A&E Flashcards

(105 cards)

1
Q

Causes of non visible haematuria

A

Transient/spurious
- UTI
- Menstruation
- Vigorous exercise (settles in 3 days)
- Sex

Persistent
- Cancer (bladder, renal, prostate)
- Stones
- BPH
- Prostatits
- Urethritis
- Renal disease

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2
Q

What can cause blood to appear red in absence of blood

A

Food
- Beetroot, rhubarb
Drugs
- Rifampicin
- Doxorubicin

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3
Q

Investigations for non visible haematuria

+ how do you diagnose persistent

A

Urine dip for testing
- Persistent diagnosed if blood present in 2/3 samples tested 2-3 weeks apart

Also test renal function, ACR and blood pressure

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4
Q

What does haematuria + ACR suggest

A

Glomerular disease (increased permeability)
- IgA nephropathy
- Thin basement membrane disease
- Alport syndrome

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5
Q

When should haematuria be referred (Urgent)

A

Urgent 2 week

Aged 45+ and
- Unexplained visible haematuria without UTI
- Visible haematuria that persists after UTI treatment

Aged 60+ and
- Unexplained non visible haematuria and dysuria or raised WCC

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6
Q

When should haematuria be referred (non urgent)

A

Aged 60+ with recurrent or persistent UTI

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7
Q

How do you interpret ABG
4 steps

A
  1. pH
  2. Respiratory or metabolic? Look at PaCO2 and HCO3-
    - If CO2 deranged (CO2 acidic), then respiratory issue
    - If HCO3- deranged (Basic) then metabolic issue
  3. Acidosis can be due to high CO2 OR low HCO3-
  4. Compensated or Uncompensated?
    - In metabolic acidosis, the PaCO2 will be decreased to compensate
    - In respiratory acidosis the HCO3- will be increased to compensate
    - And vice versa.
    - If within normal ranges, no compensation
    - If compensation but pH is still outside of normal range, compensation is only partial.
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8
Q

What is an anion gap in metabolic acidosis

A

(Na+ + K+) - (HCO3- + Cl-) = AG (how many more cations than anions - Normal 8-14 mmol/L) *sometimes K+ is excluded

Serum is normally kept neutral. Many anions aren’t included in calculation (albumin, phosphates, sulphates, lactate, ketones), these are the “gap” (cations - anions - AG = 0)

If AG is high, this suggests a more serious life threatening cause of metabolic acidosis.

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9
Q

Causes of metabolic acidosis with a normal anion gap (AKA Hyperchloraemic)

A
  • GI bicarb loss (prolonged diarrhoea etc)
  • Renal tubular acidosis
  • Ammonium chloride injection
  • Addison’s disease
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10
Q

Causes of metabolic acidosis with a raised anion gap

A

Lactic acidosis (↑ lactate)
- Shock
- Sepsis
- Hypoxia

Ketotic acidosis (↑ Ketones)
- Diabetic acidosis
- Alcohol

Urate
- Renal failure

Acid poisoning
- Salicylates
- Methanol

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11
Q

What are the 2 types of metabolic acidosis due to high lactate levels

A

Lactic acidosis:

Type A - Sepsis, shock, hypoxia, burns
Type B - Metformin

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12
Q

What is the mechanism behind metabolic alkalosis

A

Key principle is: RAAS System activated, and aldosterone causes reabsorption of Na+ in exchange for H+ DST.

Examples
- ECF depletion - Sodium and chloride ion loss. -> activation of RAAS system -> Raised aldosterone level
- Hypokalaemia - K+ shift from cells to ECF, exchanges for H+ (H+/K+ pump), causing loss of hydrogen ions in serum.

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13
Q

Causes of metabolic alkalosis

A

Vomiting/aspiration
Diuretic use
Hypokalaemia
Primary hyperaldosteronism
Cushing’s
Liquorice, carbenoxolone

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14
Q

Causes of respiratory alkalosis

A

Hyperventilation (increased CO2 expulsion, less in blood, so blood less acidic)

  • Anxiety
  • PE
  • Salicylate poisoning
  • Altitude
  • Pregnancy
  • Sepsis
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15
Q

Causes of respiratory acidosis

A

Hypoventilation (CO2 not being expelled)

  • COPD
  • Decompensation in other resp conditions (Asthma, pulmonary oedema)
  • Neuromuscular disease
  • Obesity hypoventilation syndrome (excess adipose tissue restricts lung expansion)
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16
Q

In metabolic alkalosis why should chlorine be given in fluid

A

Enables kidneys to reabsorb sodium without HCO3- and allows kidney to excrete bicarbonate

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17
Q

What electrolyte should be given with insulin and why

A

Potassium. Insulin causes inward shift of potassium

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18
Q

Treatment approaches to acid base disorders

A

MAc - Replace buffer or remove acid (treat cause, fluid, oxygen (Lactate), insulin (DKA))

MAl - Correct volume, potassium and chloride. Stop diuretics.

