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ACC > ACC general > Flashcards

ACC general Flashcards

1
Q

Definition of AAA?

A

dilatation of greater than 50% diameter (>3cm)

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2
Q

Surgery performed electively for which aneurysms?

A

> 5.5cm or expanding more than 1cm per year, can do EVAR

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3
Q

Signs of ruptured AAA?

A

Shock, expansile mass, collapse abdo pain often radiates to the back and groins

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4
Q

When to consider AAA diagnosis clinically?

A

> 50 with abdo pain/back pain/hypotensive
Known AAA and collapse/pain
AAA must be excluded where another diagnosis is more likely.

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5
Q

Emergency management of AAA?

A

Vascular surgeon, ECG, blood Xmatch (10) consider FFP and haemhorrage protocol, catheter and wide bore cannulae. Shock treated with 0 neg.
Try keep systolic <100 to avoid rupturing leak.

Cef n Met

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6
Q

Appendicitis msot common what ages and sex?

A

10-20 rare under 2 males slightly more.

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7
Q

Risk factors appendicitis?

A

Frequent ABX smoking

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8
Q

Complications from appendicitis, perforation likely after how long?

A

Mass abscess, peritonitis and rupture more likely >12hrs

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9
Q

Suspect appendicitis?

A

Abdo pain, epigastric and umbilical worsens and migrates to RIF. Movement worsens pain.
Anorexia, nausea constipation vomiting. Low grade fever

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10
Q

Maximal tenderness in appendicitis where?

A

Mcburneys point

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11
Q

What is rosvigs sign?

A

palpate left quadrant gives pain in right

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12
Q

Psoas sign in appendicitis ?

A

right thigh extended when in left lat causes right quadrant pain

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13
Q

Initial investigations in appendicitis?

A

Pregnancy test (exclude ectopic) Urine dip but may be abnormal due to inflammation. FBC and CRP 80-90% neutrophillia and leukocytosis

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14
Q

Main cause of cholecystitis?

A

Stones, 90-95% only 0.5% no stones

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15
Q

Risk factors for cholecystitis?

A

Age, female, obesity, ^cholesterol, smoking, crohns, diabetes

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16
Q

Complications of cholecystitis?

A

necrosis, perforation, peritonitis, jaundice

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17
Q

Cholecystitis symptoms?

A

Severe sudden RUQ pain, anorexia, nausea vomiting.

Fever, tenderness RUQ +- murphys. Referred pain scapular.

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18
Q

Management of cholecystitis?

A

Abdo USS, FBC, CRP amylase, ABX, analgesia and fluids

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19
Q

What is charcots triad?

A

Fever, jaundice and RUQ pain (cholangitis)

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20
Q

Most common cause of cholecystitis?

A

Obstruction

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21
Q

Key features of cholangitis?

A

Age >50 with risks, jaundice, pruritis, clay stools, fever and chills, dark urine, mental state changes, hypotension

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22
Q

Diagnosis of cholangitis?

A

FBC, urea, creatinine, ABG, MRCP, CT USS

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23
Q

Bowel obstruction features?

A

N&V, anorexia, colicky pain, constipation and distention. tinkling bowel sounds.

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24
Q

Causes of small bowel obstruction?

A

Hernias and adhesion(75%) malignancy rare

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25
Q

Causes of large bowel obstruction?

A

Usually malignancy and aged over 70, can be sigmoid volvulus

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26
Q

Bowel sounds and symptoms in ileus?

A

Painless no bowel sounds

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27
Q

Strangulated obstruction symptoms?

A

Pt more ill than expected, sharp constant pain. Peritonism is cardinal. fever WCC and signs of mesenteric ischaemia

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28
Q

Xray findings SBO?

A

Small bowel obstruction- valvulae commintantes completely cross lumen, lack of gas in large bowel.

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29
Q

Xray findings LBO?

A

peripheral gas shadow proximal to the blockage but not in the rectum. Large bowel haustra do not cross the lumens width

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30
Q

Immediate action bowel obstructions?

A

NG tube free drainage, iv fluids for electrolyte abnormalities, analgesia. FBC AXR and erect chest plus catheter

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31
Q

AXR sign with sigmoid volvulus?

