med feb Flashcards

(218 cards)

1
Q

ECG features of hypoK?

A
  • Prolonged PR
  • Prominent U waves
  • Flattened T waves
  • ST depression
  • Possibilitity of re-entrant arrhythmias
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2
Q

Some important side effects of thiazide diuretics?

A
  • Impaired glucose tolerance
  • Low K, Na
  • High Ca
  • Gout
  • Dehydration
  • postural hypotension
  • Impotence
  • Rare- pancreatitis
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3
Q

What is the consequence of left ventricular free wall rupture following an MI?

A
  • 3% MIs
  • after 1-2wks
  • Acute HF secondary to cardiac tamponade (raised JVP, pulsus paradoxus, diminished HS)
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4
Q

Clinical features of Henoch-Schonlein purpura?

A

APGAR
* Arthralgia
* Palpable purpuric rash, periarticular oedema
* Glomerulonephritis (nephritic)
* Abdo pain
* Renal involvement

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5
Q

Who to refer 2ww for bladder cancer?

A

Age over 45 and unexplained haematuria w/o UTI
or visible haematuria that persists or recurs after treatment of UTI
or age over 60 and unexplained non visible haematuria + dysuria / raised wcc

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6
Q

Gold standard dx for bladder Ca

A

Cystoscopy

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7
Q

how to investigate aki of unknown aetiology

A

Urinary tract USS- check for obstruction- within 24hrs of assessment

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8
Q

Monitoring for henoch schonlein purpura

A

BP and urinalysis for renal impairment

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9
Q

What happens in CKD bone disease and how to manage it?

A
  • Low vit D, high phosphate, drags Ca out of bone, results in osteomalacia, low Ca, secondary hyperPTH
  • Main aim of mx is to reduce phosphate and PTH levels
  • Reduced dietary phosphate is 1st line
  • Phosphate binders
  • Vit D: alfacalcidol, calcitriol
  • Parathyroidectomy may be required
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10
Q

When to give IV calcium gluconate as the first option in hyperK?

A

When the K is > 6.5 mmol/L or if there are ECG changes (do an ecg first if K is less than 6.5)

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11
Q

How to diagnose CKD?

A

Patients should only be diagnosed with CKD stage 1 if eGFR >90ml/min or stage 2 if eGFR 60-90ml/min if there are markers of kidney disease including proteinuria, haematuria, electrolyte abnormalities or structural abnormalities detected

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12
Q

Causes of renal artery stenosis?

A
  • Atherosclerosis
  • Fibromuscular dysplasia- young women esp.
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13
Q

Large volumes of 0.9% NaCl can lead to what?

A

Hyperchloraemic metabolic acidosis - use hartmanns

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14
Q

When to refer CKD from primary care to secondary care?

A
  • if eGFR falls below 30 or progressively by > 15 in a year
  • ACR 70 or more
  • uncontrolled resistant htn
  • suspected genetic cause
  • suspected RAS
  • suspected CKD complication
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15
Q

How is diabetes insipidus treated

A
  • Cranial- synthetic forms of vasopressin - desmopressin
  • Nephrogenic- thiazide diuretic- helps polyuria
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16
Q

Vomiting acid base disturbance

A

Metabolic alkalosis
- loss of hydrochloric acid
- loss of potassium and sodium
- kidneys compensate by retaining sodium at the expense of hydrogen ions

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17
Q

Diarrhoea acid base disturbance

A

normal anion gap acidosis
- GI loss of bicarbonate results in metabolic acidosis
- Normal anion gap due to excretion of bicarb increased
- Hypokalaemia

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18
Q

extra-renal manifestations of ADPKD

A
  • liver cysts- hepatomegaly
  • berry aneurysms - SAH
  • mitral valve prolapse, aortic root dilatation, aortic dissection
  • cysts in other organs such as pancreas and spleen
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19
Q

Lab findings in Paget’s disease of the bone?

A
  • Raised ALP
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20
Q

X-ray in psuedogout

A

Chondrocalcinosis

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21
Q

Osteoporosis in a man… what to check?

A

Testosterone- associated w/ higher bone turnover and therefore osteoporosis

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22
Q

Pleural effusion: exudative vs transudative

A

Exudative- infections pnumonia and TB, malignancy
Transudative- hypoalbuminaemia, ccf, hypothyroid, meig’s

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23
Q

Causes of upper lung fibrosis

A

CHARTS
C - Coal worker’s pneumoconiosis
H - Histiocytosis/ hypersensitivity pneumonitis
A - Ankylosing spondylitis
R - Radiation
T - Tuberculosis
S - Silicosis/sarcoidosis

