GP part 1 Flashcards

1
Q

what is bronchitis

A

this is when the trachea and bronchi become inflamed, swell and fill with mucus causing a chough

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2
Q

what is acute bronchitis caused by

A

this is usually caused by a viral infection and lasts a few weeks
- most people wont need treatment

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3
Q

what is chronic bronchitis

A

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

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4
Q

who is at higher risk of developing bronchitis

A

smokers
asthma, COPD or other breathing conditions
GORD
autoimmune disorders
around a high level of air pollutants

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5
Q

what are the symptoms of bronchitis

A

persistent cough that lasts one to three weeks
may bring up mucus
dyspnoea
fever
runny nose
fatigue

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6
Q

what causes bronchitis

A

Viruses - Influenza, respiratory syncytial virus, adenovirus, rhinovirus, coronavirus
bacteria- Bordetella pertussis, Mycoplasma pneumonia, chlarmydia pneumonia
pollution
smoke

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7
Q

how is bronchitis diagnosed

A

clinical diagnosis
respiratory examination
nasal swab
chest X ray of more chronic
bloods
sputum sample
pulmonary function tests

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8
Q

how is bronchitis treated

A

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

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9
Q

what is anaemia

A

it is defined as a low concentration of haemoglobin in the blood

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10
Q

what are the normal ranges of haemaglobin in
1. women
2. men

A
  1. 120-165g/L
  2. 130-180g/L
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11
Q

what is the normal MCV range in
1. women
2. men

A
  1. 80-100 femtoliters
  2. 80-100 femtoliters
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12
Q

what are the three categories anaemia is divided into

A
  1. microcytic anaemia
  2. normocytic anaemia
  3. macrocytic anaemia
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13
Q

what are the causes of microcytic anaemia

A

TAILS
Thalassaemia
Anaemia of chronic disease
Iron deficiency anaemia
Lead poisoning
Sideroblastic anaemia

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14
Q

what is a common cause of anaemia of chronic disease

A

Chronic kidney disease - reduced production of erythropoietin by the kidneys, the hormone responsible for stimulating red blood cell production. Treatment is with erythropoietin.

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15
Q

what are the causes of normocytic anaemia

A

3 As and 2 Hs
Acute blood loss
Anaemia of chronic disease
Aplastic anaemia
Haemolytic anaemia
Hypothyroidism

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16
Q

what are the two types of macrocytic anaemia

A

Megaloblastic or normoblastic

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17
Q

what is the cause of megaloblastic macrocytic anaemia

A

it is due to impaired DNA synthesis which prevents cells from dividing normally. Rather than dividing the cells grow into large abnormal cells

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18
Q

what are the causes of megaloblastic anaemi

A

B12 deficiency
Folate deficiency

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19
Q

what are the causes of normoblastic macrocytic anaemia

A

Alcohol
Reticulocytosis (normally from haemolytic anaemia or blood loss)
hypothyroidism
liver disease
drugs such as azathioprine

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20
Q

what is reticulocytosis

A

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.

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21
Q

what are generic symptoms of anaemia

A

Tiredness
Shortness of breath
Headaches
Dizziness
Palpitations
Worsening of other conditions, such as angina, heart failure or peripheral arterial disease

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22
Q

what are some specific symptoms of iron deficiency anaemia

A

Pica
hair loss

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23
Q

what are generic signs of anaemia

A

pale skin
conjunctival pallor
tachycardia
raised respiratory rate

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24
Q

what are specific signs of iron deficiency anaemia

A

Koilonychia - spoon shaped nails
angular cheilitis
atrophic glossitis - smooth tongue
brittle hair and nails