A

Coffee bean sign

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32
Q

Sigmoid volvulus treatments?

A

Flatus tube, sigmoidoscopy

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33
Q

Diverticulitis symptoms?

A

Altered bowel habit, left sided colic relieved by defecation, nausea and flatulence, pyrexia, possible tender colon?

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34
Q

Diverticulitis investigations?

A

Erect CXR for perf, USS bloods wcc, crp.

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35
Q

Diverticulitis management?

A

Mild treated at home with fluids and abx, admit if bad for nbm and iv fluids. Surgery for peritonitis and purulence. Elective resection if severe or stenosed or fistulae

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36
Q

Causes of pancreatitis?

A

Gallstones, ethanol. trauma, steroids, mumps, autoimmune, ERCP, drugs hyperlipid.

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37
Q

Signs and symptoms of pancreatitis?

A

Gradual or sudden severe epigastric pain, radiates to back. Vomiting, tachy, fever jaundice, rigid abdomen,

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38
Q

Cullen’s sign?

A

periumbilical brusing

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39
Q

Grey-turners sign?

A

Flank bruising retroperitoneal haemorrhage

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40
Q

Investigations for pancreatitis?

A

> 1000 amylase, lipase(more specific) ABG, AXR, erect CXR USS, ERCP

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41
Q

Management of pancreatitis?

A

NBM likely NG tube needed. IV fluids ensure urine 30ml/hr

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42
Q

How do you assess pancreatitis severity?

A

Glasgow modified criteria >3 prompts ITU/HDU

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43
Q

Symptoms of peptic ulcer disease?

A

Epigastric pain, often hunger related or food or time of day. Fullness, heartburn, tender epigastrium,

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44
Q

Peptic ulcer red flags? ALARMS

A

anaemia, loss of weight, anorexia, recent onset, melena, swallowing difficulty

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45
Q

Which is more common gastric or duodenal ulcer?

A

Duodenal 4X more

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46
Q

Risk factors for duodenal ulcers?

A

H.pylori, nsaids, ssris, steroids. Pain before meals relieved by drinking milk/meals

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47
Q

Gastric ulcers most common in who? where?

A

Elderly, lesser curvature.

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48
Q

Gastric ulcer risks?

A

H pylori, NSAIDS,smoking, burns. relieved by antacid related to food.

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49
Q

Gastric ulcer complications?

A

Bleeding, perf, malignancy, reduced gastric outflow

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50
Q

What happens in AKI?

A

Rapid reduction (hours to days) in the eGFR due to renal hypoperfusion, damage to the glomeruli, tubules, interstitial or the obstruction to urine outflow.

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51
Q

When is it diagnosed (AKI)?

A

is an ^ serum creatinine concentration with or without a decrease in urine production. (inverse proportion to eGFR)

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52
Q

Causes of AKI broadly?

A

Pre-renal, Renal, Post-renal

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53
Q

Pre-renal causes AKI?

A
  • Hypovolaemia
  • Reduced cardiac output- liver failure, cardiac failure
  • Sepsis
  • Renal artery stenosis
  • ACE inhibitors
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54
Q

Renal causes of AKI?

A

Ischaemic, cytotoxic or inflammatory processes in urinary tract.

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55
Q

Post renal causes of AKi?

A
  • Luminal- stones, clots and sloughed papillae
  • Mural- malignancy (ureteric, bladder and prostate), BPH and strictures
  • Extrinsic compression- malignancy (pelvic) and retroperitoneal fibrosis
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56
Q

Stages of AKI?

A

1= 1.5 X creat 0.5ml/kg urine 6hr

2= 2-2.9 times base 0.5ml/kg >12hrs

3 = 3x creat0.3ml/kg >24 hr or anuria for 12hr

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57
Q

Risk factors for AKI?

A

> 75 years, CKD, cardiac failure. liver and vascular disease DIABETES! drugs, sepsis, poor fluid

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58
Q

AKI assessment?

A

A-E assess volume status, check K urgently. Dip urine (infection or blood)

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59
Q

Bence jones proteins assoc with?

