Core Conditions Continued Flashcards

1
Q

What are the 5 most common causes of AF?

A

mrs SMITH:
Sepsis
Mitral valve stenosis or regurgitation
Ichaemic heart disease
Thyrotoxicosis
Hypertension

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2
Q

Rate control is the first line treatment for AF, unless….(4)

In which case, you can offer…?

A
  1. There is a reversible underlying cause
  2. New onset (within 48 hours)
  3. Heart failure caused by AF
  4. Symptomatic despite effective rate control

In which case you offer rhythm control (pharmacological or electrical cardioversion)

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3
Q

What metabolic abnormalities arise in refeeding syndrome? (4)

What does this increase your risk of? (3)

A
  1. Hypophosphataemia
  2. Hypokalaemia
  3. Hypomagnesaemia (→toursades de pointes)
  4. Abnormal fluid balance
    //
  5. Cardiac arrhythmias
  6. Heart failure
  7. Fluid overload
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4
Q

What medications can you give for rate control in AF?
Why does rate control help treat AF?

A

1st line = betablocker e.g. atenolol 50-100 mg OD
CCB e.g. diltiazem (avoid in heart failure)
Digoxin (only used in sedentary people, risk of toxcitiy, needs monitoring)

Aim is to get HR to <100 bpm to allow better ventricular filling during diastole

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5
Q

What medication is used for pharmacological cardioversion in AF?

A

Flecainide
Amiodarone (preferred if there is evidence of structural heart disease)

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6
Q

What medication might be given as long term rhythm control for AF?

A

1st line = beta-blocker
2nd line = dronadrone after successful cardioversion

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7
Q

What is polycythaemia vera?

A

A myeloproliferative disorder caused by clonal proliferation of a marrow stem cell.

Results in increased numbers of red blood cells.

Associated with JAK2 mutation.

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8
Q

Px of polycythaemia vera:

A
  1. Pruitus, typically after a hot bath
  2. Splenomegaly
  3. HTN
  4. Hyperviscosity leading to arterial and venous thrombosis
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9
Q

In a patient with AF who has just had a stroke, should you offer anticoagulation?

A

TIA:
1. Exclude haemorrhagic stroke
2. Start anticoagulation immediately (warfarin/apixaban)
Stroke:
1. Exclude haemorrhagic stroke
2. Treat with aspirin for 2 weeks before starting anticoagulation (warfarin/apixaban)

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10
Q

How do you treat an ischaemic stroke?

A

R/o haemorrhagic stroke
Symptom onset <4.5 hours ago? → thrombolysis with alteplase
Unsuitable for thrombolysis? → thrombectomy

+ Aspirin 300 mg OD for two weeks
+ Then start secondary prevention: clopidogrel 75mg OD and atorvastatin

Also found to have AF? Start an anticoagulant after two weeks e.g. warfarin or apixaban

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11
Q

How long should you not drive for following a TIA?

A

4 weeks

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12
Q

How do you treat a TIA?

A

300mg aspirin daily
Start secondary stroke prevention within 24 hours: clopidogrel + atorvastatin

Consider carotid artery endartectomy if >70% (ECST) or >50% (NASCET) stenosed)

Don’t forget to also anticoagulate if in AF!

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13
Q

Other than heart failure, what can cause a raised BNP?

A

MI
Valvular disease
CKD

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14
Q

How does acute mesenteric ischaemia present?
Give one key risk factor:

A
  1. Central abdominal pain
  2. Diarrhoea ± rectal bleeding
  3. Metabolic acidosis (due to dying tissue)

AF! Thrombus forms in LA and travels to superior mesenteric artery

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15
Q

How does chronic mesenteric ischaemia present?

A
  1. Central colicky pain afer eating
  2. Weight loss
  3. Abdominal bruit

Diagnosed with CT angiography

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16
Q

Right sided heart murmurs are heard loudest on..?

A

Inspiration

E.g. tricuspid regurg, pulmonary stenosis

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17
Q

Left sided heart murmurs are heard loudest on..?

A

Expiration
e.g. mitral stenosis, mitral regurg, aortic stenosis, aortic regurg

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18
Q

A patient with CKD needs a CT with contrast - what can you do to reduce the risk of contrast nephropathy?

A

Give IV 0.9% saline - some trusts also recommend oral actylcysteine but never IV as this can cause anaphylaxis

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19
Q

How high is CK in rhabdomyolysis?

A

> 10,000

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20
Q

What is primary sclerosing cholangitis?

A

A condition where intrahepatic or extrahepatic ducts become strictured and fibrotic.
This causes an obstruction to the outflow of bile out of the liver and into the intestines.
The cause is mostly unclear but there is an established association with ulcerative colitis.

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21
Q

What would a ‘cholestatic pattern’ on LFTs be?

A

ALP is the most deranged/only deranged LFT

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22
Q

What is the diagnostic investigation for primary sclerosing cholangitis?

A

Magnetic resonance cholagiopancreatography - involves an MRI of the liver/bile ducts/pancreas

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23
Q

A biopsy of a carcinoma will show these 3 features, regardless of location in the body:

A

Nuclei hyperchromasia (excessive pigmentation with staining)
Nuclei pleomorphism (multiple varying shapes and sizes)
Nuclei enlargement (

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24
Q

What is non-invasive ventilation?

A

An alternative to full intubation and ventilation to support the lungs in respiratory failure to due obstructive lung disease.

Can either be BiPAP or CPAP.

BiPAP: bilevel positive airway pressure
CPAP: continuous positive airway pressure

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25
Q

Give 3 indications for CPAP:

A

Used as an alternative to full intubation/ventilation to support the lungs and maintain the airway in conditions where they are prone to collapse. Such as:
- Obstructive sleep apnoea
- Congestive heart failure
- Acute pulmonary oedema

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26
Q

What are the criteria for initiating BiPAP?