RAc - Improve ventilation +- oxygen (NIV)

RAl - Reduce hyperventilation stimulus

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19
Q

In what patient groups should urine dip not be used for UTI diagnosis, what should be done instead

A

Women >65 - Urine culture
Men - MSU culture. Investigate for prostatitis too
Catheterised patients - Urine culture from fresh catheter or via catheter port.

These groups have asymptomatic bacteriuria and sensitivity and specificity are low. Catheters usually harmlessly colonised.

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20
Q

Nephrotic syndrome triad

A
  • Proteinuria >3g/24hr
  • Hypoalbuminaemia <30g/L
  • Oedema
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21
Q

What antibiotic can be used for acute bronchitis

A

Doxycycline
- If CRP>100 offer immediately
- If systemically unwell or pre existing comorbidities

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22
Q

What suggests pneumonia instead of bronchitis

A

Features like
- Sputum, wheeze, breathlessness
- Malaise, myalgia, fever
- Focal chest signs OE

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23
Q

Leads showing change, site of heart and coronary artery affected in ECG

A

Septal - V1, V2 - Left anterior descending

Anterior - V3, V4 - Left anterior descending

Inferior - II,III, aVF - Right coronary

Lateral- I, aVL, aVR, V5, V6 - Left circumflex

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24
Q

How can you differentiate the ACS conditions?

What are their differences in occlusion, and what are the implications for the heart in each

