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year 5 flashcards HY > med feb > Flashcards

med feb Flashcards

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
Q

thyrotoxicosis + tender goitre

A

De quervains thyroiditis (subacute thyroiditis)

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26
Q

DM diagnosis

A

fasting > 7
random glucose > 11
asymptomatic - 2 readings
hba1c > 48

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27
Q

most sensitivie lab finding in chronic liver disease that can indicate liver cirrhosis?

A

platelet count
thrombocytopenia

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28
Q

according to bts guidelines, who should have an abg in an acute asthma attack

A

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

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29
Q

describe the histology of coeliacs

A

villous atrophy, raised intra-epithelial lymphocytes, and crypt hyperplasia
(typically duodenum, jejunal biopsy may be done)

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30
Q

what cancer are coeliacs at a risk of developing

A

enteropathy-associated T cell lymphoma

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31
Q

what to investigate in high serum calcium

A

pth

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32
Q

liver + neuro problems…

A

Wilsons disease

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33
Q

keiser fleischer rings in cornea

A

green brown rings in periphery of iris
copper accumulation in descemet membrane
wilsons disease!

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34
Q

when are NG tubes safe to use

A

pH of aspirate < 5.5

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35
Q

how to work out alcohol units

A

Alcohol units = volume (ml) * ABV / 1,000

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36
Q

What are the 2 main factors contributing to diabetic foot disease

A

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.

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37
Q

primary hyperaldosteronism…

A

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

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38
Q

secondary hyperaldosteronism causes

A

renal artery stenosis
hf

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39
Q

Hydroxychloroquine monitoring

A

baseline ophthalmological examination
Annual screning thereafter
Can cause bulls eye retinopathy - reduced colour differentiation, reduced central visual acuity, floaters

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40
Q

how does chemo increase gout risk

A

from increased urate production
Cytotoxic drugs cause increase in cell breakdown, releasing products that are degraded into uric acid

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41
Q

feltys syndrome

A

RA
splenomegaly
low wcc

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42
Q

Typical presentation of pagets disease of the bone

A

Older male
Bone Pain
isolated raised ALP

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43
Q

who needs bisphoshphonate when on steroids

A

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

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44
Q

psuedogout aspiration

A

weakly positively birefringent rhomboid shaped crystals

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45
Q

prophylaxis of gout

A

Allopurinol + colchicine cover for 6/52

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46
Q

Who needs urate lowering therapy

A

> 2 attacks in 12 months, tophi, renal disease,
uric acid renal stones, cytotoxic drugs or diuretics

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47
Q

temporal arteritis vision changes

A

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

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48
Q

ank spond plain xray features

A

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

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49
Q

what to do if pt suffers significant upper GI S/E w/ alendronate

A

Switch to risedronate or etidronate

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50
Q

pts who are allergic to aspirin may also react to what?

A

sulfasalazine

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51
Q

most common joint for septic arthritis

A

knee

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52
Q

behcets syndrome triad

A

oral ulcers, genital ulcers, anterior uveitis

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53
Q

RA joint aspirate

A

Joint aspirate in rheumatoid arthritis shows a high WBC count, predominantly PMNs. Appearance is typically yellow and cloudy with absence of crystals

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54
Q

The concurrent use of methotrexate and trimethoprim containing antibiotics may cause …

A

bone marrow suppression and severe or fatal pancytopaenia

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55
Q

drug induced lupus

A

procainamide
hydralazine
less commonly isoniazid/ minocycline/ phenytoin

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56
Q

what needs correcting prior to starting bisphosphonate

A

calcium and vit D deficiency

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57
Q

pagets disease xray

A

mixed lytic and sclerotic lesions

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58
Q

marfan syndrome- defect in which protein?

A

fibrillin

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59
Q

ehlers danlos-defect in which protein

A

collagen III
autosomal recessive
widespread elasticity of tissue

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60
Q

main immunoglobulin found in breast milk

A

igA

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61
Q

main immunoglobulin found in breast milk

A

igA

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62
Q

systemic sclerosis features

A

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)

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63
Q

ank spond associated features

A

Apical fibrosis
Anterior uveitis
Aortic regurgitation
Achilles tendonitis
AV node block
Amyloidosis