A

Used in type 2 respiratory failure, criteria for initiation is: respiratory acidosis despite adequate medical tx.

Decision must be made by a reg or above. CI in untreated pneumothorax, or any structural abnormality affecting the face/airway/gi tract.

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27
Q

What is the most common organism that causes infective endocarditis?

Name one other organism that can cause IE

A

Staph. aureus - associated with IVDU and prosthetic valves

Strep. viridans - associated with sub-acute IE

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28
Q

6 signs/symptoms of infective endocarditis:

A
  1. Fever + new murmur = IE until proven otherwise
  2. Signs of sepsis
  3. Janeway lesions - non-painful erythematous macules on palms
  4. osler nodes - painful nodules on finger tips/toes
  5. roth spots - retinal haemorrhages with pale centres
  6. splinter haemorrhages
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29
Q

3 important investigations in infective endocarditis:

A
  1. Transoesophageal echo - vegetations >3mm
  2. Blood cultures - repeated at least 3 times from different sites
  3. ECG - might show heart block
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30
Q

Which criteria are used to diagnose infective endocariditis?

A

Duke’s criteria

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31
Q

What are the three big causes of bowel obstruction?

A
  1. Adhesions (small bowel)
  2. Hernia (small bowel)
  3. Malignancy (large bowel)
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32
Q

Signs/symptoms of bowel obstruction:

How might paralytic ileus present differently?

A

Bowel obstruction: bilious green vomiting, abdo distention, diffuse abdominal pain, absolute constipation and lack of flactulence, ‘tinkling’ bowel sounds early on

Paralytic ileus presents basically exactly the same, except you’re more likely to get completely absent bowel sounds (no tinkling). The hx will be helpful to differentiate e.g. most commonly a complication of handling the bowel during surgery.

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33
Q

How do you manage a bowel obstruction?

A

“Drip and suck”: IV fluids and TPN, NG tube with free drainage, +/- surgery

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34
Q

Where is Wernicke’s area? What does it do?

A

Wernicke’s area is in the temporal lobe (left/dominant hemisphere), it is involved in language comprehension.

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35
Q

Where is Broca’s area? What does it do?

A

Broca’s area is in the frontal lobe (left/dominant hemisphere), it is involved in producing fluent speech.

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36
Q

What is a case-control study?

A

Compares people with a disease to those without a disease. Retrospective.

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37
Q

A researcher is seeking to examine whether long-term mobile phone use is linked to acoustic neuroma risk. The information on mobile phone usage is collected from participants with acoustic neuroma and a comparable group of participants without acoustic neuroma, selected from the general practice register.

What kind of study design is this?

A

Case-control study

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38
Q

What are the cut-offs for stage 1, 2 and severe hypertension?

A

1 = clinic BP≥140/90, ABPM ≥135/85
2 = clinic BP ≥160/100, ABPM≥150/90
Severe = clinic systolic ≥180, or clinic diastolic ≥110

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39
Q

When should you treat stage 1 hypertension?

A

If <80 years old and has any one of:
- end organ damage
- established CVS disease
- renal disease
- diabetes
- 10 year CVS risk equivalent to 10% or more

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40
Q

Lifestyle advice for hypertension:

A

Reduce salt intake
Reduce caffiene intake
Stop smoking
Increase exercise (60 mins/day moderate, 3 days/week vigorous)

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41
Q

Draw out the NICE HTN flowchart:

A
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42
Q

Give an example of an ACEi, ARB, CCB and thiazide-like diuretic:

A

ACEi = ramipril
ARB = candesartan, valsartan, losartan
CCB = amlodipine, verapimil, nifedipine
Thiazide like diuretic = indapamide

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43
Q

Give 3 drugs that can cause pulmonary fibrosis:

A

Amiodarone
Cyclophosamide
Methotrexate
Nitrofurantoin

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44
Q

Give 4 psychiatric and 4 physical symptoms of delirium tremens:

When does delirium tremens normally occur?

A

Psych:
1. Visual hallucinations
2. Confusion
3. Agitation
4. Delusions
Physical:
1. Seizures
2. tachycardia
3. Tremor
4. Excessive sweating

24 to 72 hours after alcohol consumption is stopped/reduced

(6-12 hours: tremor, sweating, headache, craving and anxiety
12-24 hours: hallucinations
24-48 hours: seizures
24-72 hours: “delirium tremens”)

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45
Q

How do you treat delirium tremens?

A

Medical emergency, 35% mortality if untreated!

  1. Chlordiazepoxide - a benzo to combat effects of alcohol withdrawal
  2. IV high-dose B vitamins (pabrinex) to prevent Wernicke’s encephalopathy
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46
Q

What is SIADH? How does it affect urine concentration?

A

Syndrome of inappropriate ADH secretion:
- Too much ADH is secreted
- ADH stimulates too much water to be absorbed in the collecting ducts
- Leads to very dilute plasma and very concentrated urine
-> dilutional hyponatraemia

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47
Q

5 causes of SIADH:

A

S = small cell lung cancer
I = infection (TB, pneumonia, meningitis)
A = abcess
D = drugs (especially carbamazepine and antipsychotics)
H = head injury

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48
Q

Diagnostic criteria for SIADH: (4)

A
  1. Concentrated urine
  2. Hyponatraemia
  3. Low plasma osmolarity
  4. Clinically and biochemically euvolemic
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49
Q

Tx of SIADH: (4)

A
  1. Tx underlying cause
  2. Restrict fluids (1L/day)
  3. Tolvaptan 15 mg OD to block the affect of ADH on the kidneys
  4. Demeclocycline to make kindeys resistant to ADH
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50
Q

Investigations for DVT:

A

Investigations are dependent on the well’s score!