A

ECG, Troponins

  • Unstable Angina: Partial occlusion, no infarction (just ischaemia), ECG usually normal (can show ST depression/T wave inversion), troponin normal
  • NSTEMI: Major occlusion, subendothelial infarction, ST depression/T wave inversion/Pathological Q waves, troponin elevated
  • STEMI: Total occlusion, transmural infarction, ST elevation/T wave inversion/New LBBB, troponin elevated
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25
Initial ACS management
MONA Aspirin 300mg Oxygen (if <94% sats) Nitrates (sublingual/IV if pain, caution if hypotensive) Morphine if severe pain
26
What are the ECG criteria for a STEMI
Clinical symptoms >20 mins, with persistent (>20 mins) ECG features in 2 or more leads - 2.5mm ST elevation in V2-3 in men under 40, 2mm over 40. - 1.5mm ST elevation in V2-3 women - 1mm ST elevation in other leads - New LBBB
27
Management of STEMI
Aspirin 300mg straight away For patients presenting within 12 hours, is PCI possible within 120 mins? YES: Do PCI: - Give praugrel (P2Y12 inhibitor), radial access, give unfractioned heparin + bailout glycoprotein IIb/IIIa inhibitor (antiplatelet - e.g. Abciximab) - Give clopidogrel instead of praugrel if already on anticoagulation NO: Fibrinolysis AKA thrombolysis - Give alteplase (tissue plasminogen activator - binds to fibrin and converts plasminogen to plasmin, breaking down fibrin). - Give heparin with. - Ticagrelor given after. If >12 hours, medical therapy: - Dual antiplatelet (aspirin + P2Y12 inhibitor) - BB, ACEi, statins, nitrates - Anticoagulation - If ongoing ischaemia and pain you can do PCI
28
Management of NSTEMI/Unstable angina
Aspirin 300mg (Fondaparinux if no immediate PCI planned) Estimate 6 month mortality - GRACE Score Low risk (<3%) - Ticagrelor High risk (>3%) - PCI - Give prasugrel or ticagrelor - Give unfractionated heparin - Drug-eluting stents should be used If patient high bleeding risk - Swap fondaparinux for alternative antithrombin - Swap prasugrel for ticagrelor/ swap ticagrelor for clopidogrel If on anticoagulants - Swap prasugrel/ticagrelor for clopidogrel
29
What is a GRACE score
Global Registry of Acute Coronary Events - Age - Heart rate/BP - Cardiac and renal function (cardiac function measured with Kilip classification of heart failure - I - no signs, IV - Cardiogenic shock) - Cardiac arrest - ECG findings - Troponin levels
30
When is coronary angiography indicated in patients with NSTEMI/unstable angina
Immediate: If unstable (e.g. hypotensive) Within 72 hrs: GRACE>3% (intermediate, high, highest risk)
31
Kilip classification
used to assess the severity of heart failure in patients presenting with acute myocardial infarction I - No heart failure II - Lung crackles, S3 sound III - Frank pulmonary oedema IV - Cardiogenic shock (80% 30 day mortality)
32
Complications post MI
Ventricular fibrillation - most common cause of death following an MI. Leads to cardiac arrest. Cardiogenic shock - If large part of myocardium is damaged, ejection fraction is decreased such that heart cant pump to body's needs. Causes dropped BP, cold, clammy skin, confusion, low urine output, tachycardia and oedema. Bradyarrhythmias (AV block more common post inferior MI) Pericarditis - Common post transmural MI. Pain worse lying flat, pericardial rub can be heard and effusion seen on echocardiogram. - Dressler's syndrome, 2-6 weeks post MI, characterised by fever, pleuritic pain, pericardial effusion and raised ESR. Treat with NSAID
33
What is a left ventriculawr free wall rupture
Occurs in 3% of MIs 1-2 weeks post MI, patient presents with acute heart failure, secondary to cardiac tamponade (raised JVP, pulsus paradoxus, diminished heart sounds)
34
4 drugs given as secondary prevention of MI
Dual antiplatelet (Aspirin + antiplatelet (prasugrel etc)) ACEi BB Statin
35
Lifestyle advice post MI
Mediterranean diet Dont recommend omega 3 or oily fish Exercise 20-30 mins until slightly breathless Sex may resume after 4 weeks. PDE5 inhibitor (sildenafil) can be used 6 months post MI. Avoid if on nitrates
36
Whats the normal urine output for an adult
0.5-1.5 mL/kg/hr
37
Normal O2 sats for normal adult, older adult and those with chronic disease
95-100% on air Older: Depends on baseline, but 92-96% can be acceptable Chronic (COPD etc): 88-92%
38
What O2 sats warrant intervention?
Below 92 in most adults requires further assessment and oxygen therapy Below 88-90 in those with chronic respiratory disease, to avoid co2 retention Severe hypoxia <85%, urgent immediate intervention
39
How is oxygen therapy conducted and what are the targets