A

Multiple myeloma

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60
Q

Drugh overdoese treated with dialysis? (BLAST)

A

barbiturates, lithium, alcohol, salicylates and theophylline)

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61
Q

Indications for renal replacement therapy?

A

Uraemic complications, acidosis, pulmonary oedema, hyperkalaemia >7

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62
Q

Management of post renal aki?

A

: catheterise and consider CT of the renal tract and urology referral if obstruction is most likely

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63
Q

Why is ketamine good in asthma?

A

Smooth muscle relaxation

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64
Q

How does ketamine work?

A

Non competitive NMDA antagonist brain and spine.

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65
Q

Ventricular rate in AF?

A

160-180bpm

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66
Q

Define paroxysmal AF?

A

> 30s less than 7days

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67
Q

Persistent AF?

A

> 7days

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68
Q

Permanent AF?

A

Not terminated by cardioversion, or relapses <24hrs

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69
Q

Causes of AF?

A

Most have a cause-

IHD, HTN, Hyperthy, rhematic, WPW, heart failure, caffeine, drugs, infection

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70
Q

AF complications?

A

Stroke and emboli, HF, Tachy induced myopathy and ischaemia

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71
Q

ECG AF?

A

Absent P chaotic baseline

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72
Q

AF treatment?

A

Rate control - atenolol or diltiazem/verapamil)

cardioversion new onset or reversible cause/HF

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73
Q

CHADVASc score for anticoag ?

A

1= antiplatelet or anticoag, 2 = anticoag

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74
Q

Atrial flutter?

A

Atrial tachy usually 250-300bpm

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75
Q

Causes of atrial flutter?

A

CHD, Open heart, HTN, obesity, WPW, etoh, thyrotox, copd

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76
Q

ECG atrial flutter

A

Saw tooth, no p waves but regular

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77
Q

Treatment of atrial flutter?

A

reversible causes, if unstable cardiovert, anticoag, able, amiodarone, flecainide, also rate control!

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78
Q

What typically required to initiate svt?

A

Extrasystole makes re entrant circuit.

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79
Q

ECG SVT?

A

narrow complex, QRS<120ms rate greater than 100 p absent or inverted

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80
Q

SVT management?

A

Vagal manouvres first if stable, then adenosine 6mg with flush. Then verapamil, then cardiovert DC (if unstable)

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81
Q

Ventricular tachycardia?

A

Vent rhythm >100bpm wide QRS or needing termination due to instability

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82
Q

Deviation in VT?

A

Left axis

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83
Q

Management of VT?

A

Give 02, IV, ECG, ABG, Amiodarone, if torsades give MGSO4 - may need defib inplant

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84
Q

Why does torsades come about?

A

Prolonged QT

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85
Q

Triad of DKA?

A

Ketonaemia, Hyperglycaemia, Acidaemia (metabolic)

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86
Q

Features of DKA?

A

Malaise, polyuria, dipsia, abdo pain, laboured breathing, dehydration, pear drops, N&V

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87
Q

Diagnostic criteria DKA?

A

pH<7.3 or bicarb <15 kotnes >3 or marked on urine, glucose >11mmol

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88
Q

Investigations in DKA?

A

Bloods, leucocytosis common not usually infection, ECG to check for hyper or hypo kal. Can be silent MI

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89
Q

Rate of fixed insulin per hour in DKA?

A

0.1units per kg/hr

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90
Q

DKA, pH <7.1 Ketones >6 GCS <12 02 <92 consider what?

A

ITU admission

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91
Q

DKA management?

A

Large bore cannulae, fluid challenge, to restore bp >90

92
Q

If bp >90 in DKA how to replace fluids?

A

NaCl over 1 hour or to replace deficit

93
Q

What to include in fluids for DKA?

A

KCL if anuria not suspected

94
Q

How much should values fall per hour in dka treatment?

A

Ketone 0.5, and glucose 3mmol per hour

95
Q

What glucose level do you start to give glucose in dka?

A

14mmol

96
Q

How long to continue insulin infusion in DKA?

A

until pH >7.3 ketones <0.3 and pt can then eat

97
Q

DKA complications?