  1. Suspected DVT + wells score≥2 → USS doppler
    - USS doppler +ve → treat for DVT
    - USS doppler -ve → check d-dimer (if raised, repeat USS in 6-8 days)
    - USS not available within 4 hours → treat and scan later
  2. Suspected DVT + wells score <2 → D-dimer
    - D-dimer positive → USS doppler
    - D-dimer negative → consider alternative diagnosis
  3. Offer all patients with an unprovoked DVT or PE the following investigations for cancer: physical exam, CXR, blood tests, urinalysis. If over 40, also get an abdo-pelvis CT scan.

(NB: you may also want to check for antiphospholipid antibodies or hereditary thrombophilia)

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51
Q

What is a prospective cohort study?

A

A study where a group of individuals, who differ with respect to one or more factors, are followed to determine who these factors affect outcomes.

E.g. Pregnant mothers followed from the first prenatal visit until after delivery to investigate the association between maternal smoking and birth weight.

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52
Q

Symptoms of hyperprolactinaemia:

A
  1. Menstrual irregularity/amennohrea
  2. Reduced libido
  3. Erectile dysfunction
  4. Galactorhea
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53
Q

How do you treat a prolactinoma?

A

First line: dopamine agonist to block prolactin effects e.g. cabergoline

Second line: surgical resection via transphenoidal surgery

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54
Q

Which type of airway is best for protecting against aspiration?

A

Tracheal tube - seals off the tracheal and protects against aspiration

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55
Q

What is haemochromatosis?

A

An autosomal recessive genetic disease where iron accumulates in tissues, especially the liver, due to increased absorption in the gut.

Asymptomatic until late stage, signs/symptoms usually begin around 40-60 years in men, and after menopause in women.

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56
Q

What tests can confirm haemochromatosis?

A

serum ferritin (shows iron overload) and transferrin saturation

if transferrin saturation is increased -> HFE genetic testing

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57
Q

A 78 year old man has type 2 diabetes. His clinician does not invite him to join
an internet-based self-monitoring programme because she considers him to
be too old to engage with it effectively.

What is this clinician’s behaviour defined as?

A

Discrimination: the unjust or prejudicial treatment of different categories of people.

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58
Q

How does cocaine cause an MI?

A

Causes coronary artery spasm

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59
Q

What are the maintenence fluid requirements for someone with underlying cardiac disease?

A

20-25 ml/kg

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60
Q

Myasthenia gravis can cause acute respiratory failure - how should you monitor respiratory function in a patient with this condition?

A

Monitor FVC!

Also keep an eye on ABG (will show hypercapnia first, then hypoxia), a weak cough also indicates weakness of expiratory muscles. Have a low threshold for endotracheal intubation due to rapid deterioration of bulbar and resp muscles.

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61
Q

What is the first line treatment for sinus bradycardia?

A

Atropine sulfate

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62
Q

GO OVER RINNE’S AND WEBER’S

A
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63
Q

3 common causes of cellulitis:

A

Staph. aureus
Group A strep. pyogenes (common in leg cellulitis and post-op cellulitis)
Group C strep. dysgalactiae

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64
Q

What is superficial thrombophlebitis?

A

Inflammation and clotting in a superficial vein. May be spontaneous or assocaited with risk factors e.g. varicose veins, IVDU

Treat with a topical anti-inflammatory cream and oral NSAID for pain relief

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65
Q

Why should you consider stopping metformin before a surgery?

When is it ok to continue it?

When must it be stopped?

What are the consequences for stopping metformin for surgery?

A

It is renally excreted, renal impairment will lead to accumulation and lactic acidosis during surgery.

If only one meal will be missed AND eGFR > 60, AND low risk of AKI you may be able to continue metformin.

If a patient will miss more than one meal OR there is significant risk of an AKI, you must stop metformin when the pre-operative fast begins.

If the patient has more than one dose/day OR CBG is >12 on two occasions - you will need to start a variable insulin infusion.

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66
Q

A patient has foot drop due to the loss of active dorsiflexion. What nerve is most likely to be affected?

A

common peroneal

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67
Q

Ovarian cancer most commonly spreads to which regional lymph nodes?

A

Para-aortic nodes - the main lymphatic drainage of the ovaries is to these nodes

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68
Q

CSF findings for bacterial meningitis:

A

Cloudy and turbid
High opening pressure
High WBCs (leukocytes)
Low glucose
High protein

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69
Q

CSF findings for viral meningitis:

A

Clear
Normal or high opening pressure
High WBCs (lymphocytes)
Normal glucose
High protein

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70
Q

CSF findings for SAH:

A

Blood stained initially, then xanthochromia
High opening pressure
High WBCs
High RBCs
Normal glucose
High protein

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71
Q

4 causes of an SAH:

A
  1. Berry aneurysm
  2. Clotting disorder
  3. Ateriovenous malformation
  4. Trauma

NB: Don’t forget PKD is strongly associated with blood vessel malformations leading to SAH

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72
Q

What is terson’s syndrome?

A

An intraoccular vitreous haemorrhage resulting from raised ICP due to a SAH or subdural haemorrhage.

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73
Q

Tx of an SAH:

A

Nimodipine to prevent vasospasm
Endovascular coiling or neurosurgical clipping

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74
Q

Which type of intracranial haemorrhage is associated with old age and alcoholism?

A

Subdural haemorrhage - bridging veins are stretched and vulnerable due to brain atrophy, trauma causes them to shear

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75
Q

How does a subdural haemorrhage present?