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24
Q

Causes of lower zone lung fibrosis

A

Idiopathic
asbestosis
lupus
drugs

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25
thyrotoxicosis + tender goitre
De quervains thyroiditis (subacute thyroiditis)
26
DM diagnosis
fasting > 7 random glucose > 11 asymptomatic - 2 readings hba1c > 48
27
most sensitivie lab finding in chronic liver disease that can indicate liver cirrhosis?
platelet count thrombocytopenia
28
according to bts guidelines, who should have an abg in an acute asthma attack
when o2 sats < 92% abg is useful to differentiate severe from life threatening as paco2 will be normal or high in life threatening when the pt gets exhausted
29
describe the histology of coeliacs
villous atrophy, raised intra-epithelial lymphocytes, and crypt hyperplasia (typically duodenum, jejunal biopsy may be done)
30
what cancer are coeliacs at a risk of developing
enteropathy-associated T cell lymphoma
31
what to investigate in high serum calcium
pth
32
liver + neuro problems...
Wilsons disease
33
keiser fleischer rings in cornea
green brown rings in periphery of iris copper accumulation in descemet membrane wilsons disease!
34
when are NG tubes safe to use
pH of aspirate < 5.5
35
how to work out alcohol units
Alcohol units = volume (ml) * ABV / 1,000
36
What are the 2 main factors contributing to diabetic foot disease
Loss of sensation and peripheral arterial disease is correct. Loss of sensation is due to diabetic neuropathy and results in the loss of protective sensation of the foot - for example, a patient may not notice a stone in their shoe, leading to tissue damage. Chronic high blood sugar levels also cause damage to blood vessels leading to peripheral arterial disease - this causes ischaemia and poor healing of the tissues in the foot.
37
primary hyperaldosteronism...
high aldosterone: renin ratio hypertension low na low k ct abdomen with contrast bilateral venous sampling most common cause is bilateral adrenal hyperplasia and then adrenal adenoma
38
secondary hyperaldosteronism causes
renal artery stenosis hf
39
Hydroxychloroquine monitoring
baseline ophthalmological examination Annual screning thereafter Can cause bulls eye retinopathy - reduced colour differentiation, reduced central visual acuity, floaters
40
how does chemo increase gout risk
from increased urate production Cytotoxic drugs cause increase in cell breakdown, releasing products that are degraded into uric acid
41
feltys syndrome
RA splenomegaly low wcc
42
Typical presentation of pagets disease of the bone
Older male Bone Pain isolated raised ALP
43
who needs bisphoshphonate when on steroids
offer if T score <1.5 if they are on steroids for >3 months even if < 65yo high doses of oral steroids- more than 7.5mg prednisolone daily for >3/12
44
psuedogout aspiration
weakly positively birefringent rhomboid shaped crystals
45
prophylaxis of gout
Allopurinol + colchicine cover for 6/52
46
Who needs urate lowering therapy
>2 attacks in 12 months, tophi, renal disease, uric acid renal stones, cytotoxic drugs or diuretics
47
temporal arteritis vision changes
anterior ischaemic optic neuropathy - occlusion of posterior ciliary artery (a branch of the ophthalmic artery) resulting in ischaemic of the optic nerve head fundoscopy shows a swollen pale disc and blurred margins Temporal arteritis can also result in amaurosis fugax
48
ank spond plain xray features
syndesmophytes- ossifications inside spinal ligaments or of the annulus fibrosus of the intervertebral discs sacroiliitis- subchondral erosions, sclerosis squaring of lumbar vertebrae bamboo spine is late and uncommon
49
what to do if pt suffers significant upper GI S/E w/ alendronate
Switch to risedronate or etidronate
50
pts who are allergic to aspirin may also react to what?
sulfasalazine
51
most common joint for septic arthritis
knee
52
behcets syndrome triad
oral ulcers, genital ulcers, anterior uveitis
53
RA joint aspirate
Joint aspirate in rheumatoid arthritis shows a high WBC count, predominantly PMNs. Appearance is typically yellow and cloudy with absence of crystals
54
The concurrent use of methotrexate and trimethoprim containing antibiotics may cause ...
bone marrow suppression and severe or fatal pancytopaenia
55
drug induced lupus
procainamide hydralazine less commonly isoniazid/ minocycline/ phenytoin
56
what needs correcting prior to starting bisphosphonate
calcium and vit D deficiency
57
pagets disease xray
mixed lytic and sclerotic lesions
58
marfan syndrome- defect in which protein?
fibrillin
59
ehlers danlos-defect in which protein
collagen III autosomal recessive widespread elasticity of tissue
60
main immunoglobulin found in breast milk
igA
61
main immunoglobulin found in breast milk
igA
62
systemic sclerosis features
Calcinosis (white deposits) Raynaud’s (cold, white fingertips precipitated by cold weather) oEsophogeal dysmotility (dysphagia) Sclerodactyly (thickened skin on top of hands and inability to straighten fingers) Telangiectasia (excessive number of spider naevi)
63
ank spond associated features
Apical fibrosis Anterior uveitis Aortic regurgitation Achilles tendonitis AV node block Amyloidosis
64
septic arthritis causes
staph aureus young, sexually active- neisseria gonorrhoeae
65
pts w/ sjogrens have an increased risk of what malignancies