Supplemental oxygen through nasal cannula, face mask, etc. Targets: Healthy adult: 94-98% COPD or CO2 retention: 88-92% Older adults: Individualised to baseline.
40
KDIGO staging criteria for AKI
KDIGO criteria Stage 1 - Creatinine >26 or 1.5-1.9x baseline in <48hr - Urine output <0.5ml/kg/hr for 6-12 hours Stage 2 - >2-2.9x baseline creatinine - Urine output <0.5ml/kg/hr for >12 hours Stage 3 >353 or 3x reference creatinine <0.3ml/kg/hr for >24 hours or anuria for >12
41
Drugs to stop in AKI
DAAMN D - Diuretics A - ACEi/ARB A - Aminoglycosides (Gentamicin, Tobramycin etc) M - Metformin N - NSAIDs ACEi/ARB protective in Chronic
42
What is AKI
An acute reduction in renal function following an insult to the kidneys (usually physical not verbal). Pre renal Intra renal Post renal Prolonged pre or post can causes secondary intrarenal damage
43
Pre renal causes of AKI
Before blood reaches kidney -> low renal blood flow -> reduced GFR - Hypovolemia (haemorrhage, burns, vomiting, diarrhoea) - Hypotension/shock (sepsis, anaphylaxis, cardiogenic shock) - Renal artery issues (renal artery stenosis, thrombosis, aortic dissection) - Drugs (NSAIDs reduce prostaglandin mediated afferent dilation), ACEi, ARB (efferent constriction),
44
Intra renal causes of AKI
Problems within Kidney Tubular - Acute tubular necrosis (either ischaemic or nephrotoxic (toxins - Aminoglycosides, radiocontrast, cisplatin, myoglobin, haemoglobin) Interstitial - Acute interstitial nephritis (drug allergy, penicillin, NSAID, PPI, infection and autoimmunity) Glomerular - Post strep, IgA nephropathy, rapidly progressive GN Vascular - Thrombotic microangiopathies (HUS, TTP), malignant HTN, vasculitis
45
Post renal causes of AKI
Outflow blockage - Renal pelvis/ureter blockage: Stones, clots, tumours - Bladder outlet obstruction: BPH, prostate cancer, bladder cancer, neurogenic bladder - Urethra: stricture, phimosis
46
Initial investigations for AKI
Baseline bloods - U&E (renal function and electrolytes), FBC (haemolysis or anaemia), LFT (hepatorenal syndrome or systematic disease), Calcium, phosphate, albumin, CRP - Urinalysis (dipstick, MSU, blood = glomerulonephritis?, absence of abnormality means pre/post renal?) - Urine output monitoring (accurate fluid balance, oliguria (<0.5mL/kg/hour for >6 hrs) is used for AKI diagnosis
47
What imaging is used for AKI
Renal USS within 24 hours if obstruction suspected or no identifiable cause - May find hydronephrosis, renal size, cortical thickness CT Urogram if stones or malignancy suspected. Renal doppler to assess vascular causes in select cases
48
Risk factors for AKI
- CKD - Other organ failure - History of AKI - Nephrotoxic drugs (DAAMN) - Iodinated contrast agents within past week - Age > 65
49
Main 2 functions of the kidney that are stunted when they stop working
Main 2: Fluid balance, maintaining homeostasis - Reduced urine output (oliguria @ <0.5mL/kg/hr >6 hours) - Fluid overload - Rise in molecules that the kidney normally excretes/balances (K+, urea, creatinine)
50
Signs and symptoms of AKI
Early - asymptomatic - Reduced urine output - Pulmonary and peripheral oedema - Arrhythmia (secondary to K+ and acid-base balance changes) - Features of uraemia (encephalopathy, pericarditis)
51
What common drugs are safe to continue during AKI
Paracetamol Warfarin Statins Aspirin (cardioprotective dose of 75mg) Clopidogrel Beta blockers
52
What drugs should be stopped and what are the 2 main reasons
Worsen renal function - NSAIDs - Aminoglycosides - ACEi - ARBs - Diuretics Increased risk of toxicity - Metformin - Lithium - Digoxin
53
Treatments for hyperkalaemia and reasons for giving
Stabilise cardiac membrane - IV Calcium gluconate Short term inward shift of potassium - Combined insulin/dextrose infusion, nebulised salbutamol Removal of potassium from body - Calcium resonium (oral or enema) - Loop diuretic - Dialysis
54
Referral reasons in AKI
- Cause unknown or severe AKI - Where AKI is secondary to obstruction - Transplant - ITU patient with unknwon cause - (Where haemodialysis may be needed) patient not responding to treatment of complications - Stage 3 AKI - CKD 4 or 5 - Complications of AKI
55
Complications of AKI
Fluid overload - Pulmonary oedema, peripheral oedema - Hypertension Electrolyte disturbance - Hyperkalaemia - Hyponatraemia (fluid overload or inappropriate use of IV fluid) - Hyperphosphataemia, hypocalcaemia (reduced vit D activation and phosphate retention) Acid-base imbalance - Metabolic acidosis - reduced cardiac contractility, K+ shifts, bone demineralisation Uraemic - Encephalopathy - Pericarditis - Nausea/vomiting/anorexia/pruritus Hyperkalaemia and pulmonary oedema most life threatening