A

Fluctuating consciousness levels
Headaches
Drowsiness
Symptoms may be present for weeks as ICP rises

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76
Q

What does a subdural haemorrhage look like on a CT head?

A

Crescent shape

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77
Q

What does an extradural haemorrhage look like on a head ct?

A

lemon shape

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78
Q

How does an extradural haemorrhage present?

A

Deterioration in consciousness level
Associated with focal neurological signs
Can have a lucid interval

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79
Q

What is heliballismus?

A

A lesion in the subthalamic nucleus causing uncontrollable thrashing movements.

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80
Q

Which anti-emetic is safe to use in Parkinson’s disease?

A

Domperidone - does not cross the BBB

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81
Q

What is the classic triad of normal pressure hydrocephalus?

A
  1. urinary incontinence
  2. Dementia and bradyphenia (slow processing/thinking)
  3. Gait abnormality
    Sx typically develop over a few months.
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82
Q

What is normal pressure hydrocephalus?

A

An abnormal build up of CSF in the brain’s ventricles, possibly due to reduced CSF absorption at the arachnoid villi.
It is a reversible cause of dementia in elderly patients.
It can also be secondary to head injury, SAH or meningitis.

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83
Q

What is Bell’s palsy?
Which demographic are most commonly affected?

A

Idiopathic acute unilateral paralysis of the facial nerve.

LMN lesion resulting in facial drooping, and in severe cases disturbance to taste sensation in the anterior 2/3rds of the tongue and intolerance of loud noises.

Pregnant women and adults aged 20-40.

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3
4
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84
Q

Px of Bell’s palsy:

A
  1. Drooping eyelid
  2. Hyeracusis (sensitivity to loud noises)
  3. Loss of taste sensation on anterior 2/3rds of tongue
  4. Forehead is affected (LMN palsy)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

Guillain-barre is typically triggered by an infection with what organism?

A

Campylobacter-jejuni

86
Q

How do you manage an acute cluster headache?

A

High flow oxygen + SC or nasal triptan

87
Q

Features of essential tremor:

A

Worse if arm is outstretched
Improved by alcohol and rest

88
Q

What features are associated with the following types of seizure:
Frontal lobe?
Temporal lobe?
Parietal lobe?

A

Frontal = motor abnormalities (jacksonian movements)
Temporal = aura, deja vu, pulling at clothes
Partieal = sensory abnormalities

89
Q

How do you investigate narcolepsy?

A

multiple sleep latency EEG (checks for daytime sleepiness)
polysomnography (sleep study)

90
Q

How can you trigger an absence seizure?

A

Hyperventilation e.g. blow on this windmill toy

91
Q

What does right homonymous hemianopia mean?

A

Loss of vision on the right side of the visual field in both eyes.

92
Q

How does the Oxford/Bamford stroke classification differentiate between total and partial circulation strokes?

A

Total = all 3 criteria present
Partial = 2 criteria present

Criteria:
1. Unilateral hemiparesis or hemisensory loss of the face, arm and leg
2. Homonymous hemianopia
3. Higher cognitive dysfunction e.g. dysphagia

93
Q

What does the middle cerebral artery supply? (3)

A

Majority of the lateral brain
Primary motor cortex
Primary somatosensory cortex

94
Q

What does the anterior cerebral artery supply? (2)

A

Anteromedial portions of the cerebrum
The leg, foot and trunk portion of the primary motor and somatosensory cortex (imagine the motor and sensory homonculuses with their leg dangling into the central sulcus)

95
Q

Give 3 features of an ischaemic stroke of the anterior cerebral artery:

A
  1. Contralateral hemiparesis
  2. Contralateral sensory loss
  3. Affects lower extremities > upper
96
Q

Give 3 features of an ischaemic stroke of the middle cerebral artery:

A
  1. Contralateral hemiparesis
  2. Contralateral sensory loss
  3. Contralateral homonymous hemianopia
  4. Aphasia (if affecting the dominant side?)
97
Q

What does the posterior cerebral artery supply?

A

Occipital lobe
Inferomedial surface of the temporal lobe
Midbrain, thalamus, choroid plexus
Third and lateral ventricles

98
Q

2 features of a stroke in the posterior cerebral artery:

A

contralateral hemianopia with macular sparing
visual agnosia

99
Q

What is Horner’s syndrome?

A

Miosis
Ptosis
Anhidrosis
(associated with squamous cell lung carcinoma at the apex of the lung/close to the mediastinum and pressing on the cervical sympathetic ganglia)

100
Q

An infarct in which artery can cause locked-in syndrome?

A

Basilar artery

101
Q

What is Beck’s triad of cardiac tamponade?

A

Hypotension
Raised JVP
Muffled heart sounds

102
Q

What is pulsus paradoxus? Name a condition in which it is seen:

A

An abnormally large drop in BP during inspiration

Seen in cardiac tamponade

103
Q

JVP has its own waveform which consists of five parts, what does each part show?

A

A wave - contraction of the right atrium, blood forced upwards towards the IJV

X descent (1) - relaxation of the right atrium, blood fills the right atrium and leaves the IJV

C wave - contraction of the right ventricle, upwards force causes a temporary rise in the IJV

X descent (2) - final stage of right ventricular contraction, JVP falls again

V wave - relaxation of right atrium with tricuspid valve closed, temporary rise in JVP

Y descent - tricuspid valve opens, blood fills RA and RV, JVP decreases

104
Q

How do caridac tamponade and constrictive pericarditis affect JVP waveform differently?

A

Cardiac tamponande: absent Y descent
Constrictive pericarditis: X+Y present

105
Q

How do you treat cardiac tamponade?

