GP Flashcards

(407 cards)

1
Q

what is the pathophys of acne vulgaris 3

A

formation of acne lesions due to three contributing factors:
1. follicular hyperkeratinization: formation of keratinous plug due to an abnormal keratinization process= skin cells do not shed as normal leading to the proliferation of P. acnes
2. increased sebum production: sebum acts as a nutrient for P.acne and forms a favourable anaerobic environment
3. Propionibacterium acnes colonization: this bacteria contributes to inflammation by releasing pro inflammatory mediators eg chemokines, cytokines and reactive oxygen species

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2
Q

Where does acne act? 1

A

on pilosebaceous unit

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3
Q

What are the different types of acne lesions seen in acne vulgaris pts 4

A

comedones= dilated sebaceous follicle (whitehead is closed and blackhead is open)
inflammatory lesions= papules and pustules
due to excessive inflammatory response= nodules and cysts
scars: ice-pick scars and hypertrophic scars

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4
Q

How is acne vulgaris classified 3

A

mild: open and closed comedones with or without sparse inflammatory lesions
moderate acne: mild + numerous papules and pustules
severe acne: extensive inflammatory lesions, which may include and scarring

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5
Q

How is acne vulgaris treated?

A

Mild/ moderate:
12 week topical combination therapy: any 2 of the following in combination:
Topical benzoyl peroxide.
Topical antibiotics (clindamycin)
Topical retinoids (tretinoin/adapalene)

Mod/ severe:
12 week course of one of the following:
-> a fixed combination of topical adapalene with topical benzoyl peroxide + either oral lymecycline or oral doxycycline
-> a topical azelaic acid + either oral lymecycline or oral doxycycline

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6
Q

When can patients be referred with acne? 6

A
  1. Acne fulminans.
  2. Mild-moderate acne not responding to two 12 week courses of treatment as above.
  3. Moderate-severe acne not responding to one 12 week course of treatment as above, including an oral antibiotic.
  4. Psychological distress/mental health disorder contributed to by acne.
  5. Acne with persistent pigmentary changes.
  6. Acne with scarring.
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7
Q

What is a specific complication of long term abx use in acne, causes and what treatment can be given?

A

Gram-negative folliculitis (caused by e.coli/ kleb/ proteus/ pseudomonas)
high dose oral trimethoprim

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8
Q

What is acute bronchitis and timeline

A

inflammation of bronchi which is mainly virally caused (common cold eg rhino/ coronavirus)
resolves in 3 week but can have persistant cough

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9
Q

Presentation of acute bronchitis 3

A
  1. cough
  2. wheeze
  3. sore throat

inflammation in bronchi= increased mucus production= cough to clear it

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10
Q

How can acute bronchitis be differentiated from pneumonia 2

A

no focal chest signs apart from wheeze in acute bronchitis
systemic features are more indicative of pneumonia

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11
Q

What is the management of acute bronchitis 2

A
  1. supportive (fluids and analgesia at home)
  2. only consider abx (doxycyline) if systemic unwell, co-morbidities or CRP of over 100
    -> cannot use doxycycline in children/ pregnant so use amoxicillin instead
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12
Q

What is acute stress reaction and features 4

A

occurs in first 4 weeks after a traumatic event
features: sleep disturbance, hypervigilance, flashbacks, dissociation

(imagine a person sleeping then suddenly waking with hypervigilance, looking around the rooms- they dissociate whilst looking at the drawers in the room and get flashbacks looking at the floor)

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13
Q

What is the mangement for acute stress reaction 3

A

1st line: CBT
2. benzodiazipines: ONLY for acute anxiety, not recommended by WHO
3. encourage sleep hygeine and relaxation techniques

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14
Q

What is an anal fissure, 3 causes and classification

A

a tear in the mucosal lining of the distal anal canal
main cause= trauma from defecation of hard stool (constipation and dehydration), alternatively IBD or rectal cancer
acute= present for less than 6 weeks
chronic= present for over 6 weeks

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15
Q

What are the features of anal fissures 3

A
  1. intense pain post defecation, which is out of proportion to the size of the fissure
  2. bright red rectal bleeds
  3. itching typically post defecation
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16
Q

How are anal fissures investigated and diagnosed

A

In the likely event of a DRE being declined due to pain, an EUA and proctoscopy can be done to identify the fissure

EUA= examination under anaesthesia

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17
Q

how to differentiate between anal fissures and haemorrhoids 2

A

fissures are more more painful during bowel movements and bleed more than haemorrhoids

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18
Q

What is the management of acute and chronic anal fissures (5,3)

A

acute:
1. high fibre diet and high fluid intake
2. bulk forming laxatives (isphagula husk)
3. lubricants eg petroleum jelly before defecation
4. using simple analgesia eg paracetomol
5. topical anaesthetic eg lidocaine gel/ ointment

chronic:
1. topical GTN
2. diltiazem cream (CCB), second line to GTN
3. botox injections into internal anal sphincter (to encourage relaxation and healing
3. referral for lateral sphincterotomy (division of the internal anal sphincter muscle to release tension in anal sphincter muscle)

GTN + CCB relaxes internal anal sphincter= reduced anal pressure= increases blood circulation= allows for for healing and reduced pain

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19
Q

What is the pathophys of bacterial vaginosis, is it an STI?

A

overgrowth of anaerobic organisms eg gardnerella vaginalis (normally found in the flora), leading to the increase of vaginal pH
not an STI, but seen mostly in sexually active women

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20
Q

What is the diagnosis criteria of bacterial vaginosis and what is this criteria called

A

Amsel’s criteria for diagnosis of BV - 3 of the following 4 points should be present
-> thin, white homogenous discharge
-> clue cells on microscopy: stippled vaginal epithelial cells (from high vaginal swab)
-> vaginal pH > 4.5 (swab on pH paper)
-> positive whiff test (addition of potassium hydroxide results in fishy odour)

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21
Q

What is the management for bacterial vaginosis 2

A
  1. asymptomatic= no tx required
  2. symptomatic= oral metronidazole for 5-7 days
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22
Q

What are the main risk factors of benign prostatic hyperplasia 2

A
  1. age: around 80% of 80-year-old men have evidence of BPH
  2. ethnicity: black > white > Asian
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23
Q

What is the presentation of BPH 8

A

LUTS symptoms:
issues with both storage and voiding (voiding is more common)
storage: frequency, urgency, nocturne, incontinence
voiding: poor stream, hesitancy, incomplete emptying, dribbling