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64
Q

septic arthritis causes

A

staph aureus
young, sexually active- neisseria gonorrhoeae

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65
Q

pts w/ sjogrens have an increased risk of what malignancies

A

lymphoid

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66
Q

causes of gout

A

DART
diuretics, alcohol, renal disease, trauma

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67
Q

osteomalacia bloods

A

raised alp
low calcium
low phos
raised pth

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68
Q

drug induced lupus antibodies

A

anti histone antibodies

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69
Q

psa vs ra

A

psa asymmetrical, less likely
ra symmetrical, less likely dactylitis

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70
Q

sle flare monitoring

A

c4- will be low during flares

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71
Q

what to do if pt in gp suspected pmr but no response to steroid
refer to specialist

A

consider different diagnosis- PMR very responsive to steroids
- needs to have 70% improvement

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72
Q

polymyositis features

A

proximal muscle weakness
raised ck
no rash

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73
Q

when prescribing methotrexate what add on therapy should be initiated

A

folate to reduce BM suppression

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74
Q

dermatomysotis antibodies

A

ANA
anti jo –> lung fibrosis subtype
anti mil2

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75
Q

Differential diagnoses of polymyalgia rheumatica

A

rheumatoid arthritis, hypothyroidism, fibromyalgia, and polymyositis.

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76
Q

what type of hypersensitivity is sle

A

III

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77
Q

sle mnemonic

A

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)

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78
Q

pts w/ suspected visual loss secondary to GCA

A

IV methylpred

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79
Q

allergic contact dermatitis type of hs

A

type IV hypersensitivty

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80
Q

Bone pain, tenderness and proximal myopathy (→ waddling gait)

A

?osteomalacia

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81
Q

insulin users sick day rules

A

same dose
check blood sugars more frequently

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82
Q

copd pts with acute exacerbation & resp acidosis is persisting despite immediate maximum standard medical treatment… what to do

A

. 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.

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83
Q

empyeme pleural effusion aspirate findings

A
  • 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
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84
Q

cushings syndrome u&es findings

A

hypokalaemia metabolic alkalosis

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85
Q

aspiration pneumonia location & causative agent

A

right upper zone
klebsiella
produces a red currant jelly sputum

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86
Q

sbp prophylaxis

A

anyone whos had an sbp episode needs abx prophylaxis to selectively decontaminate the GIT
usually ciprofloxacin is used (or norfloxacin)

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87
Q

what medication should be given to ADPKD to slow down CKD progression

A

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

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87
Q

what medication should be given to ADPKD to slow down CKD progression

A

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
Q

RF aspiration pneumonia

A

neuro injury
supported feeding
tracheostomy
swallowing difficulty
poor dental hygiene
impaired mucocilliary clearance
(R bases affected, absence of infective cause- no fever)

88
Q

RF aspiration pneumonia

A

neuro injury
supported feeding
tracheostomy
swallowing difficulty
poor dental hygiene
impaired mucocilliary clearance
(R bases affected, absence of infective cause- no fever)

89
Q

subclinical hypothyroidism dx & mx

A
  • 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
Q

right sided abdo tenderness on dre…

A

think appendicitis

91
Q

cxr copd

A
  • hyperinflation
  • flattened hemidiaphragms
  • hyperlucent lung fields
    *
92
Q

drug causes of cholestasis

A
  • cocp
  • abx- co amox, fluclox
  • testosterone
  • sulphonylurea
93
Q

Iron defiency anaemia vs. anaemia of chronic disease:

A

TIBC is high in IDA, and low/normal in anaemia of chronic disease

94
Q

raised ferritin causes & how to differentiate?

A

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
Q

use of lactulose in liver disease

A

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
Q

features to suggest alcoholic liver disease

A

ratio ast:alt >2
(>3 is strongly suggestive)
raised gamma GT

97
Q

Metabolic alkalosis + hypokalaemia →

A

prolonged vomiting

98
Q

which UC pts should have regular meds

A

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
Q

IBS treatments? (pain/ constip/ diarrhoea)

A
  • pain: antispasmodic agents
  • constipation: laxatives but avoid lactulose
  • diarrhoea: loperamide is first-line
100
Q

globus pharyngitis features

A
  • persistent sensation of lump in throat- relieved by swallowing food and drink
  • intermittent
  • particularly swallowing saliva is difficult
101
Q

what weight loss is diagnostic of malnutrition

A

Unintentional weight loss greater than 10% within the last 3-6 months is diagnostic of malnutrition

102
Q

s/e metoclopramide

A
  • extrapyramidal effects
  • acute dystonia e.g. oculogyric crisis
  • this is particularly a problem in children and young adults
  • diarrhoea
  • hyperprolactinaemia
  • tardive dyskinesia
  • parkinsonism
103
Q

severe flare of uc mx

A
  • hosp admission
  • iv steroids
  • iv ciclosporin alt.
  • if no improvement within 72hrs give iv ciclosporin too/ consider surgery
104
Q

