GP Flashcards
1
Q
What questions should be asked as part of a history of a newborn?
A
- pregnancy details
- family history
- feeding pattern
- urination/pooing
- parental concerns
2
Q
What are the general inspections that need to be carried out on a newborn?
A
- weight/length/height
- colour: pallor (pale), cyanosis (blue), jaundice (yellow)
- posture
- tone
3
Q
What aspects of the head of a newborn should be examined?
A
- size/circumference (micro/macrocephaly)
- shape (lumps, sutures)
- fontanelle (flat, sunken, or buldging)
4
Q
What aspects of the skin should be examined on a newborn?
A
- birthmarks or bruising/lacerations from birth
- colour
- vernix
5
Q
What common birth marks may be present on a newborn?
A
- salmon patch (red/pink patches often on eyelids)
- hemangioma (strawberry marks)
6
Q
What aspects of the face should be examined on a newborn?
A
- appearance, any dysmorphia
- any asymmetry
- trauma
- nose (assess patency)
7
Q
What aspects of the eyes and ears should be inspected on a newborn?
A
- erythema or discharge
- inspect sclera
- fundal reflex (when light shone into eye, reflection is red/orange)
- inspect pinna and hearing test
8
Q
What are you checking for in the mouth of newborns?
A
Any clefts of the hard or soft palate. Check tongue for tongue/tie.
9
Q
What are you assessing the upper limbs for in newborns?
A
- symmetry
- number of fingers/toes
- check for two palmar creases
10
Q
What should be checked for in the chest of a newborn?
A
- respiratory rate (40-60 breaths per min)
- assess any increased work of breathing:
> difficulty feeding, expiratory grunting,
abdominal breathing, nasal flaring, recession
11
Q
What is checked for in auscultation of heart/lungs in newborns?
A
LUNGS - inspiratory/expiratory sounds, quality and volume of sounds
HEART - mitral/tricuspid/pulmonary/aortic valves. HR = 120-150 bpm
12
Q
What is inspected for in the abdomen of newborn babies?
A
- abdominal distension
- normal umbilicus
- inguinal hernia
- organomegaly
13
Q
What is assessed for in male and female genitalia of newborns?
A
- urethral meatus position
- size of penis (at least 2cm)
- testicular swelling
- palpate scrotum to check both testes present
- labia not fused
- clitoris present
14
Q
What abnormalities are you checking for in the lower limbs of newborns?
A
- asymmetry
- oedema
- ankle deformities
- missing digits
assess: tone, movement, range of knee joint movemement, femoral pulse
15
Q
What is Barlow’s test of the hips?
A
Hips adducted (thigh towards midline) whilst applying pressure on knee.
If hip is dislocatable, femoral head will slip over posterior rim of acetabulum
16
Q
What is Ortolani’s test of hips?
A
With hips/knees at 90 degrees, abduct legs. Will clunk when femoral head relocates.
17
Q
What is the palmar grasp reflex of a newborn?
A
Object placed in hand and palm stroked, fingers will close and grasp
18
Q
What is sucking reflex of newborn?
A
Child will suck anything that touches roof of mouth
19
Q
What is rooting reflex of newborns?
A
Newborn will turn head toward anything that strokes its cheek or mouth to aid breastfeeding.
20
Q
What is the stepping reflex of newborns?
A
Soles of feet will appear to walk when placed on a flat surface
21
Q
What is moro reflex of newborns?
A
Newborn dropped in hands quickly. Legs and head will extend, hands clench into fist
22
Q
What routes of administration can paracetamol be given to a baby? How much for neonate/1-2 months/3-5 months?
A
Suspension, IV, supposatary, effervescent tablets. 20mg/kg –> 30mg –> 60mg –> increase by 60 each time.
23
Q
What are the vaccinations given in the 6 in 1 vaccine?
A
- diphtheria
- tetanus
- polio
- whooping cough (pertussis)
- Hib
- (Hep B not always given)
24
Q
When are the 6 in 1 vaccine doses given to newborns?
A
8 weeks, 12 weeks, 16 weeks. Pre school booster at 3 years and 4 months. Teenage booster at 14 years
25
When is MenB given?
8 weeks, 16 weeks, 1 year
26
When is rotavirus given?
8 weeks, 12 weeks
27
When is MMR given?
1 year and 3 years, 4 months
28
When is Men C given?
