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random Flashcards

1
Q

CHA2DS2-VASc score?

A

Used to determine the need to anticoagulate a patient in atrial fibrillation

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2
Q

ABCD2 score?

A

Prognostic score for risk stratifying patients who’ve had a suspected TIA

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3
Q

NYHA score?

A

Heart failure severity scale

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4
Q

DAS28 score?

A

Measure of disease activity in rheumatoid arthritis

DAS stands for ‘disease activity score’ and the number 28 refers to the 28 joints that are examined in this assessment.

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5
Q

Child-Pugh classification?

A

A scoring system used to assess the severity of liver cirrhosis

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6
Q

Wells score?

A

Helps estimate the risk of a patient having a deep vein thrombosis

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7
Q

MMSE?

A

Mini-mental state examination - used to assess cognitive impairment

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8
Q

HAD scale?

A

Hospital Anxiety and Depression (HAD) scale - assesses severity of anxiety and depression symptoms

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9
Q

PHQ-9?

A

Patient Health Questionnaire - assesses severity of depression symptoms

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10
Q

GAD-7?

A

Used as a screening tool and severity measure for generalised anxiety disorder

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11
Q

Edinburgh Postnatal Depression Score?

A

Used to screen for postnatal depression

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12
Q

SCOFF score?

A

Questionnaire used to detect eating disorders and aid treatment

Sick

Control

One stone (14 lbs./6.5 kg.)

Fat

Food

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13
Q

AUDIT scoring?

A

Alcohol screening tool

Alcohol Use Disorders Identification Test

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14
Q

CAGE questionnaire?

A

alcohol screening tool

cut down/ annoyed/ guilty/ eye-opener

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15
Q

FAST screening?

A

alcohol screening tool

(also a mnemonic to rmb symptoms of stroke)

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16
Q

CURB-65 score?

A

Used to assess the prognosis of a patient with pneumonia

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17
Q

Epworth Sleepiness Scale?

A

Used in the assessment of suspected obstructive sleep apnoea

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18
Q

IPSS?

A

International prostate symptom score

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19
Q

Gleason score?

A

Indicates prognosis in prostate cancer

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20
Q

Bishop score?

A

Used to help assess the whether induction of labour will be required

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21
Q

Waterlow score?

A

Assesses the risk of a patient developing a pressure sore

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22
Q

FRAX score?

A

Risk assessment tool developed by WHO which calculates a patients 10-year risk of developing an osteoporosis related fracture

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23
Q

Ranson criteria?

A

Acute pancreatitis

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24
Q

ratio of chest compressions to ventilation?

A

30:2

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25
Q

Defibrillator assesses a rhythm of PEA/ asystole

-> mx?

A

continue CPR for 2 mins then reassess rhythm

IV adrenaline every 3-5 min

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26
Q

defibrillator assess a shockable rhythm ie. pulseless VT/VF

mx?

A

a single shock followed by 2 mins of CPR

adrenaline 1 mg is given once chest compressions have restarted after the third shock and then every 3-5 minutes.

give amiodarone after 3 shocks

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27
Q

Biochemistry of dehydration?

A

↑↑ U, ↑Cr

↑albumin

↑HCT

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28
Q

Biochemistry of Low GFR?

A

↑U, ↑Cr, ↑H, ↑K, ↑urate

↑PO4, ↓Ca

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29
Q

Biochemistry of tubular dysfunction?

A

Normal U and Cr
↓K, ↓urate, ↓PO4, ↓HCO3

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30
Q

biochemistry of SIADH?

A

↓Na

↓ serum osmolality, ↑ urine osmolality (>500), ↑ urine Na

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31
Q

Biochemistry of DI?

A

↑Na, ↑ serum osmolality, ↓ urine osmolality

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32
Q

Biochemistry of Conn’s?

A

↓K, ↑Na, ↑HCO3

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33
Q

Biochemistry of Addisons?

A

↑K, ↓Na

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34
Q

Biochemistry of cholestasis?

A

↑↑ALP, ↑↑GGT, ↑Bilirubin, ↑AST

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35
Q

biochemistry of alcoholic hepatocellular disease?