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25
what are specific signs of haemolytic anaemia
jaundice
26
what are specific signs of thalassaemia
bone deformities
27
what signs can indicate chronic kidney disease
oedema hypertension excoriations on the skin
28
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
29
what are causes of iron deficiency anaemia
insufficient dietary iron reduced iron absorption increased iron requirements - pregnancy loss of iron through bleeding - cancer/ulcer
30
what is the most common cause of iron deficiency in adults
blood loss - menstruation - cancer - oesophagitis or gastritis - peptic ulcers - inflammatory bowel disease - angiodysplasia
31
what is the most common cause of iron deficiency anaemia in children
dietary insufficiency
32
what medications can interferes with iron absorption
anything that reduces stomach acid - PPIs
33
where is iron absorbed
duodenum and jejunum
34
what can cause raised ferritin
inflammation liver disease iron supplements haemochromotosis
35
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.
36
what is the equation for working out transferrin saturation
serum iron/total iron binding capacity
37
what is ferritin
it is a protein that stores iron inside cells it is an acute phase protein released with inflammation
38
what is the transferrin saturation
this indicates the total iron in the body
39
what can cause iron overload in the body
haemochromotosis iron supplements acute liver damage
40
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
41
what are common side effects of oral iron
black stools constipation
42
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
43
what are key causes of B12 deficiency
pernicious anaemia insufficient dietary B12 medications that reduce absorption (PPI and metformin )
44
what is pernicious anaemia
Pernicious anaemia is an autoimmune condition involving antibodies against the parietal cells or intrinsic factor.
45
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.
46
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
47
what antibodies are used to diagnose pernicious anaemia
Intrinsic factor antibodies - first line Gastric parietal cell antibodies
48
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
49
what is the maintenance therapy for B12 deficiency
pernicious anaemia: 2-3 monthly injections for life diet related - oral cyanocobalamin or twice yearly injections
50
what do you treat first if a patient has both B12 and folate deficiency
the B12 deficiency
51
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
52
what is haemolytic anaemia
this is anaemia caused by the destruction of red blood cells, resulting in a low haemoglobin concentration
53
what inherited conditions can cause chronic haemolytic anaemia
hereditary spherocytosis hereditary elliptocytosis thalassaemia sickle cell anaemia G6DP deficiency
54
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
55
what are features of haemolytic anaemia
anaemia splenomegaly - filled with destroyed red blood cells jaundice
56
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
57
what is the most common inherited haemolytic anameia in northern europeans
hereditary spherocytosis
58
what is the inheritance pattern of hereditary spherocytosis
autosomal dominant
59
what is hereditary spherocytosis
a genetic condition which causes fragile, sphere shaped red blood cells that easily break down when passing through the spleen
60
what is the presentation of hereditary spherocytosis
anaemia jaundice gallstones splenomegaly aplastic crisis in the presence of parvovirus
61
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
62
what is the treatment of hereditary spherocytosis
folate supplementation blood transfusions when required splenectomy cholecystectomy if gallstones become a problem
63
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
64
how is G6PD deficiency inherited
in an X linked recessive pattern
65
in what groups of people is G6PD deficiency more common in
mediterranean, asian and african patients
66
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
67
what are key medications that can cause acute episodes of haemolytic anaemia in G6PD deficiency
ciprofloxacin sulfonylureas sulfasalazine
68
how does G6PD deficiency present
jaundice gallstones anaemia splenomegaly
69
what is seen on a blood film in someone with G6PD deficiency
Heinz bodies
70
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
71
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
72
what is warm autoimmune haemolytic anaemia
haemolysis occurs at normal or above normal temperatures - usually idiopathic
73
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
74
what can cold autoimmune haemolytic anaemia be secondary to
lymphoma leukaemia SLE infections - mycoplasma, EBV, CMV, HIV
75
what is the management of autoimmune haemolytic anaemia
blood transfusions prednisolone rituximab splenectomy
76
what is alloimmune haemolytic anaemia
this occurs due to foreign red blood cells or foreign antibodies
77
what are the two scenarios where alloimmune haemolytic anaemia occurs
transfusions reactions haemolytic disease of the newborn
78
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
79
what is the characteristic presenting feature of paroxysmal nocturnal haemoglobinuria
red urine in the morning - contains haemoglobin and haemosiderin anaemia thrombosis smooth muscle dystonia
80
what is the management of paroxysmal nocturnal haemoglobinuria
eculizumab - monoclonal antibody which targets complement component C5 bone marrow transplant
81
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
82
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
83
what is a key blood film finding of someone with microangiopathic haemolytic anaemia
schistocytes
84
what is prosthetic valve haemolysis
it is a key complication of prosthetic hear valves, which can occur in both bioprosthetic and metallic valve replacement
85
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
86
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
87
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
88
what is the inheritance pattern on sickle cell anaemia
autosomal recessive
89
what chromosome is affected in sickle cell anaemia
chromosome 11
90
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
90
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)
91
what is a sickle cell crisis
it refers to a spectrum of acute exacerbations caused by sickle cell disease
92
what can trigger a sickle cell crisis
dehydration infection stress cold weather
93
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)
94
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
95
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
96
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
97
what is the management of splenic crisis
emergency - ABCDE blood transfusions fluid resuscitation
98
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
99
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
100
how does acute chest syndrome present
fever shortness of breath chest pain cough hypoxia
101
what will a chest X ray show in acute chest syndrome
pulmonary infiltrates
102
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
103
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
104
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
105
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
106
what is acute stress reaction/disorder
this is a stress response that can happen within a month of experiencing a traumatic event
107
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.
108
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.
109
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
110
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
111
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
112
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).
113
what are risk factors for acute stress reaction
history of prior mental health conditions catastrophic worry avoidant coping style minimal support system
114
how is acute stress reaction diagnosed
clinical diagnosis = DSM-5
115
how is acute stress reaction treated
psychotherapy - CBT exposure therapy may offer SSRI/SNRI
116
what is an anal fissure
it is a crack or tear in the lining of your anal canal
117
what are causes of anal fissure
chronic constipation and straining obstructed defecation syndrome infant dyschezia chronic diarrhoea childbirth penetration
118
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
119
what are possible contributing factors to the development of anal fissures
prior surgery STIs IBD anal cancer TB diaper rash
120
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
121
how are anal fissures diagnosed
clinical diagnosis plus examination DRE
122
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
123
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
124
what are the principals of anaphylaxis management
ABCDE IM adrenaline - repeated after 5 minutes if necessary antihistamines can be given steroids can be given
125
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
126
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
127
how do you use an adrenaline auto-injector
1. prepare the devise - remove the safety cap on the non needle end 2. grip the device with needle end pointing down 3. administer the injection by firmly jabbing the device into the outer portion of the mid thigh until the device clicks 4. remove the device and gently massage the area for 10 seconds 5. phone an ambulance
128
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)
129
what are the four main differentials for a narrow complex tachycardia
sinus tachycardia supraventricular tachycardia atrial fibrillation atrial flutter
130
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
131
how is supraventricular tachycardia treated
vagal manoeuvers adenosine
132
what does atrial fibrillation look like on ECG
absent P waves irregularly irregular ventricular rhythm
133
how is atrial fibrillation treated
rate control/rhythm control
134
what does atrial flutter look like on ECG
atrial rate is normally around 300 bpm saw tooth pattern QRS at regular intervals
135
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
136
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
137
how is ventricular tachycardia treated
IV amiodarone
138
how is polymorphic ventricular tachycardia treated
IV magnesium
139
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
140
what can offer a permanent solution to atrial flutter
radiofrequency ablation
141
when is a QT interval considered prolonged
when its more than 440 milliseconds in men more than 460 milliseconds in women
142
what does a prolonged QT interval represent
prolonged repolarisation of the heart muscle cells after contraction
143
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
144
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
145
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
146
what is acute management of torsades de pointes
correcting the underlying issue magnesium infusion defibrillation
147
what are ventricular ectopics
these are premature ventricular beats caused by random electrical discharges outside the atria
148
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
149
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
150
on ECG how does first degree heart block present
PR interval greater than 0.2 seconds (5 small or 1 big)
151
what is second degree heart block
some atrial impulses done make it through the atrioventricular node to the ventricles
152
what are the types of second degree heart block
mobitz type 1 mobitz type 2
153
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
154
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
155
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
156
what is bradycardia
slow heart rate typically less than 60 bpm
157
what can cause bradycardia
medications - beta blockers heart block sick sinus syndrome
158
what is sick sinus syndrome