lymphoid
66
causes of gout
DART diuretics, alcohol, renal disease, trauma
67
osteomalacia bloods
raised alp low calcium low phos raised pth
68
drug induced lupus antibodies
anti histone antibodies
69
psa vs ra
psa asymmetrical, less likely ra symmetrical, less likely dactylitis
70
sle flare monitoring
c4- will be low during flares
71
what to do if pt in gp suspected pmr but no response to steroid refer to specialist
consider different diagnosis- PMR very responsive to steroids - needs to have 70% improvement
72
polymyositis features
proximal muscle weakness raised ck no rash
73
when prescribing methotrexate what add on therapy should be initiated
folate to reduce BM suppression
74
dermatomysotis antibodies
ANA anti jo --> lung fibrosis subtype anti mil2
75
Differential diagnoses of polymyalgia rheumatica
rheumatoid arthritis, hypothyroidism, fibromyalgia, and polymyositis.
76
what type of hypersensitivity is sle
III
77
sle mnemonic
MD SOAP BRAIN -Malar Rash -Discoid Rash -Serositis (Pericarditis/Pleuritis) -Oral ulcers -Arthritis -Photosensitivity -Blood disturbance (i.e. anaemia of chronic disease/thrombocytopaenia) -Renal -ANA+ -Immunological investigations (dsDNA-ABs/cadiolipin-ABs) -Neurological (seizures)
78
pts w/ suspected visual loss secondary to GCA
IV methylpred
79
allergic contact dermatitis type of hs
type IV hypersensitivty
80
Bone pain, tenderness and proximal myopathy (→ waddling gait)
?osteomalacia
81
insulin users sick day rules
same dose check blood sugars more frequently
82
copd pts with acute exacerbation & resp acidosis is persisting despite immediate maximum standard medical treatment... what to do
. NIV is required in COPD patients who develop acute respiratory acidosis despite maximum standard medical treatment. NIV increases tidal volume, decreases the respiratory rate and reduces work of breathing. This results in improved oxygenation and decreased hypercapnia.
83
empyeme pleural effusion aspirate findings
- low glucose because bacteria use it for respiration - low pH (<7.2) because bacteria producing CO2 in repsiration - high LDH because lactate dehydrogenase is needed for the bacteria to convert glucose into energy
84
cushings syndrome u&es findings
hypokalaemia metabolic alkalosis
85
aspiration pneumonia location & causative agent
right upper zone klebsiella produces a red currant jelly sputum
86
sbp prophylaxis
anyone whos had an sbp episode needs abx prophylaxis to selectively decontaminate the GIT usually ciprofloxacin is used (or norfloxacin)
87
what medication should be given to ADPKD to slow down CKD progression
tolvaptan - selective vasopressin antagonist inhibits the binding of vasopressin to V2 receptors, reduces cell proliferation, cyst fomation, and fluid excretion this reduces kidney growth (due to cysts, they become ballotable), and protects kidney function this is the only medication shown to reduce disease progression rather than just symptoms reduction
87
what medication should be given to ADPKD to slow down CKD progression
tolvaptan - selective vasopressin antagonist inhibits the binding of vasopressin to V2 receptors, reduces cell proliferation, cyst fomation, and fluid excretion this reduces kidney growth (due to cysts, they become ballotable), and protects kidney function this is the only medication shown to reduce disease progression rather than just symptoms reduction
88
RF aspiration pneumonia
neuro injury supported feeding tracheostomy swallowing difficulty poor dental hygiene impaired mucocilliary clearance (R bases affected, absence of infective cause- no fever)
88
RF aspiration pneumonia
neuro injury supported feeding tracheostomy swallowing difficulty poor dental hygiene impaired mucocilliary clearance (R bases affected, absence of infective cause- no fever)
89
subclinical hypothyroidism dx & mx
* TSH raised * normal thyroid hormones * no sx * if tsh remains high on 2 occasions 3 months apart, then offer levothyroxine for 6 months if age < 65
90
right sided abdo tenderness on dre...
think appendicitis
91
cxr copd
* hyperinflation * flattened hemidiaphragms * hyperlucent lung fields *
92
drug causes of cholestasis
* cocp * abx- co amox, fluclox * testosterone * sulphonylurea
93
Iron defiency anaemia vs. anaemia of chronic disease:
TIBC is high in IDA, and low/normal in anaemia of chronic disease
94
raised ferritin causes & how to differentiate?
If transferrin saturation is high, consider iron overload, 10% cases * hereditary haemochromatosis * secondary iron overload eg following repeated transfusions if transferrin is low, then high ferritin can be due to: * inflammation- ferritin is an acute phase reactant * alcohol excess * liver disease * ckd * malignancy
95
use of lactulose in liver disease
used in cirrhosis to ensure 2-3 loose stools a day to treat and prevent cases of hepatic encephalopathy helps clear ammonia from the gut ammonia builds up in gut for 2 reasons in cirrhosis 1. functional impairment of liver cells preventing them metabolising the ammonia into harmless waste products 2. collateral vessels between the portal and systemic circulation meaning the ammonia bypasses the liver altogether and enters the systemic system directly
96
features to suggest alcoholic liver disease
ratio ast:alt >2 (>3 is strongly suggestive) raised gamma GT