A

AST:ALT>2, ↑GGT

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36
Q

biochemistry of viral hepatocellular disease?

A

ALT>AST

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37
Q

biochemistry of thiazide and loop diuretics?

A

↓Na, ↓K, ↑HCO3, ↑U

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38
Q

presentation of hypoNa?

A

<135: n/v, anorexia, malaise

<130: headache, confusion, irritability

<125: seizures, non-cardiogenic pulmonary oedema

<115: coma and death

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39
Q

Causes of hypovolaemia hypoNa?

A

Urine Na > 20 mM (= renal loss)

  • diuretics
  • addisons
  • osmolar diuresis e.g. glucose
  • renal failure

Urine Na < 20 mM

diarrhoea

vomiting

burns

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40
Q

Causes of hypervolaemic hypoNa?

A

Cardiac failure

Renal failure

Nephrotic syndrome

Cirrhosis

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41
Q

causes of euvolaemic hypoNa?

A

urine osmolality >500

SIADH

urine osmolality <500

  • water overload
  • severe hypothyroidism
  • Addisons
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42
Q

Mx of hyponatraemia?

A

Correct the underlying cause

Replace Na and water at the same rate they were lost

  • Too fast → central pontine myelinolysis
  • Chronic: 10mM/d
  • Acute: 1mM/hr

Asymptomatic chronic hyponatraemia -> Fluid restrict

Symptomatic / acute hyponatraemia / dehydrated -> Cautious rehydration with 0.9% NS

If hypervolaemic consider frusemide

Emergency: seizures, coma -> Consider hypertonic saline (e.g. 1.8%)

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43
Q

features of SIADH?

A

Concentrated urine: Na>20mM, osmolality >500

HypoNa or plasma osmolality <275

Absence of hypovolaemia, oedema or diuretics

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44
Q

causes of SIADH?

A

Resp: SCLC, pneumonia, TB

CNS: meningoencephalitis, head injury, SAH

Endo: hypothyroidism

Drugs: cyclophosphamide, SSRIs, CBZ

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45
Q

Mx of SIADH?

A

Rx cause and fluid restrict

Vasopressin receptor antagonists

  • Demeclocycline
  • Vaptans
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46
Q

presentation of hyperNa?

A

Thirst
Lethargy
Weakness
Irritability
Confusion, fits, coma

Signs of dehydration

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47
Q

Causes of hyperNa?

A

Usually caused by dehydration (↓ intake or ↑ loss)

Hypovolaemic

GI loss: diarrhoea, vomiting

Renal loss: diuretics, osmotic diuresis (e.g. DM)

Skin: sweating, burns

Euvolaemic

↓ fluid intake

DI

Fever

Hypervolaemic

Hyperaldosteronism (↑BP, ↓K, alkalosis)

Hypertonic saline

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48
Q

Mx of hyperNa?

A

Give water PO if possible

Otherwise, 5% dextrose IV slowly

Use 0.9% NS if hypovolaemic or Na >170mM

-> Causes less marked fluid shifts

Aim for Na ↓ ≤12mM/d

Too fast → cerebral oedema

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49
Q

Causes of Hyperkalaemia?

A

artefact:

haemolysis

K2EDTA contamination from FBC bottle

Leucocytosis, thrombocytosis

Drip arm

internal distribution

acidosis

low insulin

cell death/ tissue trauma/ burns

digoxin poisoning

suxamethonium

decreased excretion:

oliguric renal failure

Addisons

Drugs: ACEi, NSAIDs, K+ sparing diuretics

increased input:

massive transfusion

excessive K therapy

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50
Q

Mx of hyperkalaemia?

A

non-urgent: if K+ 6-6.5 w no ECG changes

  • Stop all K containing/ sparing drugs
  • Low K diet
  • Ensure adequate hydration and monitor UO
  • Tx hypotension
  • Give iv fluids if dehydrated
  • Monitor renal fn
  • consider Calcium resonium to decrease K

Emergency: evidence of myocardial instability or K>6.5

  • 10ml 10% calcium gluconate
  • 100ml 20% glucose + 10u insulin (Actrapid)
  • Salbutamol 5mg nebulizer
  • Haemofiltration (usually needed if anuric)
  • Calcium resonium 15g PO or 30g PR
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51
Q

symptoms of hypoK?