A

Urgent drainage = peridcardiocentesis

106
Q

What is the most common ECG change seen in a PE?
Give one other possible ECG change seen in a PE:

A

Sinus tachycardia

Right axis deviation - seen in 16% of cases due to increasing strain and demand on the right ventricle to overcome the pulmonary occlusion

107
Q

What is Buerger’s disease? How does it present?

A

A small and medium vessel vasculitis that is strongly associated with smoking.

Px:
- Affects young men predominately
- Raynaud’s
- Extremity ischaemia: intermittent claudication, ischaemic ulcers
- Superficial thrombophlebitis

108
Q

What ECG change might you see in cardiac tamponade?

A

Electrical alternans: beat to beat variation in QRS amplitutde and morphology (due to the heart “swinging” in pericardial fluid)

109
Q

What is Wolff-Parkinson White Syndrome?

What is the definitive treatment?

A

An extra electrical pathway connects the atria and ventricles.
Causes AV re-entrant tachycardia.

Radiofrequency ablation of the accessory pathway.

110
Q

What ECG changes would you see in Wolff-Parkinson White Syndrome?

A

Short PR interval <0.12 seconds
Wide QRS complex >0.12 secondas
Delta wave (slurred upstroke on the QRS complex)

111
Q

T wave inversion in leads II, III, and AVF is high suggestive of what condition?

A

An inferior MI

112
Q

What is the mechanism of action of fondaparinux?

A

Activates antithrombin III, which in turn potentiates the inhibition of coagulation factors Xa

113
Q

What is the mechanism of action of warfarin?

A

Inhibits the activation of vitamin K, in turn inhibiting clotting factors 2, 7, 9 and 10

114
Q

What is the mechanism of action of DOACs?

A

Direct inhibition of factor Xa

115
Q

Definition of orthostatic hypertension:

A

A drop in systolic BP of at least 20 mmHg and/or diastolic BP of at least 10 mmHg after THREE minutes of standing

116
Q

Give 3 possible causes of a new LBBB:

A

ALWAYS pathological!
MI
HTN
Cardiomyopathy

117
Q

Give 4 causes of RBBB:

A

Normal variant (increasing incidence with age)
RVH
Cor pulmonale
PE
MI
ASD (ostium secundum)
Cardiomyopathy, myocarditis

118
Q

What ECG changes are seen in acute pericarditis?

A

Throughout most leads:
Saddle-shaped ST elevation
PR depression (most specific marker for pericarditis)
(May see reciprocal ST depression and PR elevation in lead aVR)

119
Q

4 ECG changes seen in hypokalaemia:

A

Long QT interval
Long PR interval
ST depression
U waves

120
Q

What does PCI involve?

A

Give praugrel
Gain radial access
Give unfractionated heparin and bailout glycoprotein IIb/IIIa inhibitor
Drug-eluting stents should be used in preference

121
Q

4 features of Klebsiella pneumonia:

A
  1. More common in alcoholics and diabetics
  2. May occur following aspiration
  3. “red-currant jelly” sputum
  4. Often affects upper lobes
  5. Commonly causes lung abcess formation and empyema
  6. Mortality is 30-50%
122
Q

3 features of legionella pneumophilia pneumonia:

A

Atypical pneumonia associated with:
- Hyponatraemia
- Lymphopenia
- Infected air conditioning units

123
Q

What is mesothelioma?

A

Malignant disease of the pleura, caused by exposure to asbestos, most commonly crocidolite (blue) asbestos.

Prognosis is poor, median survival is 8-14 months.

124
Q

What is asbestosis? Give 4 features:

A

Lung fibrosis related to the inhalation of asbestos.
Features:
- Lower lobe fibrosis
- Dyspnoea and reduced exercise tolerance
- Clubbing
- Bilateral end-inspiratory crackles
- Restrictive pattern on spirometry and reduced gas transfer

125
Q

What are pleural plaques?

A

Benign plaques caused by asbestos exposure, generally after a latent period of 20-40 years.

Will no undergo malignant change, do not require follow up.

126
Q

Small cell lung cancer is associated with which paraneoplastic syndrome?

A

Hyponatraemia due to ADH secretion

127
Q

Squamous cell lung cancer is associated with which paraneoplastic syndrome?

A

Hypercalcaemia secondary to PTH-rp (parathyroid related protein)

128
Q

Describe pleuritic chest pain:

A

Sharp chest pain, worse on inspiration

129
Q

What are bronchial breath sounds?

A

Harsh breath sounds equally loud on inspiration and expiration - due to consolidation.

130
Q

3 characteristic chest signs on auscultation/percussion that indicate pneumonia:

A

Bronchial breath sounds
Focal coarse crackles
Dullness to percussion

131
Q

CURB65:

A

Confusion
Urea >7
Resp rate ≥ to 30
BP <90 systolic or ≤ diastolic
Age ≥ 65

Score 1 = under 5% mortality
Score 3 = 15%
Score 4.5 = over 25%

Score 0-1 = at home care
≥ 2 = hospital admission
≥ 3 = ?ICU assessment

132
Q

The following bugs commonly cause pneumonia in which groups of patients?
Streptococcus pneumoniae
Haemophilus influenzae
Moraxella catarrhalis
Pseudomonas aeruginosa
Staph aureus

A

Streptococcus pneumoniae = common cause of CAP
Haemophilus influenzae = infective exacerbation of COPD

Moraxella catarrhalis = pneumonia in immunocompromised patients

Pseudomonas aeruginosa
Staph aureus = patients with cystic fibrosis OR after recovery influenza infection

133
Q

What is the definition of an atypical pneumonia?