97
Metabolic alkalosis + hypokalaemia →
prolonged vomiting
98
which UC pts should have regular meds
If a patient with ulcerative colitis has had a severe relapse or >=2 exacerbations in the past year they should be given either oral azathioprine or oral mercaptopurine to maintain remission check tpmt- risk of BM supression if low/ OD
99
IBS treatments? (pain/ constip/ diarrhoea)
* pain: antispasmodic agents * constipation: laxatives but avoid lactulose * diarrhoea: loperamide is first-line
100
globus pharyngitis features
* persistent sensation of lump in throat- relieved by swallowing food and drink * intermittent * particularly swallowing saliva is difficult
101
what weight loss is diagnostic of malnutrition
Unintentional weight loss greater than 10% within the last 3-6 months is diagnostic of malnutrition
102
s/e metoclopramide
* extrapyramidal effects * acute dystonia e.g. oculogyric crisis * this is particularly a problem in children and young adults * diarrhoea * hyperprolactinaemia * tardive dyskinesia * parkinsonism
103
severe flare of uc mx
* hosp admission * iv steroids * iv ciclosporin alt. * if no improvement within 72hrs give iv ciclosporin too/ consider surgery
104
TIPSS which vessels
connects hepatic v to portal vein
105
child with sudden onset dysphagia... what you thinking
benign oeseophageal stricture rf- tracheo oeseophageal fistula which was repaired
106
what is asorbic acid
vitamin c
107
acute mesenteric ischaemia 1st line ix
raised alctate (abg/vbg)
108
most common cause hepatocellular carcinoma
hepatitis B most common cause worldwide hepatitis C most common cause in Europe
109
Budd-Chiari syndrome
triad of sudden onset abdominal pain, ascites, and tender hepatomegaly (hepativ vein thrombosis causing portal hypertension)
110
Budd-Chiari syndrome
triad of sudden onset abdominal pain, ascites, and tender hepatomegaly (hepativ vein thrombosis causing portal hypertension)
111
recurrent c diff mx
* within 12 wks- oral fidaxomycin * after 12 wks- oral fidax or oral vanc
112
pigment laden macrophages within mucosa on PAS staining of colon
laxative abuse causing melanosis coli abnormal pigmentation of the large bowel due to the presence of pigment-laden macrophages may be associated with ileal ulcers, polyps and adenomas
113
monitoring in HH
serum ferritin transferrin saturation
114
how can crohns cause gallstones
* terminal ileitis- this is where bile salts are reabsorbed- so messes up the absorption predisposing pts to gallstones
115
nafld associated factors
* obesity * type 2 diabetes mellitus * hyperlipidaemia * jejunoileal bypass * sudden weight loss/starvation
116
ix + mx for mallory weiss syndrome
repeated vomiting- mucour membrane lacerations at the gastroesophageal junction ix- endoscopy mx- ablation
117
R vs L sided colon cancers
* Right-sided colon cancers – abdominal pain, iron-deficiency anaemia, palpable mass in right iliac fossa, often present late * Left-sided colon cancers – rectal bleeding, change in bowel habit, tenesmus, palpable mass in left iliac fossa or on PR exam
118
3 features to assess severity of UC
1) number of loose stools a day, blood? 2) systemic features such as fever, tachycardia, abdo tenderness/ distension/ reduced bowel sound 3) ESR/ CRP raised?
119
extra-intestinal manifestations of UC
arthritis psc uveitis
120
apart from endoscopic intestinal biopsy, what other ix can be done for coeliacs?
* serology- tissue transglutaminase (TTG) antibodies (igA) * endomyseal antibody )igA) * check iga levels too * Genetic screen- HLA DQ2/ DQ8
121
give 4 mx strategies of LBP
1) nsaids are 1st line- paracetamol monotherapy has been shown to be relatively ineffective. co-prescribe ppi if age > 45 2) exercise programme- group exercise programme within the NHS 3) manual therapy- spinal manipulation, mobilisation or soft tissue techniques such as massage 4) radiofrequency denervations 5) epidural injections of local anaesthetic and steroid for acute and severe sciatica
121
give 4 mx strategies of LBP
1) nsaids are 1st line- paracetamol monotherapy has been shown to be relatively ineffective. co-prescribe ppi if age > 45 2) exercise programme- group exercise programme within the NHS 3) manual therapy- spinal manipulation, mobilisation or soft tissue techniques such as massage 4) radiofrequency denervations 5) epidural injections of local anaesthetic and steroid for acute and severe sciatica
122
initial therapy for RA
In 2018 NICE updated their rheumatoid arthritis guidelines. They now recommend DMARD monotherapy +/- a short-course of bridging prednisolone. In the past dual DMARD therapy was advocated as the initial step.
123
monitoring of response to treatment in RA
* CRP and disease activity score DAS 28
124
pt with RA, tried 2 DMARDs, inadequate response, what now?
* TNF inhibitors * etanercept: recombinant human protein, acts as a decoy receptor for TNF-α, subcutaneous administration, can cause demyelination, risks include reactivation of tuberculosis * infliximab: monoclonal antibody, binds to TNF-α and prevents it from binding with TNF receptors, intravenous administration, risks include reactivation of tuberculosis * adalimumab: monoclonal antibody, subcutaneous administration
125
sclerodactyly hand changes