1 year and 14 years in Men ACWY
29
What is depression?
Mood affective disorder characterised by persistant low mood, low energy, and loss of interest in everyday activities.
30
What are some biological risk factors for depression?
- family history
- anxious or dependent personality
- chronic physical illness
- biochemical deficiencies
- medications
31
What are some psychological risk factors for depression?
- traumatic life events/childhood
- environmental factors
- low self esteem
- lack of education
32
What are some social risk factors for depression?
- poor social support
- poor economic status or support
- marital status
33
What are the 3 MAIN clinical features needed for a diagnosis of depression?
1. low mood
2. feeling tired all the time
3. low interest or pleasure in normally enjoyable activities
34
How long do symtpoms need to last to be classed as depressive epsiode?
- 2 weeks
- not attributable to other causes (eg. bereavement)
- impair daily function and cause distress
35
What are some other symptoms that people suffering from depression may be experiencing?
- weight change
- disturbed sleep (insomnia or hypersomnia)
- slowed actions or increased restlessness
- reduced libido
- worthlessness or guilt feelings
- decreased concentration
- recurring thoughts of harm or suicide
36
What are some more somatic symptoms of depression?
- loss of emotional reactivity
- diurnal mood changes
- early morning wakening
- appetite loss
37
What should be looked for in risk assessment of patient presenting with depression?
- risk to self (harm, neglect, suicide)
- risk to others (hallucinations)
- risk from others (abuse, neglect etc)
38
Which questionnaire is used to screen for depression?
PHQ-9 questionnaire
39
What are non-pharmacological treatments of depression?
- guided self-help
- CBT
- mindfulness and meditation
- psychotherapy
- counselling
40
How should depression be reviewed?
- ongoing to check compliance and symptoms
- relapse prevention plan
- safety netting
41
What are SSRIs? and how do they work? and examples?
selective serotonin reuptake inhibitors
- most widely prescribed as fewer side effects
- increase levels of serotonin in brain by blocking reuptake into neurons
- eg. fluocetine, citalopram, sertraline
42
What are SNRIs? how do they work? example?
serotonin-noradrenaline reuptake inhibitors
- more effective but maybe more side effects
- block reuptake of serotonin and noradrenaline into nerve cells, so more active in brain
- eg. duloxetine, venlafaxine
43
What are TCAs? how do they work? example?
Tricyclic antidepressant
- older so no longer first line as more dangerous/more side effects
- block reuptake of serotonin and noradrenaline into presynaptic terminals so more in synaptic cleft
- eg. amitriptyline
44
What is St John's Wort?
herbal medicine used to treat mental health - similar action to SSRIs.
Should ask patient whether using St John's wort in history - could interact with other medications.
45
What is the difference between type 1 and 2 diabetes?
Type 1 is inability of pancreas to produce insulin, resulting in rising glucose levels. Type 2 is defect in secretion of insulin
46
What is the difference in pathology of Type 1 and Type 2 diabetes
Type 1 involves destruction of beta cells. Type 2 is due to repeated exposure to glucose/insulin, so beta cells become resistant and pancrease becomes fatigued.
47
What are the diagnostic levels of HbA1c, random glucose, and fasting glucose for diabetes?
HbA1c = > 48 mmol/mol
Random glucose = > 11 mmol/l
Fasting glucose = > 7 mmol/l
48
What are the key presentations for diabetes?
- polyuria and polydispia
- weight loss
- slow wound healing
- visual blurring
- fatigue
- recurrent infections
- loss of sensation
49
What is 1st line treatment for diabetes?
lifestyle modification:
- healthier diet (low carbs/glucose, high fibre)
- exercise and weight loss
- stop smoking and reduce alcohol
50
What is the 1st line medical management for type 2 diabetes?
metformin - complications include diarrhoea, abdo pain
51
What is 2nd line treatment for type 2 diabetes?
ADD
- sulfonylurea - complications of weight gain, hypoglycaemia
- DPP 4 inhibitor - stops DPP4 inhibiting incretins. complications of GI upset
- pioglitazone - complications of weight gain, fluid retension, heart failure
- SGLT2 inhibitor - stop glucose being reabsorbed. complications of glucosuria, increased UTIs, weight loss.
52
Examples of rapid acting insulin?
novorapid and Humalog
53
Examples of short acting insulin?
Humulin S
54
Example of intermediate acting insulin?
