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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
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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
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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)
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4
Q

What aspects of the skin should be examined on a newborn?

A
  • birthmarks or bruising/lacerations from birth
  • colour
  • vernix
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5
Q

What common birth marks may be present on a newborn?

A
  • salmon patch (red/pink patches often on eyelids)
  • hemangioma (strawberry marks)
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6
Q

What aspects of the face should be examined on a newborn?

A
  • appearance, any dysmorphia
  • any asymmetry
  • trauma
  • nose (assess patency)
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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
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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.

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9
Q

What are you assessing the upper limbs for in newborns?

A
  • symmetry
  • number of fingers/toes
  • check for two palmar creases
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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
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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

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12
Q

What is inspected for in the abdomen of newborn babies?

A
  • abdominal distension
  • normal umbilicus
  • inguinal hernia
  • organomegaly
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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
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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

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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

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16
Q

What is Ortolani’s test of hips?

A

With hips/knees at 90 degrees, abduct legs. Will clunk when femoral head relocates.

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17
Q

What is the palmar grasp reflex of a newborn?

A

Object placed in hand and palm stroked, fingers will close and grasp

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18
Q

What is sucking reflex of newborn?

A

Child will suck anything that touches roof of mouth

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19
Q

What is rooting reflex of newborns?

A

Newborn will turn head toward anything that strokes its cheek or mouth to aid breastfeeding.

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20
Q

What is the stepping reflex of newborns?

A

Soles of feet will appear to walk when placed on a flat surface

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21
Q

What is moro reflex of newborns?

A

Newborn dropped in hands quickly. Legs and head will extend, hands clench into fist

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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.

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23
Q

What are the vaccinations given in the 6 in 1 vaccine?

A
  1. diphtheria
  2. tetanus
  3. polio
  4. whooping cough (pertussis)
  5. Hib
  6. (Hep B not always given)
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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

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25
Q

When is MenB given?

A

8 weeks, 16 weeks, 1 year

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26
Q

When is rotavirus given?

A

8 weeks, 12 weeks

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27
Q

When is MMR given?

A

1 year and 3 years, 4 months

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28
Q

When is Men C given?

A

1 year and 14 years in Men ACWY

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29
Q

What is depression?

A

Mood affective disorder characterised by persistant low mood, low energy, and loss of interest in everyday activities.

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30
Q

What are some biological risk factors for depression?

A
  • family history
  • anxious or dependent personality
  • chronic physical illness
  • biochemical deficiencies
  • medications
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31
Q

What are some psychological risk factors for depression?

A
  • traumatic life events/childhood
  • environmental factors
  • low self esteem
  • lack of education
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32
Q

What are some social risk factors for depression?

A
  • poor social support
  • poor economic status or support
  • marital status
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33
Q

What are the 3 MAIN clinical features needed for a diagnosis of depression?

A
  1. low mood
  2. feeling tired all the time
  3. low interest or pleasure in normally enjoyable activities
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34
Q

How long do symtpoms need to last to be classed as depressive epsiode?

A
  • 2 weeks
  • not attributable to other causes (eg. bereavement)
  • impair daily function and cause distress
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35
Q

What are some other symptoms that people suffering from depression may be experiencing?

A
  • 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
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36
Q

What are some more somatic symptoms of depression?

A
  • loss of emotional reactivity
  • diurnal mood changes
  • early morning wakening
  • appetite loss
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37
Q

What should be looked for in risk assessment of patient presenting with depression?

A
  • risk to self (harm, neglect, suicide)
  • risk to others (hallucinations)
  • risk from others (abuse, neglect etc)
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38
Q

Which questionnaire is used to screen for depression?

A

PHQ-9 questionnaire

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39
Q

What are non-pharmacological treatments of depression?

A
  • guided self-help
  • CBT
  • mindfulness and meditation
  • psychotherapy
  • counselling
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40
Q

How should depression be reviewed?

A
  • ongoing to check compliance and symptoms
  • relapse prevention plan
  • safety netting
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41
Q

What are SSRIs? and how do they work? and examples?

A

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
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42
Q

What are SNRIs? how do they work? example?

A

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
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43
Q

What are TCAs? how do they work? example?