* puffy swollen hands- dactylitis * thickening and hardening of skin due to fibrosis- sclerodactyly- firstly in fingers then hands and face * contractures- claw deformities
126
causes of raynauds
* rheumatological- RA, SLE, scleroderma is most common * leukaemia * use of vibrating tools * oral contraceptive pill * cervical rib
127
name 4 drugs causing PF
* methotrexate * cyclophosphamide * amiodarone * nitrofurantoin
128
rash in reactive arthritis
circinate balanitis (painless vesicles on the coronal margin of the prepuce) keratoderma blenorrhagica (waxy yellow/brown papules on palms and soles)
129
virchows triad
hypercoaguable stasis of blood flow endothelial injury
130
explain SVTs briefly
you have an electrical signal re-entering the atria, causing an extra ventricular contraction if the source is AVN = avnrt if the source is an accessory pathway = avrt = eg WPW if the source is somewhere in the atria itself = atrial tachycardia/ flutter/ fibrillation. and then the pathway tachycardia als for acute. for chronic main thing is wpw's mx as radiofrequency ablation
131
WPW ecg
short PR wide QRS delta wave
132
causes of infective endocarditis related to their relations
* staph aureus- most common overall * strep viridans- poor dental hygiene * staph epidermidis- for 2/12 following prosthetic valve replacement * strep bovis- colorectal ca * SLE (non infective)
133
cardiac tamponade
becks triad hypotension + muffled (distant) heart sounds + elevated JVP dyspnoea tachycardia an absent Y descent on the JVP - this is due to the limited right ventricular filling pulsus paradoxus - an abnormally large drop in BP during inspiration Kussmaul's sign - much debate about this ECG: electrical alternans
134
posterior MI ecg- which coronary artery
* reciprocal stemi changes in v1-v3 i.e. st depression, tall R waves, dominant r wave V2 * st elevation seen in v7-9 * usually left cx * sometimes rca
135
causes of lbbb
new lbbb= myocardial infarction diagnosing a myocardial infarction for patients with existing LBBB is difficult rhe Sgarbossa criteria can help with this - please see the link for more details hypertension aortic stenosis cardiomyopathy rare: idiopathic fibrosis, digoxin toxicity, hyperkalaemia
136
causes of rbbb
normal variant - more common with increasing age right ventricular hypertrophy chronically increased right ventricular pressure - e.g. cor pulmonale pulmonary embolism myocardial infarction atrial septal defect (ostium secundum) cardiomyopathy or myocarditis
137
causes of rbbb
normal variant - more common with increasing age right ventricular hypertrophy chronically increased right ventricular pressure - e.g. cor pulmonale pulmonary embolism myocardial infarction atrial septal defect (ostium secundum) cardiomyopathy or myocarditis
138
s/e doxazosin
postural hypotension drowsiness dyspnoea cough
139
if a pt declines statin, are there any alternative drugs that can be used?
fenofibrate
140
surgical options for aortic stenosis
options for aortic valve replacement (AVR) include: surgical AVR is the treatment of choice for young, low/medium operative risk patients. Cardiovascular disease may coexist. For this reason, an angiogram is often done prior to surgery so that the procedures can be combined transcatheter AVR (TAVR) is used for patients with a high operative risk balloon valvuloplasty may be used in children with no aortic valve calcification in adults limited to patients with critical aortic stenosis who are not fit for valve replacement
141
criteria for stemi
2.5 mm (i.e ≥ 2.5 small squares) ST elevation in leads V2-3 in men under 40 years, or ≥ 2.0 mm (i.e ≥ 2 small squares) ST elevation in leads V2-3 in men over 40 years 1.5 mm ST elevation in V2-3 in women 1 mm ST elevation in other leads new LBBB (LBBB should be considered new unless there is evidence otherwise)
142
bp 180/ 120 who to refer for same day assessment
* retinal haemorrhage or papilloedema (accelerated hypertension) or * life-threatening symptoms or * suspected pheochromocytoma
143
htn bp targets
below 135/85 mmHg for adults aged under 80 below 145/85 mmHg for adults aged 80 and over.
144
signs of infective endocarditis
cardiac murmur- Ar/ MR signs of HF janeway lesions- palm/ soles of feet- painless osler nodes- ouch- fingertips roth spots- in the retina splinter haemorrhages- nail splenomegaly- splenic abscess
145
bb or ccb od
glucagon
146
ix for aaa rupture
ct angiogram chest/abdo/pelvis - false lumen if too unstable- toe cxr- widened mediastinum
147
nicorandil- use & s/e?
stable angina- 3rd line when ace/bb not tolerated ulceration anywhere in git- mouth to anus
148
Diastolic murmur + AF →
?mitral stenosis may present with stroke/tia
149
Causes of AR
can be due to valve disease (e.g. bicuspid aortic valve, aortic dissection, spondyloarthropathies (e.g. ankylosing spondylitis) and connective tissue disease) or due to aortic root disease (e.g. rheumatic fever, calcific valve disease, infective endocarditis and connective tissue diseases).
150
what murmur can cause haemoptysis
mitral stenosis
151
loud s1 with opening snap
mitral stenosis rheumatic fever
152
statins moa
Statins inhibit HMG-CoA reductase, the rate-limiting enzyme in hepatic cholesterol synthesis
153
recurrent episodes of collapse and a normal resting ECG- what to do now?