A
  • Cannot be cultured or detected using gram staining
  • Does not respond to penecillins
134
Q

5 causes of atypical pneumonia:

A

“Legions of psittaci MCQs”
Legionella
Chalmydia psittaci - from infected birds (parrot owner)
Mycoplasma pneumoniae
Chlamydophilia pneumoniae
Q fever/Coxiella burnetii - from animal bodily fluids (farmer with flu)

135
Q

Mycoplasma pneumoniae is an atypical cause of pneumonia - give 3 features:

A
  1. Mild pneumonia
  2. Erythema multiforme rash: varying sized target lesions formed by pink rings with pale centres
  3. Neurological symptoms in young patients
136
Q

How do you treat CAP?

A

Low severity: 5 days oral amoxicillin
Moderate/severe: 7-10 days amoxicillin + macrolide (e.g. co-amoxiclav)

137
Q

What is sarcoidosis?

A

A granulomatous inflammatory condition of unknown cause.

Associated with chest symptoms and extra-pulmonary manifestations such as erythema nodosum and lymphadenopathy.

NB: granulomas are nodules of inflammation full of macrophages

138
Q

Px of sarcoidosis: (lungs, systemic, liver, eyes, heart)

A

Affects any organ in the body!

Lungs:
- Mediastinal lymphadenopathy
- Pulmonary fibrosis (UPPER LOBES)
- Pulmonary nodules
Systemic sx:
- fever
- weight loss
-fatigue
Liver:
- liver nodules
- cirrhosis
- cholestasis
Eyes
- urveitis
- conjunctivitis
skin
- erythema nodosum
- granulomas develop in scar tissue
-lupud pernio
Heart:
- BBB
- Heart block
- Myocardial muscle involvement

139
Q

Blood results for sarcoidosis: (5)

A

Raised serum ACE
Hypercalcaemia
Raise serum soluble interleukin-2 receptor
Raised CRP
Raised immunoglobulins

140
Q

What is the gold standard diagnostic test for sarcoidosis?

A

Bronchoscopy to obtain a lung biopsy
Histology shows non-caseating granulomas with epitheliod cells

141
Q

How is latent TB treated?

A

Isoniazid and rifampicin for 3 months

(or just isoniazid for 6 months)

142
Q

How is active TB treated?
Give a side effect of each drug:

A

Rifampicin - orange urine
Isoniazid - peripheral neuropathy (co-prescribe pyridoxine)
Pyrazinamide - hyperuricaemia
Ethambutal - colour blindness/decreased visual acuity
ALL also cause hepatotoxicity

143
Q

What is Kartagener’s syndrome?

A

Dextrocardia + bronchiecstasis + recurrent sinusitis + subfertility

144
Q

Px of cholangiocarcinoma:

A
  • Biliary colic
  • Anorexia
  • Weight loss
  • Jaundice
  • Palpable RUQ mass (courvoisier sign)
  • Left supraclavicular adenopathy (Virchow’s node)
145
Q

Which types of cancer is most associated with helicobacter pylori infection?

A

gastric cancer

146
Q

50 year old presents with constant RUQ pain, pyrexia and raised inflammatory markers. She has a history of gallstones. What’s the diagnosis?

A

Acute cholecystitis

147
Q

40 year olds man with a history of back pain presents with epigastric pain and passing black, tarry stools. His pain is relieved by eating. What’s the diagnosis?

A

Duodenal ulcer

148
Q

40 year old man presents with severe pain on the right side of his back. It comes in waves. On examination he is restless and his urine dipstick is +blood. What’s the diagnosis?

A

Renal colic

149
Q

A 70 year old woman with a history of AF presents with central abdominal pain and diarrhoea. ABG showed metabolic acidosis. What is the diagnosis?

A

Mesenteric ischaemia

150
Q

How do you treat a life-threatening C.diff infection?

A

oral vancomycin and IV metronidazole

151
Q

How do you treat a recurrent episode of c.diff within 12 weeks of symptom resolution?

A

Oral fidaxomicin

152
Q

Name 5 patient groups that might benefit from being screened for coeliac disease:

A
  • Patients with AI thyroid disease
  • Patients with dermatitis herpetiformis
  • Patients with IBS
  • Patients with DM1
  • First degree relatives
153
Q

6 complications of coeliac disease:

A
  1. Anaemia
  2. Hyposplenism
  3. Osteoporosis, osteomalacia
  4. Lactose intolerance
  5. Enteropathy-assocaited T-cell lymphoma of the small intenstine
  6. Subfertility
  7. Rare: oesophageal cancer
154
Q

Histology of coeliac disease:

A

Villous atrophy
Flat mucosa
Crypt hypertrophy
Intraepithelial lymphocytosis

155
Q

What viral markers would you check when looking for active hep B infection? What would they show?

A

HBsAg - hepatitis B surface antigen = positive (present for 1-6 months, >6 months implies chronic infection)
HBcAb - hepatitis B core antibodies = positive
HBeAg - hepatitis E antigen = positive if high infectivity, negative if past the viral replication stage

156
Q

Which is the most common cause of viral hepatitis? What kind of virus is this? How is it transmitted?

A

Hep A
RNA virus
Faecal-oral route (contaminated food or water)

157
Q

How does Hep A present? (4)
How is it managed?

A

Px:
- N&V
- Anorexia
- Jaundice
- Can cause cholestasis (dark urin, pale stools, moderate hepatomegaly)

Mx:
Self-resolves within 1-3 months

158
Q

Hep A, B, C, D and E are what kind of viruses?

A

A, C, D, E = RNA viruses
B = DNA virus

159
Q

Which antibiotic is a well known cause of cholestasis?

A

Co-amoxiclav

160
Q

How can serum ascites albumin (SAAG) can be used to find the cause of ascites?