it encompasses many conditions that causes dysfunction in the sinoatrial node
159
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
160
what is asystole
it is the absence of electrical activity in the heart
161
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
162
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)
163
what are options for temporary cardiac pacing
transcutaneous pacing - pads on patients chest transvenous pacing - catheter fed through venous system to stimulate the heart
164
what is atropine
it is an antimuscarinic medication that works by inhibiting the parasympathetic nervous system
165
what are side effects of atropine
pupil dilation dry mouth urinary retention constipation
166
what is atopic dermatitis
it is a long lasting skin condition leading to dry, itchy and inflamed skin
167
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
168
what age does atopic dermatitis begin at
before the age of 5 and may continue into teen and adult years
169
what are the different types of dermatitis
atopic dermatitis - eczema contact dermatitis seborrheic dermatitis - dandruff
170
what are risk factors for atopic dermatitis
having had eczema, allergies, hay fever or asthma in the past family history
171
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
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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
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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
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how is atopic dermatitis diagnosed
clinical history and examination of the skin patch testing
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what is the treatment for atopic dermatitis
emollients topical steroids 'wet wraps' treating any complications such as bacterial or viral infection
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what are specialised treatments used in severe eczema
zinc impregnated bandages topical tacrolimus phototherapy systemic immunosuppressants - corticosteroids, methotrexate and azathioprine
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what are examples of thin emollient creams
E45 Diprobase cream Oilatum cream Aveeno cream Cetraben cream Epaderm cream
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what are examples of thick emollient creams
50:50 ointment (50% liquid paraffin) Hydromol ointment Diprobase ointment Cetraben ointment Epaderm ointment
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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%)
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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
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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
182
when does atopic dermatitis typically present
in childhood, usually in the first 6 months of life
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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
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what are the main two types of contact dermatitis
irritant allergic
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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
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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
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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
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how is contact dermatitis treated
hydrocortisone and other steroids identify and avoid irritant
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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
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what can trigger dyshidrotic eczema
metals - nickel stress laundry detergent hot, humid weather sweaty palms
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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
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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
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what is neurodermatitis
neurodermatitis is extremely itchy patches of skin which is confined to one or two patches of skin on the body
194
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
195
how is neurodermatitis treated
healing the skin and ending the scratch itch cycle - corticosteroids, and non steroidal topicals (calcineurin inhibitors/salicylic acid) lidocaine
196
what is nummular eczema
it is also known as discoid eczema and features scattered circular, often itchy and sometimes oozing patches
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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
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how is nummular eczema treated
mid to high potency topical corticosteroid with a topical antibiotic
199
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
200
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
201
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.
202
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
203
what is stasis dermatitis
this is when there is venous insufficiency or poor circulation in the lower legs causing changes to the skin
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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
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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
206
what is atrophic vaginitis
dryness and atrophy of the vaginal mucosa related to a lack of oestrogen
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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
208
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
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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
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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)
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what contraindications does topical oestrogens have
breast cancer angina venous thromboembolism
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what is bacterial vaginosis
it is an overgrowth of bacteria in the vagina, specifically anaerobic bacteria
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what is the pathophysiology of bacterial vaginosis
loss of the lactobacilli in the vagina, which produce lactic acid and maintains the low vaginal pH as the low pH prevents other bacteria growing. When there is a loss in lactobacilli the pH rises, allowing anaerobic bacteria to multiply
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what bacteria are associated with bacterial vaginosis
Gardnerella vaginalis (mc) mycoplasma hominis prevotella species
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what are risk factors for developing bacterial vaginosis
multiple sexual partners (not an STI) excessive vaginal cleaning recent antibiotics smoking copper coil
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how does bacterial vaginosis present
fishy smelling watery grey or white discharge half of women with BV and asymptomatic
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what will a speculum examination on a women with bacterial vaginosis show
confirm typical discharge can be used to complete a high vaginal swab
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what investigations should be done on a women with suspected bacterial vaginosis
vaginal pH can be tested via swab or pH paper charcoal vaginal swab for microscopy - will give 'clue cells' on microscopy
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what is the management for bacterial vaginosis
asymptomatic BV doesnt normally require treatment metronidazole is 1st line - can be given orally or via vaginal gel clindamycin is 2nd but less optimal choice always assess risk of additional pelvic infections
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when must you advise parents about when prescribing metronidazole
they should avoid alcohol for the duration of the treatment as it can cause a disulfiram like reaction, with nausea, vomiting and sometimes severe symptoms of shock and angioedema
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what are complications of bacterial vaginosis
increased risk of STI it is also associated with several complications in pregnant women: Miscarriage Preterm delivery Premature rupture of membranes Chorioamnionitis Low birth weight Postpartum endometritis
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what is blepharitis
it refers to inflammation of the eyelid margins
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what is the typical presentation of blepharitis
bilateral symptoms of; ocular irritation foreign body sensation burning redness sandy feeling crusting there may be paradoxical watering of the eye due to the reflex tear secretion
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what are causes of blepharitis
atrophic dermatitis (staphylococcal) seborrheic dermatitis acne rosecea demodex infestation (mites)
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what is blepharitis associated with
dysfunction of the meibomian glands which are responsible for secreting meibum (oil) into the surface of the eye
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what is the treatment for blepharitis
lid hygiene: warm compression of the eyelids eyelid massage to empty glands of debris eyelid cleaning with cotton wool topical antibiotic ointments (chloramphenicol) extended course of low dose oral tetracyclines and regular omega 3 fatty acid supplements may have a useful anti-inflammatory effect
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what is a hordeolum
external hordeolum is caused by a staphylococcal infection of an eyelid follicle and is more commonly known as a stye internal hordeolum is an infection of a meibomian gland and is less common
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what is hordeolum externum an infection o
glands of Zeis which are sebaceous glands at the base of the eyelashes glands of moll which are sweat glands at the base of the eyelashes
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how does a stye present
tender, red lump along the eyelid which may contain pus
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how are styes treated
hot compresses and analgesia removal of the eyelash associated with it topical antibiotics (chloramphenicol) or oral antibiotics (co-amoxiclav) if the style is recurrent or severe
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what is a chalazion
it is a granulomatous inflammatory lesion that forms in an obstructed meibomian gland - non infectious
232
how does a chalazia present
presents as a painless red eyelid cyst in the internal eyelid if they are infected they may become an internal hordeolum
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what is the management of a chalazion
often resolve spontaneously patients should be encouraged to perform warm compression of the eyelid and eyelid massage persistent chalazion should be referred to ophthalmology for consideration of incision and curettage
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what is an entropion
an entropion is an inward turning of the eyelid, with inward turning eyelashes which may irritate the eye causing ulceration and risk of sight loss
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what are the causes of entropion
age related degenerative changes eyelid irritation scarring trachoma - bacterial eye infection
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what is the management of entropion
examination for any corneal abrasions and ulcers prescribed frequent lubricants to reduce the risk of corneal abrasions and advised to perform eyelid taping as a temporary measure refer to ophthalmology for surgical correction
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what is ectropion of the eye