24-hour Holter monitor would be pertinent to investigate for any abnormal arrhythmias causing recurrent collapse. Findings on a 24-hour Holter may reveal; sinus pauses, abnormal bradycardia, supraventricular tachycardia or non-sustained ventricular tachycardia. Further investigations will be guided on the 24-hour Holter monitor findings. For example recurrent episodes of non-sustained ventricular tachycardia may warrant a coronary angiogram to investigate for underlying coronary artery disease as a potential precipitant.
154
do beta blockers cause prolonged qt
not usually however sotalol does
155
acute asthma mx
1. High flow O2 to achieve sats 94-98% 2. 5mg salbutamol, via O2-driven nebuliser, repeat every 20-30 mins 3. 40-50mg prednisolone PO (continued for at least 5 days) 4. Add nebulised ipratropium bromide 500mcg (SAMA) to SABA treatment 5. IV magnesium sulphate single dose (1.2-2g infusion over 20 mins) 6. IV aminophylline (following senior discussion) 7. ITU/ HDU input  intubation + ventilation, ECMO a. For pts failing to respond to therapies, evidenced by: deteriorating PEF, persistent/ worsening hypoxia, hypercapnia, ABG showing acidosis, exhaustion, feeble respiration, drowsy, confused, altered consciousness, respiratory address 8. Continue normal ICS as per usual dose
156
criteria for discharge following acute asthma admission
stable on discharge meds for 12-24 hrs (i.e. no nebs or o2 required) inhaler technique checked and recorded pef >75% best or predicted
157
criteria for discharge following acute asthma admission
stable on discharge meds for 12-24 hrs (i.e. no nebs or o2 required) inhaler technique checked and recorded pef >75% best or predicted
158
who gets ltot copd
Offer LTOT to patients with a pO2 of < 7.3 kPa or to those with a pO2 of 7.3 - 8 kPa and one of the following: * secondary polycythaemia * peripheral oedema * pulmonary hypertension
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histological features of chronic asthma
i. Smooth muscle cells hypertrophy ii. Thickened basement membrane iii. Goblet cell hyperplasia
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a. How do you differentiate pleural effusion from consolidation?
i. Pleural effusion: homogenous opacification, meniscus ii. Consolidation: heterogenous opacification
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c. What are the specific risks of bronchoalveolar lavage that you warn this patient about?
can diagnose pneumonia or ILD- extrinsiv allergic alveolitis as a cause of ILD will show raised lymphocytes and mast cells (hypersensitivity pneumonitis) risks- haemoptysis, sore throat, pneumothorax, infection
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name 3 hereditary causes of thrombosis
* antiphospholipid syndrome * antithrombin deficiency * protein C or S deficiency * factor V Leiden * polycythaemia rubra vera
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what needle for pleural effusion aspiration & where to put the needle?
i. Patient is sat upright with their back slightly flexed ii. 21g needle placed 2-3 spaces below the level of the meniscus
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Organisms which may colonise CF patients
Staphylococcus aureus Pseudomonas aeruginosa Burkholderia cepacia* Aspergillus
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CAP causes
* Streptococcus pneumoniae (accounts for around 80% of cases) * Haemophilus influenzae * Staphylococcus aureus: commonly after influenza infection * atypical pneumonias (e.g. Due to Mycoplasma pneumoniae) * viruses
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PE ECG
i. Tachycardia ii. Right sided heart strain – T-wave inversion iii. S1Q3T3 – S wave depression in lead 1, pathological q wave and T-wave inversion in leads 3
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tb mx & a/e
Drug adverse effects rifampicin potent liver enzyme inducer hepatitis, orange secretions flu-like symptoms isoniazid peripheral neuropathy: prevent with pyridoxine (Vitamin B6) hepatitis, agranulocytosis liver enzyme inhibitor pyrazinamide hyperuricaemia causing gout arthralgia, myalgia hepatitis ethambutol optic neuritis: check visual acuity before and during treatment
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causes of copd infective exacerbation
bacteria Haemophilus influenzae (most common cause) Streptococcus pneumoniae Moraxella catarrhalis respiratory viruses account for around 30% of exacerbations human rhinovirus is the most important pathogen
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eosinophilia + bronchiectasis...
* Allergic bronchopulmonary aspergillosis * allergy to Aspergillus spores * eosinophilia and bronchiectasis * mx- glucocorticoids; itroconazole
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atelectasis mx
positioning the patient upright chest physiotherapy: breathing exercises (occurs 72hrs post op where alveoli collapse)
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causes of bilateral hilar lymphadenopathy
The most common causes of bilateral hilar lymphadenopathy are sarcoidosis and tuberculosis. Other causes include: lymphoma/other malignancy pneumoconiosis e.g. berylliosis fungi e.g. histoplasmosis, coccidioidomycosis
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chest drain location