A

SAAG > 11g/L = liver disorder e.g. alcoholic liver disease, acute liver failure, liver metastases, right heart failure, constrictive pericarditis

SAAG<11g/L = nephrotic sydrome, malignancy, severe malnutrition, pancreatitis, bowel obstruction, biliary ascites

161
Q

What is actelectasis?
Give 3 causes:

A

Partially (or rarely whole) collapse of a lung.
Occurs when the alveoli deflate or become filled with fluid.

  1. Early post-operative complication
  2. Inhaled foreign object
  3. Cystic fibrosis
  4. Lung tumours
162
Q

What is spinal stenosis?

A

Narrowing of part of the spinal canal, resulting in compression of the spinal cord or nerve roots.
Most commonly affects the lumbar spine.

163
Q

Causes of spinal stenosis (5):

A

Congenital spinal stenosis
Degenerative changes including facet joint changes, disc disease and bone spurs
Herniated discs
Thickening of the spinal ligaments
Spinal fractures
Tumours

164
Q

Three types of spinal stenosis:

A

Central stenosis = narrowing of central spinal canal
Lateral stenosis = narrowing of nerve root canals
Foramina stenosis = narrowing of intervertebral foramina

165
Q

Px of lumbar spinal stenosis:

A
  • Gradual onset
  • Intermittent neurogenic claudication (in central stenosis)
  • Lower back pain
  • Buttock and leg pain
  • Leg weakness
166
Q

What are the criteria needed to refer a patient for a 2 week wait CXR for suspected lung cancer?

A

> 40 years old with 2 or more of the following unexplained symptoms:
- cough
- fatigue
- SOB
- chest pain
- weight loss
- appetite loss
OR >40 with a history of smoking and 1 of the above unexplained symptoms.

OR >40 with any of:
- clubbing
- lymphadenopathy
- recurrent or persistent chest infections
- raised platelets
- chest signs of lung cancer

167
Q

After a CXR, what imaging investigation should a patient with suspected lung cancer have?

A

CT chest, abdo, pelvis for staging - contrast enhanced

168
Q

4 causes of DIC:

A

Sepsis
Trauma
Obstetric complications (HELLP syndrome)
Malignancy

169
Q

How does DIC affect the following:
Platelets
Fibrinogen
PT
APPT
Fibrinogen degradation products

A

Platelets = low
Fibrinogen = low
PT = high
APPT = high
Fibrinogen degradation products = high

170
Q

Why might an anaethestist apply pressure to the cricoid cartilage during induction?

A

To seal off the oesophagus and prevent the passage of gastric contents into the airway

171
Q

What is vestibular neuronitis?
How does it present (4)

A

Inflammation of the vestibular nerve. A cause of vertigo that often develops after a viral infection.
Px:
- Recurrent vertigo attacks lasting hours or days
- N&V
- Horizontal nystagmus
- No hearing loss or tinnitus

172
Q

How do you manage vestibular neuronitis?

A

Rapid relief in severe cases: buccal/IM prochlorperazine
Short course of prochlorperazine or antihistamine

173
Q

What is meniere’s disease?
How does it present?

A

A disorder of the inner ear, charactertised by excessive build up of endolymph in the labyrinth. Cause is unknown.
Px:
- Recurrent episodes of vertigo, tinnitus and sensorineural hearing loss
- A sensation of aural fullness/pressure
- Episodes last mins-hours
- Typically unilateral but can develop into bilateral symptoms over a number of years

174
Q

What does tripple assessment in breast clinic involve?

A

Clinical examination
Breast imaging (mamography and USS)
Biopsy

175
Q

3 features of lithium toxicity:

A
  • Coarse tremor
  • Jerky movements
  • Confusion
176
Q

Primary biliary cirrhosis is associated with which patients? (3)

A

Middle aged women
Patients with other autoimmune diseases
Patients with rheumatoid conditions

177
Q

Which antibodies do you check for in primary biliary cirrhosis? Which is the most specific for diagnosis?

A

Anti-mitochondrial antibodies = most specific
Anti-nuclear antibodies = present ins ~30% of cases

178
Q

How do you treat primary biliary cirrhosis? (2)

A

Ursodeoxylcholic acid
Colestyramine

179
Q

What is the typical presentation for EBV infection? (5)

A
  • Young adult with a sore throat
  • Lymphadenopathy
  • Enlarged tonsils
  • Fever
  • Malaise
  • Intense itchy rash in response to amoxicillin or cefalosporin
180
Q

Which genes are associated with type 1 diabetes?

A

HLA-DR4 and HLA-DR3

181
Q

What results do you need to diagnose type 1 diabetes for the following:
- Fasting glucose
- Random glucose
- OGTT
What other blood tests are used? (4)

A

Fasting glucose >7
Random glucose >11
OGTT: >11.1 at 2 hours

Islet cell antibodies
Anti-glutamic acid decarboxylase antibodies (GAD)
C-peptide - measure endogenous insulin production (useful to differentiate between DM1 and DM2)

182
Q

What is the target HbA1c for DM1?