this is when the eyelid turns outwards exposing the inner aspect of the lid
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what is ectropion of the eye most commonly caused by
age related degenerative disorder to the lower lid facial palsy (bells palsy)
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what is the risk involved with ectropion of the eye
can result in exposure keratopathy, which is damage to the cornea due to ocular dryness caused by inadequate lid closure - can cause sight loss
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what is the management of ectropion
lubricating eye drops and taping the eyes shut at night severe cases may need corrective surgery patients should be referred to ophthalmology if there is evidence of exposure keratopathy
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what is trichiasis
this is when eyelashes grow inwards due to damaged eyelid follicles which can irritate the cornea and result in ulceration and risk of sight loss
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what is the cause of trichiasis
mostly caused by eyelid inflammation
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how is trichiasis treated
epilating the eyelash however recurrence may occur electrolysis or laser ablation can destroy the lash follicle and may provide a permanent solution same day referral to ophthalmology if there is a risk to sight
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what is periorbital cellulitis
it is an eyelid and skin infection in front of the orbital septum (in front of the eye)
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how does periorbital cellulitis present
swollen, hot, red skin around the eyelid and the eye
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what is the treatment for periorbital cellulitis
need to distinguish it from orbital cellulitis systemic antibiotics - oral or IV
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what is orbital cellulitis
it is an infection around the eyeball involving the tissues behind the orbital septum
248
what are symptoms of orbital cellulitis
pain with eye movement reduced eye movements vision changes abnormal pupil reactions proptosis
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what is the treatment for orbital cellulitis
emergency admission under ophthalmology and intravenous antibiotics surgical drainage may be needed if an abscess forms
250
what is benign prostatic hyperplasia
it is a condition which causes hyperplasia of the stromal and epithelial cells of the prostate and usually presents with lower urinary tract symptoms
251
what symptoms does someone with BPH present with
lower urinary tract symptoms : hesitancy weak flow urgency frequency intermittency straining terminal dribbling incomplete emptying nocturia
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what score can be used to asses the severity of lower urinary tract symptoms
international prostate symptom score
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how do you assess someone with symptoms of BPH
Digital rectal examination abdominal examination urinary frequency volume urine dipstick prostate specific antigen
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what do you have to be careful with when monitoring prostate specific antigen
it is known to be unreliable with a high rate of false positives (75%) and false negatives (15%)
255
what are common causes for a raised PSA
Prostate cancer Benign prostatic hyperplasia Prostatitis Urinary tract infections Vigorous exercise (notably cycling) Recent ejaculation or prostate stimulation
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what would you feel on a prostate examination in someone with BPH
smooth symmetrical and slightly soft prostate which has a maintained central sulcus
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what might a cancerous prostate feel line on a DRE
firm or hard asymmetrical craggy irregular loss of the central sulcus
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what is the management for someone with benign prostatic hyperplasia
patients with mild and manageable symptoms may not require interventions medical options are: alpha blockers (tamsulosin) to relax the smooth muscle 5-alpha reductase inhibitors (finasteride) which will reduce the size of the prostate surgery
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how long does it take for 5-alpha reductase inhibitors to have an affect on symptoms
takes up to 6 months
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what are the surgical options for treating benign prostatic hyperplasia
transurethral resection of the prostate transurethral electrovaporisation of the prostate holmium laser enucleation of the prostate open prostatectomy
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what is a side effect of tamsulosin
postural hypotension
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what is transurethral resection of the prostate
this is where parts of the prostate are removed from inside the urethra using a resectoscope - uses a diathermy loop
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what are the major complications of transurethral resection of the prostate
Bleeding Infection Urinary incontinence Erectile dysfunction Retrograde ejaculation (semen goes backwards and is not produced from the urethra) Urethral strictures Failure to resolve symptoms
264
what is mastitis
it is inflammation of the breast tissue and is a common complication of breastfeeding it can occur with or without infection
265
what can cause mastitis
obstruction in the ducts and accumulation of the milk infection where bacteria enters at the nipple and back tracks into the ducts
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what is the most common cause of bacterial mastitis
staphylococcus aureus
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how does mastitis present
Breast pain and tenderness (unilateral) Erythema in a focal area of breast tissue Local warmth and inflammation Nipple discharge Fever
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what is the management of mastitis
where is is caused by a blockage, management is conservative with continued breastfeeding, expressing milk and massage heat packs, showers and simple analgesia can help symptoms where conservative management isnt working or infection is suspected antibiotics should be started: flucloxacillin first line fluconazole can be used in suspected candida
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what is a rare complication of mastitis
breast abscess if the mastitis isnt properly treated and will require incision and drainage to treat it
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what is candida of the nipple
this is candidal infection of the nipple which can occur after a course of antibiotics and lead to recurrent mastitis
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how does candida of the nipple present
cracked skin on the nipple oral thrush and nappy rash in the infant sore nipples bilaterally particularly after feeding nipple tenderness and itching cracked, flaky or shiny areola
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how is candida of the nipple treated
both mother and baby need treatment - topical miconazole 2% on the nipple after each breastfeed - treatment for the baby is either oral miconazole gel or nystatin
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what is bursitis
it is a painful swelling in a small fluid filled sac called a bursa, usually around your joints. it is more common in the shoulders, elbows, knees and feet
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what is the cause of bursitis
the most common cause it overuse and putting too much pressure on a bursa - repetitive motions - spending time in positions that put pressure on a specific part of your body
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what are the different types of bursitis
shoulders - subacromial bursitis elbow - olecranon bursitis knees - prepatellar bursitis feet - heel, big toe or ball of foot hips - iliopectineal or trochanteric buttocks - ischial
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what are symptoms of bursitis
pain especially when moving affected area limited range of motion swelling if infected you may have dicolouration or redness of the skin, heat, fever
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what are risk factors which can lead to bursitis
athletes physical or manual labour musicians those with arthritis, diabetes and thyroid disease
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how is bursitis diagnosed
physical examination and clinical history X ray Ultrasound or MRI to detect swollen bursae bloods to look for infection aspiration if infection is suspected
279
how are bursitis treated
avoid the activity/positions that irritate the bursa elevate the area over the counter analgesia ice area/apply heat to area support injured area with brace or sling antibiotics if infection suspected - flucloxacillin first line with clarithromycin as alternative physical therapy corticosteroids surgery to resect bursa if other treatments are not effective and still experiencing symptoms for 6 months or longer
280
what causes vaginal candidiasis
vaginal infection with a yeast of the candida family, most commonly candida albicans
281
what are risk factors for developing thrush
increased oestrogen (higher in pregnancy, lower in pre-puberty and menopause) poorly controlled diabetes immunosuppression broad spectrum antibiotics
282
how does thrush present
thick white discharge that doesnt typically smell vulval and vaginal itching, irritation or discomfort erythema fissures oedema dyspareunia dysuria excoriation
283
what investigations are done in someone with suspected candida infection
often treat empirically based on presentation testing the vaginal pH using swabs and pH paper may be helpful differentiating between thrush, BV and trichomonas charcoal swab and microscopy
284
how is thrush managed
antifungals: antifungal cream (clotrimazole) inserted into the vagina - single dose at night (5g 10% cream) antifungal pessary - single dose at night (500mg) or three doses over three nights (200mg) oral antifungal tablets (fluconazole) - single dose (150mg)
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what is an over the counter thrush treatment
canesten Duo - has single dose fluconazole and clotrimazole cream to use externally
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when is thrush considered recurrent
when there is more than 4 a year - can be treated with induction and maintenance regime over 6 months with oral or vaginal antifungals (of label use)
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what is important to say when prescribing antifungal creams
that it can damage latex condoms and prevent spermicides from working so alternative contraception is required for at least 5 days after use
288
what is chronic kidney disease
it is defined as abnormal kidney function or structure present for greater than three months, with subsequent implications for health
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what are the most common causes of chronic kidney disease
diabetes vascular disease
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what are causes of chronic kidney disease
glomerular disease - IgA nephropathy, membranous nephropathy, focal segmental glomerulosclerosis nephrotic drugs obstructive uropathy or reflux nephropathy multisystem diseases with renal involvement hereditary kidney disease
291
what are examples of nephrotoxic drugs which can cause CKD
aminoglycosides bisphosphonates calcineurin inhibitors (ciclosporin) lithium proton pump inhibitors mesalazine NSAIDs
292
what obstructive uropathy can cause CKD
structural renal tract disease neurogenic bladder benign prostatic hypertrophy urinary diversion surgery recurrent urinary tract infections pathology inside the urinary tract such as malignancy or retroperitoneal fibrosis