safe triangle The triangle is located in the mid axillary line of the 5th intercostal space. It is bordered by: Anterior edge latissimus dorsi, the lateral border of pectoralis major, a line superior to the horizontal level of the nipple, and the apex below the axilla
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cxr-cavitating lung lesion
abscess (Staph aureus, Klebsiella and Pseudomonas) squamous cell lung cancer tuberculosis Wegener's granulomatosis pulmonary embolism rheumatoid arthritis aspergillosis, histoplasmosis, coccidioidomycosis
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give 3 causes of clubbing
Cardiac causes cyanotic congenital heart disease (Fallot's, TGA) bacterial endocarditis atrial myxoma Respiratory causes lung cancer pyogenic conditions: cystic fibrosis, bronchiectasis, abscess, empyema tuberculosis asbestosis, mesothelioma fibrosing alveolitis Other causes Crohn's, to a lesser extent UC cirrhosis, primary biliary cirrhosis Graves' disease (thyroid acropachy) rare: Whipple's disease
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key indications for NIV
COPD with respiratory acidosis pH 7.25-7.35 the BTS guidelines state that NIV can be used in patients who are more acidotic (i.e. pH < 7.25) but that a greater degree of monitoring is required (e.g. HDU) and a lower threshold for intubation and ventilation should be used type II respiratory failure secondary to chest wall deformity, neuromuscular disease or obstructive sleep apnoea cardiogenic pulmonary oedema unresponsive to CPAP weaning from tracheal intubation
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3 complications following thyroid surgery
* Anatomical such as recurrent laryngeal nerve damage. * Bleeding. Owing to the confined space haematoma's may rapidly lead to respiratory compromise owing to laryngeal oedema. * Damage to the parathyroid glands resulting in hypocalcaemia.
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precipitants for DKA
The most common precipitating factors of DKA are infection, missed insulin doses and myocardial infarction.
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adverse effects of thiazide diuretics
dehydration postural hypotension hyponatraemia, hypokalaemia, hypercalcaemia gout impaired glucose tolerance impotence rare- pancreatitis
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persistent ST elevation following MI
LV aneurysm The ischaemic damage sustained may weaken the myocardium resulting in aneurysm formation. This is typically associated with persistent ST elevation and left ventricular failure. Thrombus may form within the aneurysm increasing the risk of stroke. Patients are therefore anticoagulated.
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what are bronchial breath sounds
harsh breath sounds equally loud on inspiration and expiration
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define cerebral palsy
Fixed (non-progressive) neurodevelopmental insult causing abnormalities in development, posture and movement. (can occur between conception and 3 years of age, while the brain is still developing)
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define eisenmenger's syndrome
W h e n a le ft-to -rig h t sh u n t leads to pulm onary hypertension and sh u n t reversal, therefore tu rn in g an acyanotic h eart defect into a cyanotic h eart defect
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clcnical features of decompensated cardiac congenital disease
P o o r feeding, dypnoea, tachycardia, w eak pulse, cold peripheries, hepatom egaly, engorged neck veins, sw eating, gallop rhythm (third h eart sound)
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what enzymes do you expect to be risen following cardiac damage
Troponin (I/T), CK-MB, CK, AST, LDH.
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ecg changes in MI pt prior to discharge
inverted T waves pathological Q waves
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besides exertion what can trigger angina
Cold/windy weather, emotion (anger/excitement), lying down (decubitus angina), vivid dreams (nocturnal angina).
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signs of pulmonary oedema
Tachypnoea, tachycardia, raised JVP, fine lung crepitations, wheeze, additional heart sounds/gallop rhythm , dull percussion of bases, cyanosis, decreased tactile/vocal fremitus. (
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complications of htn
hypertensive retinopathy hypertensisive nephropathy, ckd mi hf stroke, haemorrhage
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common causes of af
P neum onia, m ocardial infarction, pulmonary embolism , hyperthyroidism , alcohol excess, heart failure, endocarditis.
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other than ivdu, give rf for infective endocarditis
Prosthetic valves, patent ductus arteriosis, VSD, coarctation, mitral valve disease, aortic valve disease (e.g. bicuspid aortic valve).
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what is used to grade severity in copd
fev>80- mild 50-79%- mod 30-49- sev <30- vsevere
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signs of consolidation on resp examination
Reduced chest expansion, dull percussion note, increased tactile vocal fremitus, increased vocal resonance, bronchial breathing.