A

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
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44
Q

What is St John’s Wort?

A

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.

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45
Q

What is the difference between type 1 and 2 diabetes?

A

Type 1 is inability of pancreas to produce insulin, resulting in rising glucose levels. Type 2 is defect in secretion of insulin

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46
Q

What is the difference in pathology of Type 1 and Type 2 diabetes

A

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.

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47
Q

What are the diagnostic levels of HbA1c, random glucose, and fasting glucose for diabetes?

A

HbA1c = > 48 mmol/mol
Random glucose = > 11 mmol/l
Fasting glucose = > 7 mmol/l

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48
Q

What are the key presentations for diabetes?

A
  • polyuria and polydispia
  • weight loss
  • slow wound healing
  • visual blurring
  • fatigue
  • recurrent infections
  • loss of sensation
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49
Q

What is 1st line treatment for diabetes?

A

lifestyle modification:
- healthier diet (low carbs/glucose, high fibre)
- exercise and weight loss
- stop smoking and reduce alcohol

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50
Q

What is the 1st line medical management for type 2 diabetes?

A

metformin - complications include diarrhoea, abdo pain

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51
Q

What is 2nd line treatment for type 2 diabetes?

A

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.

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52
Q

Examples of rapid acting insulin?

A

novorapid and Humalog

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53
Q

Examples of short acting insulin?

A

Humulin S

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54
Q

Example of intermediate acting insulin?

A

Humulin I

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55
Q

Example of long acting insulin?

A

levemir

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56
Q

What sequence of insulin is given in type 2 diabetics?

A

Basal followed by prandial. Bi-phasal can be made by mixing two together

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57
Q

What are macrovascular complications of type 2 diabetes?

A

atherosclerotic cardiovascular disease, increased risk of stroke/MI/heart failure

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58
Q

What are microvascular problems of type 2 diabetes?

A
  • retinopathy
  • nephropathy
  • peripheral neuropathy
  • autonomic neuropathy
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59
Q

Why are foot problems common in type 2 diabetes?

A

loss of sensation so foot ulceration more common –> gangrene and ischaemia

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60
Q

What are metabolic complications of diabetes?

A

dyslipidaemia, hyperosmolar hyperglycaemic state, diabetic ketoacidosis

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61
Q

What is hyperosmolar hyperglycaemic state?

A

Fluid lost through urine during high glucose levels –> dehydration and electrolyte imbalance –> urine becomes hyperosmolar

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62
Q

Why does diabetic ketoacidosis occur?

A

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.

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63
Q

What combination of insulin is given in type 1 diabetes?

A

Combination of background, long-acting given once a day, and short acting given around mealtimes

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64
Q

Define Atrial Fibrillation (AF).

A

Uncontrolled, rapid, and irregular contraction of the atria

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65
Q

What is the aetiology of AF? (mrs SMITH)

A

Sepsis, Mitral valve disease, IHD, Thyrotoxicosis, Hypertension

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66
Q

What are the risk factors for AF?

A

Age, existing heart conditions, T2DM, alcohol/caffeine/drugs/smoking, obesity

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67
Q

What is the pathology of AF?

A

Disorganised electrical activity overrides normal SA node.

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68
Q

Most common type of AF?

A

paroxysmal (episodic)

69
Q

Key presentations of AF?

A

PALPITATIONS, syncope, SOB, chest pain, dizziness, faitgue

70
Q

Signs of AF?

A

Irregularly irregular pulse, absence of P waves, narrow QRS complex tachycardia

71
Q

What is the first line and gold standard investigation for AF?

72
Q

What are some other investigations that can be done for AF?

A
  • echocardiogram
  • CXR
  • U&Es, TFTs, troponin, calcium/magnesium
73
Q

What drugs are used to control rate in AF?

A

Beta blockers are 1st line. Also CCBs and digoxin.

74
Q

What is used to control rhythm in AF?

A

Cardioversion - immediately or can be delayed

75
Q

What are the two different types of cardioversion?

A

Pharmacological - amiodarone
Electrical - heart shocked back into sinys rhythm using defibrillator, pacemaker

76
Q

What anticoagulants are used to control AF?

A

Warfarin and DOACs (eg. apixaban)

77
Q

What is CHA2DS2VASc?