293
what is the pathophysiology of chronic kidney disease
chronic kidney disease us the end stage for any cause of severe and or long standing kidney injury damage to the kidneys reduces the number of functioning nephrons. This leads to hyperfiltration at the glomeruli, and increased permeability leading to proteinuria it also causes activation of the renin angiotensin aldosterone system causing an increase in blood pressure which furthers the hyperfiltration the increase in the capillary pressure within the glomerulus and inflammatory mediators causes chronic inflammation, reducing the filtration ability of the glomerulus
294
what is chronic kidney disease classified by
the eGFR and the amount of proteinuria
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what is stage 1 CKD
this is when the GFR is normal with the filtration rate being >90 mL/min/1.73m2
295
what is stage 2 CKD
when there is mild impairment GFR is between 60-89 mL/min/1.73m2
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what is stage 3a CKD
when there is mild-moderate impairment GFR is between 45-59 mL/min/1.73m2
297
what is stage 3b CKD
when there is moderate to severe impairment GFR is between 30-44 mL/min/1.73m2
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what is stage 4 CKD
when there is severe impairment GFR is between 15-29 mL/min/1.73m2
299
what are risk factors for developing chronic kidney disease
age greater than 50 history of acute kidney injury history of childhood kidney disease family history of CKD stage 5 diabetes mellitus cardiovascular disease obesity with metabolic syndrome gout solitary functioning kidney smoking black or Hispanic ethnicity male gender
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what is stage 5 CKD
when there is established renal failure GFR is < 15mL/min/1.73m2 or they are on renal replacement therapy
300
what are the clinical features of someone with CKD
it is primarily asymptomatic and symptoms develop in advanced stages fatigue nausea cramps insomnia restless legs taste disturbance bone pain pruritis oliguria, polyuria, nocturia dyspnoea and orthorpnoea sexual dysfunction severe uraemia can cause hiccups, pericarditis, coma and seizure
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what clinical findings in CKD may be found
ammonia like smell on the breath pallor due to anaemia cachexia cognitive impairment tachypnoea due to fluid overload or anaemia hypertension volume disturbance - overload or depletion peripheral neuropathy fundoscopy may reveal microvascular damage in patients with diabetes or hypertension
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what specific clinical findings may you get in chronic kidney disease
bilateral masses suggestive of polycystic kidney disease palpable bladder suggestive of obstructive uropathy, with prostatic enlargement in men
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how is CKD usually detected
though the presence of hypertension, haematuria and or proteinuria, reduction in the GFR with an increase in serum creatinine
304
what investigations should be done in someone with suspected CKD
bedside investigations: blood pressure, urinalysis, plasma glucose, ECG labs: Bloods - FBC, U+E, serum albumin, calcium, phosphate, PTH, alkaline phosphatase, cholesterol and triglycerides urinary albumin serology hepatitis B, C and HIV imaging: abdominal radiograph, renal ultrasound, CT or MRI
305
how is CKD diagnosed
A diagnosis of CKD requires evidence of kidney damage and/or a persistent reduction in renal function. CKD stages 3-5 can be diagnosed based on the eGFR alone stages 1-2 require additional evidence of renal disease
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what is accelerated progression of CKD
this is defined as a persistent decrease in eGFR of 25% or more and a change in CKD category within 12 months, or a persistent decrease in eGFR of 15mL/min/1.73m2 within 12 months
307
what are general measures for the management of CKD
exercise weight loss smoking cessation good glycaemic control control of blood pressure immunisations: influenza and pneumococcus avoidance of nephrotoxic medication diet: adequate protein intake, restricted sodium and phosphate intake
308
what are medications used in the treatment of chronic kidney disease
1. statins and antiplatelet drugs for prevention of CVD 2. ACEi or ARB to aid blood pressure control in those with diabetic renal disease or significant proteinuria 2. SGLT2 inhibitor if ACEi or ARB is not doing enough 4. dietary phosphate restriction and phosphate binders (calcium acetate) to control hyperphosphataemia 5. 1-alpha-hydroxycholecalciferol given if secondary hyperparathyroidism is present
309
how is CKD monitored in patients
monitoring requirements include full blood count and iron studies, serum calcium, phosphate and PTH levels monitoring level is done dependent on the risk level (determined by eGFR and albuminuria) low-moderate: monitor annually high risk: monitor every 6 months very high: monitor ever 3-4 months
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what is renal replacement therapy
this is an important aspect in the treatment of end stage CKD and includes dialysis and kidney transplantation
311
when do patients generally begin dialysis
when there eGFR reaches approximately 5-10 mL/min/1.73m2
312
what is haemodialysis
this involves pumping blood from the patients body through a dialyser, and solutes from the blood diffuse into the dialysate and are removed together with fluid - typically 4 hours three times a week
313
what do patients require in order to have haemodialysis
they require a good blood flow and so they need either an arterio-venous fistula or a tunnelled central venous catheter
314
what are complications of haemodialysis
access related: infection, venous stenosis or access failure haemodynamic instability nausea and vomiting, headache, cramp reactions to dialysis membranes
315
what is peritoneal dialysis
it involves infusing dialysate into the peritoneal cavity through a tunnelled catheter. Solutes and fluid from the peritoneal vessels move across the peritoneal membrane into the dialysate and are removed
316
what are the two typical regimes which comes with peritoneal dialysis
continuous ambulatory peritoneal dialysis: manual dialysate exchanges performed about four times per day automated dialysis: a machine performed the exchange overnight
317
what restrictions are there for patients wanting peritoneal dialysis
patients may not be suitable if they have had any previous intra-abdominal pathology like peritonitis, surgery or adhesions as a functional peritoneal membrane is needed
318
what are complications of peritoneal dialysis
Bacterial or fungal peritonitis Catheter problems: infection, blockage, kinking, leaks, displacement (more likely if a patient becomes constipated) Weight gain Worsening glycaemic control in patients with diabetes Failure of peritoneal membrane requiring a switch to haemodialysis Encapsulating peritoneal sclerosis
319
what provides the best long term outcome in patients with end stage chronic kidney disease
transplantation
320
what are contraindications to kidney transplantation
active or recent malignancy active infection significant co-morbidity such as heart disease
321
what are complications of renal transplantation
operative complications: infection, bleeding, thrombosis, problems with ureteric anastomosis stenosis of graft vessels or ureter side effects from immunosuppressive therapy opportunistic infections malignancy recurrent of original disease in the transplant graft rejection (hyperacute or acute) chronic allograft nephropathy
322
what are complications of CKD
A WET BED 1. Acid base balance - metabolic acidosis 2. Water removal - pulmonary oedema 3. Erythropoiesis - anaemia of chronic disease 4. Toxin removal - uraemic encephalopathy 5. BP control - cardiovascular disease 5. Electrolyte balance - hyperkalaemia 6. Vitamin D - bone mineral disorder of CKD
323
what is chronic obstructive pulmonary disease
it is a lung disease characterised by persistent respiratory symptoms and airflow obstruction
324
what is chronic obstructive pulmonary disease a triad of
emphysema chronic bronchitis small airway fibrosis
325
what is chronic bronchitis
it is a productive cough for at least three months in 2 consecutive years
326
what are risk factors for developing chronic obstructive pulmonary disease
tobacco smoking indoor air pollution alpha 1 antitrypsin deficiency
327
what is alpha 1 anti-trypsin deficiency
it is an autosomal dominant condition which presents in younger patients, caused by a deficiency in alpha 1 antitrypsin, a protease inhibitor
328
what is the pathophysiology of alpha 1 antitrypsin deficiency
alpha 1 antitrypsin is a protease inhibitor which prevents neutrophil elastase breaking down alveolar structures. In alpha 1 antitrypsin there is increased destruction of alveolar structures and results in early onset emphysema it also leads to cirrhosis of the liver
329
what is the presentation of chronic obstructive pulmonary disease
progressive dyspnoea - initially exertional but can progress to resting chronic productive cough - usually colourless sputum recurrent lower respiratory tract infections fatigue headache due to CO2 retention
330
what is the MRC dyspnoea scale and what are the different grades
it is a scale used to measure level of dyspnoea grade 1 = breathlessness during strenuous exercise only grade 2 = breathlessness when hurrying or walking up a slight incline grade 3 = walks slower than other people of the same age, or needs to pause for breath when walking at own pace grade 4 = pauses after walking 100m/a few minutes on the level grade 5 = too breathless to leave house, or breathless when dressing
331
what is the COPD assessment test
this is a test used to assess the impact of the patients COPD on their wellbeing and daily life the score ranges from 0-40 with 40 being the highest score you can get the higher the score the greater the impact on a patients life
332
what might be seen on an examination of a patient with COPD
tachypnoea wheeze on auscultation pursed lip breathing barrel chest peripheral cyanosis cor pulmonale CO2 retention flap
333
what are differential diagnosis for COPD
asthma bronchiectasis congestive heart failure lung cancer tuberculosis
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what investigations are done on someone with suspected COPD
spirometry - FEV1/FVC <70% pulse oximetry - aim for SpO2 = 88-92% sputum culture ECG Bloods, ABG imaging: Chest X ray
335
what are the FEV1 levels used to classify severity of COPD
mild = <80% moderate = 50-80% severe = 30-50% very severe = <30%
336
what is conservative management for COPD
smoking cessation pulmonary rehabilitation annual influenza vaccine and one off pneumococcal vaccine personalised self management plan
337
what is the medical management for COPD
inhalers 1. starts with SAMA or SABA when needed 2. if having exacerbations still with asthmatic features then add LABA and ICS. If having exacerbations with no asthmatic features add LABA and LAMA 3. if there are still daily symptoms then do LABA, LAMA and ICS Long term oxygen therapy surgical management - lung volume reduction surgery or lung transplant
338
what are indications for someone with chronic obstructive pulmonary disease to go on long term oxygen therapy
if their SpO2 is <88% or PaO2 is <7.3 kPa
339
what are complications of chronic obstructive pulmonary disease
hypercapnic respiratory failure secondary polycythaemia due to chronic hypoxia cor pulmonale bronchiectasis anxiety and depression osteoporosis sleep disturbance
340
what is conjunctivitis
itis inflammation of the conjunctiva, the external layer covering the outer surface of the globe and the inner surface of the eyelids
341
what are the two types of conjunctivitis
infections and non infectious
342
what are causes of infectious conjunctivitis
viral bacterial
343
what are causes of viral conjunctivitis
