema
atopic dermatitis
contact dermatitis
dyshidrotic eczema - dries out skin and can cause burning sensation, blisters and rashes
neurodermatitis - small patches of skin
nummular eczema - small, rounded lesions all over the body but especially on arms and legs
seborrheic dermatitis
stasis dermatitis - skin discolouration on the legs which looks similar to varicose veins
what is the pathophysiology behind atopic dermatitis
some people with atopic dermatitis have a mutation in a gene responsible for filaggrin, a protein which helps to maintain a healthy skin barrier. Without which moisture can escape and pathogens can enter
in those with atopic dermatitis the immune system becomes disordered, and damages the skin barrier leaving it dry and prone to itching/rashes
when does atopic dermatitis typically present
in childhood, usually in the first 6 months of life
what is contact dermatitis
this is when the skin becomes irritated or inflamed after coming into contact with a substance that triggers an allergic reaction
- doesnt run in families and isnt linked to other allergic conditions
what are the main two types of contact dermatitis
irritant
allergic
what is irritant contact dermatitis
doesnt involve an allergic reaction
occurs when skin cells are damaged by exposure to irritating substances such as solvents, detergents, soaps, bleach or nickel containing jewelry
what is allergic contact dermatitis
this is a delayed allergic reaction that appears a day or two after the skin is exposed to an allergen. common examples are poison ivy, nail polish and poison oak
what are symptoms of contact dermatitis
itchy, crusty or scaly skin and lesions and vesicles in affected areas
hypersensitivity to the sun
increased risk of sunburn and irritation from suncream
how is contact dermatitis treated
hydrocortisone and other steroids
identify and avoid irritant
what is dyshidrotic eczema
this is a skin condition causing small blisters on the palms of the hands, soles of the feet and edges of the fingers and toes
what can trigger dyshidrotic eczema
metals - nickel
stress
laundry detergent
hot, humid weather
sweaty palms
what are the symptoms of dyshidrotic eczema
flares only happen on the hands and the feet
begin with a rash of painful deep seated blisters
as the blisters heal, the skin dries and often reddens and peels
how is dyshidrotic eczema treated
wash the affected skin with mild cleanser and pat dry
apply heavy emollient creams to repair skin
remove jewelry when washing hands
stress management
steroids
what is neurodermatitis
neurodermatitis is extremely itchy patches of skin which is confined to one or two patches of skin on the body
what are symptoms of neurodermatitis
occurs most commonly on feet, ankles, hands, wrists, elbows, shoulders, neck and scalp
itching can com and go, and people often feel itchiest when relaxing or trying to sleep, or when they are stressed or anxious
develops as thick leathery patches of skin
pronounced skin lines, scales and discolouration thats often red, brown or gray
scratching can cause bleeding and scarring
how is neurodermatitis treated
healing the skin and ending the scratch itch cycle - corticosteroids, and non steroidal topicals (calcineurin inhibitors/salicylic acid)
lidocaine
what is nummular eczema
it is also known as discoid eczema and features scattered circular, often itchy and sometimes oozing patches
what are the symptoms of nummular eczema
coin shaped lesions on the arms, legs, torso or hands
itching and burning
lesions that are oozing liquid or have crusted over
red, pinkish or brown scaly inflamed skin around the lesions
how is nummular eczema treated
mid to high potency topical corticosteroid with a topical antibiotic
what is seborrheic dermatitis
eczema that occurs on the body where there are a lot of sebaceous glands like the upper back, nose and scalp
what are triggers of seborrheic dermatitis
stress
recovery from a stressful life event, like losing a loved one or a heart attack
hormonal changes or illness
harsh detergents, solvents, chemicals and soaps
cold, dry weather or a change in the season
some medications, including psoralen, interferon and lithium
certain medical conditions, such as HIV and Parkinson’s disease
what are common symptoms of seborrheic dermatitis
Flaking skin or dandruff;
Patchy of flaky white or yellow scales on top of greasy skin;
A irritable rash which looks dark in brown and Black skin and lighter in white skin;
Ring-shaped rash for those with petaloid seborrheic dermatitis;
Itchiness.
how is seborrheic eczema treated
wash affected areas with gently, zinc containing cleanser
dandruff shampoo which should include:
Pyrithione zinc. Selenium sulfide;
Ketoconazole 1%;
Tar;
Salicylic acid
if the condition is more severe topical corticosteroids may be required
what is stasis dermatitis
this is when there is venous insufficiency or poor circulation in the lower legs causing changes to the skin
what are symptoms of stasis dermatitis
ankle swelling
orange-brown discolouration (cayenne pepper spots)
redness in lighter skin tones, may appear brown, purple or gray in darker tones
itching
scaliness
dryness
heavy or aching feeling after long periods of sitting or standing
increased risk of developing contact dermatitis
how is stasis dermatitis treated
compression stockings to reduce swelling
elevating legs above heart every two hours to reduce swelling
avoid foods high in salt
supplementation of vitamin C and rutin
topical cortcosteroids
topical or oral antibiotics
what is atrophic vaginitis
dryness and atrophy of the vaginal mucosa related to a lack of oestrogen
what is the pathophysiology of atrophic vaginitis
the epithelial lining of the vagina and urinary tract responds to oestrogen by becoming thicker, more elastic and producing secretions
as women enter menopause, oestrogen levels fall, resulting in the mucosa becoming thinner, less elastic and more dry
there are also changes in the vaginal pH and microbial flora that can contribute to localised infections
how does atrophic vaginitis present
itching
dryness
dyspareunia (discomfort or pain during sex)
bleeding due to localised inflammation
also consider it in older women presenting with recurrent UTI, stress incontinence or pelvic organ prolapse
what will examination of the labia and vagina show in someone with atrophic vaginitis
pale mucosa
thin skin
reduced skin folds
erythema and inflammation
dryness
sparse pubic hair
what is the management of atrophic vaginitis
vaginal lubricants can help symptoms of dryness - sylk, replens and YES
topical oestrogens - estriol cream, pessaries, tablets (vagiem) or ring (estring)
what contraindications does topical oestrogens have
breast cancer
angina
venous thromboembolism