A

Muscle weakness

Hypotonia

Hyporeflexia

Cramps

Tetany

Palpitations

Arrhythmias

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52
Q

ECG changes of hypoK?

A

Result from delayed ventricular repolarisation

Flattened / inverted T waves

Prominent U waves (after T waves)

ST depression

Long PR interval

Long QT interval

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53
Q

causes of HypoK?

A

Internal Distribution

Alkalosis

↑ insulin
β-agonists

↑ Excretion

GI: vomiting, diarrhoea, rectal villous adenoma

Renal: RTA (esp. type 2), Bartter syn.

Drugs: diuretics, steroids

Endo: Conn’s syn., Cushing’s syn.

↓ Input

Inappropriate IV fluid management

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54
Q

Mx of hypoK?

A

1mM K ↓ = ~200-300mmol total deficit

Don’t give K if oliguric

Never give STAT fast bolus

Mild: K >2.5

Oral K supplements

≥80mmol/d

Severe: K <2.5 and/or dangerous symptoms

IV KCl cautiously

10mmol/h (20mmol/h max)

Best to give centrally (burning sensation peripherally)

Max central conc: 60mM
Max peripheral conc: 40mM

Mg Replacement

Pts. are often Mg deplete too
Until Mg is replaced the K will not return to normal levels despite K replacement
Give empiric Mg replacement

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55
Q

in hypoK, what other electrolyte do u also need to correct?

A

Mg replacement

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56
Q

Role of Mg in PTH release?

A

low Mg prevents PTH release

may -> low Ca

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57
Q

symptoms of hypocalcaemia?

A

tetany

perioral parasthesiae

carpopedal spasms

Cardiomyopathy (↑ QTc -> TdP)

seizures

confusion

dermatitis: atopic, exfoliative

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58
Q

signs of HypoCa?

A

Trousseau’s sign:

BP cuff inflated + held in place for 3 minutes-> occlude the brachial artery. In the absence of blood flow, the patient’s hypocalcemia and subsequent neuromuscular irritability will induce spasm of the muscles of the hand and forearm

Chvostek’s sign: facial n is tapped in front of tragus -> facial muscles on the same side of the face will contract momentarily due to hyperexcitability of nerves.

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59
Q

causes of hypoCa?

A

With ↑ PO4

CKD

Hypoparathyroidism / pseudoyhpoparathyroidism

↓Mg
 Acute rhabdomyolysis (muscle Ca deposition)

With normal or ↓ PO4

Osteomalacia
Active pancreatitis
Respiratory alkalosis

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60
Q

Mx of hypoCa?

A

Mild

Ca 5mmol QDS PO

Daily Ca levels

CKD

Alfacalcidol (1-OH-Vit D3)

Severe

10ml 10% Ca gluconate IV (2.25mmol) over 30min

Repeat as necessary

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61
Q

presentation of hyperCa?

A

Stones
Renal stones

Polyuria and polydipsia (nephrogenic DI)

Nephrocalcinosis

Bones

Bone pain

Pathological #s

Moans: depression, confusion

Groans

Abdo pain
n/v and constipation
Pancreatitis
PUD (↑gastrin secretion)

high BP

decreased QT interval

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62
Q

Causes of hyperCa?

A

Most commonly malignancy or 1O HPT

With ↑ PO4
↑ ALP (e.g. ↑ bone turnover)

Bone mets: thyroid, breast, lung, kidney, prostate, colon

Sarcoidosis
Thyrotoxicosis

Lithium

Normal ALP
Myeloma

Hypervitaminosis D

Sarcoidosis

Milk alkali syn.

With normal or ↓ PO4

1O or 3O HPT

Familial benign hypercalciuria: AD, ↑ Ca-sensing receptor set-point

Paraneoplastic: PTHrP (but ↓PTH)

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63
Q

Ix of HyperCa?