TIPSS which vessels

A

connects hepatic v to portal vein

105
Q

child with sudden onset dysphagia… what you thinking

A

benign oeseophageal stricture
rf- tracheo oeseophageal fistula which was repaired

106
Q

what is asorbic acid

A

vitamin c

107
Q

acute mesenteric ischaemia 1st line ix

A

raised alctate (abg/vbg)

108
Q

most common cause hepatocellular carcinoma

A

hepatitis B most common cause worldwide
hepatitis C most common cause in Europe

109
Q

Budd-Chiari syndrome

A

triad of sudden onset abdominal pain, ascites, and tender hepatomegaly
(hepativ vein thrombosis causing portal hypertension)

110
Q

Budd-Chiari syndrome

A

triad of sudden onset abdominal pain, ascites, and tender hepatomegaly
(hepativ vein thrombosis causing portal hypertension)

111
Q

recurrent c diff mx

A
  • within 12 wks- oral fidaxomycin
  • after 12 wks- oral fidax or oral vanc
112
Q

pigment laden macrophages within mucosa on PAS staining of colon

A

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
Q

monitoring in HH

A

serum ferritin
transferrin saturation

114
Q

how can crohns cause gallstones

A
  • terminal ileitis- this is where bile salts are reabsorbed- so messes up the absorption predisposing pts to gallstones
115
Q

nafld associated factors

A
  • obesity
  • type 2 diabetes mellitus
  • hyperlipidaemia
  • jejunoileal bypass
  • sudden weight loss/starvation
116
Q

ix + mx for mallory weiss syndrome

A

repeated vomiting- mucour membrane lacerations at the gastroesophageal junction
ix- endoscopy
mx- ablation

117
Q

R vs L sided colon cancers

A
  • 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
Q

3 features to assess severity of UC

A

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
Q

extra-intestinal manifestations of UC

A

arthritis
psc
uveitis

120
Q

apart from endoscopic intestinal biopsy, what other ix can be done for coeliacs?

A
  • serology- tissue transglutaminase (TTG) antibodies (igA)
  • endomyseal antibody )igA)
  • check iga levels too
  • Genetic screen- HLA DQ2/ DQ8
121
Q

give 4 mx strategies of LBP

A

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
Q

give 4 mx strategies of LBP

A

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
Q

initial therapy for RA

A

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
Q

monitoring of response to treatment in RA

A
  • CRP and disease activity score DAS 28
124
Q

pt with RA, tried 2 DMARDs, inadequate response, what now?

A
  • 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
Q

sclerodactyly hand changes

A
  • puffy swollen hands- dactylitis
  • thickening and hardening of skin due to fibrosis- sclerodactyly- firstly in fingers then hands and face
  • contractures- claw deformities
126
Q

causes of raynauds

A
  • rheumatological- RA, SLE, scleroderma is most common
  • leukaemia
  • use of vibrating tools
  • oral contraceptive pill
  • cervical rib
127
Q

name 4 drugs causing PF

A
  • methotrexate
  • cyclophosphamide
  • amiodarone
  • nitrofurantoin
128
Q

rash in reactive arthritis

A

circinate balanitis (painless vesicles on the coronal margin of the prepuce)
keratoderma blenorrhagica (waxy yellow/brown papules on palms and soles)

129
Q

virchows triad

A

hypercoaguable
stasis of blood flow
endothelial injury

130
Q

explain SVTs briefly

A

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
Q

WPW ecg

A

short PR
wide QRS
delta wave

132
Q

causes of infective endocarditis related to their relations

A
  • 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
Q

cardiac tamponade

A

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
Q

posterior MI ecg- which coronary artery

A
  • 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
Q

causes of lbbb

A

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
Q

causes of rbbb

A

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
Q

causes of rbbb

A

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
Q

s/e doxazosin

A

postural hypotension
drowsiness
dyspnoea
cough

139
Q

if a pt declines statin, are there any alternative drugs that can be used?

A

fenofibrate

140
Q

surgical options for aortic stenosis

A

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
Q

criteria for stemi

A

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
Q

bp 180/ 120 who to refer for same day assessment

A
  • retinal haemorrhage or papilloedema
    (accelerated hypertension) or
  • life-threatening symptoms or
  • suspected pheochromocytoma
143
Q

htn bp targets

A

below 135/85 mmHg for adults aged under 80

below 145/85 mmHg for adults aged 80 and over.