A

Scoring system to assess risk of AF patients developing stroke or TIA

78
Q

What does CHA2DS2VASc stand for?

A

Congestive heart failire, Hypertension, Age (>75 = 2), Diabetes, Stroke or TIA previously (=2), Vascular disease, Age 65-74, Sex (female)

79
Q

What is ORBIT?

A

Scoring system to assess someone’s risk of bleeding whilst on anticoagulation

80
Q

What is ORBIT based on?

A
  • low haemoglobin/haematocrit
  • age > 75
  • previous bleeding
  • renal function GFR < 60
  • antiplatelet meds
81
Q

What are the two types of IBD, and which parts of the GI tract do they affect?

A

Crohn’s - any part (espec. ileum)
UC - only affects colon and rectum, starting at rectum (espec. sigmoid?)

82
Q

Why does inflammatory bowel disease occur?

A

Mucosal immune system exerts inappropriate response to luminal antigens which enter mucosa via leaky epithelium.

83
Q

What gene is the Crohn’s mutation on?

84
Q

How does smoking affect Crohns and UC?

A

Exacerbates Crohns but relieves UC

85
Q

What is the difference macroscopically between Crohns and UC?

A

Crohns - skip lesions, cobblestone appearance (due to ulcers and fissures
UC - continuous inflammation and pseudopolyps

86
Q

What is the difference microscopically between Crohns and UC?

A

Crohns - transmural, non-caseating granulomas, has goblet cells
UC - inflammation limited to mucosa, depleted goblet cells, increased crypt abscesses, no granulomas

87
Q

What is the difference in key presentation between Crohns and UC?

A

Crohns is diarrhoea and RLQ pain. UC is bloody/mucus diarrhoea and LLQ pain

88
Q

What are some other signs of IBD?

A

Malabsorptions, mouth ulcers, erythema nodosum, episcleritis/uveitis, arthritis, rectal tenesmus

89
Q

What is the first line investigations for IBD?

A

FBC showing raised ESR/CRP. pANCA is positive in UC and negative in Crohns

90
Q

What is the gold standard investigation for IBD?

A

Endoscopy, sigmoidoscopy, colonscopy - bipsies taken and histology examined

91
Q

What is the first line treatment for Crohns?

A

Steroids - eg. prednisolone.

If steroids alone don’t work, add immunosuppressant eg. azathioprine

92
Q

How is remission maintained in Crohns?

A

immunosuppressants, eg. azathioprine

93
Q

What is the first line treatment for mild/moderate and severe UC?

A

Mild/Moderate = Aminosalicylate, eg. mesalazine
(second line are corticosteorids)

Severe = IV corticosteroids

94
Q

How is remission maintained in UC?

A

Aminosalicylates and azathioprine

95
Q

What is the difference between IBD and IBS?

A

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
Q

What are red flag symptoms for iBD?

A

rectal bleeding, weight loss, anaemia, fever, chronic abdo pain

97
Q

What are the NICE criteria for Acute Kidney Injury (AKI)?

A

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
Q

What are the three types of AKI?

A

Pre-renal, renal, and post-renal

99
Q

What are some examples for each of the types/causes of AKI?

A

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
Q

What investigations are used for AKIs?

A

Serum Creatinine and GFR

Urinalysis:
- leukocytes and nitrites = infection
- protein and blood = infection or nephritis
- glucose = diabetes

USS to look for obstruction

101
Q

What are 4 main treatment steps that can be undertaken in AKI?

A
  1. fluid rehydration (for pre renal)
  2. stop nephrotoxic drugs
  3. relieve obstruction (for post renal)
  4. consider dialysis
102
Q

Why are NSAIDs nephrotoxic?

A

Cause vasoconstriction of afferent arteriole (into glomerulus) = reduced GFR

103
Q

Why are ACE Inhibitors nephrotoxic in AKI?

A

Cause vasodilation of efferent arteriole (after glomerulus) = reduced GFR.

However, they are renoprotective in diabetic patients

104
Q

What changes can be made to drug administration in patients with renal impairement?

A
  1. increase interval between doses
  2. decrease dose
  3. combination of both
105
Q

What are examples of nephrotoxic drugs?