Humulin I
55
Example of long acting insulin?
levemir
56
What sequence of insulin is given in type 2 diabetics?
Basal followed by prandial. Bi-phasal can be made by mixing two together
57
What are macrovascular complications of type 2 diabetes?
atherosclerotic cardiovascular disease, increased risk of stroke/MI/heart failure
58
What are microvascular problems of type 2 diabetes?
- retinopathy
- nephropathy
- peripheral neuropathy
- autonomic neuropathy
59
Why are foot problems common in type 2 diabetes?
loss of sensation so foot ulceration more common --> gangrene and ischaemia
60
What are metabolic complications of diabetes?
dyslipidaemia, hyperosmolar hyperglycaemic state, diabetic ketoacidosis
61
What is hyperosmolar hyperglycaemic state?
Fluid lost through urine during high glucose levels --> dehydration and electrolyte imbalance --> urine becomes hyperosmolar
62
Why does diabetic ketoacidosis occur?
Massive perceived lack of glucose, so fatty acids metabolise and produce ketones (acetone). Number of blood ketones exceed those metabolised and K+ forces H+ into cells so more K+ in blood.
Causes vomiting, reduced perfusion of kidneys, inability to excrete excess, dehydration, electrolyte loss.
63
What combination of insulin is given in type 1 diabetes?
Combination of background, long-acting given once a day, and short acting given around mealtimes
64
Define Atrial Fibrillation (AF).
Uncontrolled, rapid, and irregular contraction of the atria
65
What is the aetiology of AF? (mrs SMITH)
Sepsis, Mitral valve disease, IHD, Thyrotoxicosis, Hypertension
66
What are the risk factors for AF?
Age, existing heart conditions, T2DM, alcohol/caffeine/drugs/smoking, obesity
67
What is the pathology of AF?
Disorganised electrical activity overrides normal SA node.
68
Most common type of AF?
paroxysmal (episodic)
69
Key presentations of AF?
PALPITATIONS, syncope, SOB, chest pain, dizziness, faitgue
70
Signs of AF?
Irregularly irregular pulse, absence of P waves, narrow QRS complex tachycardia
71
What is the first line and gold standard investigation for AF?
ECGs
72
What are some other investigations that can be done for AF?
- echocardiogram
- CXR
- U&Es, TFTs, troponin, calcium/magnesium
73
What drugs are used to control rate in AF?
Beta blockers are 1st line. Also CCBs and digoxin.
74
What is used to control rhythm in AF?
Cardioversion - immediately or can be delayed
75
What are the two different types of cardioversion?
Pharmacological - amiodarone
Electrical - heart shocked back into sinys rhythm using defibrillator, pacemaker
76
What anticoagulants are used to control AF?
Warfarin and DOACs (eg. apixaban)
77
What is CHA2DS2VASc?
Scoring system to assess risk of AF patients developing stroke or TIA
78
What does CHA2DS2VASc stand for?
Congestive heart failire, Hypertension, Age (>75 = 2), Diabetes, Stroke or TIA previously (=2), Vascular disease, Age 65-74, Sex (female)
79
What is ORBIT?
Scoring system to assess someone's risk of bleeding whilst on anticoagulation
80
What is ORBIT based on?
- low haemoglobin/haematocrit
- age > 75
- previous bleeding
- renal function GFR < 60
- antiplatelet meds
81
What are the two types of IBD, and which parts of the GI tract do they affect?
Crohn's - any part (espec. ileum)
UC - only affects colon and rectum, starting at rectum (espec. sigmoid?)
82
Why does inflammatory bowel disease occur?
Mucosal immune system exerts inappropriate response to luminal antigens which enter mucosa via leaky epithelium.
83
What gene is the Crohn's mutation on?
NOD2
84
How does smoking affect Crohns and UC?
Exacerbates Crohns but relieves UC
85
What is the difference macroscopically between Crohns and UC?
Crohns - skip lesions, cobblestone appearance (due to ulcers and fissures
UC - continuous inflammation and pseudopolyps
86
What is the difference microscopically between Crohns and UC?
Crohns - transmural, non-caseating granulomas, has goblet cells
UC - inflammation limited to mucosa, depleted goblet cells, increased crypt abscesses, no granulomas
87
What is the difference in key presentation between Crohns and UC?
Crohns is diarrhoea and RLQ pain. UC is bloody/mucus diarrhoea and LLQ pain
88
What are some other signs of IBD?