A

↑PTH = 1o or 3O HPT

↓PTH: most likely Ca

FBC, protein electrophoresis, CXR, bone scan

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64
Q

mx of hyperCa?

A

Dx and Rx underlying cause

Rehydrate

1L 0.9% NS/4h

Monitor pts. hydration state

Frusemide

Only start once pt. is volume replete

Calciuric + makes room for more fluids

Bisphosphonates:

Ca bisphosphonate can’t be resorbed by osteoclasts

Only used in hypercalcaemia of malignancy

Can obscure Dx as → ↓Ca, ↓PO4 and ↑PTH

E.g. Pamidronate, Zoledronate (IV)

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65
Q

risk factors of osteoporosis?

A

SHATTERED

Steroids

Hyperthyroidism, HPT, HIV

Alcohol and Cigarettes

Thin (BMI <22)

Testosterone Low

Early Menopause

Renal / liver failure

Erosive / inflam bone disease (e.g. RA, myeloma)

Dietary Ca low / malabsorption

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66
Q

T score vs Z score?

A

T: no. of SDs away from youthful average

Z: no. of SDs away from age-matched average

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67
Q

indications for DEXA scan?

A

Low-trauma #
Women ≥65yrs w one or more risk factors

Before giving long-term steroids (>3mo)

Parathyroid disorders, myeloma, HIV

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68
Q

Bisphosphonates SEs?

A

GI upset

Oesophageal ulceration / erosion: Take w plenty of water on an empty stomach and refrain from lying and don’t eat for 30min.

Diffuse musculoskeletal pain

Osteonecrosis of the jaw

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69
Q

Mx of osteoporosis?

A

Decision to instigate pharmacological Rx is based upon age, RFs, and BMD.

FRAX can estimate 10yr # risk

Conservative

Stop smoking, ↓ EtOH

Wt. bearing or balancing exercise (e.g. Tai Chi)

Ca and vit-D rich diet

Home-based fall-prevention program w visual assessment.

Primary and secondary prevention of #s

Bisphosphonates: alendronate is 1st line

Ca and Vit D supplements: e.g Calcium D3 Forte

Strontium ranelate: bisphosphonate alternative

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70
Q

Alternative medications for 2O prevention of osteoporotic #s?

A

Raloxifene: SERM, ↓ breast Ca risk cf. HRT
Teriparetide: PTH analogue → new bone formation

Denosumab: anti-RANKL → ↓ osteoclast activation

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71
Q

diagnostic ix of Hereditary spherocytosis?

A

cryohaemolysis test snd EMA binding test

Osmotic fragility test

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72
Q

mx of osteomalacia?

A

Dietary: Calcium D3 Forte

Malabsorption or hepatic disease: Vit D2 (ergocalciferol) PO, Parenteral calcitriol

Renal disease or vit D resistance:

1α-OH-Vit D3 (alfacalcidol)

↓1,25-(OH)2 Vit D3 (calcitriol)

Monitor plasma Ca

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73
Q

Ix of Heart Failure?

A

Previous myocardial infarction

arrange echocardiogram within 2 weeks

No previous myocardial infarction

measure serum natriuretic peptides (BNP)

if levels are ‘high’ arrange echocardiogram within 2 weeks

if levels are ‘raised’ arrange echocardiogram within 6 weeks

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74
Q

in tumour lysis syndrome, apart from high K+, phosphate and low Ca

what else do u need?

A

one or more of:

increased serum creatinine (1.5 times upper limit of normal)

cardiac arrhythmia or sudden death

seizure

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75
Q

what supportive therapy can you provide to pt w dementia?

A

offer ‘a range of activities to promote wellbeing that are tailored to the person’s preference’

cognitive stimulation therapy

reminiscence therapy and cognitive rehabilitation

memory clinic

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76
Q

mx of mumps?

A

rest

paracetamol for high fever/discomfort

notifiable disease

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77
Q

what antibiotic can cause a disulfiram-like reaction when combined w ethanol?