A

Contrast media, ACE-I, NSAIDs, Diuretics

106
Q

Symptoms of AKI?

A
  • oliguria
  • uraemia (anorexia, lethargy)
  • sepsis signs
  • postural hypotension
  • weak/rapid pulse
  • low JVP
107
Q

What is the main complication of AKI?

A

Hyperkalaemia - tall T waves, flat p waves, prolonged PR interval, wide QRS, ST depression

108
Q

What is used to treat hyperkalaemia?

A

Insulin - shifts potassium until cells by stimulating Na+/H+ antiporter.
Adminitstered with dextrose to avoid hypoglycaemia.

109
Q

What are LUTS?

A

Lower urinary tract symptoms associated with problems with bladder and urethra

110
Q

What are examples of storage LUTS symptoms?

A

Frequency, urgency, nocturia, incontinence

111
Q

What are examples of voiding LUTS symptoms?

A

Slow stream, splitting/fraying, intermittency, hesitance, straining

112
Q

What are post-micturition LUTS symptoms?

A

Dribble, sensation of incomplete emptying

113
Q

What are the primary investigations for LUTS symptoms?

A

Urodynamics and bladder diary DRE

114
Q

What are the main causes of LUTS?

A

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
Q

What is difference in texture of prostate in BPH and malignancy?

A

BPH = smooth/soft, symmetrical, enlarged
Malignancy = firm/hard, asymmetrical, craggy, irregular, loss of central sulcus

116
Q

What are the problems of PSA testing?

A

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
Q

What is the management of prostate cancer?

A

watchful waiting, external beam radiotherapy, brachytgerapy, hormone therapy, surgery

118
Q

What grading system is used for prostate cancer?

A

Gleason grading and TNM

119
Q

What is the management for BPH?

A

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
Q

What is the main difference between RA and OA?

A

RA is inflammatory and autoimmune. OA is non-inflammatory and wear and tear.

121
Q

What type of joints does arthritis usually affects?

A

Synovial lining/synovial joints

122
Q

What genes are associated with RA?

A

HLA DR4 and HLA DR1

123
Q

What is the pathophysiology of OA?

A

Imbalance between cartilage being worn down and chondrocytes repairing it - OA pain due to irritation of bone after cartilage has worn away

124
Q

What is the pathophysiology of RA?

A

Rheumatoid factor antibody targets IgG and causes activation of immune system against own IgG –> inflammation

125
Q

What type of antibodies are most specific/sensitive in RA?

A

Cyclic citrullinated peptide antibodies (anti -CCPs)

126
Q

What is the difference in joints affected between RA and OA?

A

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
Q

Difference in pain types between OA and RA?

A

RA better with movement (morning stiffness), OA worse with movement (no morning stiffness).

128
Q

What are the Xray signs seen with OA? (LOSS)

A
  • loss of joint space
  • osteophytes
  • subchondral sclerosis
  • subchondral cysts
129
Q

What are the classic signs in the hands in RA?

A
  • 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
Q

What are the common signs in hands of OA?

A

Nodes - (Heberdens in DIP, Bouchards in PIP)

131
Q

What is the first line and gold standard investigation for OA?

A

Xray - but diagnosis can be made without investigation if patient >45, typical activity related pain, and no morning stiffness

132
Q

What is the first line and GS investigations for RA?

A

First = check RF –> check anti-CCP. Inflammatory markers (ESR, CRP). Xray (joint destruction/deformity, swelling, bony erosions)

Gold = anti-CCP

133
Q

Treatment options for OA?

A
  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
Q

Treatment options for RA?

A
  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
Q

What is methotrexate MOA?

A

Inhibits enzymes responsible for nucleotide synthesis. Prevents cell division so leads to anti-inflammatory actions.

136
Q

What is the difference between gout and pseudogout?

A

Gout = high blood uric acid levels. M>F.
Pseudogout = high calcium pyrophosphate crystals in joints. F>M>.

137
Q

Big risk factor for gout?

138
Q

Difference in presentation of gout and pseudogout?

A

gout - single, acute, hot, swollen joint
pseudogout - knees, older adults

139
Q

Difference in Xray signs between gout and pseudogout?