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24
Q

What are the Ix for BPH 5

A
  1. DRE (rectal exam)- smooth enlarged- prostatic cancer is hard and irregular
  2. PSA (for ruling out prostate cancer but can be raised in both)
  3. urine dipstick
  4. international prostate symptom score (IPSS) to assess impact of LUTSon QOL-
    Score 20-35: severely symptomatic
    Score 8-19: moderately symptomatic
    Score 0-7: mildly symptomatic
  5. transrectal ultrasound to determine size (can determine tx options)
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25
What is the management for BPH 5
1. lifestyle changes and watchful waiting: decrease caffeine intake 2. 1st line- alpha 1 antagonist eg tamsulosin which relaxes bladder neck 3. 2nd line- 5 alpha reductase inhibitor eg finasteride which decreases testosterones production and therefore decreases prostate size 4. combination therapy of 2 & 3 5. surgery (last resort): transurethral resection of prostate (main complication= retrograde ejaculation)
26
What is vaginal candidiasis, cause 2 and risk factors 4
'vaginal thrush' mostly candida albicans and rest by other candida species long term abx/ steroids, diabetes mellitus, immunocompromised
27
What is the normal vaginal flora compromised of and how does this maintain a healthy environment. What happens when this is lacking?
lactobacillus- releases lactic acid to maintain low ph= prevents growth of bacteria
28
What is the presentation of vaginal candidiasis 2
cottage cheese but non-offensive discharge vulvitis- itching and vulval erythema
29
What are the investigations for vaginal candidiasis
swab not indicated if consistent clinical features with candidiasis | otherwise black charcoal swab
30
What is the management of recurrent vaginal candidiasis 4 and what is classed as recurrent
classified as 4+ episodes a year 1. check compliance with treatment 2. confirm candidiasis with high vaginal swab for microscopy and culture 3. glucose test to exclude diabetes 4. induction-maintenance regime -> induction: oral fluconazole every 3 days for 3 doses -> maintenance: oral fluconazole weekly for 6 months
31
What is the management vaginal candidiasis 3
1. first line: oral fluconazole 150 mg as a single dose 2. if allergy/ pregnant: clotrimazole 500 mg intravaginal pessary 3. if vulval sx then add topical imidazole in combination with oral/ intravaginal antifungal
32
What is the cause of Chlamydia and why is it relevant in the UK
Chlamydia trachomatis the most prevalent sexually transmitted infection in the UK
33
What is the presentation of chlamydia 3
1. asymptomatic in around 70% of women and 50% of men 2. women: cervicitis (discharge, bleeding), dysuria 3. men: urethral discharge, dysuria
34
How is chlamydia diagnosed 4
test done 2 weeks after exposure women: low vaginal swab is first-line men: the urine test is first-line (first morning void urine sample) both of these samples are tested via NAATs
35
What is the screening for chlamydia
National Chlamydia Screening Programme for 15-24 years, open to all sexually active pts
36
What is the Mx for chlamydia 3
1. 7 days doxycycline 100mg BD 2. if CI or pregnant, then azithromycin 3. all contacts (men in 4 weeks before sx and women in 6 months before) can be offered support/ referral with GUM- if pt has confirmed chlamydia case then treat their contacts with doxycycline before testing them
37
What are the complications of chlamydia? 4
infertility (both) PID (f) epididymo-orchitis (m) reactive arthritis (both)
38
What is chronic fatigue syndrome
3 months of disabling fatigue affecting mental and physical function more than 50% of the time with no other diseases causing this
39
What are the features of chronic fatigue syndrome 5
1. fatigue (main one) 2. sleep problems 3. muscle/ joint pains 4. headaches 5. cognitive dysfunction (inability to concentrate, difficulty with thinking and word-finding) | (Feeling Sleepy, Might Just Head (c)Out)
40
What is the ix for chronic fatigue syndrome and diagnostic criteria?
1. bloods to exclude pathology: FBC, U&E, LFT, TFT, CRP, ESR, ferratin, coeliac, calcium, CK, glucose 2. nice criteria to diagnose- fatigue not caused by any other condition, post-exertional malaise that is disproportionate to activity and with a prolonged recovery time, sleep disturbance, cognitive dysfunction for more than 3 months
41
What is the Mx for chronic fatigue syndrome 4
1. refer to specialist chronic fatigue syndrome service 2. energy management to stay within energy limit (strategy supported by CFS specialist) 3. cognitive behavioral therapy 4. do not encourage exercise unless part of programme with CFC specialist team
42
What are the two types of conjunctivitis
allergic infective (split into bacterial and viral)
43
What are the features 2 and mx of allergic conjunctivitis 2
features: ->bilateral conjunctival erythema and swelling -> itching Mx: first line: topical/ oral antihistamines eg cetirizine 2nd line: topical mast cell stabilisers eg sodium cromoglicate
44
Compare the sx of bacterial and viral conjunctivitis
bacterial: purulent discharge, eyes stuck together in morning viral: serous discharge, recent URTI
45
How is infective conjunctivitis managed 2
1. topical abc chloramphenicol eye drops, 2/3 hourly 2. topical fusidic acid eye drops or pregnant women BD
46
What classifies as constipation
unsatisfactory defecation due to : infrequent stools (<3 times weekly) difficult stool passage (with straining or discomfort) seemingly incomplete defecation
47
What is the management of constipation 5
1 month of increased fibre, fluids and exercise 2 months of bulk forming laxative eg isphagula husk 2 months of osmotic laxartive eg lactulose/ macrogol 2 months of stimulant laxative eg senna/ sodium picosulfate if still constipated, stop all laxatives and take prucalopride 1mg
48
What is contact dermatitis types, which is more common, locations of each
irritant contact dermatitis: inflammation of skin due to direct contact with irritants (more common) -> on hands/ where contact was with irritant allergic contact dermatitis: inflammation of skin due to a type 4 hypersensitivity reaction (less common) -> expands to area past contact with trigger
49
what r the best readings to quantify CKD 2
eGFR and albumin: creatinine ratio
50
what is CKD
eGFR of <60mL/min/1.73m2 for 3 or more months
51
what are the stages of CKD 5 and their values
stage 1: >90mL/min eGFR stage 2: 60-89 mL/min eGFR stage 3A: 45-59mL/min eGFR stage 3B: 30-44mL/min eGFR stage 4: 15-29mL/min eGFR stage 5: less than 15mL/min eGFR (end stage CKD)
52
what is the pathophys of CKD 4 and explain why proteins and blood can get into urine
low GFR= lots to damaged nephrons this increases burden on remaining nephrons this also increases RAAS activation to increase GFR but this increases pressure this causes loss of basement membranes selective permeability= blood and protein in urine
53
what are the 2 most common risk factors for CKD
diabetes mellitus hypertension
54
why is CKD initially asymptomatic 1 and why does CKD become symptomatic 1
asymptomatic- lots of nephrons as a reserve symptomatic- due to substance accumulation
55
What are the Ix for CKD 3
1. FBC (CKD= kidnyes produce less EPO= less RBC made= anaemia) and U&Es 2. Urinalysis - haematuria, proteinuria, glycosuria, albumin: creatine ratio 3. Renal ultrasound: shows bilateral small atrophied kidneys
56
treatment for CKD 4 (what is the aim of treatment, example, when to refer and last resort treatment)
Irreversible so treat to prevent progression of disease and symptom control: eg Oedema - fluid and sodium restriction furosemide Referral to nephrology if eGFR < 30 (stage 4) or A:CR>70 last resort- renal replacement therapy
57
what is gout’s pathophysiology 3
1. uric acid build up 2. leads to monosodium urate monohydrate crystal deposition along joints 3. =joints symtoms in gout
58
risk factors for gout 2
1. purine rich food: high meat, seafood, alcohol diet 2. middle aged overweight man
59
What are the medicines that increase risk of gout
1. low dose aspirin eg 75mg 2. thiazide like diuretics
60
presentation of gout 2 and what joint is usually affected 1
1. sudden onset 2. painful swollen red joint 3. usually big toe (metatarsophalangeal joint)
61
investigations for gout 2 and result
1. joint aspiration and polorised light microscopy showed needle shaped negatively birefringent crystals 2. bloods: high uric acid
62
treatment for acute gout 3
1st line NSAIDs eg diclonefac PLUS PPI 2nd line colchicine (alternative to NSAIDs for patients on anticoagulants) 3rd line IM corticosteroid injection
63
prophylactic treatment for gout 2
1. allopurinol 2. lifestyle changes: decrease meat, seafood and alcohol
64
how does allopurinol prevent gout 2
it is a xanthine oxidase inhibitor which reduces uric acid production
65
what is the crystal composition for gout and pseudogout?
gout= monosodium urate monohydrate crystals pseudogout= calcium pyrophosphate crystals
66
What is pseudogout
calcium pyrophosphate crystals deposits along joint capsule
67
risk factors for pseudogout 3
1. hypercalcaemia 2. hyperparathyroidism 3. hyperthyroidism
68
investigations for pseudogout 3
1. joint aspiration and polarised light microscopy shows positively birefringent, rhomboid shaped crystals 2. bloods show high calcium 3. joint x-ray to differentiate from rheumatoid/ osteoathritis
69
presentation of pseudogout 2
1. swollen red hot joint 2. multiple widespread joints affected (MC is the knee)
70
treatment for pseudogout 2
1. same acute management as gout- NSAIDs, colchicine and corticosteroids 2. joint aspiration in severe cases
71
What is the prophylactic treatment for pseudogout 1
daily low dose colchicine if no SE
72
what type of disease is type 1 diabetes mellitus, what does it cause destruction of and what is the consequence of this (3)
autoimmune disease causes destruction of beta cells in pancreas causes absolute insulin deficiency
73
what type of reaction is T1DM
type 4 hypersensitivity
74
what are the causes of T1DM 2
combination of genetics and environmental triggers
75
what are the consequences of the body not making insulin in T1DM (4 steps), start with body being unable to produce insulin to digest carbohydrates
2. cells cannot take in glucose so the body thinks it is being fasted 3. gluconeogenesis occurs in liver 4. causing more hyperglycaemia
76
when does T1DM usually manifest and what does it present in the form of
in childhood diabetes ketoacidosis
77
what are 5 symptoms of T1DM
polyuria, polydipsia, lethargy, thursh, sudden weight loss (thirst, toilet, tired, thrush, weight loss)
78
explain polyuria in diabetes 1 reason only explain polydipsia in diabetes
glucose excretion in urine draws water with it because glucose is osmotically active extreme thirst due to fluid loss via urine
79
explain sudden weight loss in T1DM
due to breakdown of adipose and muscle tissue as an alternative energy source to glucose
80
Explain recurrent thrush in diabetics
due to high sugar levels which is an optimal environment for candida
81
what is the max reabsorption value for glucose in the kidneys
10mmol/L
82
what is required for a diagnosis of T1DM 2
one abnormal glucose value and symptoms or two abnormal glucose values in asymptomatic
83
what is fasting glucose value determines diabetes mellitus and units
> =7mmol/L
84
what is fasting glucose value determines pre diabetes and units
> 6mmol/L
85