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signs of consolidation on resp examination
Reduced chest expansion, dull percussion note, increased tactile vocal fremitus, increased vocal resonance, bronchial breathing.
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complications bronchiectasis
P neum onia, septicaem ia, recu rren t pneumonia/L R T Is, haemoptysis, respiratory failure, cor pulmonale, pneumothorax
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pul fibrosis cxr
R educed lung volum e, reticulonodular shadow ing (often w orse in low er zones), honeycom b lung (advanced disease).
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OSA questionnaire
epworth sleepiness scale
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OSA rf beside obesity
Acromegaly, enlarged tonsils, enlarged adenoids, nasal polyps, alcohol.
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sarcoidosis biopsy
noncaseating granulomas
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intermittent claudication in right calf, what artery is likely stenosed
superficial femoral artery or popliteal artery
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rf for intermittent claudication
hyperlipidaemia lack of exercise diet high in saturated and trans fats fhx smoking
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what process in the arterial tree can allow intermittent claudication to improve over time
development/ opening up of collateral vessels
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how does aspirin work- pharmacological and therapeutic action (2 marks)
irreversible cox inhibitor, which prevents further production from TXA2 (thrmboxane A20 from platelets as they dont have a nucleus therapeutic actgion- prevents platelet aggregation
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where in the lower limb does rest pain typically occur and below what abpi
below 0.5 toes, foot, forefoot
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when pt lies on couch, pt with peripheral arterial disease, leg becomes pale when he stands up again it becomes red explain this
* when he lies down, the perfusion pressure of the leg is reduced on elevation * severe ischaemia during elevatin leads to release of local vasodilators eg ADP, potassium CO2, this increases the perfusion of the ischaemc foot when the foot becomes dependent again on returning to the chair
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pt with cellulitis has hypotension and tachycardia explain the pathophys of this
* bacterial factors (eg exotoxins), induce host inflammatory response * inflammatory mediators/ cytokines released * leads to systemic vascular resistance reduced/ increased systemic vascular permeability/ myocardial depression which reduces systemic bp * in response, activation of sympathetic nervous system, leads to tachycardia, to maintain cardiac output
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most common organisms for cellulitis
staphylococcus aureus grp A strep or streptococcus pyogenes
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surgical procedure for improving hearing loss caused by OME
* myringotomy- drains fluid * grommet insertion- ventilates & equalises pressure across eustachian tube * adenoidectomy- removes source of infection in the oropharynx
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ix for palpitations & why?
* U&Es- ckd or hypoK associated w/ palpitations * TFTs- hyperthyroidism associated with AF * echo-structural heart disease or LVH * ambulatory BP monitoring- look for htn * ambulating heart rate or rhythm monitoring to look for arrhythmias * overnight pulse oximetry look for hypoxia overnight
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what biochemical abnormality is responsible for the specific damage caused by paracetmaol overdose
glutathione depletion
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features of untreated paracetamol OD
HEPATIC ENCEPHALOPATHY The aetiology is not fully understood but is thought to include excess absorption of ammonia and glutamine from bacterial breakdown of proteins in the gut. * nausea * malaise * jaundice * confusion * bleeding
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problems with peritoneal dialysis
* bacterial peritonitis * peritoneal sclerosis * constipayion * ultrafiltration failure * psychosocial effects- changing the dialysis solution and sleeping with a machine each night
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risk facgtors for peptic ulcer disease
H. pylori infection, m edications: N S A ID s/steroids, sm oking, delayed gastric em ptying, physiological stress, e.g. in I T U patients, hypercalcaem ia, chronic renal failure.
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suspected perforated peptic ulcer ix
erect cxr pneumoperitoneum is seen as free air under the diaphragm
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causes of papilloedema
space-occupying lesion: neoplastic, vascular malignant hypertension idiopathic intracranial hypertension hydrocephalus hypercapnia
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causes of tunnel vision
papilloedema glaucoma retinitis pigmentosa choroidoretinitis optic atrophy secondary to tabes dorsalis hysteria