A

gout - maintained joint space, lytic lesions, punched out erosions
pseudogout - chondracalcinosis and LOSS

140
Q

Difference in joint fluid aspiration between gout and pseudogout?

A

gout - needle shaped crystals. negative birefringement of polarised light.

pseudogout - rhomboid shaped crystals. positive birefringement of polarised light

141
Q

How are gout and pseudogout treated?

A

NSAIDs, Colchicine, Steroids. Allopurinol in long term for gout.

142
Q

What is the definition of epilepsy?

A

Paroxysmal event in which changes of behaviour, sensation, or cognitive processes are caused by excessive neuronal discharges. Associated with seizures.

143
Q

What kind of receptors can be affected in epilepsy?

A

excitatory NMDA or inhibitory GABA

144
Q

What happens during a seizure?

A

Clusters of neurones become temporarily impaired and send out excitatory, paroxysmal electrical discharges - too much excitation or too little inhibition

145
Q

What are the different types of seizures?

A
  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
Q

Difference in presentation between focal and generalised seizures?

A

Focal - hallucinations, memory flashbacks, doing strange things
Generalised - tongue biting, incontinence, groaning, convulsions

147
Q

What are the phases of seizures and how long do they last for?

A
  1. prodromal (confusion, irritability, mood change)
  2. early ictal (aura)
  3. ictal
  4. post-ictal (drowsy, confused, depression)
148
Q

First line and gold investigation for epilepsy?

A

Electroencephalogram (EEG)

149
Q

First line treatment for Generalised seizures in non-pregnant?

A

Sodium valproate - increases activity of GABA

150
Q

First line treatment for Generalised seizures in women of child bearing age?

A

Lamotrigine - inhibits sodium currents and suppreses glutamate release.

Valproate contraindicated because teratogenic

151
Q

First line treatment for Focal seizures in all non-pregnant?

A

Carbamazepine - sodium channel blocker that prevents firing of action potentials

152
Q

First line treatment for Focal seizures in women of child bearing age?

A

Lamotrigine.

Carbamazepine is tertogenic

153
Q

Definition of asthma?

A

Chronic inflammatory airway disease characterised by airway obstruction (bronchoconstriction) and hyper-reactivity

154
Q

When does asthma commonly present?

A

Childhood, 3-5 years and peaks 5-15 years

155
Q

What gene is associated with airway hyper-responsiveness and tissue remodelling in asthma?

156
Q

What is asthma caused by?

A

Genetic susceptibility predisposes patients to hyper-responsiveness, which is then triggered by environmental factors

157
Q

What are some risk factors for asthma?

A

Atopy, FHx, allergens, upper resp infections, medications (bb)

158
Q

What type of hypersensitivity reaction is asthma?

159
Q

What is the brief pathophysiology of asthma?

A
  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
Q

What are the main symptoms of asthma?

A

Dysponoea, expiratory wheeze, chest tightness, episodic SOB, history of triggers, sputum

161
Q

What is Samter’s triad (asthma)?

A
  1. Nasal polyps
  2. Aspirin sensitivity
  3. Asthma
162
Q

What are the first line and gold investigations for asthma?

A

Spirometry: FEV1/FVC < 0.7
Fractional Exhaled Nitric Oxide (FeNO): > 40 ppb

163
Q

What are some additional asthma tests?

A

Peak expiratory flow rate, allergy testing, CXR

164
Q

What is the stepwise approach of asthma management? 7 steps.

A
  1. SABA (salbutamol)
    • low dose ICS (budesonide)
    • leukotriene receptor antagonist (LTRA, Montelukast)
    • 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
Q

What are some exacerbations of asthma?

A

Infection, exercise, cold weather

166
Q

What PEFR is moderate asthma? Treatment?

A

50-75%. SABA, ipratropium bromide, and steroids.

167
Q

What PEFR is severe asthma?

A

33-50% + resp rate >25 + HR >110 + unable to complete sentences. Oxygen, IV salbutamol, IV aminophylline

168
Q

What PEFR is life-threatening asthma?

A

<33% + sats <92% + tired + silent chest + haemodynamocally unstable. IV magnesium sulphate, ICU, intubation

ICS/GP/ILA (9 decks)

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