most cases of viral conjunctivitis is caused by adenovirus, with herpes virus causing it as well other less frequent causes include measles, mums, rubella, enterovirus and coxsackievirus
344
what are risk factors for viral conjunctivitis
direct contact with contaminated skin or objects lead to spread of infection
345
what are the clinical features of viral conjunctivitis
both eyes affected profuse watery discharge tender preauricular lymphadenopathy concurrent upper resp tract infection (sometimes)
346
what are features of adenoviral conjunctivitis
pharyngoconjunctival fever: pharyngitis, conjunctivitis and fever epidemic keratoconjunctivitis: more severe with corneal involvement and photophobia
347
how is viral conjunctivitis diagnosed
clinical history and examination occasionally swabs are required
348
what is the management of viral conjunctivitis
tends to be self limiting and rarely requires treatment important to adopt hygiene measures to prevent the spread
349
what are the causative organisms of bacterial conjunctivitis
staphylococcus streptococcus haemophilus chlamydia trachomatis neisseria gonorrhoea
350
what are risk factors for developing bacterial conjunctivitis
contact with contaminated skin and objects in cases o chlamydia and gonorrohea unprotected sexual intercourse
351
what are clinical features of bacterial conjunctivitis
one eye affected develops rapidly very inflamed conjunctiva sticky purulent discharge gonococcal infections associated with very profuse discharge chlamydia conjunctivitis tend to be associated with follicles and pre-auricular lymphadenopathy
352
what investigations are done for bacterial conjunctivitis
clinical history and examination conjunctival scrapes in patients with high risk of atypical organisms
353
what is the management of bacterial conjunctivitis
supportive and antibiotic drops (chloramphenicol) are used rarely in cases secondary to gonorrhoea and chlamydia azithromycin is used
354
what are complications of bacterial conjunctivitis
Certain bacteria such as Neisseria have a propensity to invade the cornea, which can lead to keratitis and endophthalmitis.2 These conditions can subsequently cause reduced vision or blindness if not treated promptly.
355
what are types of non infectious conjunctivitis
allergic chemical injury
356
what is allergic conjunctivitis
it is the most common type of non infective cause and occurs secondary to a type 1 hypersensitivity reaction
357
what are the clinical features of allergic conjunctivitis
itching both eyes affected diffuse redness and watery discharge papillae in the eyelid which can give a cobblestone appearance
358
what are the subtypes of allergic conjunctivitis
Seasonal allergic conjunctivitis: secondary to hay fever, therefore most common in summer months due to the presence of pollen Perennial allergic conjunctivitis: caused by allergens such as house dust mite Vernal keratoconjunctivitis: most common in young males living in hot dry climates Atopic keratoconjunctivitis: most common in middle-aged men
359
what is the management of allergic conjunctivitis
Treatment includes allergen avoidance, topical and oral antihistamine as well as topical mast-cell stabilisers and occasionally, mild steroids
360
what chemicals can result in conjunctivitis
alkaline - more significant damage acids - denature and precipitate proteins in the cornea both are an ophthalmic emergency
361
how is short term (less than 3 months) constipation managed
investigate any underlying cause identify any faecal impaction advise lifestyle measures - drink more water, increase dietary fibre, exercise oral laxatives - bulk forming first line such as ispaghula, if stools remain hard then switch to osmotic laxative such as macrogol. If stools are soft but difficult to pass then add stimulant laxative
362
what should be prescribed if someone has opioid induced constipation
dont prescribe bulk forming laxatives offer osmotic or stimulant laxative
363
how is chronic constipation managed
consider secondary causes identify faecal loading or impaction advise on lifestyle measures laxatives - same as in acute consider treatment with prucalopride if at least two laxatives from different classes have been tried at the highest tolerated recommended doses for at least 6 months
364
how do you manage faecal loading or impaction
if there are hard stools, consider prescribing a high dose of oral macrogol if there is ongoing hard stools with oral macrogol consider starting or adding oral stimulant laxative if its inadequate or too slow consider prescribing suppository or mini enema if it is still slow then sodium phosphate or arachis oil retention enema
365
how do bulk forming laxatives work
act by retaining fluid within the stool and increasing faecal mass, stimulated peristalsis - ispaghula husk - methylcellulose
366
how do osmotic laxatives work
increasing the amount of the fluid in the large bowel producing distension, which leads to stimulation of peristalsis - lactulose - macrogols - phosphate and sodium citrate enemas
367
how do stimulant laxatives work
cause peristalsis by stimulating colonic nerves or colonic and rectal nerves - senna - bisacodyl and sodium Picosulfate - docusate
368
what is crystal arthropathy
they are a group of joint disorders due to the deposition of crystals in and around joints which lead to joint destruction and soft tissue masses
369
what are different crystal arthropathies
gout pseudogout and other rarer causes
370
what is gout
it is a crystal arthropathy caused by urate crystals depositing in joints causing them to become inflamed
371
what are risk factors for gout
Male Family history Obesity High purine diet (e.g., meat and seafood) Alcohol Diuretics Cardiovascular disease Kidney disease
372
what are typical joints which are affected by gout
The base of the big toe – the metatarsophalangeal joint (MTP joint) The base of the thumb – the carpometacarpal joint (CMC joint) Wrist
373
how does gout present
single acute hot swollen and painful joint
374
how is gout diagnosed
made clinically, supported by a raised serum urate level on blood tests it is essential to exclude septic arthritis aspiration - shows monosodium urate crystals which are needle shaped and negatives birefringent of polarised light
375
what will an X-ray of a joint with gout show
Maintained joint space (no loss of joint space) Lytic lesions in the bone Punched out erosions Erosions can have sclerotic borders with overhanding edges
376
how are acute flares of gout managed
NSAIDS first line (co-prescribed with a PPI) colchicine second line oral steroids third line
377
what are side effects of colchicine
abdominal symptoms diarrhoea
378
what is prophylaxis for gout
xanthine oxidase inhibitors allopurinol febuxostat
379
what lifestyle changes can reduce the risk of gout
losing weight staying hydrated minimising the consumption of alcohol and purine based food such as meat and seafood
380
what is pseudogout caused by
calcium pyrophosphate crystals collecting in the joints
381
how does pseudogout present
many patient are asymptomatic chronic pain and stiffness in multiple joints over 65 years old with a rapid onset hot, swollen, stiff and painful knee
382
how is pseudogout diagnosed
need to exclude a medical emergency joint aspiration - calcium pyrophosphate crystals which are rhomboid shaped and positively birefringent of polarised light
383
what is a sign of pseudogout on Xray
chondrocalcinosis - calcium deposits in the joint cartilage show up as a thin white line in the middle of the joint space
384
what are the types of fungal infection
superficial fungal infections subcutaneous fungal infections deep fungal infections
385
what are types of superficial fungal infections
ringworm (dermatophytosis) - skin, hair and nails onychomycosis - fingernails and toenails candidiasis tinea versicolor/pityriasis versicolor
386
what are examples of subcutaneous fungal infections
under the surface of the skin sporotrichosis chromoblastomycosis eumycetoma
387
what are symptoms of superficial or subcutaneous infections
itching, soreness, redness or rash on the affected area discoloured, thick or cracked nails pain while eating, loss of taste or white patches in the mouth or throat painless limp under skin
388
what are common causes of fungal infection
dermatophytes - live off keratin in hair, nails and skin candida environmental fungi - Histoplasma, Coccidioides, Blastomyces and Aspergillus.
389
how is a fungal infection diagnosed
clinical history and examination samples of skin or other affected tissue, nails, blood, sputum, secretions, urine, discharge
390
what are general measures when treating fungal infection
keep affected area dry and clean - wash daily clean shower/bath hot wash socks, bathmats, towels etc
391
when might oral antifungals be used
It is extensive or severe. It resists topical antifungal therapy. It affects hair bearing areas (tinea capitis and tinea barbae).
392
what are medications which can be used for candida and dermatophytes
Itraconazole ketoconazole fluconazole
393
what are application regiments for treatment of fungal infection on the body
- terbinafine 1% cream (once or twice a day for 1-2 weeks) - clotrimazole 1% cream (2-3 times a day for at least 4 weeks) - miconazole 2% cream (twice a day for 10 days) - econazole 1% cream (twice a day until healed)
394
what are cutaneous warts
these are small, rough growths that are caused by infection of keratinocytes with HPV
395
what is a verruca
this is a wart that is on the sole of your foot
396
what can cutaneous warts be classified as
Common wart (Verruca vulgaris). Flat wart or plane wart (Verruca plana). Plantar wart — wart on the sole of the foot (Verruca plantaris). Periungual wart — wart around the fingernails or toenails.
397
how are warts spread
they are spread by direct skin to skin contact or indirectly via contact with contaminated floors or surfaces
398
how do you increase the risk of developing cutaneous warts
if skin is damaged a wart is scratched or knocked and bleeds occupation involves regular handling of meat or fish if the person is immunosuppressed
399
how long does it take for warts to clear
can clear spontaneously at any time or persist for years about 60-70% resolve within 2 years and 95% within 4 years
400
how are warts diagnosed
typical appearance and usually clinical if there is any diagnostic doubt then referral can occur
401
what do common warts look like
firm, raised papules with rough surface which resembles a cauliflower
402
when should warts and verrucae be treated
for most people there is not a strong case for treatment consider treating if the wart is painful, the wart is cosmetically unsightly or if the person request treatment and the wart is persisting
403
what treatments are recommended for warts
facial warts - referral to dermatology non facial warts: - topical salicylic acid applied daily for 12 weeks - cryotherapy - combination of salicylic acid and cryotherapy (not to use cryotherapy in younger children)
404
what is a diverticulum
it is a pouch or pocket in the bowel wall, ranging in size from 0.5-1cm
405
what is diverticulosis
it refers to the presence of diverticula without inflammation or infection. it may be referred to as diverticular disease when patients experience symptoms
406
what is diverticulitis
inflammation and infection of diverticula
407
what is the pathophysiology of diverticular disease
the wall of the large intestine contains a layer of muscle called circular muscle the points where this muscle layer is penetrated by blood vessels are areas of weakness increased pressure in the lumen can cause a gap to form in these areas of the muscle these gaps allow the mucosa to herniate though the muscle layer and pouches to form diverticula
408
why dont diverticula form in the rectum
because it had an outer longitudinal muscle layer that surrounds the diameter of the rectum adding extra support
409
what are risk factors for the development of diverticulosis
increased age low fibre diets obesity use of NSAIDs