56
How is pulmonary oedema treated
Fluid restriction Loop diuretics (furosemide) (only used in AKI IF secondary fluid overload) Supplemental oxygen - NIV (CPAP, BiPAP) Sit them upright. IF hypertensive and stable, can give nitroglycerin (vasodilator)
57
What is Acute Interstitial Nephritis and what are its causes
Inflammation of renal interstitium - 25% of drug induced AKI Normally immune mediated hypersensitivity to drugs but can also be due to infection or autoimmunity Mainly antibiotics - Penicillin - Rifampicin But also: - NSAIDs - Allopurinol - Furosemide - Systemic disease (SLE, Sjogrens, Sarcoidosis) - Infection (hantavirus, staph)
58
Features of acute interstitial nephritis
- Fever, maculopapular rash, athralgia - Eosinophilia! (increased eosinophil WBCs) - Mild renal impairment and hypertension
59
Investigations to do in Acute interstitial nephritis
Sterile pyuria White cell casts
60
What is tubulointerstitial nephritis with uveitis (TINU)
TINU usually occurs in young females. Symptoms - Fever - Weight loss - Painful, red eyes Urinalysis - Leukocytes and protein
61
What is the most common cause of AKI
Acute tubular necrosis Necrosis of renal tubular epithelial cells severely affects the functioning of the kidney. Reversible at early stage.
62
Main causes of ATN
Ischaemia (Shock, sepsis) Nephrotoxins - DAAMN drugs - Myoglobin secondary to rhabdomyolysis - Radiocontrast agents - Lead
63
Features of ATN
Raised Urea, creatinine and potassium Muddy brown casts in urine
64
What are casts, what do they suggest
Casts are formed when proteins or cellular elements take the shape of the renal tubules, where they form. Usually Tamm-Horsfall protein which precipitates in acidic urine. Suggests an intrarenal cause of AKI
65
What happens histologically in ATN
Tubular epithelium necrosis - Loss of nuclei and detachment from basement membrane - Dilation of tubules - Necrotic cells obstruct tubule lumen
66
What is rhabdomyolysis
Skeletal muscle fibre breakdown, releasing intracellular contents (Myoglobin, CK, potassium) into bloodstream. This can lead to AKI as myoglobin is filtered by the kidney, precipitates in the tubules and causes AKI
67
Causes of Rhabdomyolysis
- Collapse (especially in an older person) - Seizure - Ecstasy - Crush injury - McArdle's syndrome - Statins (especially if co-prescribed with clarithromycin)
68
Signs/symptoms of rhabdomyolysis
- AKI with high CK >5000. (AKI risk at >15000) CK 5x Baseline - Myoglobinuria (dark/reddish-brown colour) - Hypocalcaemia (myoglobin binds to calcium) - Elevated phosphate - Hyperkalaemia - Metabolic acidosis Urine dip is positive for blood but microscopy shows no RBCs
69
Management of rhabdomyolysis
IV fluids and fuckin lots of em
70
Acute tubular necrosis vs prerenal uraemia
Urine normal/bland sediment in PRU. Brown granular casts in ATN Urine Sodium PRU: Low ATN: High Urine osmolality PRU: >500 ATN <350 Serum urea:creatinine ratio PRU Raised ATN Normal
71
How to do an A-E assessment
Airway - Patent? Talking? Stridor? Noisy breathing? Obstruction (vomit, blood etc) Breathing - Look: Resp rate, IWOB, Chest expansion, cyanosis, O2 sats - Listen: Wheeze, crackles, stridor - Feel: Trachea, chest wall movement, percussion Circulation - Look: Colour, cap refill, sweating, obvious bleeding - Feel: Pulse, temperature of peripheries - Measure: BP, HR, ECG, Urine output, IV access, bloods Disability - GCS Scale - Pupils - Blood glucose Exposure - Expose patient, maintain dignity and warmth - Look for rashes, bleeding, trauma, surgical wounds etc
72
A-E interventions
Airway - Head tilt/chin lift, jaw thrust, suction, airway support, call anaesthetics Breathing - Oxygen, nebulisers, physio, ventilation support Circulation - IV fluids, stop bleeding Disability - Correct hypoglycaemia, protect airway Exposure - Remove exposure
73
Features of anaphylaxis
Rapid onset of airway breathing circulation symptoms A - Swelling of throat and tongue (hoarse voice, stridor) B - IWOB, wheeze, dyspnoea, cyanosis, reduced O2 sats C - Hypotension, Tachycardia, reduced consciousness Also pruritus, widespread urticaria
74
Management of anaphylaxis
1. Remove exposure 2. 500mcg adrenaline, IM, anterolateral aspect of middle third of thigh 3. IV Fluid challenge with crystalloid (500-1000mL in adults, 10mL/kg in children)
75
Age doses of adrenaline in Anaphylaxis
Adult/child >12 years - 500 mcg 6-12 years - 300 mcg 6 month- 6 years - 150 mcg <6 months - 100-150 mcg Can be repeated every 5 mins. Usually done on the anterolateral aspect of the middle third of the thigh. Always done at 1mg/mL