what HbA1c value determines diabetes mellitus and units
> =48mmol/mol
86
what HbA1c value determines pre diabetes and units
> 41mmol/mol
87
what is the gold standard investigation test for diabetes mellitus
HbA1c test
88
what random glucose value/ glucose tolerance test value determines diabetes mellitus and units
> =11.1mmol/L
89
what is the GS treatment for T1DM (2)
combination of long lasting 12-24 hour basal insulin dose and a short acting bolus injected 30 mins before meals
90
what is vital for treating T1DM patients 2
patient education- to monitor dietary glucose intake TREATMENT IS LIFELONG
91
what can diabetic ketoacidosis be classed as
a life threatening medical emergency
92
explain the pathophysiology of DKA starting with insulin deficiency
glucose not able to be absorbed alternative sources of energy is to break down free fatty acids from adipose tissue this is oxidised to acetyl coA to produce ketones ketones are acidic and cause blood acidosis
93
what is the compensation for DKA and what is this due to/ countering
respiratory compensation due to metabolic acidosis
94
symptoms of DKA (3) signs of DKA (2)
nausea, vomiting, dehydration, acetone-smelling breath, Kaussmal’s breathing
95
what 3 things are required for a DKA diagnosis (not specific values)
1. symptoms 2. hyperglycaemia 3. blood gas sample showing metabolic acidosis with respiratory compensation
96
what value dictates acidosis in the blood
pH <7.3
97
what test can be done to identify ketone levels and what value is DKA
blood ketone test >3mmol/L
98
what is treatment for DKA (4 steps)
1. ABC 2. 0.9% NaCl infusion 3. give insulin and glucose simultaneously 4. correct hypokalaemia if this occurs
99
what are the three complications of DKA treatment
1. cerebral oedema 2. hypokalaemia (insulin treatment for DKA causes intracellular shift of K+ which can cause muscle weakness) 3. hypoglycaemia (insulin treatment can cause glucose levels to drop rapidly into hypoglycaemia)
100
Name 4 non modifiable and 4 modifiable risk factors for T2DM
Non: age, family history, male, ethnicity modifiable: obesity, hypertension, sedentary lifestyle, high carb diet
101
what is T2DM’s insulin deficiency and how does T2 cause hyperglycaemia
relative insulin deficiency insulin resistance in liver and muscle cells causes hyperglycaemia
102
what are the diagnosis and investigations for T2DM
exactly the same as T1DM
103
explain the pathophysiology of T2DM starting with hyperglycaemia, including the role of the pancreas
hyperglycaemia causes increased insulin resistance in cells pancreas compensates by producing large volumes of insulin but is damaged by overworking and toxic glucose levels
104
what are the 4 lines of treatment for T2DM (1,1,4,1)
1st: lifestyle modifications eg lose weight 2nd: metformin 3rd: add sulfonylurea, PIOGLITAZONE, DPP-4 inhibitor or SGLT-2 inhibitor 4th: insulin
105
What is the second line medication for T2DM after metformin
ifno co-morbidiites= solfonylurea-gliciazide if CV co-morbidiity= SGLT2- dapagloflozin as it is cardioprotective
106
how does the SGLT2 inhibitor work? and name examples
inhibits reabsorption of glucose in the proximal tubule via the sodium-glucose transporter, resulting in more glucose to be excreted eg empagliflozen/ dapagliflozen
107
how does the DPP4 inhibitor work? and name an example
DPP4 inhibitor blocks DPP4 enzyme which prevents inhibition of GLP1. Overall effect= increased insulin production in response to a meal being sensed by the body (eg chewing) eg sitagliptin
108
how do sulfonylureas work and give an example
sulfonylurea binds to bind to K+ channels on beta pancreatic cells, reducing K+ efflux which causes depolarisation of the cell. There is a Ca2+ influx due to the action potential which stimulates insulin release from vesicles in the cell eg Gliciazide
109
how does metformin work
inhibits the AMPK enzyme in the liver which inhibits gluconeogensis, decreases intestinal glucose absorption and increases insulin sensitivity
110
what are the 3 microvascular complications of DM
retinopathy peripheral neuropathy nephropathy
111
what are the 4 macrovascular complications of DM
stroke hypertension peripheral artery disease coronary artery disease
112
explain retinopathy associated with diabetes and what can this lead to
high blood pressure and glucose levels damages retina= blindness/ cotton wool spots
113
explain peripheral neuropathy associated with diabetes and what can this lead to
high glucose levels damage blood vessels supplying nerves= pain/ numbness can lead to HTN as more likely to get atherosclerosis which can narrow blood vessels and cause hypertension
114
explain coronary artery disease associated with diabetic hypertension
hypertension caused by diabetes causes increased force exerted on artery walls which can damage them= atherosclerosis and embolism
115
what can hyperosmolar hyperglycaemic state be classed as and who typically presents with hyperosmolar hyperglycaemic state 2
a life threatening medical emergency elderly with T2DM
116
explain the pathophysiology of hyperosmolar hyperglycaemic state starting with hyperglycaemia and ending with what this does to the blood
hyperglycaemia causes osmotic diuresis and the volume depletion in the body increases the serum osmolarity causing hyperviscosity of blood
117
how can you diagnose hyperosmolar hyperglycaemic state (3)
1. severe hyperglycaemia (>30mmol/L) 2. hyperosmolarity (>320mosmol/kg) 3. no acidosis or ketosis
118
what is the presentation of hyperosmolar hyperglycaemic state (6) 2 signs and 3 symptoms
nausea, vomiting, dehydration, HYPOTENSION, TACHYCARDIA
119
what is osmotic diuresis and how does it cause electrolyte imbalances
increased urination in response to hyperglycaemia: excreted glucose in urine takes water with it so sodium and potassium follow the water and are excreted in the urine
120
what are the 3 haematological complications of hyperviscosity of blood and what condition does this occur in
MI, stroke, peripheral arterial thrombosis hyperosmolar hyperglycaemic state
121
what is the treatment for hyperosmolar hyperglycaemic state (4)
1. fluid replacement with saline 2. venous thromboembolism prophylaxis eg LWMH like enoxaparin 3. give insulin if glucose levels do not decrease 4. give K+ if K+ levels aren’t naturally corrected SLIK
122
what are the two complications related to treatment of hyperosmolar hyperglycaemic state
1. insulin related hypoglycaemia (due to excessive high-dose insulin therapy) 2. treatment related hypokalaemia (due to high-dose insulin therapy)
123
what is fibromyalgia and two risk factors
chronic widespread MSK pain for 3+ months 1. females 2. stress
124
presentation of fibromyalgia 3
widespread pain fatigue sleep difficulties
125
investigations of fibromyalgia 2 and how is it diagnosed
pain or tenderness in 11 or more out of 18 sites palpated bloods for exclusion: FBC, UE, LFT, TSH, CRP, calcium, glucose, B12 folate, urine dip (all normal in fibromyalgia) Diagnosis criteria: 1. more than 3 months 2. generalised pain 3. fibromyalgia pain of 12+/31 (consists of widespread pain index and symptom severity score)
126
treatment for fibromyalgia 2
1. encourage exercise, CBT 2. tricyclic antidepressants for severe pain
127
what is GORD and what does it stand for what causes the reflux
LOS relaxation causes reflux of gastric contents into the oesophagus Gastro-Oesophageal Reflux Disease
128
risk factors for GORD 3 and which sex is more likely to get this by how much and why
1. increased abdo pressure eg obesity & pregnancy 2. Sliding Hiatus hernia (LOS slides up into chest) 3. LOS relaxants: Caffeine Alcohol Males x2 risk than females (eostrogen is protective)
129
signs and symptoms 2 of GORD including 3 red flags and 3 extra-oesophageal signs GORD
1. Heartburn (main symptom) which is exacerbated when lying down as reflux more easily occurs 2. Dyspepsia (indigestion) 3. Extra-oseophageal signs: cough, asthma, dental erosion (due to acid eroding teeth) 4. Red flags: dysphagia, weight loss, haematemesis
130
investigations for GORD 2
1. GS and diagnostic: 24 hour pH monitoring (abnormal if pH <4 more than 4% of the time) 2. Endoscopy to look for Barrett’s, especially in those with chronic heartburn symptoms
131
treatment for GORD 2
1st line: PPI Lifestyle changes: smaller meals, avoid food from 3 hours before bed
132
1 complication for GORD and show the disease pathway
Gastric adenocarcinoma GORD-> barretts-> oesophageal adenocarcinoma
133
what is barretts oesophagus and where does this occur, Ix 1 and Mx 2
Metaplasia from stratified squamous to simple columnar epithelium (has to occur within 1cm of the gastro-oesophageal junction) Ix: Endoscopy with biopsy which should show metaplasia within 1cm of the GOJ Tx: PPI + regular endoscopic surveillance
134
what is diverticular disease and where do they usually form
multiple outpouches of the colon wall with symptom sigmoid colon
135
explain the pathophysiology of diverticulitis 2 steps
1. high pressure in colon/ weak wall= diverticula formed 2. inflammation if bacteria/ faecal matter gathers in diverticula (diverticular disease with infection)
136
signs and symptoms of diverticular disease 3
divertiCuLaR constipation, lower left quadrant pain, rectal bleeding (haematochezia)
137
investigation for diverticular disease (GS)
CT abdomen and pelvis with contract GS
138
treatment for diverticular disease (2, GS)
bulk forming laxative eg isphagula husk and antibiotics (if signs of infection) GS= surgery
139
what value is defined to be hypertension and define malignant HTN and value
140/90+ very high blood pressure that develops quickly and causes organ damage 180/110+
140
what are the categories of hypertension and how many cases are in each category and describe the difference between the two
primary 90% secondary 10% primary has no known cause and secondary has known causes
141
what are the causes of secondary hypertension (6) 3 Cs, 2Ps, 1R
renal disease (MC) pregnancy phaechromocytoma cushings conns coarctation of the aorta (congenital narrowing of the aorta)
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what are the 4 main areas that malignant hypertension has symptoms in and how can this be assessed
brain (cerebral oedema, stroke), eye (papilloedema/ cotton wool spots), heart (HF, MI) and kidneys (AKI) fundoscopy= for papilloedema urinalysis= for renal function Echo/ECG= assesses left ventricular hypertrophy
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if the bp is measured at GP and is 140/90 then what is the next step
check ambulatory blood pressure at home
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how is hypertension staged and what are the actions for each stage (3)
stage 1: 135/85 (assess risks- including assessing organ damage) stage 2: 150/95 (lifestyle changes + medications) stage 3: 180/110 (malignant- same day admission and start antihypertensive medication ASAP)
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what is the treatment approach for stage 1 hypertension 1
BP monitored every 5 years
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what two things are offered to a person who has been diagnosed with hypertension
assessment of Cv risk investigation for secondary hypertension
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what is the treatment for under 55s and not of African/ Caribbean origin (2)
ace inhibitor or angiotensin receptor blocker