Malabsorptions, mouth ulcers, erythema nodosum, episcleritis/uveitis, arthritis, rectal tenesmus
89
What is the first line investigations for IBD?
FBC showing raised ESR/CRP. pANCA is positive in UC and negative in Crohns
90
What is the gold standard investigation for IBD?
Endoscopy, sigmoidoscopy, colonscopy - bipsies taken and histology examined
91
What is the first line treatment for Crohns?
Steroids - eg. prednisolone.
If steroids alone don't work, add immunosuppressant eg. azathioprine
92
How is remission maintained in Crohns?
immunosuppressants, eg. azathioprine
93
What is the first line treatment for mild/moderate and severe UC?
Mild/Moderate = Aminosalicylate, eg. mesalazine
(second line are corticosteorids)
Severe = IV corticosteroids
94
How is remission maintained in UC?
Aminosalicylates and azathioprine
95
What is the difference between IBD and IBS?
IBD is a chronic autoimmune condition resulting in inflammation and swelling. IBS is a functional bowel disorder made up of a group of abdominal symptoms
96
What are red flag symptoms for iBD?
rectal bleeding, weight loss, anaemia, fever, chronic abdo pain
97
What are the NICE criteria for Acute Kidney Injury (AKI)?
Acute drop in kidney function:
1. rise in creatinine of >25 ug/L in 48 hours
2. rise in creatinine of >50% in 7 days
3. urine output < 0.5ml/kg/hr for > 6 hrs
98
What are the three types of AKI?
Pre-renal, renal, and post-renal
99
What are some examples for each of the types/causes of AKI?
Pre-renal: dehydration, hypotension/sepsis, HF
Renal: glomerulonephritis, interstitial nephritis, acute tubular necrosis
Post-renal: obstruction (causing back pressure) such as kidney stones, cancer masses, ureter/urethral strictures, enlarged prostate
100
What investigations are used for AKIs?
Serum Creatinine and GFR
Urinalysis:
- leukocytes and nitrites = infection
- protein and blood = infection or nephritis
- glucose = diabetes
USS to look for obstruction
101
What are 4 main treatment steps that can be undertaken in AKI?
1. fluid rehydration (for pre renal)
2. stop nephrotoxic drugs
3. relieve obstruction (for post renal)
4. consider dialysis
102
Why are NSAIDs nephrotoxic?
Cause vasoconstriction of afferent arteriole (into glomerulus) = reduced GFR
103
Why are ACE Inhibitors nephrotoxic in AKI?
Cause vasodilation of efferent arteriole (after glomerulus) = reduced GFR.
However, they are renoprotective in diabetic patients
104
What changes can be made to drug administration in patients with renal impairement?
1. increase interval between doses
2. decrease dose
3. combination of both
105
What are examples of nephrotoxic drugs?
Contrast media, ACE-I, NSAIDs, Diuretics
106
Symptoms of AKI?
- oliguria
- uraemia (anorexia, lethargy)
- sepsis signs
- postural hypotension
- weak/rapid pulse
- low JVP
107
What is the main complication of AKI?
Hyperkalaemia - tall T waves, flat p waves, prolonged PR interval, wide QRS, ST depression
108
What is used to treat hyperkalaemia?
Insulin - shifts potassium until cells by stimulating Na+/H+ antiporter.
Adminitstered with dextrose to avoid hypoglycaemia.
109
What are LUTS?
Lower urinary tract symptoms associated with problems with bladder and urethra
110
What are examples of storage LUTS symptoms?
Frequency, urgency, nocturia, incontinence
111
What are examples of voiding LUTS symptoms?
Slow stream, splitting/fraying, intermittency, hesitance, straining
112
What are post-micturition LUTS symptoms?
Dribble, sensation of incomplete emptying
113
What are the primary investigations for LUTS symptoms?
Urodynamics and bladder diary DRE
114
What are the main causes of LUTS?
Obstruction - BPH, kidney/bladder stones, urethral strictures, bladder/prostate malignancy
Infection - UTI, prostatitis
Primary pathology - overactive bladder, detrusor underactivity
Other - dementia, drugs, eg. diuretics
115
What is difference in texture of prostate in BPH and malignancy?
BPH = smooth/soft, symmetrical, enlarged
Malignancy = firm/hard, asymmetrical, craggy, irregular, loss of central sulcus
116
What are the problems of PSA testing?