410
what are symptoms of diverticulosis
lower left abdominal pain constipation rectal bleeding
411
what is management of diverticulosis
increase fibre in diet bulk forming laxatives surgery to avoid affected area
412
what laxatives should be avoided in diverticulosis
stimulant laxatives
413
what is acute diverticulitis
inflammation in the diverticula
414
how does diverticulitis present
Pain and tenderness in the left iliac fossa / lower left abdomen Fever Diarrhoea Nausea and vomiting Rectal bleeding Palpable abdominal mass (if an abscess has formed) Raised inflammatory markers (e.g., CRP) and white blood cells
415
what is the management of uncomplicated diverticulitis in primary care
Oral co-amoxiclav (at least 5 days) Analgesia (avoiding NSAIDs and opiates, if possible) Only taking clear liquids (avoiding solid food) until symptoms improve (usually 2-3 days) Follow-up within 2 days to review symptoms
416
what is hospital treatment of diverticulitis
happens when a patient is in severe pain or complications Nil by mouth or clear fluids only IV antibiotics IV fluids Analgesia Urgent investigations (e.g., CT scan) Urgent surgery may be required for complications
417
what are complications of acute diverticulitis
Perforation Peritonitis Peridiverticular abscess Large haemorrhage requiring blood transfusions Fistula (e.g., between the colon and the bladder or vagina) Ileus / obstruction
418
what are non modifiable risk factors for the development of type 2 diabetes
Age: >40 years old, although now being seen more in younger people Sex: slightly more common in men than women Ethnicity: South Asian, Black African and Black-Caribbean groups have a higher risk Family history: especially having first-degree relatives with T2DM
419
what are modifiable risk factors for the development of type 2 diabetes
Obesity: encompasses increased body mass index (BMI)/waist circumference, sedentary lifestyle and consumption of processed carbohydrate/sugary foods. Alcohol excess: beer and cocktails are high in calories and sugar, and alcoholism causes liver damage, which reduces the hepatic uptake of glucose. Smoking: a potent CVD risk factor itself and also associated with insulin resistance. Poor sleep/stress: both promote insulin resistance and increase hyperglycaemia through chronically raised cortisol levels and poor dietary/exercise habits.
420
what medical conditions increase the risk of type 2 diabetes
PCOS gestational diabetes mental health conditions steroid induced diabetes
421
what might be seen on a physical exam on someone with suspected type 2 diabetes
raised BMI and waist circumference acanthosis nigricans diabetic retinopathy on fundoscopy diabetic neuropathy and PVD on foot exam
422
what investigations should be done on someone with suspected type 2 diabetes
Capillary blood glucose urinary glucose, ketones and protein HbA1C U+E, LFT, cholesterol and lipid urine albumin creatinine ratio
423
when is someone diagnosed with diabetes
if their HbA1C is above 48mmol/mol - if symptomatic one result is significant - if asymptomatic then repeat HbA1C in two weeks
424
what is lifestyle management for someone with type 2 diabetes
weight loss of >5% diet - low sugar especially with low carbohydrate and low ultra processed diet foods exercise reduced alcohol intake stop smoking improve sleep and stress
425
what is the first line drug offered to patients with type 2 diabetes
metformin - reduces insulin resistance of target cells - reduces liver gluconeogenesis
426
what are other medications used in diabetes control in type 2 diabetes
SGLT2 inhibitors (dapagliflozin) 2nd line Sulfonylureas (gliclazide) DPP4 inhibitors (sitagliptin) GLP-1 analogues (liraglutide)
427
what is the method of action of SGLT2 inhibitors
reduce renal glucose reabsorption
428
what are side effects of SGLT2 inhibitors
UTI and genital thrush doesnt cause hypoglycaemia itself but should be paused in acute illness
429
what are side effects of metformin
GI upset dont use in renal failure or post MI due to risk of lactic acidosis
430
what is the method of action sulfonylureas
increase endogenous insulin secretion by stimulating pancreatic B islet cells causes rapid reduction in HbA1C
431
what are side effects of sulfonylureas
hypoglycaemia weight gain abnormal LFTs hyponatraemia
432
what is the mode of action of DPP4 inhibitors
blocks dipeptidyl peptidase 4 which would normally break down GLP-1 increasing the insulin release effect
433
what are the side effects of DPP4 inhibitors
weight neutral can cause pancreatitis has less effect in reducing HbA1C compared with other options
434
what is the most of action of GLP-1 analogues
also work on the incretin effect to enhance GLP-1 action major weight loss effect
435
what are side effects of GLP-1 analogues
significant weight loss can cause pancreatitis harder to access currently
436
when would someone with type 2 diabetes be put on insulin
if above treatment fails (already on triple therapy) or rapid control is required then subcut insulin injections may be needed
437
what are complications of type 2 diabetes
Macrovascular - MI, TIA/stroke, peripheral vascular disease Microvascular - diabetic nephropathy, retinopathy and neuropathy
438
what is the diabetes annual review checklist
HbA1C and individualised target lifestyle advice and education bedside parameters - BP, BMI, urine dip labs - U+E, lipids, QRISK diabetic foot review annual diabetic retinopathy screen
439
what are the implications of driving with type 2 diabetes
DVLA has specific driving regulations for diabetes - if it is managed with lifestyle alone or medications done cause hypoglycaemia the DVLA does not need to be informed - if they are on hypoglycaemic drugs (gliclazide, insulin) then the DVLA needs to know
440
when is someone diagnosed with hypertension
it is when there is a blood pressure above 140/90 in the clinical setting, confirmed with ambulatory or home readings above 135/85
441
what is essential hypertension
also known as primary hypertension and means a high blood pressure has developed on its own and does not have a secondary cause - accounts for 90% of hypertension
442
what are secondary causes of hypertension
ROPED Renal disease Obesity Pregnancy induced or Pre eclampsia Endocrine Drugs (alcohol, steroids, NSAIDs, oestrogen and liquorice)
443
what is the most common cause of secondary hypertension
renal disease - when blood pressure is very high or doesnt respond to treatment consider renal artery stenosis
444
what is an important cause of endocrine caused hypertension
hyperaldosteronism
445
what are complications of high blood pressure
Ischaemic heart disease (angina and acute coronary syndrome) Cerebrovascular accident (stroke or intracranial haemorrhage) Vascular disease (peripheral arterial disease, aortic dissection and aortic aneurysms) Hypertensive retinopathy Hypertensive nephropathy Vascular dementia Left ventricular hypertrophy Heart failure
446
what might be seen on examination if someone has left ventricular hypertrophy
sustained and forceful apex beat felt
447
how is hypertension diagnosed
NICE recommends measuring BP every 5 years to screen for htn (should be measured more in borderline cases and every year in patients with T2DM) patients with a clinic BP between 140/90-180/120 should have a 24 hour BP or home readings to confirm the diagnosis
448
what is stage 1 hypertension
clinic reading - above 140/90 ambulatory or home reading - above 135/85
449
what is stage 2 hypertension
clinic reading - above 160/100 ambulatory or home reading - above 150/95
450
what is stage 3 hypertension
clinic reading - above 180/120 no at home reading
451
what needs to be checked for in patients with hypertension
end organ damage
452
how is end organ damage checked for in patients with hypertension
urine albumin creatinine ratio for proteinuria and dipstick for microscopic haematuria bloods for HbA1C, renal function and lipids fundus examination for hypertensive retinopathy ECG for cardiac abnormalities including left ventricular hypertrophy
453
what risk score should be calculated in someone with hypertension
QRISK which estimates the percentage risk a patient will have a stroke or MI in the next 10 years
454
if a QRISK score is above 10% what medication should the patient be offered
should be offered a statin - atorvastatin 20mg daily
455
what lifestyle advice is given to those with hypertension
healthy diet stop smoking reduce alcohol reduce caffeine reduce salt intake regular exercise
456
what is the treatment for hypertension
step 1. Aged under 55 or type 2 diabetic of any age or family origin, use ACE inhibitors. Aged over 55 or black african use Calcium channel blocker step 2. ACEi plus CCB. Alternatively ACEi + Thiazide like diuretic or CCB + diuretic step 3. ACEi + CCB + thiazide like diuretic step 4. ACEi + CCB+ diuretic + fourth agent which depends on potassium levels in all of this ARBs are recommended instead of ACEi in patients of black african or african caribbean family origin and in those than cant tolerate ACEi
457
what medications are used as a fourth agent for hypertension regulation
dependent on serum potassium level 1. less than or equal to 4.5mmol/L consider a potassium sparing diuretic like spironolactone 2. more than 4.5mmol/L consider an alpha blocker or a beta blocker
458
why is it important to regularly measure U+E when using certain medications for hypertension
spironolactone is potassium sparing and can cause hyperkalaemia ACE inhibitors can also cause hyperkalaemia thiazide like diuretics can cause electrolyte disturbances and hypokalaemia
459
what are the blood pressure targets when treating hypertension
under 80 - below 140/90 over 80 - below 150/90
460
what is a hypertensive emergency
also referred to as malignant hypertension it refers to blood pressure above 180/120 with retinal haemorrhages or papilloedema - need same day referral !
461
how is a hypertensive emergency managed
1. patients need same day assessment for confusion, heart failure, suspected acute coronary syndrome or AKI 2. patients need assessing for secondary causes and end organ damage 3. IV sodium nitroprusside, labetalol, glyceryl trinitrate and nicardipine can be used
462
what is folliculitis
it is a common skin condition where the hair follicles become infected or inflamed
463
what can cause folliculitis
activities such as shaving, hot tub, excess sweating bacterial infection
464
what are the types of folliculitis you can get
1. Staphylococcus aureus folliculitis 2. Pseudomonas aeruginosa (hot tub) 3. Malassezia folliculitis (yeast) 4. Pseudofolliculitis barbae (razor bumps) 5. Sycosis barbae (severe shaving related) 6. Gram negative folliculitis (antibiotic use) 7. Boils (furuncles - deep infection) 8. Carbuncles (several boils in one spot) 9. Eosinophilic folliculitis (immunosuppressed)
465
what are symptoms of folliculitis
red bumps that look like pimples can look like while filled bumps or can be pustules itchy and uncomfortable
466
what are risks for developing folliculitis
frequent shaving oral antibiotics for long period of time overweight or obese diabetes activities where you sweat a lot and dont fully shower off after spending time in hot tum or sauna that isnt properly cleaned
467
What is Gastro-oesophageal reflux disease
it is where the acid from the stomach flows through the lower oesophageal sphincter and into the oesophagus, where it irritates the lining and causes symptoms
468
what is the lining of the oesophagus
squamous epithelial lining
469
what are causes and triggers of GORD
greasy and spicy food coffee and tea alcohol non steroidal anti-inflammatory drugs stress smoking obesity hiatus hernia
470
how does GORD present
dyspepsia heartburn acid regurgitation retrosternal or epigastric pain bloating nocturnal cough hoarse voice
471
what are red flag symptoms of GORD
dysphagia - difficulty swallowing at any age aged over 55 weight loss upper abdominal pain reflux treatment resistant dyspepsia nausea and vomiting upper abdominal mass on palpation low haemoglobin raised platelet count