A

Cerebral oedema, hypokal, pneumonia, hypomag, VTE

98
Q

Define hypoglycaemia?

A

<4plasma glucose

99
Q

Symptoms of hypoglycaemia?

A

Sweating, hunger, anxiety, tremor, confusion drowsiness, eventually coma

100
Q

Causes of Hypo? (ExPLAIN)

A

Exogenous drugs- oral antidiabetics, aspirin, betablockers acei, alcohol.

Pituatary insufficiency
liver failure
addisons
islet cell
non pancreatic neoplasm
101
Q

Treating hypo?

A

initial 10-20g glucose in drink or solid then give carbs If cannot swallow IV glucose 200ml 10% 100ml 20%

102
Q

Hypo unconscious?

A

Glucagon 0.5-2mg IM

103
Q

Hyperglycaemic hyperosmolar state?

A

Symptoms present over days not hours and it is mostly a complication of type 2 diabetes. Typically older pts higher mortality than DKA

104
Q

Diagnosis of HHS?

A

hypovolaemia, severe, glucose up to and over 30, no significant acidosis or ketones, osmalality raised >320

105
Q

Treatment of HHS?

A

ketones <1 use fluids, ketones >1 start fixed rate insulin look for infection,

106
Q

What do inotropes do?

A

Increase cardiac contractility and thus output.

107
Q

Main receptor to affect rate and force of contraction in heart?

A

B1

108
Q

How and on what does dobutamine work?

A

Predominant B1 increase contractility, and HR also B2 increases afterload

109
Q

Isoprenaline can cause what?

A

Tachy

110
Q

Noradrenaline is primarily what?

A

Vasopressor- maintains BP often used with others

111
Q

What does witholding treatment entail?

A

Not starting or increasing interventions

112
Q

Withdrawing treatment means?

A

actively stopping a life sustaining intervention (passive euthanasia)
**Both withholding and withdrawing treatment are accepted to be equally morally and ethically the same

113
Q

Define death?

A

irreversible loss of the capacity for consciousness combined with the irreversible loss of the capacity to breathe

114
Q

Confirming death?

A
  • Observed for a minimum of 5 mins
  • Absence of a central pulse and absence of heart sounds on auscultation
  • Asystole on continuous ECG
  • After 5 minutes of CPR confirm absence of pupillary light reflexes, corneal reflexes and motor response to supra-orbital pressure
115
Q

Diagnosisng brain death what should be considered?

A

Potential reversible causes-

depressant drugs

  • hypothermia- core temp should be >34 at testing
  • metabolic/endocrine disturbance
  • neuromuscular blocking agents and high cervical cord injury can cause apnoea
116
Q

Criteria for brain death?

A

¬ The pupils are fixed and do not repond to light
¬ There is no corneal reflex
¬ The oculo-vestibular reflexes are absent
¬ No motor response within the cranial nerve distribution (supra-orbital pressure)
No cough reflex to bronchial stimulation or gag reflex to pharyngeal stimulation

117
Q

Over what age can adult brainstem testing be used?

A

> 2months

118
Q

How many years registered to certify brain death?

A

At least 5 and 1 doctor must be consultant

119
Q

What should happen if you suspect a pt may be eligible for donating?

A

Contact SNOD in first instance

120
Q

Trauma triangle of death?

A

Coagulopathy, acidosis, hypothermia

121
Q

Clinically relevant hypothermia?

A

<36 for >4hrs

122
Q

What is cerebral perfusion pressure?

A

MAP-ICP

123
Q

How is CPP usually controlled in practice?

A

Raising MAP ICP should be <20

124
Q

What is the cushings response?

A

HTN, Bradycardia and irregular respiration - pre terminal sign

125
Q

Managing ICP?

A

Head elevated, Mannitol boluses 0.5-1g/kg (no good if renal problems) hypervent (controversial) RSI

126
Q

Head injury history?

A

Mechanism, LOC, amnesia, vom and headache any alcohol or drugs and anticoag, pre-injury functioning

127
Q

Examination head injury?