Early detection but unreliable as high rate of false positives and false negatives - may lead to unecessary and invasive investigations of a cancer that would've been unproblematic
117
What is the management of prostate cancer?
watchful waiting, external beam radiotherapy, brachytgerapy, hormone therapy, surgery
118
What grading system is used for prostate cancer?
Gleason grading and TNM
119
What is the management for BPH?
Lifestyle mod - reduce natural diuretics, avoid large volume intake, bladder training
Medical - alpha blockers (eg. tamsulosin) to relax smooth muscle, and 5-alpha reductase inhibitors (eg. finasteride) to reduce size
120
What is the main difference between RA and OA?
RA is inflammatory and autoimmune. OA is non-inflammatory and wear and tear.
121
What type of joints does arthritis usually affects?
Synovial lining/synovial joints
122
What genes are associated with RA?
HLA DR4 and HLA DR1
123
What is the pathophysiology of OA?
Imbalance between cartilage being worn down and chondrocytes repairing it - OA pain due to irritation of bone after cartilage has worn away
124
What is the pathophysiology of RA?
Rheumatoid factor antibody targets IgG and causes activation of immune system against own IgG --> inflammation
125
What type of antibodies are most specific/sensitive in RA?
Cyclic citrullinated peptide antibodies (anti -CCPs)
126
What is the difference in joints affected between RA and OA?
RA: symmetrical. PROXIMAL interphalangeal, metacarphophalangeal, wrists, ankles, metatarsophalangeals
OA: weight bearing joints. Hips, knees, sacro-iliac, DISTAL interphalangeal, CMC at thumb base, wrist, spine
127
Difference in pain types between OA and RA?
RA better with movement (morning stiffness), OA worse with movement (no morning stiffness).
128
What are the Xray signs seen with OA? (LOSS)
- loss of joint space
- osteophytes
- subchondral sclerosis
- subchondral cysts
129
What are the classic signs in the hands in RA?
- Z-shaped thumb deformity
- Swan-neck deformity (hyperextended PIP with flexed DIP)
- Boutonnieres deformity (hyperextended DIP with flexed PIP)
- Ulnar deviation
- Decreased fist squeeze
130
What are the common signs in hands of OA?
Nodes - (Heberdens in DIP, Bouchards in PIP)
131
What is the first line and gold standard investigation for OA?
Xray - but diagnosis can be made without investigation if patient >45, typical activity related pain, and no morning stiffness
132
What is the first line and GS investigations for RA?
First = check RF --> check anti-CCP. Inflammatory markers (ESR, CRP). Xray (joint destruction/deformity, swelling, bony erosions)
Gold = anti-CCP
133
Treatment options for OA?
1. lifestyle changes and physio
2. stepwise analgesia:
- oral paracetamol and topical NSAIDs
- + oral NSAIDS w/ PPI
- opiates such as codeine or morphine
3. intra-articular steroid injections
4. joint replacement
134
Treatment options for RA?
1. Supportive - physio, occupational therapy
2. Analgesics - paracetamol, NSAIDs, steroids (tablet, injection. used to bridge until DMARD)
3. DMARD - methotrexate, sulfasalazine (1st line)
4. Biological treatments - adalimumab (if DMARD ineffective/contraindicated)
5. JAK Inhibitors
6. Surgery - joint replacement, athroscopy
Also consider dietary changes - mediterranean diet, folic acid, supplements
135
What is methotrexate MOA?
Inhibits enzymes responsible for nucleotide synthesis. Prevents cell division so leads to anti-inflammatory actions.
136
What is the difference between gout and pseudogout?
Gout = high blood uric acid levels. M>F.
Pseudogout = high calcium pyrophosphate crystals in joints. F>M>.
137
Big risk factor for gout?
alcohol
138
Difference in presentation of gout and pseudogout?
gout - single, acute, hot, swollen joint
pseudogout - knees, older adults
139
Difference in Xray signs between gout and pseudogout?
gout - maintained joint space, lytic lesions, punched out erosions
pseudogout - chondracalcinosis and LOSS
140
Difference in joint fluid aspiration between gout and pseudogout?
gout - needle shaped crystals. negative birefringement of polarised light.
pseudogout - rhomboid shaped crystals. positive birefringement of polarised light
141
How are gout and pseudogout treated?
NSAIDs, Colchicine, Steroids. Allopurinol in long term for gout.