A

Metronidazole

+ Cefoperazone, a cephalosporin

Clinical features of this include head and neck flushing, nausea and vomiting, sweatiness, headache and palpitations.

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78
Q

mx of secondary pneumothorax <1cm and asymptomatic?

A

management is with admission, high flow oxygen, and reassessment in 24 hours.

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79
Q

what should you assess for before offering a pt azathioprine or mercaptopurine?

A

TPMT activity

thiopurine methyltransferase

defect-> enhanced bone marrow toxicity which may cause myelosuppression, anemia, bleeding tendency, leukopenia & infection

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80
Q

Strong assoc of syringomyelia with?

A

Arnold-Chiari malformation

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81
Q

mx of essential tremor?

A

propranolol is first-line

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82
Q

most common cause of titubation (head tremor)?

A

essential tremor

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83
Q

1st line mx of chronic heart failure?

A

ACEi + BB

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84
Q

first line ix of acute mesenteric ischaemia (before CT)?

A

bloods: raised lactate (lactic acidosis)

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85
Q

mx of acute haemolytic transfusion reaction?

A

immediate transfusion termination, generous fluid resuscitation with saline solution and informing the lab

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86
Q

mx of latent TB?

A

3 months of isoniazid (with pyridoxine) and rifampicin OR 6 months of isoniazid (with pyridoxine)

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87
Q

concurrent use of BB and verapamil?

A

may precipitate severe bradycardia

Non-dihydropyridine calcium channel blockers (verapamil, diltiazem) and beta blockers are both negatively inotropic and their combined effects can cause severe bradycardia and even asystole.

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88
Q

main indications for placing a chest tube in pleural infection?

A

frankly purulent or turbid/cloudy pleural fluid

The presence of organisms identified by Gram stain and/or culture

Pleural fluid pH < 7.2

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89
Q

predisposing factors to obstructive sleep apnoea?

A

obesity

macroglossia: acromegaly, hypothyroidism, amyloidosis

large tonsils

Marfan’s syndrome

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90
Q

mx of obstructive sleep apnoea?

A

weight loss

CPAP is first line for moderate or severe OSAHS

intra-oral devices (e.g. mandibular advancement) may be used if CPAP is not tolerated or for patients with mild OSAHS where there is no daytime sleepiness

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91
Q

which bones does Pagets disease tend to affect?

A

axial skeleton

  • ie pelvis, lumbar spine, skull, femur, tibia
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92
Q

complications of Paget’s disease?

A

Nerve compression: deafness, radiculopathy

High output CCF

Osteosarcoma (<1% after 10yrs) -> sudden onset or worsening of bone pain

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93
Q

Ix of Pagets Disease?

A

HIGH ALP

Bone scan: hot spots

X-ray:

bone enlargement, sclerosis, patchy cortical thickening, deformity, wedge-shaped lytic lesions, osteoporosis circumscripta (well defined lytic skull lesions)

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94
Q

Biochemistry of pts w osteoporosis?

A

usually Ca, PO4, Alk Phos, PTH all normal

*Alk Phos may be raised if recent #

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95
Q

Looser’s zones on Xrays?

A

pseudofractures

found in osteomalacia/ Rickets

A band of bone material of decreased density may form alongside the surface of the bone. Thickening of the periosteum occurs. The formation of callouses in the affected area is also common. This gives the appearance of a false fracture.

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96
Q

Biochemistry of Osteomalacia?

A

Ca LOW

PO4 Low

PTH high

Alk Phos high

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97
Q

Biochemistry of Rickets

A

Ca Normal or Low

PO4 low

PTH high

ALk phos High

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98
Q

Biochemistry of primary hyperparathyroidism?

A

Ca high

PO4 low

PTH inappropriately normal/ High

Alk phos High

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99
Q

causes of primary hyperPTH?

A

most common 80% Parathyroid adenomas

20% gland hyperplasia

<0.5% parathyroid ca

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100
Q

Biochemistry of secondary HyperPTH

A

Ca low

PO4 high

PTH high

Alk Phos high

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101
Q

Biochemistry of tertiary hyperPTH?