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what is the treatment for over 55s and of African/ Caribbean origin (1)
calcium channel blocker
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what is the 2nd step if one drug is not controlling hypertension for the two categories of people to treat
<55 not A/C origin= CCB or thiazide like diuretic eg indapamide can be added >55 of A/C origin= ACEi or ARB or thiazide like diuretic eg indapamide can be added
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if a patient is on ACEi and CCB and indapamide already but still symptomatic what should be given to them 1 (and normal potassium levels)
low dose spironolactone
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what is a side effect of ACEi and what can be given instead
dry long term cough ARB- losartan
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give an example of an ARB, ACEI, beta blocker, calcium channel blocker
losartan, ramipril, bisoprolol, amlodipine
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what is ACEi contradicted in 3
asthma and pregnancy and renal stenosis
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side effect of beta blockers 1 and what can this cause 1
postural hypotension which cause cause loss of consciousness
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SE of CCB
ankle swelling
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what is the first line medication for diabetics with hypertension
ACEi
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what happens when hypertension persists even when multiple medications are prescribed (2)
1. talk about adherence 2. add a beta blocker (potassium above 4.5) or spironolactone (potassium below 4.5)
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what are haemorrhoids
enlarged veins around anus
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3 causes of haemorrhoids and main cause
MC: constipation obesity pregnancy
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What are the two types of haemorrhoid
External originate below the dentate line prone to thrombosis, may be painful Internal originate above the dentate line do not generally cause pain
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grades of haemorrhoids 4
1. No prolapse 2. Prolapse when straining and return on relaxation 3. Prolapse when straining and can be manually pushed back in 4. Prolapse permanently
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signs and symptoms of haemorrhoids 2
painless haematachezia (fresh bleeding from rectum) Puritis anus
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What is the mx of haemorrhoids 3, 2
symptom mx: 1. high fibre diet and high fluid intake 2. bulk forming laxatives (isphagula husk) 3. topical treatment eg hydrocortisone cream (anusol) escalation: 1. rubber band ligation (outpt tx) for internal only 2. haemorrhoidectomy (for large symptomatic haemorrhoids that do not respond to outpt tx)
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what are rolling hiatal hernias
where the lower gastro-osophageal junction remains the the abdomen but a bulge of stomach (typically fundus) herniates up into the chest via the oesophageal hiatus
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what is a hiatal hernia and what r the two types of hiatal hernias and which is MC
stomach hernia through diaphragm aperture sliding (MC) and rolling
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what r sliding hiatal hernias and what is a consequence of this
where the lower gastro-osophageal junction slides up into the chest, above the diaphragm acid reflux
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investigations for hiatal hernia
barium swallow + x-ray for diagnosis
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Mx for hiatal hernia 3
1. conservatives: encourage weight loss, treat heartburn with gaviscon 2. PPI 3. laproscopic hiatal hernia repair
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what is hypothyroidism and what does is generally cause
thyroid hormone deficiency generalised slowing of processes
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what are the two types of hypothyroidism and how do they each cause hypothyroidism
primary- issue with thryoid gland, lack of T3/4 (one i in thyroid= 1) secondary- issue with pituitary, lack of TSH (two i in pituitary= 2)
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what are the causes of primary hypothyroidism (4) and secondary (1)
Hashimotos thyroiditis, De Quervain’s thyroiditis, dietary iodine deficiency, carbimazole pituitary adenoma
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6 symptoms of hypothyroidism
weight gain, lethargy, cold intolernace, loss of lateral aspect of eyebrow, constipation, fluid retention
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what three diseases are associated with hypothyrodism
downs and turners syndrome and coeliac disease (DOWN the stairs, TURN the corner and you’ll SEE it)
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what are the investigations for hypothyroidism (3)
1st line: thyroid function test 2. antithyroid peroxidase antibody levels for autoimmune causes 3. fasting blood glucose in patients with non-specific fatigue and weight gain due to association with T1DM
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what are the thyroid function test results for primary and secondary hypothyroidism
primary: low T3, high TSH secondary: low T3, low TSH
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treatment for hypothyroidism and how does this work
levothyroxine synthetic T4
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what is hashimotos thyroiditis, what does it lead to and what type of hypothyroidism does it cause
thyroid gland is attacked by immune system via antithyroid antibodies and leads to loss of function primary hypothyroidism
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what is the presentation of hashimotos like 2 and what does this progress to
same as hypothyroidism plus goitre of thyroid gland which progresses to atrophy
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what is the gold standard investigation for hashimotos
antithyroid peroxidase antibodies test should be positive (anti-TPO)
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What are the two strain of herpes simplex virus that affects humans, how does each spread and what is particular to note about herpes virus?
HSV-1, HSV-2 1= orally (more likely to be responsible for cold sores) 2= sexual contact (more likely to be responsible for genital ulceration) can be latent and reinfect body
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What are the features of HSV infection.
1. cold sores 2. painful genital ulceration (can happen repeatedly but **first is worst**) 3. severe gingivostomatitis
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What is the ix for a HSV genital ulcer
swab + NAAT test
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What is the mx for herpes simplex virus?
1. for gingivostomatitis: oral aciclovir, chlorhexidine mouthwash 2. for cold sores: topical aciclovir 3. for genital herpes: oral aciclovir, especially if multiple episodes
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What is the appearance of HSV on a pap smear? 3
3 Ms Multinucleated giant cells Margination of the chromatin Molding of the nuclei
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What is the cause and acute infection location of gonorrhoea
Gram-negative diplococcus Neisseria gonorrhoeae on any mucous membrane surface, typically genitourinary but also rectum and pharynx
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Features of gonorrhoea
males: urethral discharge, dysuria females: cervicitis e.g. leading to vaginal discharge rectal and pharyngeal infection is usually asymptomatic
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Why can we not immunise or prevent reinfections of gonorrhoea
due to antigen variation of type IV pili (proteins which adhere to surfaces) and Opa proteins (surface proteins which bind to receptors on immune cells)
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What is the Mx of gonorrhoea
1st line single dose 1g ceftrioxone IM
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What is Blepharitis, features, progression and mx
inflammation of the eyelid margins with lots of crusting at the base of eyelids features: dry and itchy eyes this can lead to styes and chalazions mx: warm compresses and gentle cleaning of eyelid margins
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What are styes, pathophys and mx
infection of sweat glands on eyelid, mc staph aureas mx: warm compresses and analgesia, chloramphenicol if conjunctivitis sx/ persist
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What is a chalazion and difference to styes. Mx
blocked and swollen meibomian gland typically on inside of eyelid mx: warm compresses and gentle massaging towards eyelashes
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What is entropian and mx
when eyelid turns inwards, causing lashes to press against the eye Mx: taping eyelid down, lubricating eye drops and surgical resolvement
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What is Ectropion
when the eyelid turns outwards, exposing the conjunctiva and means the eyeball is not adequately lubricated and protected
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What is the mx for any benign eyelid disorders that cause a risk to sight
same-day referral to ophthalmology
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What is thrichiasis and Mx
inward growth of eyelashes which causes corneal damage and ulceration mX; remove affected eyelashes
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What is periorbital cellulitis, features and mx
infection in front of the orbital septum (in front of the eye) features: swollen, red, hot skin around the eyelid and eye Mx: urgent referral to opthamology, CT to distinguish from orbital cellulitis, systemic oral abx
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What is orbital cellulitis
infection of tissues behind the orbital septum features: pain with eye movement, reduced eye movements, vision changes, abnormal pupil reactions, and proptosis (bulging forward of the eyeball) Mx: emergency opthamology admission, IV abx LIFE THREATENING
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What is atrophic vaginitis, who does it affect 1, features, tx 3
atrophy (thinning, drying and inflammation of vaginal walls) post-menopausal women vaginal dryness, dyspareunia and occasional spotting Tx: vaginal lubricants and moisturisers, if these do not help then topical oestrogen cream can be used
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define IBS 3
Chronic functional bowel disorder characterised by abdominal pain and change in bowel habits
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3 risk factors for IBS
Stress/ anxiety Female Younger age (peak at 20-30 year olds)
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5 investigations for IBS and what is the general investigation aim for IBS
Exclude coeliacs with serology (anti-tTG or anti-EMA) Exclude IBD with faecal calprotectin Exclude infections with ESR/CRP/ blood cultures Exclude colorectal cancer with FIT test Exclude hyperthyroidism with tfts Process of exclusion of other conditions