A

GCS, cranial nerves, focal neurology, neck tender

128
Q

Ct scan within 1 hour of head injury if …

A

GCS <13 at time, <15 2 hrs post, suspected fractures, battles sign or panda eyes, seizure, >1 vomit

129
Q

How many hours for ct if head injury on warfarin?

A

Within 8 hrs and report within 1 of doing scan

130
Q

Psych disorder linked to head injury?

A

PTSD

131
Q

Where is fast scan looking?

A

Liver, spleen, pelvic, pericardiac and anterior chest

132
Q

Brief canadian c spine rules?

A

IF suspect need radiology immobilise! or if high risk mechanism of injury. If no pain and was ambulatory and can move neck is fine,

133
Q

Broadly speaking what is resp failure (Pa02)

A

<8 divided in to 2

134
Q

What is type 1 resp failure?

A

Pa02< 8 with normal or low CO2

135
Q

Causes of type 1 resp failure?

A

Asthma, PE, oedema, Pneumonia, ARDS, Fibrosis

136
Q

What is type 2 resp failure?

A

pa02 <8 and co2 >6

137
Q

Causes of type 2 resp failure?

A

COPD, asthma, pneomonia fibrosis, reduced resp drive, neuromuscular disease and lesion, myasthenia gravis and guillan barre thoracic wall defects

138
Q

Management of type 1 resp failure?

A

Treat underlying give oxygen 35-60% face mask assited vent if pa02 low despite 60% oxygen

139
Q

Which NIV used for type 1 failure?

A

CPAP

140
Q

Which NIV used for type 2 failure?

A

Bipap

141
Q

Type 2 resp failure treatment?

A

Underlying causes, then start 24% oxygen and titrate up, check abg 20mins if paco2 continues to rise and hypoxic consider support

142
Q

ARDS?

A

May be caused by direct lung injury or occur secondary to severe systemic illness. Lung damage and release of inflammatory mediators

143
Q

Causes of ARDS?

A

Aspiration, vaculitis, shock, sepsis, DIC, pancreatitis, liver failure, fat embolism, burns, drugs

144
Q

Management of ARDS?

A

resp support with cpap, if cant keep pa02 >8.3 with 60% oxygen
may need circulatory support and organ support

145
Q

When should u give nasal cannulae as well as nebuliser?

A

If copd to maintain sats as neb through air (1-6l)

146
Q

What does CPAP increase in the lungs?

A

Functional residual capacity reduces atelectasis

147
Q

Anterior or anteroseptal Mi casued by which vessel occlusion?

A

LAD

148
Q

Lateral infarction caused by occlusion of?

A

Circumflex

149
Q

Chest pain investigations?

A

ECG, ST elevation, or new BBB

150
Q

Changes after MI?

A

New LBBB, Hyper acute t waves

151
Q

Days after Mi ecg changes?

A

pathological Q waves or t wave inversion

152
Q

Normal ecg and normal troponin more than 6 hrs after pain?

A

Unlikely to be MI

153
Q

How quickly for primary PCi?

A

2hrs

154
Q

NSTEMI management?

A 
Morphine plus antiemetic
aspirin followed by 75mg daily or clopi
GTN
B Blocker (metoprolol/bisop)
Fondaparinux
155
Q

STEMI management?

A

Morphine plus antiemetic, , aspirin clopidogrel 300mg (ticagrelor) GTN oxygen if needed

156
Q

What is unstable angina?

A

pain on minimal exertion and angina that seems to be progressing rapidly despite increasing medical treatment. Is an acute coronary syndrome that is defined by the absence of biochemical evidence of myocardial damage

157
Q

What is nicorandil?

A

Long acting nitrate for angina

158
Q

Wells score >what do CTPA?

A

4

159
Q

Wells score <4 do what?

A

Arrange d dimer, if neg consider alternative if pos do ctpa

160
Q

When is a v/q scan used?

A

Pregnancy, renal impairment and dye allergies

161
Q

CXR finding in PE?

A

Normal in context of hypoxaemia suggests PE

162
Q

Ecg changes in PE?

A

RBBB Right axis deviation t wave inversion (right sided strain)

163
Q

IS d-dimer sensitive or specific?