76
What is refractory anaphylaxis
When symptoms persist despite 2 doses of IM adrenaline
77
Management algorithm of refractory anaphylaxis
1. Establish IV access and seek expert help so they can do IV adrenaline infusion 2. Rapid fluid bolus (Crystalloid e.g. 0.9% sodium chloride) 3. Keep giving IM adrenaline every 5 mins till infusion started. Give high flow oxygen and monitor If BP goes crazy high, may indicate adrenaline overdose
78
Post anaphylaxis management
Non sedating oral antihistamines Serum tryptase to confirm anaphylaxis (stay raised 12 hours post anaphylaxis) Refer to allergy clinic Give adrenaline injector (epipen) and train on use
79
How is adult life support done
1) CPR 30 compressions:2 breaths 2) Assess rhythm 3) If rhythm shockable (VF or pulseless VT), 1 shock then 2 mins of CPR If not shockable (PEA or asystole) continue for 2 mins before assessing again
80
Define antepartum haemorrhage
Vaginal bleeding post 24 weeks
81
What are the differences between placental abruption and placenta praevia
Placental abruption - Shock out of keeping with visible loss - Constant pain - Woody, hard, tender, tense uterus. Firm and constant tone all round - Normal lie and presentation - Fetal heartbeat absent or distressed - Have coagulation issues Praevia - Shock in proportion to visible loss - No pain - Non tender uterus - Lie and presentation abnormal - Fetal heart normal - Dont normally have coagulation issues - Small bleeds before large
81
Define placental abruption and praevia
Praevia - When the placenta lies wholly or partly over the cervical os. Major cause of mortality and morbidity, and is indication for C section. It is a worse version of a low lying placenta, as low lying placentas usually resolve upwards. Abruption - When compromise of the vascular structures supporting the placenta separate from the wall of the uterus causing bleeding into the new space under attachment site. Causes a solid woody feeling abdomen
82
Whats the most common isolated organism that implicated in dog or cat bites, how is it treated?
Pasteurella multocida Cleanse, (Dont suture puncture wounds), co amoxiclav Wound should undergo irrigation and debridement, and be left open 3-5 days if no infection. Tetanus status should be checked.
83
Whats the risk and treatment for human bites? What microbes?
Organisms: - Streptococci - Staph aureus - Eikenella - Fusobacterium - Prevotella HIV and Hep C risk Treated with co amoxiclav
84
What is Lyme Disease, whats it spread by, and how does it present early
Spirochaete infection (Borrelia burgdorferi), spread by ticks. <30 days Erythema migrans - Bullseye rash typically at site of tick bite - 1-4 weeks after initial bite - Painless, >5cm, slowly increases Systemic features - Headache - Lethargy - Fever - Arthralgia
85
Later features of lyme disease
>30 days Cardiovascular - Heart block - Peri/myocarditis Neurological - Facial nerve palsy - Radicular Pain - Meningitis
86
How is Lyme disease diagnosed and treated
Diagnosed clinically if erythema migrans present, start antibiotics ELISA antibodies to Borrelia burgdorferi first line test. If negative but suspected, repeat in 4-6 weeks. If positive, immunoblot test. Treat with doxycycline. Amox as alternative, ceftriaxone if disseminated.
87
Management of asymptomatic tick bites
If the tick still present, best way to remove is with tweezers, grasping as close to the skin as possible. Wash following, abx not needed
88
What is a Jarisch-Herxheimer reaction
Fever, rash, tachycardia after first dose of antibiotics (more commonly in syphilis but also in lyme disease) Rash is sometimes worsening of maculopapular rash (classically secondary syphilis) and sometimes urticarial/erythematous Resolves in 24 hours
89
Methods to assess the extent of a burn
Assess Total Body Surface Area (TBSA). The surface of your palm is equivalent to ~1% Wallace's Rule of 9s - Head and neck = 9% - Anterior or posterior chest = 9% each - Each arm = 9% each - Anterior or posterior leg = 9% each - Anterior or posterior abdomen = 9% each Lund and Browder chart (more precise and better in children)
90
How is burn depth classified? How does each look?
1) First degree - Superficial epidermis - Red and painful with no blisters 2) Second degree - Partial thickness (superficial dermal) - Pale pink, painful, blistered, slow cap refill 2.5) Second degree - Partial thickness (deep dermal) - Typically white but may have patches of non blanching erythema. Reduced sensation and painful to deep pressure. May or may not need grafting. Heals in 2-3 weeks. 3) Third degree - Full thickness - White (Waxy)/Brown (leathery)/ black, no blisters and no pain (nerve endings destroyed). Requires grafting. 4) Affects tendon, muscle, bone. May require debridement, amputation etc.