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diagnosis checklist for IBS 3
Diagnosis checklist= 1. recurrent abdominal pain for at least 1 day weekly for past 3 months 2. symptoms from 6 months ago 3. one of the following -Symptoms relieved by defecation -Change in bowel appearance -Change in bowel frequency
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conservative treatment for IBS 2
Reassure patient Advise to avoid trigger foods eg caffeine/ alcohol and short chain carbohydrate
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mild treatment of IBS 2
Anti mobility eg Loperamide for diarrhoea Laxatives eg Senna for constipation
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severe treatment of IBS 3
Tricyclic antidepressants eg amitriptyline CBT GI referral
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what is osteoarthritis 1 and what happens 1
degenerative disease of joint due to mechanical erosion of the cartilage in the joint
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symptoms of osteoarthritis 2
1. painful joints (typically high usage joints- worse towards end of day/ after usage) 2. morning stiffness for less than 30 mins
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state and explain two clinical signs of osteoarthritis
Bouchards nodes (bony growths on PIP joints= proximal) Heberdens nodes (bony growths on DIP joints=distal)
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2 investigations into osteoarthritis and results
bloods= normal x-ray of joint (LOSS- loss of joint space, osteophytes (bony growths on joints), subchondral sclerosis (increased density bone along joint line), subchondral cysts (fluid filled holes in bone)
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what is the treatment of osteoarthritis 3
lifestyle changes: physio, weight bearing pain relief: NSAIDs last resort: joint replacement
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what is rheumatoid arthritis and what happens
inflammatory disease autoimmune destruction of synovium (soft tissue of the joints)
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compare the symmetry and number of joints affected for rheumatoid arthritis and osteoarthritis
osteoarthritis= asymmetrical, affects few joints rheumatoid= symmetrical, affects many joints
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risk factors of rheumatoid arthritis 2
HLADR4/1 women
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symptoms of rheumatoid arthritis 2 and clinical signs of RA 4
painful swollen joints morning stiffness lasting more than 30 mins rheumatoid skin nodules boutinniere deformity swan neck thumb ulnar deviation
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treatment for R arthritis 3
1. Disease modifying anti rheumatic drugs- methotrexate/ hydroxychloroquine/ sulfsalazine 2. analgesia- NSAIDs/ steroid injections 3. biologics -> 1st line: TNF alpha inhibitor infliximab (given with methotrexate) -> 2nd line: B cell inhibitor (CD20 target)- rituximab RADAB
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What is a differential for fibromyalgia
polymalgia rheumatica
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investigations for R arthritis 4 and results
1. bloods: high ESR/CRP 2. serology: positive rheumatoid factor, positive anti-CCP antibodies 3. genetic test for HLA DR1/4 4. X-ray (LESS- lost joint spaces, bony erosion, soft tissue swelling, periarticular osteopenia)
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compare polymyalgia rheumatica anad fibromyalgia 3
fibromyalgia at any age but PR over 50 Y/O PR= concentrates pain in shoulder and hips, onsest over a few days with joint stiffness PR resolves within 2 years, fibromyalgia is chronic and lifelong
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What is syphillis and cause
STI caused by the gram negative bacteria Treponema pallidum
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What is the disease progression for syphyilis
primary stage: chancre (painless ulcer at site of sexual contact/ where direct contact occured) secondary stage: 1 week after primary > systemic symptoms: fevers, lymphadenopathy > non itchy maculopapular rash on trunk, palms and soles > buccal 'snail track' ulcers (30%) > condyloma lata (painless, white lesions on the genitalia) tertiary features: type 4 hypersensitivity reaction (severe immune response) and organ damage > gummas (granulomatous lesions formed from WBC) > ascending aortic aneurysms due to aortitis > weakness and paralysis and loss of sensation (T. pallidum affects anterior spinal cord) > tabes dorsalis (T.pallidum damages dorsal column-medial lemniscus nerve pathway= loss of vibration and proprioception) > Argyll-Robertson pupil (pupil loses light reflex but does have accomodation reflex)
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Explain the latent stage of syphillis
Latent phase happens after secondary phase of syphillis infection (basically an asymptomatic stage) early latent phase: within a year of infection- T. pallidum mostly found in capillaries of organs/ tissues finds its way back into bloodstream= secondary symptoms again late latent phase: after a year of infection- T. pallidum stays in capillaries of organs/ tissues finds its way back into bloodstream
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What are the Ix for syphilis 3
1. Dark-field microscopy from swab of chancre/ secondary lesions (+ is presence of T. pallidum) 2. serology testing: treponemal eg florescent treponemal antibody (more specific and sensitive so used for diagnosis) and non-treponemal tests eg Rapid Plama Reagin blood test (screening and monitoring tx response) 3. CSF examination: Should be considered in tertiary syphilis to evaluate for CNS involvement.
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Explain serology test results for syphilis 4 and action for 1
both positive= active/ recent syphilis infection Positive non-treponemal test + negative treponemal test= no syphilis, false positive due to other causes eg SLE/ pregnancy Negative non-treponemal test + positive treponemal test = primary/ latent syphillis/ previously having treated or untreated syphilis both negative= no syphilis or incubating syphilis (should repeat after 3 months, as syphilis has an incubating time period of 3 months)
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What is the mx for syphilis 5
1. 1st line IM benzathine penicillin once confirmed 2. needs referral to GUM, with follow up at 3,6, and 12 months 2. if CI then doxycycline (14 days if early syphillis, 28 dys if late) 3. should monitor nentroponemal titres to assess response (fourfold decline in titres seen as an adequate response to treatment) 4. avoid sex until fully treated **IBANG (ive been a nasty girl)** (C)**I** then doxycycline- 14 for early, 28 dys for late **b**enpen IM injection once + results **a**void sex until fully treated **N**on treponemal titres to assess response (fourfold decline in titres= adequete response) **G**UM referral with 3,6,12 month follow up
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What is a SE of syphilis mx and mx of this
Jarisch- Herxheimer reaction: fever, rash and tachycardia several hours after treatment no treatment apart from antipyretics
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What are the causes of otitis externa and features
causes: recent swimming, staph aureaus, p.aerginosa, dermatitis features: ear pain, itch, discharge
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Mx of otitis externa 3
1. topical antimicrobial (acetic acid) plus with steroid (eg ciprofloxacin and dexamethasone combined-otomize spray) 2. oral flucox if cellulitis expanding past ear or immunocompromised/ diabetes 3. refer to ENT if do not respond to topical abx
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What is Trichomonas vaginalis and cause
STI caused by Trichomonas vaginalis: a highly motile, flagellated protozoan parasite
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What are the features of Trichomonas vaginalis 5
1. vaginal discharge: offensive, yellow/green, frothy 2. vulvovaginitis 3. strawberry cervix 4. pH > 4.5 5. in men is usually asymptomatic but may cause urethritis | 4 Vs (1-4)
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What is the Ix for Trichomonas vaginalis 2
NAAT swab (same as chlamydia + g) microscopy of a wet mount shows motile trophozoites
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What is the mx of microscopy of Trichomonas vaginalis 1
oral metronidazole 5-7 days
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What is Sinusitis
inflammatory disorder of paranasal sinuses and linings of the nasal passages
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What are the features of sinusitis 4
1. facial pain: typically frontal pressure pain which is worse on bending forward 2. nasal discharge: usually clear if allergic or vasomotor. Thicker, purulent discharge suggests secondary infection 3. nasal obstruction: e.g. 'mouth breathing' 4. post-nasal drip: may produce chronic cough
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What are the red flags for sinitis 3 and action for these
unilateral symptoms persistent symptoms despite compliance with 3 months of treatment epistaxis referral to ENT
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How is acute and chronic sinusitis managed 2 and what is the timeline for this
acute: supportive as it is self limiting, NICE avoids antibiotics chronic: 3+ months 1. intranasal corticosteroids 2. nasal irrigation with saline solution
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risk factors for prostate cancer 4
genetic BRCA1/2 and HOXB13 and lynch syndrome elderly family history A/C origin
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what is prostate cancer
proliferation of outer peripheral zone of prostate (adenocarcinoma)
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presentation of prostate cancer 2
LUTS like BPH (voiding and storage issues) but with systemic cancer symptoms eg weight loss, fatigue, night pain and bone pain
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investigations for prostate cancer 3
DRE is hard and irregular PSA in community multiparametric MRI-influenced prostate biopsy
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where does prostate cancer typically metastasise to and what is the effect of this
typically metastasises to bone= sclerotic lesions, typical lumbar back pain also metastasises to liver, lung and brain
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what determines if multiparametric MRI is offered to someone with suspected prostate cancer?
If the Likert scale is >=3 a multiparametric MRI-influenced prostate biopsy is offered If the Likert scale is 1-2 then NICE recommend discussing with the patient the pros and cons of having a biopsy.
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3 treatment approaches for prostate cancer
radical prostatectomy radiotherapy hormone therapy: only for T3/T4 and metastatic malignancy
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explain hormone therapy treatment for prostate cancer (example name, how does it work and 2 side effects)
GnRH agonist eg goserelin increases LH and FSH but results in suppression of HPG axis= less testosterone side effects= libido loss, erectile dysfunction