472
what is the course of action if someone has red flag symptoms with GORD
anything suspicious of cancer required a two week wait referral for further investigation It is also possible to refer from primary care for an urgent direct access endoscopy
473
what is endoscopy used to assess for
Gastritis Peptic ulcers Upper gastrointestinal bleeding Oesophageal varices (in liver cirrhosis) Barretts oesophagus Oesophageal stricture Malignancy of the oesophagus or stomach
474
what is a hiatus hernia
it is the herniation of the stomach through the diaphragm which can cause reflux
475
what are the four types of hiatus hernia
type 1: sliding type 2: rolling type 3: combination of sliding and rolling type 4: large opening with additional abdominal organs entering the thorax
476
what are lifestyle changes which can help GORD
reduce tea, coffee and alcohol intake weight loss avoid smoking smaller, lighter meals avoid heavy meals before bedtime stay upright after meals rather than staying flat
477
what medications can be given for GORD
antiacids - Gaviscon, Pepto-Bismol, Rennie (short term) PPIs - omeprazole and lansoprazole Histamine H2 receptor antagonists - Famotidine
478
what surgical intervention can be done for GORD
laparoscopic fundoplication - tying the fundus of the stomach around the lower oesophagus to narrow the lower oesophageal sphincter
479
how does Helicobacter pylori cause GORD
it produces ammonium hydroxide as well as several toxins. these cause gastric mucosal damage, and can cause gastritis, ulcers and increased risk of stomach cancer
480
what type of bacteria is helicobacter pylori
gram negative aerobic bacteria - has flagella
481
what are the investigations for helicobacter pylori
offer H.pylori test to anyone with dyspepsia - stool antigen test - urea breath test using radiolabelled carbon 13 - h.pylori antibody bloods - rapid urease test performed during endoscopy
482
how is H.pylori treated
triple therapy with a PPI and two antibiotics for 7 days - Omeprazole - amoxicillin - clarithromycin
483
what is barretts oesophagus
this is when the lower oesophageal epithelium changes from squamous to columnar epithelium caused by chronic acid reflux into the oesophagus (metaplasia)
484
what is the treatment for barretts oesophagus
endoscopic monitoring proton pump inhibitors endoscopic ablation - destroy abnormal cells
485
what is Zollinger-Ellison syndrome
this is a rare condition where a duodenal or pancreatic tumour secreted excessive quantities of gastrin which stimulated stomach acid secretion. This excess production results in severe dyspepsia, diarrhoea and peptic ulcers
486
what genetic condition are gastrin secreting tumours associated with
multiple endocrine neoplasia type 1 (MEN1)
487
what are haemorrhoids
they are enlarged anal vascular cushions
488
what are anal cushions
they are specialised submucosal tissue that contains connections between arteries and veins, making them very vascular. they are supported by smooth muscle and connective tissue. they help to control anal continence, along with the internal and external sphincters
489
what are the different classifications of haemorrhoids
1st degree: no prolapse 2nd degree: prolapse when straining and return on relaxing 3rd degree: prolapse when straining, do not return on relaxing but can be pushed back 4th degree: prolapsed permanently
490
what are symptoms of haemorrhoids
may be asymptomatic can be associated with constipation and straining painless bright red bleeding on the toilet tissue or seen after opening the bowels (not mixed with stool) sore/itchy anus feeling a lump around or in the anus
491
what is seen on examination in someone with haemorrhoids
External: visible on inspection as swellings covered in mucosa internal: may be felt on PR examination they may appear if the patient is asked to bear down during examination
492
what else can be used to examine a patient with haemorrhoids
proctoscopy - inserting a hollow tube into the anal cavity to visualise the mucosa
493
what are topical treatments for haemorrhoids
Anusol - contains astringents which help shrink the haemorrhoids Anusol HC - also contains hydrocortisone (only use for a short time) Germoloids cream (contains lidocaine) Proctosedyl ointment (contains cinchocaine and hydrocortisone - short term use only)
494
what are non surgical treatments for haemorrhoids
rubber band ligation (fitting a tight rubber band around the base of the haemorrhoid) injection sclerotherapy (phenol oil injection) infra-red coagulation bipolar diathermy (electrical current)
495
what are surgical treatments for haemorrhoids
haemorrhoidal artery ligation - using a proctoscope and suturing blood supply haemorrhoidectomy - can result in incontinence stapled haemorrhoidectomy
496
what can cause thrombosed haemorrhoids
these are caused by strangulation at the base of the haemorrhoid resulting in thrombosis in the haemorrhoid
497
how does a thrombosed haemorrhoid present
purplish very tender swollen PR examination unlikely due to the pain
498
what are symptoms of oral herpes
tingling and burning sensation followed by development of vesicular then ulcerative lesions involving the oropharynx and perioral mucosa
499
what virus causes herpes
HSV HSV-1 is typically associated with cold sores and can be associated with genital herpes HSV-2 typically causes genital herpes
500
what are symptoms of genital herpes
can be asymptomatic ulcers or blistering lesions burning, tingling or shooting pain flu like symptoms dysuria inguinal lymphadenopathy
501
what are risk factors for developing herpes
HIV infection immunosuppressive medications female sex higher risk sexual behaviour black race increasing age lack of condom use
502
how do you diagnose herpes
clinical history and examination - ask about sexual contacts in the case of genital herpes viral swab and PCR reaction Viral culture Glycoprotein G based type specific serology
503
How do you treat acute genital herpes
Acyclovir - 400mg orally three times daily for 7-10 days should be started 48-72 hours after symptom onset consider symptomatic treatment: paracetamol, ibuprofen, lidocaine topical (5% ointment)
504
how do you treat oral herpes
Aciclovir - 200mg orally five times daily for 7-10 days, should be started 48-72 hours after symptom onset symptomatic treatment: paracetamol, ibuprofen, lidocaine topical (5%) 2/3 times per day 2nd line: topical antivirals - docosanol topical (10%) five times a day at first sign of symptoms (also peniciclovir (1%) and aciclovir (5%) can be used)
505
what is given for ongoing/chronic genital herpes
aciclovir - 400mg orally twice daily for 12 months
506
what is given for disseminated disease: pneumonitis, hepatitis or CNS involvement in herpes
IV aciclovir
507
what is primary hypothyroidism
is where the thyroid produces inadequate thyroid hormones. THS will be raised, T3 and T4 are low
508
what is secondary hypothyroidism
central hypothyroidism, is where the pituitary behaves abnormally and produces inadequate TSH resulting in under stimulation of the thyroid gland and insufficient thyroid hormones. TSH, T3 and T4 will be low
509
what are causes of primary hypothyroidism
Hashimotos is the most common cause - presence of anti-TPO and anti-Tg antibodies iodine deficiency lithium use inhibits the production of thyroid hormones amiodarone interferes with thyroid hormone production and metabolism
510
what hyperthyroidism treatments can cause hypothyroidism
Carbimazole Propylthiouracil Radioactive iodine Thyroid surgery
511
what are causes of secondary hypothyroidism
Tumours (e.g., pituitary adenomas) Surgery to the pituitary Radiotherapy Sheehan’s syndrome (where major post-partum haemorrhage causes avascular necrosis of the pituitary gland) Trauma
512
how does hypothyroidism present
Weight gain Fatigue Dry skin Coarse hair and hair loss Fluid retention (including oedema, pleural effusions and ascites) Heavy or irregular periods Constipation iodine deficiency causes a goitre hashimotos can initially cause a goitre
513
what are diagnostic investigations for hypothyroidism
serum thyroid stimulating hormones look at free serum thyroxine, antithyroid peroxidase antibodies RBC fasting blood glucose
514
how is hypothyroidism treated
replacement dose levothyroxine: 1.6 micrograms/kg/day orally, just dose in increments of 12.5 to 25 micrograms to normalise the TSH in patients with pre existing coronary artery disease or aged over 65 use low dose levothyroxine sub-clinical hypothyroidism use low dose levothyroxine
515
What is infectious mononucleosis
it is a clinical syndrome most commonly caused by EBV, characterised by a triad of fever, pharyngitis and lymphadenopathy
516
How does infectious mononucleosis present
triad of fever, pharyngitis, cervical/generalised lymphadenopathy malaise splenomegaly rash signs of hepatitis jaundice myalgia
517
what are risk factors for infectious mononucleosis
kissing sexual behaviour
518
how do you diagnose infectious mononucleosis
clinical history and exam FBC antibodies - EBV specific antibodies LFTs PCR ultrasound/CT of abdomen
519
what is the treatment for infectious mononucleosis
supportive care - paracetamol and NSAIDs (no aspirin in children due to reyes syndrome) patient to refrain from strenuous activity and contact sports in the initial 3-4 weeks of illness if there is upper airway obstruction, haemolytic anaemia, and thrombocytopenia use corticosteroids (and IvIg)
520
when is a rash seen in patients who have been treated for infectious mononucleosis
if they have been treated with ampicillin, amoxicillin or beta-lactam antibiotics
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what are the types of influenza
A, B and C A and B are the most common type A has different H and N subtypes
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who is the yearly flu vaccination offered to for free on the NHS
people aged 65 or older young children pregnant women those with chronic health conditions such as asthma, COPD, heart failure and diabetes healthcare workers and carers
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how does influenza present
the delay between exposure and symptoms is typically 2 days: fever lethargy fatigue anorexia muscle and joint aches headache dry cough sore throat coryzal symptoms
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how is influenza diagnosed
testing may be considered to confirm diagnosis, and monitor circulation and outbreaks. The UK Health Security Agency monitors the number of flu cases and provides guidance when numbers are high point of care tests using swabs are available and give rapid results detecting viral antigens viral nasal or throat swabs can be sent for PCR analysis
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how is influenza managed
healthy patients who are not at risk of complications dont need treatment - self care, good fluid intake, rest if someone is at risk of complications there are two treatment options: - oral oseltamivir (twice daily for 5 days) - inhaled zanamivir (twice daily for 5 days) these treatments need to be started within 48 hours of onset of symptoms
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when might post exposure prophylaxis be given for influenza
when patients meet a certain criteria: - it is started within 48 hours of close contact - increased risk to the patient - the patient isnt protected by vaccination (less than 14 days since they were vaccinated/not vaccinated)
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what are the options for post influenza exposure prophylaxis
oral oseltamivir 75mg daily for 10 days inhaled zanamivir 10mg daily for 10 days
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what are complications of influenza
Otitis media, sinusitis and bronchitis Viral pneumonia Secondary bacteria pneumonia Worsening chronic health conditions, such as COPD and heart failure Febrile convulsions (young children) Encephalitis
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