A

Sensitive, negative almost excludes PE

164
Q

PE treatment?

A

LMWH for stable pts, continued for at least 5 days or until inr >2 offer rivaroaxaban or warfarin for 3 months then assess (depends if provoked)

165
Q

Renal impairment or haemodynamic instability in PE use what?

A

Unfractionated heparin

166
Q

Symptoms of aortic dissection?

A

Sudden tearing pain radiating to the back. leading to hemiplegia and unequal arm pressures and pulses limb ischaemia

167
Q

Two types of aortic dissection?

A

Type A (70%) ascending aorta consider all for surgery

Type B Ascending not involved surgery if leaking or ruptured

168
Q

Management of aortic dissection?

A

Xmatch 10 units major haemorrhage! ECG possible chest xray (widening of mediastinum) CT/MRi needs ITU keep BP 100-110 (labetolol or esmolol)

169
Q

8 signs of delirium?

DELIRIUM

A

Disordered, Euphoric, Language impaired, Illusions, Reversal(sleep), Inattention, Unaware, Memory

170
Q

Hyponatraemia definition?

A

< 135mmol/l Na

171
Q

What may plasma Na not show?

A

True depletion of Na as depends on water in plasma too so volume status important.

172
Q

Causes of hyponatraemia?

A

Decreased volume, (third space infections) SIAD, Hypothyroid, anorexia, Heart failure, Drugs (diuretics thiazide nsaids)

173
Q

Features of hyponatraemia?

A

Usually incidental, non specific and onset is unsure. Vomiting, drowsiness, headache, seizures, cerebral oedema and raised ICP. Chronic can lead to brain problems.

174
Q

Hyperkalaemia serum ?

A

> 5.5

175
Q

How is K balance achieved?

A

Through renal and gut excretion

176
Q

Causes of Hyperkalaemia?

A

massive blood transfuse, burns rhabdomyolsis, tumour lysis, drugs (spiron and digox), renal addisons, conpartment shift

177
Q

^K symptoms/signs

A

Muscle weakness ECG changes, paralysis, renal impairment, parasthaesia

178
Q

Immediate management of ^K?

A

Anatagonise cardiac toxicity with calcoium gluconate (10% 15-30ml)

179
Q

After immediate management of K^ what should you do?

A

Drive K in to cells, nebulised salbutamol(10-20mg) or insulin dextrose infusion.

180
Q

What serum K do you expect ecg changes?

A

> 6 usually, once >9 Vfib and death!

181
Q

Most common cause of SAH?

A
  • Rupture of saccular aneurysms- berry aneurysms (80%)
  • Arteriovenous malformations (15%)
  • No causes are identified in <15%
182
Q

Risks for SAH?

A
  • Smoking
  • Alcohol misuse
  • Hypertension
  • Bleeding disorders
  • Mycotic aneurysm
183
Q

What is a sentinel haemorrhage?

A
  • 50% of patients experience a warning leak (sentinel haemorrhage) in the hours to weeks before the major bleed. This headache may be mild, generalised or resolve within minutes
  • Upper neck pain or stiffness is common
184
Q

Imaging for SAH?

A

non contrast CT in first 24hrs >95% demonstrates blood after days MRI is better

185
Q

When to do LP in SAH?

A

suspicion but CT negative and no ICP^ 6-12hrs after symptoms meaning degradation of blood in csf

186
Q

Lentiform on head CT ?

A

Extradural extra lentils

187
Q

Crescent on CT head?

A

Subdural

188
Q

What is cerebral vaso spasm?

A

occurs in 20% of patients. Major cause of death and morbidity. Tends to occur 3-15 days after SAH with peak incidence 6-8 days. Vasospasm causes ischaemia or infarction

189
Q

SAH management?

A

Nimodipine prevent vasospasm

Coiling

Maintain 160BP for perfuson if clipped and 120-140 if unclipped

190
Q

Presssure and appearance of csf in bacterial meningitis?

A

High turbid

191
Q

Low glucose in csf sign of what meningitis?

A

Bacterial

192
Q

Fibrin web csf?