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What is vasovagal syncope and fully explain a vasovagal syncopal episode
transient loss of consciousness due to global cerebral hypoperfusion with rapid onset, short duration and spontaneous recovery trigerred by emotion, pain or stress EPISODE: prodrome: lightheadedness, visual disturbances, muffled hearing, nausea, pallor event: loss of postural tone and consciousness up to a minute recovery: may show signs of confusion, weakness and can recollect prodromal period but has amnesia for actual syncopal event
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What are the ix for vasovagal syncope
1. BP readings: fall BP >20 mmHg is diagnostic for postural hypotension 2. ECG
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What are the other types of syncope apart from vasovagal and explain each
REFLEX SYNCOPE: carotid sinus + vasovagal + situational situational: specifically associated with certain situations eg coughing, defecation, post-exercise carotid sinus: hypersensitivity of carotid sinus baroreceptors which stimulate bradycardia/ vasodilation when stimulated eg turning head/ tight collars. Mostly affects elderly OTHER SYNCOPE TYPES: orthostatic: due to postural BP drop eg Parkinsons and Lewy body (nervous system unable to regulate BP changes well), diarrhoea/ diuretics/ vasodilators (volume deplation) cardiac: bradycardias and arrythmias
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What is lyme disease caused by and how does it spread?
caused by the spirochaete Borrelia burgdorferi and is spread by ticks
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How does lyme disease present?
1. early features within 30 days - 'bulls-eye' rash is typically at the site of the tick bite which slowly increases in size -systemic features eg lethargy and fever 2. later features after 30 days - myocarditis/ heart block (CV) - facial nerve palsy, radicular pain, meningitis (Neuro)
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What is the mx of lyme disease 3
1. if asymptomatic tick bite just ensure you remove tick if still present with tweezers and wash area thoroughly after. no other tx 2. suspected/ confirmed lyme disease- doxycycline if early disease and ceftrioxone if disseminated disease
250
What are the Ix for lyme disease
1st line ELISA for Borrelia burgdorferi if negative, repeat after 1 month if positive, do a immunoblot test for lyme disease
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What is infectious mononucleosis caused by and what is its alternative name
Epstein-Barr virus glandular fever
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What are the features of infectious mononucleosis 7
triade: pharyngitis (with exudative tonsils), lymphadenopathy, sore throat other: palatal petechiae, maculopapular pruritic rash when being treated with amoxicillin/ penicillins (although this is not part of mx when it is known to be infectious mono, hepatitis (high ALT) LISTENING TO PEALSH FM pharyngitis (struggling to swallow) Exudate on tonsils antibiotics cause MP rash Lymphadenopathy (cervical) Sore throat Hepatitis (high ALT) FBC (haemolytic anaemia) Monospot test (2 weeks in) if pt treated for tonsillitis with abs and gets a rash, then its infectious mononucleosis
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How is infectious mononucleosis dx 3
NICE guidelines suggest FBC (can show haemolytic anaemia) and Monospot test in the 2nd week of the illness to confirm a diagnosis of glandular fever, otherwise clinical
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What is the mx for infectious mononucleosis 2
1. rest, analgesia, drink fluids 2. avoid contact sports for 4 weeks after symptoms to reduce risk of splenic rupture
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What is folliculitis
infection from a single hair follicle, causing pustule/ papule formation (pimples) which can form anywhere on the body except for hands and feet
256
Causes of folliculitis 4
bacterial: staph aureus MC or hot tub folliculitis (caused by pseudo. aeruginosa) or any gram neg bacteria after a long course of abx (eg after acne tx) yeast: malassezia (yeast from skins normal flora infecting hair follicles)
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What is the mx of folliculitis 2
1. topical antimicrobial (benzyl peroxide) + antibacterial soaps (Hibiscrub) 2. Oral antibiotics (trimethoprim for gram neg due to long term abx use for acne mx) may also be required in more severe cases or cases that don't respond to topical treatments
258
What is another name for atopic dermatitis and features
eczema pruritic, dry, erythemous patches on skin, in a typical distribution pattern in fleuxural areas (inner elbows, behind knees, armpits)
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What can cause exacerbation of atopic dermatitis 3
stress, irritants, allergens
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How is atopic dermatitis diagnosed
1. An itchy skin condition in the last 12 months Plus three or more of Onset of some sx below 2 years* (not used for kids under 4) History of flexural involvement History of generally dry skin Personal history of other atopic disease Visible flexural dermatitis
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How is atopic dermatitis managed 6, 3 community, 3 specialist
1. emollients to be liberally applied 2. topical corticosteroids for acute flares/ severe eczema (hydrocortisone 1 for face/ genitals, betamethasone valerate 0.1 for thicker areas like palms/ soles or in severe cases) 3. chloramphenamine (sedating antihistamine) to short term releive itch adn help with sleep disturbance, otherwise cetirizine if non sedating more appropriate SPECIALIST MX: 4. immunosuppressants eg tacrolimus by a specialist dermatologist 5. phototherapy in unresponsive cases 6. biologics eg dupilomab for severe unresponsive cases
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what is the MC arrythmia
atrial fibrillation
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what is the atrial firing rhythm of atrial fibrillation
irregular irregular atrial firing rhythm
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causes of atrial fibrillation (4)
heart failure hypertension secondary to mitral stenosis sometimes idiopathic
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explain the pathophysiology of atrial fibrillation and how it increases the risk of thromboembolic events (3)
1. rapid firing rate 300-600 bpm causes atrial spasm (not co-ordinated contraction like normal) 2. blood is not efficiently pumped to ventricles 3. this decreases cardiac output and increases the risk of thromboembolic events
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symptoms of A fib (6)
palpitations irregularly irregular pulse thromboemboli eg ischaemic stroke chest pain SYNCOPE HYPOTENSION 6 Ps- palpitations, pulse, pain in chest, (hy)potension, (P)FAINTING and thromPoemboli
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what are the 3 types of atrial fibrillation and what are their patterns
paroxysmal (episodic) persistant (longer than 7 days) permanent (sinus rhythm unrestorable)
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diagnostic investigation for atrial fibrillation (1, 3)
ECG is diagnostic: irregularly irregular pulse narrow QRS (less than 120ms no p waves (fibrillatory squiggles instead) acronym= PIQ
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acute treatment for atrial fibrillation
synchronised cardioversion DC (shock heart back into normal rhythm)
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long term treatment for atrial fibrillation 4
1. start anticoagulant (justify with ChadsVasc stroke risk score and ORBIT bleeding risk score) 2. offer rate control first line: eg beta blocker/ CCB (only first line if not causing HF/ new onset). Can also give digoxin for non paroxysmal, not exercising person when other rate drugs ruled out) 3. offer rhythm control: eg amiodarone (when pts have worse symptoms and HF) 4. surgical: radio frequency ablation which intends to prevent future episodes
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what is atrial flutter firing rhythm (2) and compare it for atrial fibrillation (2)
regularly irregular atrial firing less common and less severe than atrial fibrillation
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pathophysiology of atrial flutter 2
1. fast atrial ectopic firing 120-350 bpm 2. this causes atrial spasm
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symptoms of atrial flutter (2)
shortness of breath palpitations
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investigation for atrial flutter (1) and results (2)
ECG diagnostic: f wave ‘saw tooth’ pattern, often with a 2:1 blocker (2 p waves for every QRS)
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what is the wolff parkinson white AVRT and explain the pathophysiology and inheritence
accessory pathways for conduction= bundle of Kent pre-excitation syndrome (excite ventricle faster than typical pathwa) autosomal dominant
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treatment for atrial flutter that is acutely unstable treatment for atrial flutter that is stable (2) and what is the purpose of these treatments
acute: DC synchronised cardioversion stable: 1. rhythm/ rate control with beta blocker and oral anticoagulation 2. radio frequency ablation to prevent future episodes
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what are the symptoms of wolff parkinson white (3)
palpitations dizziness dyspnoea
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what are the ECG changes seen in Wolff parkinson white (3)
slurred delta waves short PR interval wide QRS complex acronym= QuPiD
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what is the treatment for wolff parkinson white (3)
1. valsalva manoeuvre and carotid massage 2. IV adenosine (temporarily ceases conduction- warn patient it feels like dying)- 6mg then 12mg, then 12 mg and additional doses if unsuccessful 3. radiofrequency ablation of bundle of Kent
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what is long QT syndrome and what type of arrythmia does this lead to? What is the interval
congenital channelopathy disorder where mutation affects cardiac ion channels =ventricular taachycardia QT interval is 480ms +
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what are the 4 causes of long QT syndrome
1. Romano Ward syndrome (autosomal dominant) 2. Jerrell Lange Nelson syndrom (autosomal recessive) 3. hypokalaemia and hypocalcaemia (not inherited) 4. drugs eg amiodarone
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what are two examples of long QT syndrome
torsades de pointes ventricular fibrillation
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what is torsades de pointes, what does this look like on an ECG, what can this progress to
polymorphic ventricular tachycardia in patients with prolong QT rapid irregular QRS completes which ‘twist’ around baseline ventricular fibrillation
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what does ventricular fibrillation look like on ECG and what can happen with ventricular fibrillation
shapeless rapid oscillations on ECG patient becomes pulseless and goes into cardiac arrest (no effective cardiac output)