A

48 or lower

183
Q

What are the target blood sugar levels for type 1 diabetes? (2)

A

Fasting of 5-7 on waking
4-7 prior to meals

184
Q

Explain 3 different insulin regimens used in type 1 diabetes:

A

Basal-bolus: intermediate/long-acting before bed, rapid/short acting before meals (this is first line)

Once-daily: one long acting at bedtime

Twice-daily: mix of short and intermediate, injected once pre-breakfast and once pre-dinner

185
Q

Three macrovascular complications of DM1:

A

Increased risk of stroke/TIA
Coronary artery disease
Peripheral vascular disease (→gangrene)

186
Q

3 microvascular complications of DM1:

A

Diabetic retinopathy
Renal nephropathy
Peripheral neuropathy

187
Q

Diagnostic criteria for type 2 diabetes: (3)

A

HbA1c of 48 or more
Fasting glucose of 7 or more
Random plasma glucose of 11.1 or more

NB: if asymptomatic do not diagnose diabetes based on a single abnormal HbA1c, repeat and monitor

188
Q

Describe the management of type 2 diabetes: (1st to 4th line)

A

1st line:
- Lifestyle changes ± metformin
- Target HbA1c = 48
2nd line:
- Initiate if HbA1c rises to 58
- Metformin + one of: DPP-4i, pioglitazone, sulfonyurea, SGLT2-i
- Target HbA1c = 53
3rd line:
- Triple therapy or switch or insulin + metformin
4th line:
- Switch one drug to a GLP-1 mimetic if BMI>35

189
Q

What is the “healthy” BMI range?

A

18.5 to 24.9

190
Q

Which of the type 2 diabetes drugs are considered weight neutral? Which can cause weight gain? Which can cause weight loss?

A

Weight neutral: metformin
Weight gain: pioglitazone, sulfonylureas (gliclazide)
Weight loss: GLP-1 mimetics (exenatide), SGLT-2 inhibtors (empagliflozin)

191
Q

Which of the DM2 medications can cause hypoglycaemia?

A

Sulfonylureas e.g. gliclazide

192
Q

What kind of drug is sitagliptin?
How does it work?

A

DPP-4 inhibitor
Inhibits DDP-4 enzyme, thereby increasing GLP-1 actvitiy.
GLP-1 is an incretin.
Incretins: increase insulin secretion, inhibit glucagon, slow GI absorption.

193
Q

How frequently should you check HbA1c in DM2?

A

Every 3-6 months until stable. The every 6 months.

194
Q

Criteria for pre-diabetes:

A

HbA1c 42-47
Fasting glucose 6.1-6.9
OGTT at 2 hours 7.8-11.1

195
Q

Explain the pathophysiology of DKA:

A

Inadequate insulin → high plasma glucose BUT low tissue/brain glucose → adipose tissue undergoes lipolysis to produce energy → produces glycerol and fatty acids → liver converts fatty acids to ketones

196
Q

Diagnostic criteria for DKA (3):

A

Hyperglycaemia >11 mmol/L or known DM
Ketones >3 mmol/L or 2+ on dipsticl
pH <7.3 or HCO3- <15 (metabolic acidosis with high anion gap)

197
Q

What would an ABG of a patient in DKA show?

A

Metabolic acidosis with high anion gap

198
Q

How do you manage DKA?

A

ABCDE approach
Fixed rate insulin infusion
Possibly switch to a sliding scale once BMs reach 15 to avoid a hypo
Continuous monitoring
Should improve within 6-24 hours

199
Q

3 complications of DKA

A

Hypokalaemia → VT
Cerebral oedema
Thrombosis/DVT

200
Q

How does hyperosmolar hyperglycaemic state present? (5)

A
  1. Slower onset (develops over a week)
  2. N&V
  3. Lethargy/weakness
  4. Dehydration
  5. Triggered by infection/stroke/MI/medications/poor diabetic control
201
Q

Investigations and results for hyperosmolar hyperglycaemic state: (5)

A

Hyperosmolar = serum osmolarity > 320
Hyperglycaemia = CBG >30
No/low ketones <3
No acidosis
Hypovolaemia

202
Q

How do you calculate serum osmolarity?

A

[Nax2] + [Kx2] + urea + glucose

203
Q

How do you manage hyperosmolar hyperglycaemic state?

A

ABCDE approach (GCS<8 → intubate!)
Replace fluids slowly
Encourage eating and drinking, monitor blood glucose
Continually assess for cerebral oedema, DVT, foot ulcers

204
Q

What is Grave’s disease?

A

An autoimmune disease in which autoantibodies to TSH receptors are produced.
These antibodies stimulate TSH receptors causing excessive T3/T4 production.

205
Q

What antibodies can you look for to diagnose Grave’s disease?

A

TSH-Rab - thyroid stimulating antibody

206
Q

How do you treat Grave’s disease? (3)

A

Carbimazole (titrate or block and replace with levothyroxine)
Beta-blockers for symptom relief
?thyroidectomy

207
Q

Give an example of a primary, secondary and congenital cause of hypothyroidism:

A

Primary: Hashimoto’s thyroiditis, idoine deficiency
Secondary: Pituitary failure e.g. tumour
Congenital: thyroid dysgenesis or dyshormogenesis

208
Q

What anti-bodies can you test for in Hashimoto’s thyroiditis?

A

Anti-TPO antibodies

209
Q

What is primary adrenal insufficieny?

A

Insufficient production of steroid hormones by the adrenal glands, most commonly caused by autoimmune damage to the adrenal glands (Addison’s)

210
Q

What is secondary adrenal insufficiency?

A

Insufficient production of ACTH therefore leading to insufficient stimulation of the adrenal glands, and insufficient production of steroid hormones.

Usually due to damage to the pituitary gland.

211
Q

Metabolic abnormalities in an addisonian crisis: (3)

A

Hyperkalaemia
Hyponatraemia
Hypoglycaemia

212
Q

With reference to each layer of the adrenal glands, what symptoms can Addison’s disease cause and why?

A

Zona Glomerulosa: low aldosterone → high potassium, low sodium, hypovolaemia, metabolic acidosis with normal anion gap

Zona fasciculata: low cortisol →low blood glucose at times of stress, ↑melanocyte stimulating hormone causing skin hyperpigmentation

Zona reticularis: low testosterone precursor → not very noticeable in men (testes produce much more testosterone), loss of pubic hair and sex drive in women