144
Q

signs of infective endocarditis

A

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
Q

bb or ccb od

A

glucagon

146
Q

ix for aaa rupture

A

ct angiogram chest/abdo/pelvis - false lumen
if too unstable- toe
cxr- widened mediastinum

147
Q

nicorandil- use & s/e?

A

stable angina- 3rd line when ace/bb not tolerated
ulceration anywhere in git- mouth to anus

148
Q

Diastolic murmur + AF →

A

?mitral stenosis
may present with stroke/tia

149
Q

Causes of AR

A

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
Q

what murmur can cause haemoptysis

A

mitral stenosis

151
Q

loud s1 with opening snap

A

mitral stenosis
rheumatic fever

152
Q

statins moa

A

Statins inhibit HMG-CoA reductase, the rate-limiting enzyme in hepatic cholesterol synthesis

153
Q

recurrent episodes of collapse and a normal resting ECG- what to do now?

A

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
Q

do beta blockers cause prolonged qt

A

not usually
however sotalol does

155
Q

acute asthma mx

A
  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
Q

criteria for discharge following acute asthma admission

A

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
Q

criteria for discharge following acute asthma admission

A

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
Q

who gets ltot copd

A

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

159
Q

histological features of chronic asthma

A

i. Smooth muscle cells hypertrophy
ii. Thickened basement membrane
iii. Goblet cell hyperplasia

160
Q

a. How do you differentiate pleural effusion from consolidation?

A

i. Pleural effusion: homogenous opacification, meniscus
ii. Consolidation: heterogenous opacification

161
Q

c. What are the specific risks of bronchoalveolar lavage that you warn this patient about?

A

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

162
Q

name 3 hereditary causes of thrombosis

A
  • antiphospholipid syndrome
  • antithrombin deficiency
  • protein C or S deficiency
  • factor V Leiden
  • polycythaemia rubra vera
163
Q

what needle for pleural effusion aspiration & where to put the needle?

A

i. Patient is sat upright with their back slightly flexed
ii. 21g needle placed 2-3 spaces below the level of the meniscus

164
Q

Organisms which may colonise CF patients

A

Staphylococcus aureus
Pseudomonas aeruginosa
Burkholderia cepacia*
Aspergillus

165
Q

CAP causes

A
  • 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
166
Q

PE ECG

A

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

167
Q

tb mx & a/e

A

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

168
Q

causes of copd infective exacerbation

A

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

169
Q

eosinophilia + bronchiectasis…

A
  • Allergic bronchopulmonary aspergillosis
  • allergy to Aspergillus spores
  • eosinophilia and bronchiectasis
  • mx- glucocorticoids; itroconazole
170
Q

atelectasis mx

A

positioning the patient upright
chest physiotherapy: breathing exercises
(occurs 72hrs post op where alveoli collapse)

171
Q

causes of bilateral hilar lymphadenopathy

A

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

172
Q

chest drain location

A

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

173
Q

cxr-cavitating lung lesion

A

abscess (Staph aureus, Klebsiella and Pseudomonas)
squamous cell lung cancer
tuberculosis
Wegener’s granulomatosis
pulmonary embolism
rheumatoid arthritis
aspergillosis, histoplasmosis, coccidioidomycosis

174
Q

give 3 causes of clubbing

A

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

175
Q

key indications for NIV

A

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

176
Q

3 complications following thyroid surgery

A
  • 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.
177
Q

precipitants for DKA

A

The most common precipitating factors of DKA are infection, missed insulin doses and myocardial infarction.

178
Q

adverse effects of thiazide diuretics

A

dehydration
postural hypotension
hyponatraemia, hypokalaemia, hypercalcaemia
gout
impaired glucose tolerance
impotence
rare- pancreatitis

179
Q

persistent ST elevation following MI

A

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.

180
Q

what are bronchial breath sounds

A

harsh breath sounds equally loud on inspiration and expiration

181
Q

define cerebral palsy

A

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)

182
Q

define eisenmenger’s syndrome

A

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

183
Q

clcnical features of decompensated cardiac congenital disease

A

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)

184
Q

what enzymes do you expect to be risen following cardiac damage

A

Troponin (I/T), CK-MB, CK, AST, LDH.

185
Q

ecg changes in MI pt prior to discharge

A

inverted T waves
pathological Q waves

186
Q

besides exertion what can trigger angina

A

Cold/windy weather, emotion (anger/excitement), lying down
(decubitus angina), vivid dreams (nocturnal angina).