91
When do burns need secondary care referrals?
- All deep dermal and full thickness burns - Superficial dermal burns of the hands, face, feet, perineum, genitals or flexures. - Inhalation injuries - Electrical, chemical burns - non accidental injury
92
Give me some complications of burns
Local progressive tissue loss and release of inflammatory cytokines Fluid loss due to increased capillary permeability and plasma leakage into interstitial space. Leads to a hypovolaemic state causing reduced stroke volume and cardiac output, burn shock, vasodilation and increased vascular permeability, compensatory tachycardia, organ dysfunction Immunosuppression +- bacterial translocation from gut, which can cause sepsis, the major cause of death in burns.
93
What should be used to fluid resuscitate in major burns cases
Parkland formula - 4mL x Body weight (kg) x %TBSA burned Use crystalloid (Ringer's lactate), with half in the first 8 hours since the burn and half in the following 16 Burn is major if >10% TBSA in children, or >15% in adults
94
How else should a major burn be managed, besides fluids
Airway (smoke inhalation causes oedema) - early intubation if deep burns to head/neck Urinary catheter + analgesia Complex burns should go to burns unit 1st or 2nd degree can be managed conservatively, will heal in 2 weeks. Excision not done due to infection risk Escharotomy indicated in circumferential full thickness burns to torso or limbs. Careful division of encasing band will improve ventilation or relieve compartment syndrome
95
GCS Scale
MVE Motor - 6. Obeys - 5. Localises to pain - 4. Withdraws from pain - 3. Abnormal flexion to pain - 2. Extending to pain - 1. No response Verbal response - 5. Orientated - 4. Confused - 3. Words - 2. Sounds - 1. Nothing Eye opening - 4. Spontaneous - 3. To speech - 2. To pain - 1. None
96
Dehydration findings
Dry mucous membranes Loss of skin turgor Sunken eyes Tachycardia Hypotension Delirium
97
How is a beta blocker overdose managed
Bradycardia - Atropine Give glucagon if resistant
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Drugs that can be cleared with haemodialysis
BLAST Barbiturates Lithium Alcohol Salicylates Theophyllines
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Adult tachycardia resus guidelines
Assess with ABCDE - O2 sats (give if less than 94), IV access, monitor ECG, identify cause Life threatening features? - Shock (hypotension <90 systolic, pallor, sweating, cold, clammy, confused), syncope, Myocardial ischaemia, heart failure. If yes, Synchronised DC shocks, up to 3 shocks. If no, is QRS Narrow (<0.12 s/120ms) If no (broad complex), and regular QRS. - VT possible, give amiodarone 300mg bolus IV over 10-60 mins. If non regular QRS - If irregular and not AF Polymorphic VT give magnesium 2g over 10 mins. If yes (narrow complex) and regular QRS, Vagal manoeuvres. If ineffective, give adenosine 6mg rapid IV bolus, increasing by 6mg up to 18 every time its ineffective. Finally, beta blocker or verapamil if doesn't work. If narrow complex and irregular, possible AFIB. Control rate with BB. Digoxin or amiodarone if heart failure. Anticoagulate if >48 hours.
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How to manage a broad complex tachycardia?
Broad = >120ms QRS Regular rhythm - Assume VT unless previously confirmed SVT with bundle branch block. Loading bolus of 300mg of IV Amiodarone over 10-60 mins, followed by 900mg IV over 24 hours.
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What are the reversible causes of tachycardia
4 H - Hypoxia - Hypovolaemia - Hypo/hyperkalaemia - Hypothermia 4 T - Tension pneumothorax - Tamponade - Toxins (drug overdose, poisoning) - Thrombosis (PE, MI)
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How is oxygen therapy given in COPD exacerbation
Initial O2 target of 88-92, due to hypercapnia risk. 1) before ABG, 28% Venturi mask at 4L/min. If pCO2 normal, increase target to 94-98 2) If type 2 resp failure (high CO2 and low O2), then NIV. BIPAP used with initial settings (EPAP 4-5cm H2O, IPAP 10cm H2O)
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Recommendations to treat COPD exacerbation
Increase frequency of bronchodilator use and consider nebuliser. Give prednisolone 30mg for 5 days Oral amoxicillin or clarithromycin or doxycycline if sputum prurulent or clinical signs of pneumonia
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