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what is the first line of treatment for ventricular fibrillation
electrical defibrillation
286
what is primary AV block
PR interval prolongation (200ms +) and every P followed by QRS
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what is the treatment for asymptomatic and symptomatic primary AV block (1, 3)
if asymptotic then no treatment symptomatic treatment= beta blocker eg atenolol, CCB eg verapamil, digoxin to block AVN conduction
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what are the two types of secondary AV block and explain what each are
Mobitz type 1 and 2 1: PR prolongation until a QRS is dropped (PR progressively elongates) 2: PR interval is consistently prolonged at the same length with random dropped QRS
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What is the tx for 2 AV block
pacemaker
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what is a tertiary AV block and explain pathophys
AV dissociation (complete heart block so atria and ventricles beat independantly of each other) ventricular escape rhythm is sustaining the heartbeat (ventricle pacemakers take over which is bad (firing rate= 20-40bpm))
291
tx for tertiary AV block
IV atropine and permanent pacemaker
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what is a bundle branch block and what are the two types and explain each
blocked bundles of His RBBB: right ventricle is activated later than left ventricle LBBB: left ventricle is activated later than right ventricle
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what is the heart sound and ECG pattern in RBBB
wide physiological S2 splitting heart sound MARROW: M in V1 (R wave), W in V6 (S wave)
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what is the heart sound and ECG pattern in LBBB
WILLIAM: W in V1 (r wave), M in V6 (s wave)
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What is MART, its use and example
combined ICS and LABA treatment in one inhaler and this inhaler is used both for daily maintenance and to relieve symptoms eg formoterol
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How much is a low and high dose of inhaled corticosteroids?
<= 400 micrograms budesonide or equivalent = low dose 400 micrograms - 800 micrograms budesonide or equivalent = moderate dose > 800 micrograms budesonide or equivalent= high dose
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How is asthma diagnosed in adults 3
1. FeNO test (40+ ppb is positive, 35+ in kids) PLUS 2. spirometry + bronchodilator reversibility test (positive if improvement of FEV1 by 12+% **and** increase in volume of 200ml+ (childrne just need 12% improvement in FEV1) 3. spirometry (FEV1:FVC less than 0.7= obstructive)
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What is balanitis and most common causes 3
inflammation of glans penis 1. candidiasis (candida albicans) 2. contact/ allergic/ eczema (look for hx of eczema elsewhere on body)/ psoriasis dermatitis 3. bacterial (staph)
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What are the clinical features of balanitis? 3
itching white/ clear non-urethral discharge if bacterial: painful, itchy and yellow non-urethral discharge
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What is the mx for balanitis?
1. gentle and thorough saline washes 2. 1% hydrocortisone for irritation and dermatitis causes 3. topical clotrimzole 2 weeks if candiasis 4. if bacterial then oral flucoxacillin
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What is Chancroid and symptoms 2
tropical disease caused by Haemophilus ducreyi -> painful genital ulcers -> unilateral painful inguinal lymph node enlargement
302
What are the classifications of heart failure? Explain each
systolic (heart unable to pump properly = reduced ejection fraction) diastolic (heart unable to relax properly= preserved ejection fraction) acute HF (new onset or acute deterioration of chronic HF) chronic HF= gradual progression and takes years to develop
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Explain the classification for HF
New York Heart Association (NYHA) Classification of HF 1. Class 1 - no limitation in physical activity, and activity does not cause undue fatigue, palpitations or dyspnoea. 2. Class 2 - slight limitation of physical activity, and comfort at rest. Ordinary physical activity causes fatigue, palpitations and/or dyspnoea. 3. Class 3 - marked limitation in physical activity, but comfort at rest. Minimal physical activity causes fatigue (less than ordinary). 4. Class 4 - inability to carry on any physical activity without discomfort, with symptoms occurring at rest. If any activity takes place, discomfort increases.
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What are two clinical signs of HF 2
1. orthopnoea (SOB when lying flat, releived by sitting/ standing up) 2. paroxysmal nocturnal dysponoea (sudden onset SOB whilst a person is sleeping, causing them to wake up from sleep)
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symptoms of left sided HF (8)
respiratory crackles (due to bilateral pleural effusions) pink-tinged sputum tachycardia fatigue CYANOSIS EXERTION DYSPNOEA cough PULMONARY oedema due to vessel backflow lungs: 4 cough, pulmonary oedema, resp crackles, cyanosis systemic: 2 tachy, fatigue, exertional dyspnoea specific: 1 pink tinged sputum
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symptoms of right sided HF (5)
ASCITES hepatosplenomegaly WEIGHT GAIN raised JVP (due to increased pressure in right atrium) PERIPHERAL OEDEMA due to systemic venous backflow
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What are the ix for HF
1. first line is NT-pro-BNP ->400-2000 refer to cardio and TTE within 6 weeks -> 2000+ urgent referral to cardio and TTE within 2 weeks -> TTE (echo) confirms ventricular dysfunction= dx 2. 12 lead ECG 3. CXR: A: Alveolar oedema (with 'batwing' perihilar shadowing) B: Kerley B lines (caused by interstitial oedema) C: Cardiomegaly (cardiothoracic ratio >0.5) D: dilated upper lobe vessels E: Pleural effusions (typically bilateral transudates) F: Fluid in the horizontal fissure
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What are the causes of HF? 5
uncontrolled HTN MI coronary heart disease valve abnormalities Arrythmias eg AF
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What is the conservative advice for HF 5
1. Weight loss if BMI >30. 2. Smoking cessation 3. Salt and fluid restriction (improves mortality) 4. Supervised exercise-based group rehabilitation programme for people with heart failure. 5. Offer annual influenza and one-off pneumococcal vaccinations for patients diagnosed with heart failure.
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What is the main symptom management for HF?
loop diuretic for fluid overload eg furosemide
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How is ventricular dysfucntion measured + classified in HF and how
Transthoracic echocardiogram (TTE) EF <40% = HF with reduced ejection fraction (systolic dysfunction) EF >40% but with raised BNP = HF with preserved ejection fraction (diastolic dysfunction)
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What are the surgical managements for HF 1
1. Cardiac resynchronisation therapy if wide QRS and above NYHA class 3 (aims to improve QoL)
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What is the mx for reduced ejection fraction HF? 6?
1st line = ACE-I (if CI then ARB) and beta-blocker (bisoprolol) if sx persist or NYHA class 3/4 then: -> add aldosterone agonist (spironolactone) -> Afro-Caribbean patients add hydralazine and a nitrate -> IvAbradine if in sinus rhythm and impaired EF. -> AF/ not sinus rhythm add digoxin -> ACEi replacement with sacubitril valsartan once pt is stable on ACE and if ejection fraction is less than 35 (stop ACEi 36 hours beforehand before starting SV due to risk of angioedema- facial oedema)
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what are the two methods the body uses to compensate for heart failure (2) and why is this only effective short term?
RAAS system activation (increased salt and water reabsorption to increase bp) sympathetic system activation (increases inotrophy and chronotrophy) short term as high RAAS and SNS activation exacerbates fluid overload
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What is the mx for preserved ejection fraction HF? and class of drug
SGLT2 inhibitors dapagliflozin
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acute heart failure treatment (4)
oxygen, morphine, furosemide, GTN spray OMFG
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What are the causes 2 and features 3 of innocent murmurs
causes: due to increased cardiac output in febrile illness/ anaemia features: soft systolic murmur, asymptomatic, loudest left sternal edge
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What are the 3 foetal circulation shunts?
Ductus venosus: shunts oxygenated blood from placenta in umbilical vein towards the fetal heart (placenta to umbilical vein to ductus venosus to skip liver straight to heart via inferior vena cava then to right atria then to left atria via foramen ovale) Foramel ovale: shunts oxygenated bloods from R to L atria to bypass lungs Ductus arteriosus: connects pulmonary artery with aorta to shunt blood away from lungs into the aorta
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what is the tetralogy of fallots pathophysiology and is it cyanotic
congenital condition with four different heart problems cyanotic due to ventricular systolic defect causes right ventricle outflow obstruction (deoxygenated blood is shunted to the systemic circulation)
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investigations for tetralogy of fallot and what do they show (2,1)
echo, chest x-ray shows a boot shaped heart
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what is a behavior of infants with tetralogy of fallot and why do they do this
infants often seen in knee to chest squatting position which increases preload and after load and improves cyanosis get tet spells where they turn blue for short periods of time
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What are the features of tetralogy of fallot
PROVe P for pulmonary stenosis R for Right ventricular hypertrophy O for overriding aorta V for Ventricular Septal Defect
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treatment for tetralogy of fallot 2
treatment: full surgical repair within 2 years of life (this gives a good prognosis if done) encourage knees to chest for tet spells and can give beta blockers to help with tet spells egp propanalol/ o2 in hospital
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what is coarctation of the aorta 1 and what is the pathophysiology of this
congenital narrowing of aorta blood is diverted through proximal aortic arch branches= increased perfusion to upper body vs lower body
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symptoms/ signs of coarctation of aorta (5)
1. upper body hypertension 2. radio-femoral delay 3. diminished femoral pulses but strong UL pulses 4. systolic murmur, loudest between scapulae 5. leg claudication during physical activities in children
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diagnostic investigation for coarctation of aorta
echocardiogram
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treatment for coarctation of the aorta
baloon angioplasty + stent insertion
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what are the cardinal signs of heart failure 3
orthopnea (difficulty breathing whilst lying down) ankle oedema fatigue
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if a patient is on ACEi and BB already for HF but still symptomatic what should be given to them 1
spironolactone
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what is the 1st line ix for IE and what is the GS
1- TTE 2- TOE
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what is a side effect of amlodipine and what alternative can be given to prevent this side effect 2
peripheral/ ankle oedema ace inhibitor (if not already given) and indapamide
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what ecg leads look at the lateral aspect of the heart, anterior, inferior and septal
I, aVL, V5, V6 V3-4 II, III, aVF V1-2 see mneumonic online when drawing up the ecg graph (like in iceland, like in spain, some amazing ass anal lois lane)
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what ecg leads looks at the LAD, RCA, Lcx. diagonal of LAD
V1-4 II, III, aVF I, aVL, V5-6
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What is the cause of mumps and method of transmission
RNA paramyxovirus resp droplets
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What are the features of mumps? 3
1. fever 2. malaise, muscular pain 3. parotitis (= earache/pain on eating: unilateral initially then becomes bilateral in 70%
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What are the features of influenza? 6
1. fever >38 2. myalgia 3. headache 4. sore throat 5. cough 6. lethargy
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is mumps a notifiable disease?
yes
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What is the mx for influenza?
only give antivirals if high risk pt presents within 48 hours from onset of sx during a flu outbreak -> antiviral= oseltamivir (zanamivir for renal impairment/ immunocompromised)
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What are the features of acute tonsillitis? 5
1. sore throat 2. fever >38 3. dysphagia 4. cough, headache (indicates viral) OR cervical lymphadenopathy (indicates bacterial) 5. white pathes on tonsils
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What is acute tonsillitis? Causes?
acute infection of the palatine tonsils MC viral: MC rhinovirus, coronavirus and parainfluenza virus (MC to LC) bacterial: group A strep MC
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How is acute tonsillitis dx?
1. physical exam: inflamed tonsils, purulent tonsils (suggests bacterial), painful and large cervical lymph nodes
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What tool is used to predict likelihood of bacterial cause of tonsillitis? Explain
CENTOR criteria: score 1 point for each (maximum score of 4) presence of tonsillar exudate tender anterior cervical lymphadenopathy or lymphadenitis history of fever absence of cough 3/4 points= more likely to be bacterial (32 to 56% chance of isolating strep in swab) CENTor Cough absent Enlarged lymph nofes Not normal temp (fever) Tonsillar pus
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What is the mx for tonsillitis 2
1. conservative: fluids and painkillers 2. if 3+ on centor criteria or immunosuppressed or feverPAIN score is 4+, give abx: -> 1st line: Phenoxymethylpenicillin for 10 days -> Clarithromycin if allergy
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What is a viral exanthma and name some causes 4
widespread rash due to virus eg: 1. chickenpox 2. hand foot and mouth disease
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Why do people get arterial and venous ulcers
arterial: peripheral arterial disease (atherosclerosis= inadequate blood supply) venous: chronic venous insufficiency (poor venous return= HTN in lower limbs)
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Compare arterial and venous ulcers
arterial: small, deep 'punched out' ulcers that do not bleed or ooze, at heel/ above foot, PAINFUL, cold, no palpable pulses venous: large and shallow, with sloping edges, and bleed or ooze, on medial side, PAINLESS