187
Q

signs of pulmonary oedema

A

Tachypnoea, tachycardia, raised JVP, fine lung crepitations,
wheeze, additional heart sounds/gallop rhythm , dull percussion of
bases, cyanosis, decreased tactile/vocal fremitus. (

188
Q

complications of htn

A

hypertensive retinopathy
hypertensisive nephropathy, ckd
mi
hf
stroke, haemorrhage

189
Q

common causes of af

A

P neum onia, m ocardial infarction, pulmonary embolism ,
hyperthyroidism , alcohol excess, heart failure, endocarditis.

190
Q

other than ivdu, give rf for infective endocarditis

A

Prosthetic valves, patent ductus arteriosis, VSD, coarctation,
mitral valve disease, aortic valve disease (e.g. bicuspid aortic valve).

191
Q

what is used to grade severity in copd

A

fev>80- mild
50-79%- mod
30-49- sev
<30- vsevere

192
Q

signs of consolidation on resp examination

A

Reduced chest expansion, dull percussion note, increased tactile
vocal fremitus, increased vocal resonance, bronchial breathing.

192
Q

signs of consolidation on resp examination

A

Reduced chest expansion, dull percussion note, increased tactile
vocal fremitus, increased vocal resonance, bronchial breathing.

193
Q

complications bronchiectasis

A

P neum onia, septicaem ia, recu rren t pneumonia/L R T Is,
haemoptysis, respiratory failure, cor pulmonale, pneumothorax

194
Q

pul fibrosis cxr

A

R educed lung volum e, reticulonodular shadow ing (often w orse
in low er zones), honeycom b lung (advanced disease).

195
Q

OSA questionnaire

A

epworth sleepiness scale

196
Q

OSA rf beside obesity

A

Acromegaly, enlarged tonsils, enlarged adenoids, nasal polyps,
alcohol.

197
Q

sarcoidosis biopsy

A

noncaseating granulomas

198
Q

intermittent claudication in right calf, what artery is likely stenosed

A

superficial femoral artery or popliteal artery

199
Q

rf for intermittent claudication

A

hyperlipidaemia
lack of exercise
diet high in saturated and trans fats
fhx
smoking

200
Q

what process in the arterial tree can allow intermittent claudication to improve over time

A

development/ opening up of collateral vessels

201
Q

how does aspirin work- pharmacological and therapeutic action (2 marks)

A

irreversible cox inhibitor, which prevents further production from TXA2 (thrmboxane A20 from platelets as they dont have a nucleus

therapeutic actgion- prevents platelet aggregation

202
Q

where in the lower limb does rest pain typically occur and below what abpi

A

below 0.5
toes, foot, forefoot

203
Q

when pt lies on couch, pt with peripheral arterial disease, leg becomes pale
when he stands up again it becomes red
explain this

A
  • 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
204
Q

pt with cellulitis
has hypotension and tachycardia
explain the pathophys of this

A
  • 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
205
Q

most common organisms for cellulitis

A

staphylococcus aureus
grp A strep or streptococcus pyogenes

206
Q

surgical procedure for improving hearing loss caused by OME

A
  • myringotomy- drains fluid
  • grommet insertion- ventilates & equalises pressure across eustachian tube
  • adenoidectomy- removes source of infection in the oropharynx
207
Q

ix for palpitations & why?

A
  • 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
208
Q

what biochemical abnormality is responsible for the specific damage caused by paracetmaol overdose

A

glutathione depletion

209
Q

features of untreated paracetamol OD

A

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

210
Q

problems with peritoneal dialysis

A
  • bacterial peritonitis
  • peritoneal sclerosis
  • constipayion
  • ultrafiltration failure
  • psychosocial effects- changing the dialysis solution and sleeping with a machine each night
211
Q

risk facgtors for peptic ulcer disease

A

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.

212
Q

suspected perforated peptic ulcer ix

A

erect cxr
pneumoperitoneum is seen as free air under the diaphragm

213
Q

causes of papilloedema

A

space-occupying lesion: neoplastic, vascular
malignant hypertension
idiopathic intracranial hypertension
hydrocephalus
hypercapnia

214
Q

causes of tunnel vision

A

papilloedema
glaucoma
retinitis pigmentosa
choroidoretinitis
optic atrophy secondary to tabes dorsalis
hysteria

year 5 flashcards HY (5 decks)

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