A

Fungal/TB

193
Q

CSF monocytes ?

A

Viral

194
Q

Protein in CSF how does it change?

A

<1 in viral >1 in bacterial

195
Q

Signs and symptoms of temporal arteritis?

A
  • New onset localised headache that is usually unilateral
  • Temporal artery abnormality such as tenderness, thickening or nodularity
  • Fever, fatigue, anorexia and weight loss

pain on eating visual disturbance

196
Q

Temporal arteritis diagnosis?

A

♣ Temporal artery biopsy. If there is visual impairment arrange an urgent (same day) assessment by an ophthalmologist

197
Q

Treatment of temporal arteritis?

A

60mg/day prednisolone

198
Q

How long is temporal arteritis treated for?

A

Can be years as reducing the steroids counsel pts about this

199
Q

FBC of temporal arteritis?

A

Normocytic normochromic anaemia and elevated platelet count

200
Q

Venous sinus thrombosis symptoms? saggital?

A

Headache, vomiting seizures, pappiloedema

201
Q

Transverse sinus thrombosis symptoms?

A

Headache mastoid pain, focal cns papilloedema

202
Q

Sigmoid sinus thrombosis symptoms?

A

cerebellar signs

203
Q

5th and 6th cranial nerve palsies with which thrombosis?

A

Inferior petrosal

204
Q

Cavernous sinus thrombosis spread from where?

A

facial pustules or folliculitis

205
Q

Common causes of sinus thromboses?

A

Pregnancy, oral contraceptive, head injury, dehydration, abscess, meningitis, tb

206
Q

Venous sinus thrombosis treatment?

A

Heparin, seek expert help

207
Q

Signs and symptoms of DVT?

A

1/3 no signs, pitting oedema, tenderness politeal or femoral veins, dull ache

208
Q

Management of DVT?

A

Acute (LMWH) warfarin or noac for 3months (lmwh in preg or cancer)

209
Q

Wells score to do d dimer?

A

<2

210
Q

Travel delayed by how long after dvt anticoag?

A

2 weeks

211
Q

Management of DVT?

A

warfarin or noac for 3months (lmwh in preg or cancer)

212
Q

Wells for pregnancy?

A

No not useful neither is D dimer

213
Q

Risk factors for cellulitis?

A

Leg ulceration, Atopic eczema, funal infection, lymphoedema, obesity venous insufficiency

214
Q

What classification is used for severity of cellulitis?

A

ERON - 4 classes

215
Q

ABX for cellulitis? Penicillin allergy too? primary care

A

Fluclox 500mg qds 7/7

Clarithro 500mg BD 7/7

216
Q

Secondary care abx for cellulitis?

A

Iv fluclox or if more severe, ben pen, cipro and cinda!

217
Q

How long can an ischaemic limb wait for revascularisation?

A

4-6hrs

218
Q

Causes of ischaemic limb?

A

Thrombosis, emboli, graft occlusion, trauma

219
Q

6 P’s of ischaemia?

A 
Pale 
Pulseless
Painful
Paralysis
Paraesthesia
Perishingly cold
220
Q

Complications of ischaemic limb treatment?

A

Reperfusion injury, compartment syndrome

221
Q

What is gout, where most common?

A

Typically presents with acute monoarthropathy with severe joint inflammation. More than 50% occurs at the metatarsophalangeal joint of the big toe.

222
Q

NSAIDS contraindicated what used for gout?

A

Colchicine

223
Q

Most common site for septic arthritis?

A

Knee >50%

224
Q

Risks for septic arthritis?

A
  • Pre existing joint disease
  • Diabetes
  • Immunosuppression
  • Chronic renal failure
  • Recent joint surgery
  • Prosthetic joints
  • IV drug abuse
    Age > 80 years
225
Q

Investigation suspected septic arthritis?

A

Urgent joint aspiration for synovial fluid microscopy and culture is the key investigation C~RP may be normal as may radiographs

226
Q

ABX for septic arthritis?

A

Fluclox, vanc, clind

227
Q

Common organisms septic arthritis?

A

Staph, strep, gonococcus,

ACC (2 decks)

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