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What are the ix for ulcers 2
1. doppler US for venous ulcers 2. ABPI for arterial
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What is the mx for arterial and venous ulcers? 3 2
arterial: need to improve arterial circulation 1. lifestyle changes 2. antiplatelets, statins 3. surgery: angioplasty/ peripheral bypass grafting venous: need to compress veins to increase venous return 1. 4 layer band compression stockings 2. If fail to heal after 12 weeks or >10cm2 skin grafting may be needed
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What are varicose veins?
dilated superficial veins that are formed due to incompetent venous valves
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What are the rfx of varicose veins? 4
elderly pregnancy (uterus compresses pelvic veins) obesity inactivity
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What is the ix for varicose veins + result? 1
venous duplex ultrasound: this will demonstrate retrograde venous flow
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What are the complications of varicose veins? 5
1. varicose eczema (also known as venous stasis) 2. haemosiderin deposition → hyperpigmentation 3. lipodermatosclerosis → hard/tight skin 4. DVT 5. venous ulcers
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What is the mx for varicose veins? 4
1. conservative: weight loss, elevation, graduated compression stockings 2. referral to 2' care if skin changes (eg eczema), ulcers or significant sx (pain/ swelling) 3. endothermal ablation 4. surgery: ligation of vein
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what is reactive arthritis
sterile inflammation of synovial membranes and tendons
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what causes reactive arthritis 3
reaction to a distant GI/GU infection normally by chlamydia trachomatis or campylobacter jejuni
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presentation of reactive arthritis 2
1. Reiters triad: can’t see, can’t pee, can’t climb a tree= uveitis, urethritis and arthritis 2. occurs a month after intiial infection onset
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investigations of reactive arthritis 1
joint aspirate: plane polarised light microscopy is negative for crystalarthropathy
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treatment for reactive arthritis 3
1. symptomatic relief: NSAIDs/ steroid injection 2. give antibiotics until septic arthritis is ruled out 3. methotrexate for chronic
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what is Psoariatic arthritis
inflammatory arthritis that 1/5 with Psoriasis get
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presentation of Psoariatic arthritis 4
1. psoriatic rash on skin: hidden sites eg behind ears, scalp 2. enthesitis (inflammation of entheses) 3. dactylitis (sausage fingers) 4. oncholysis (nail separation from nail bed)
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Describe the psoriasis rashes
well-demarcated red, scaly patches affecting the extensor surfaces and scalp
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investigations of psoariatic arthritis 1,3
x ray -> osteolysis -> dactylitis -> pencil in cup appearance
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complication of psoriatic arthritis 1
arthritis mutilans
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What is guttate psoriasis cause and appearance
psoriatic rash frequently triggered by a streptococcal infection. Multiple red, teardrop lesions appear on the body
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What is the mx for psoriasis? 6
1. regular emollients 2. hydrocortisone OD 3. vit D analogue (calcitriol) OD and if it doesn't work then vit D BD 4. short-acting dithranol (slows down the production of new skin cells) SECONDARY CARE REFERRAL 5. phototherapy UVB light 6. if associated joint disease, then NSAIDS and then if unresponsive: oral methotrexate
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what is peripheral arterial/ vascular disease
ischaemia of lower limb arteries
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general symptoms of PVD 2 and test and positive result for it 1
skin changes: pale colour, cold and ulcers pulses: weak/ absent buerger test positive: elevate leg 45 degrees for 1 min= pallor, pt to sit up with legs hanging off on the coach= blue then reactive hyperaemia (red)
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why does chronic ischaemic pain occur at night (2) and what can this lead to (2)
due to elevation of limb which can further reduce blood supply to the distal part of the limb which can cause ulcers and gangrene
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intermittent claudification: when is there pain, how occluded is the lumen and what is the cause of the occlusion
intermittent claudification pain on exertion, relieved by rest partial lumen occlusion atherosclerotic
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critical limb ischaemia: when is there pain, and what is there a risk of getting 2
pain at rest gangrene and infection
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ix for PVD 3
1. ABPI 2. colour duplex ultrasound imaging- assesses degree of stenosis 3. CT angiography if surgery is considered
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what does ABPI stand for, what is it what is classed as normal and explain what the value for results means
ankle brachial pressure index compares blood pressure in upper and lower limbs as a ratio 0.5-0.9= intermittent claudication less than 0.5= critical limb ischaemia absent/0= risk of acute limb threatening ischaemia
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treatment for intermittent claudification (5)
1. reduce risk factors eg stop smoking 2. exercise programme for intermittent which trains through the pain to stimulate collateral blood supply growth 3. meds: 80mg highest dose statin, clopidogrel is 1st line for PAD 4. according to NICE, can give naftidrofuryl oxalate: vasodilator (for pt with poor QOL) 5. if severe: percutaenous transluminal angioplasty +/- stent placement
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treatment for critical limb ischaemia (1)
surgical emergency requires revascularisation within 4-6 hours otherwise there is an increase amputation risk via percutaenous transluminal angioplasty +/- stent
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what are the 6 Ps and how can they assess the severity of the acute limb ischaemia
6 Ps: pulselessness, pallor, pain, persistently cold, paralysis, parasthesia ->the more of these 6 Ps that you have, the more severe the ischaemia
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How is BMI calculated and state the classifications
BMI = weight (kg) / height (m) squared Underweight < 18.49 Normal 18.5 - 25 Overweight 25 - 30 Obese class 1 30 - 35 Obese class 2 35 - 40 Obese class 3 > 40
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What is the mx for obesity 4
1. conservative: diet, exercise 2. orlistat -> pancreatic lipase inhibitor 3. liraglutide injections -> GLP1 4. types of bariatric surgery: -> laparoscopic-adjustable gastric banding -> sleeve gastrectomy -> Roux-en-Y gastric bypass surgery
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What are the NICE guideline criteria for medical mx of obesity
orlistat: -> BMI of 28 kg/m^2 or more with associated risk factors, or -> BMI of 30 kg/m^2 or more -> continued weight loss e.g. 5% at 3 months ->orlistat is normally used for < 1 year liraglutide (SC daily injection) -> person has a BMI of at least 35 kg/m² -> prediabetic hyperglycaemia (e.g. HbA1c 42 - 47 mmol/mol)
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What is classed as obesity in pregnancy
BMI >= 30 kg/m² at the first antenatal visit
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What is the mx for obesity in pregnancy?
1. obese women should take 5mg of folic acid, rather than 400mcg 2. screened for gestational diabetes with an oral glucose tolerance test (OGTT) at 24-28 weeks 3. if the BMI >= 35 kg/m² women should give birth in a consultant-led obstetric unit (as obesity increases risk of complications at birth and fetal complications) 4. if the BMI >= 40 kg/m² should have an antenatal consultation with an obstetric anaesthetist and a plan made (" ") | 543O
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What is the ix 1 and mx 4 for bursitis?
ix: joint aspiration for when septic bursitis/ crystal arthropathy is suspected 1. modify activities to ensure not putting pressure on affected joint 2. conservative: ice and elevation 3. NSAIDs 4. corticoid injections for chronic bursitis
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What is bursitis? What are the symptoms of bursitis? 3
Inflammation of the bursa (fluid filled sacs in joints) that become inflammed due to repetitive trauma 1. dull achy pain 2. swelling over area 3. redness
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What are the five types of bursitis?
1. prepatellar (knee) 2. olecranon (elbow) 3. trochanteric (hip) 4. subacromial (shoulder) 4. retrocalcaneal bursitis (back of heel) only one joint is affected usually on presentation
389
Explain screening for AAA
all men aged 65 offered US screening for asymptomatic AAA -> women only screened 70+ with existing co-morbidities eg fhx or CV disease -> done via abdo US -> if aorta diameter 3cm+ then refer to vascular team (urgent referral if 5.5+)
390
Explain screening for bowel cancer
FIT tests sent every 2 years for people between 60-74 -> if FIT is postiive then sent for colonoscopy -> people with rfx eg FAP, HNPCC or IBD are offered a colonoscopy at regular intervals to screen for bowel cancer
391
Explain screening for diabetic eyes and results
yearly eye checks, if last 2 tests were clear then in 2 years -> tropicamide put into eyes to make pupils large so photo can be taken of back of eye results: STAGE : background retinopathy means small changes but vision unaffected, non-proliferative STAGE 2: pre-proliferative retinopathy means widespread changes in the retina, including bleeding= more frequent screening STAGE 3: proliferative retinopathy= retinal detachment, risk of vision loss, needs referral for treatment DIABETIC MACULOPATHY: leaky/ blocked blood vessels supplying macula, risk of vision, needs more frequent testing and treatment
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What are the different types of diabetic eye disease 4
1. diabetic retinopathy (haemorrhages, cotton wool spots, aneurysm) 2. diabetic macular odema (leaky BV cause fluid build up in macula= blurry vision) 3. cataracts (high sugar levels over time damage the eye lens= less flexible and less transparent= cloudy vision and sensitivity to light/ glares) 4. glaucoma (damaged retina BV= abnormal collaterals= block fluid from draining out of eye= increased eye pressure= blurry vision)
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What is the care after newborn birth 5
1. clamp the umbilical cord 2. skin to skin, keeping baby warm 3. vitamin K injection (baby's have deficiency so this prevents bleeds and stimulates baby to cry to open up lungs) 4. measure baby's weight and length 5. screening: -> NIPE within 72 hours -> blood spot test -> newborn hearing test
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Expain the newborn spot test
-> test on day 5 with parental conset screenign for 9 congenital conditions: eg sickle cell disease, cystic fibrosis, congenital hypothyroidism, Maple syrup urine disease | 4 Ss: (S for Spot) SIckle, Systic, Slow (cong hypothyroid), Syrup
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Explain screening done in NIPE
1. oxygen sats (should be 94+) 2. head: circumference, fontanelle, red reflex, cleft lip/ palate, suckling reflex, tone 3. shoulder/ hand: shoulder symmetry for clavicle fracture, check all digits are present 4. chest: heart and breath sounds 5. abdo: check umbilicus for healing, check for hernias 6. genitals: descended testes, patent anus, check it is being cleaned well, ask if baby opened bowel yet 7. legs: check digits, symmetry of legs, Barlows (to dislocate (Dr Barlow= bad)- involves addution and putting pressure down) and Ortolani manouveres, femoral pulse 8. back: spina bifida 9. reflexes: Moro (startle), rooting (turning head towards the direction where something touched their mouth), grasp, stepping 10. any abnormalities, refer (undescended testes) or US (hip clicking)
396
What are the MC causes of COPD 2
smoking alpha 1 antitrypsin deficiency
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What are COPD CXR signs 3
barrel chest flat hemidiaphragm hyperinflation bullae (big fat heart- meaning chest)
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What are the sx of an acute exacerbation of COPD 3
1. increased green sputum 2. increase in cough 3. increase inSOB
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What are the causes of acute exacerbation of COPD 2
1. haemophilus influenza (MC) 2. strep pneumoniae
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What is the tx for acute exacerbation of COPD 3
1. pred 30mg for 5 days 2. abx only if sputum is purulent or clinical signs of pneumonia (amoxicillin) 3. admisison if severe SOB, O2 sats less than 90: give 02 with venturi mask at 4L/min with target sats of 88-92
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What is the risk for patients with acute exacerbation of COPD and how is this risk managed?
risk of developing type 2 resp failure non invasive ventilation
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What are the ix for COPD diagnosis and how does the severity scale work?
spirometry to demonstrate airflow obstruction: FEV1/FVC ratio less than 70% FEV1 is used to rank severity: >80= stage 1 mild (symptoms need to be present to diagnosed COPD in these patients) 50-79= stage 2 moderate 30-49= stage 3 severe <30= stage 4 very severe
403
What is the mx for stable COPD? 5
1. lifestyle: stop smoking 2. vaccinations: annual influenza, one off- pneumococcal vaccine 3. first line SABA 4. if asthmatic features/ features that suggest steroid responsiveness then add regular LABA + ICS, otherwise LABA + LAMA 5. prophylactic azithromycin (ECG needs to be done as azithromycin can prolong QT interval) 6. pulmonary rehabilitation for MRC 3+ individuals
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What are the extra tests for COPD? 5
1. FBC to exclude polycythaemia, anaemia and infection 2. CXR to exclude lung cancer 3. BMI (weight loss can occur in severe disease) 4. sputum culture (for recurrent infections) 5. Serum alpha-1 antitrypsin to look for alpha-1 antitrypsin deficiency
405
What are the MRC scale grades
Grade 1: Breathless on strenuous exercise Grade 2: Breathless on walking uphill Grade 3: Breathlessness that slows walking on the flat Grade 4: Breathlessness stops them from walking more than 100 meters on the flat Grade 5: Unable to leave the house due to breathlessness
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SABA, LAMA, LABA, ICS, LRA: what does each stand for and examples for each
SABA: short acting brochodilator agonist, salbutamol SAMA: short acting muscarinic agonist, ipratropium bromide LAMA: long acting muscarinic agonist, tiotropium bromide LABA: long acting brochodilator agonist, salmetorol ICS: inhaled corticosteroids, beclomethasone dipropionate LRA: leukotriene receptor antagonist, montelukast
407
What is infa