142
What is the definition of epilepsy?
Paroxysmal event in which changes of behaviour, sensation, or cognitive processes are caused by excessive neuronal discharges. Associated with seizures.
143
What kind of receptors can be affected in epilepsy?
excitatory NMDA or inhibitory GABA
144
What happens during a seizure?
Clusters of neurones become temporarily impaired and send out excitatory, paroxysmal electrical discharges - too much excitation or too little inhibition
145
What are the different types of seizures?
1. focal - limited to one hemisphere or lobe. often involves hearing and speech. with or without impaired awareness
2. generalised
- tonic: muscles stiff and flexed, fall backward
- atonic: muscles relax and floppy, fall forward
- clonic: violent contractions and convulsions
- tonic-clonic: episodes + loss of consciousness + post-ictal period
- myoclonic: short muscle twitches
- absence: impaired awareness or responsiveness
146
Difference in presentation between focal and generalised seizures?
Focal - hallucinations, memory flashbacks, doing strange things
Generalised - tongue biting, incontinence, groaning, convulsions
147
What are the phases of seizures and how long do they last for?
1. prodromal (confusion, irritability, mood change)
2. early ictal (aura)
3. ictal
4. post-ictal (drowsy, confused, depression)
148
First line and gold investigation for epilepsy?
Electroencephalogram (EEG)
149
First line treatment for Generalised seizures in non-pregnant?
Sodium valproate - increases activity of GABA
150
First line treatment for Generalised seizures in women of child bearing age?
Lamotrigine - inhibits sodium currents and suppreses glutamate release.
Valproate contraindicated because teratogenic
151
First line treatment for Focal seizures in all non-pregnant?
Carbamazepine - sodium channel blocker that prevents firing of action potentials
152
First line treatment for Focal seizures in women of child bearing age?
Lamotrigine.
Carbamazepine is tertogenic
153
Definition of asthma?
Chronic inflammatory airway disease characterised by airway obstruction (bronchoconstriction) and hyper-reactivity
154
When does asthma commonly present?
Childhood, 3-5 years and peaks 5-15 years
155
What gene is associated with airway hyper-responsiveness and tissue remodelling in asthma?
ADAM33
156
What is asthma caused by?
Genetic susceptibility predisposes patients to hyper-responsiveness, which is then triggered by environmental factors
157
What are some risk factors for asthma?
Atopy, FHx, allergens, upper resp infections, medications (bb)
158
What type of hypersensitivity reaction is asthma?
Type 1
159
What is the brief pathophysiology of asthma?
1. allergens picked up by dendritic cells and presented to Th2
2. Cytokines signalled which produce IgE antibodies
3. These coat mast cells and stimulate them to release granules (histamine)
4. Causes bronchial smooth muscle spasm and increased mucus secretion
5. Bronchoconstriction
160
What are the main symptoms of asthma?
Dysponoea, expiratory wheeze, chest tightness, episodic SOB, history of triggers, sputum
161
What is Samter's triad (asthma)?
1. Nasal polyps
2. Aspirin sensitivity
3. Asthma
162
What are the first line and gold investigations for asthma?
Spirometry: FEV1/FVC < 0.7
Fractional Exhaled Nitric Oxide (FeNO): > 40 ppb
163
What are some additional asthma tests?
Peak expiratory flow rate, allergy testing, CXR
164
What is the stepwise approach of asthma management? 7 steps.
1. SABA (salbutamol)
2. + low dose ICS (budesonide)
3. + leukotriene receptor antagonist (LTRA, Montelukast)
4. + LABA (salbutamol)
5. SABA +/- LTRA but switch ICS/LABA to MART (combined LABA and ICS)
6. SABA +/- LRTA but increase ICS dose within MART
7. SABA +/- LRTA but increase isolated ICS. Or trial theophylline or inhaled LAMA (tiotropium)
165
What are some exacerbations of asthma?
Infection, exercise, cold weather
166
What PEFR is moderate asthma? Treatment?
50-75%. SABA, ipratropium bromide, and steroids.
167
What PEFR is severe asthma?
33-50% + resp rate >25 + HR >110 + unable to complete sentences. Oxygen, IV salbutamol, IV aminophylline
168
What PEFR is life-threatening asthma?
<33% + sats <92% + tired + silent chest + haemodynamocally unstable. IV magnesium sulphate, ICU, intubation