A

Ca high

PO4 low/ n

Alk Phos high

PTH high

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102
Q

Biochemistry of hypoPTH?

A

Ca low

PO4 high

PTH inappropriately N/ low

Alk phos N

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103
Q

cause of hypoPTH?

A

surgical

autoimmune

congenital - DiGeorge’s

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104
Q

Biochemistry of Paget’s Disease?

A

Ca normal

PO4 normal

ALK phos HIGH

PTH normal

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105
Q

Classification of hyperlipidaemia?

A

Common Primary Hyperlipidaemia

  • 70%
  • Dietary and genetic factors
  • HIGH LDL only

Familial primary hyperlipidaemia

  • multiple phenotypes
  • high risk of CVD

Secondary hyperlipidaemia:

  • high LDL: nephrotic syndrome, cholestasis, hypothyroidism, Cushing’s, Drugs: thiazides, steroids

Mixed high LDL and high TG: T2DM, Alcohol, Chronic renal failure

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106
Q

Causes of secondary hyperlipidaemia?

A

high LDL: nephrotic syndrome, cholestasis, hypothyroidism, Cushing’s, Drugs: thiazides, steroids

Mixed high LDL and high TG: T2DM, Alcohol, Chronic renal failure

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107
Q

Types of Familial primary hyperlipidaemias?

A

1o hypercholesterolaemia:

commonest, ApoB (LDL receptor) defect -> high LDL-C

Combined hyperlipidaemia:

high LDL and TG

Lipoprotein lipase deficiency: high chylomicrons

Hypertriglyceridaemia

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108
Q

presentation of hyperlipidaemia?

A

CVD

Xanthomata:

  • corneal arcus
  • xanthelasma on eyelids
  • planar: orange streaks in palmar creases
  • tuberous: plaques on elbows, knees (over joints)
  • tendons

Pancreatitis

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109
Q

Ix of hyperlipidaemia?

A

Plasma cholesterol

Plasma HDL + LDL

Fasting TGs

TC:HDL ratio is best predictor of CV risk

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110
Q

Aims of tx for hyperlipidaemia?

A

Total cholesterol < 4

Total cholesterol: HDL ratio < 4

LDL < 2

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111
Q

Mx of Hyperlipidaemia?

A

Lifestyle changes: weight loss, increase exercise, diet (increase fibre, fruit and veg, less sat fat)

1st Line: Statins

e.g. Simvastatin 40mg PO nocte

HMG-CoA reductase inhibitors -> decrease cholesterol synthesis

2nd line;

fibrates: PPARa antagonists, decrease TGs

Ezetimibe: inhibits cholesterol absorption

Niacin/ Nicotinic acid: raises HDL, lowers LDL

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112
Q

What is Porphyria Cutanea Tarda?

A

Commonest porphyria

Cutaneous manifestations only

Uroporphyrinogen decarboxylase deficiency

photosensitivity: blistering skin lesions

facial hyperpigmentation and hypertrichosis

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113
Q

ix of porphyria cutanea tarda?

A

high Urine and serum porphyrins

high serum ferritin

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114
Q

Precipitants of porphyria cutanea tarda?

A

sunlight

alcohol

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115
Q

Mx of porphyria cutanea tarda?

A

Avoid sun

Phlebotomy/ iron chelators

chloroquine

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116
Q

Precipitants of acute intermittent porphyria?

A

P450 inducers: anti epileptics, alcohol, OCP/ HRT

infection/ stress

fasting

pre-menstrual

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117
Q

Ix of acute intermittent porphyria?

A

Urine sample!

keep it shielded from light

Increased ALA and PBG in urine

‘port wine urine’ as seen by person

when PBG gets oxidised to porphobilin (deep yellow -> purple)

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118
Q

what are porphyrias?

A

diseases due to deficiencies in the enzymes of the Haem biosynthesis pathway. -> overproduction of toxic haem precursors leading to 3 presentations. 1. acute neuro-visceral 2. acute cutaneous 3. chronic cutaneous

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119
Q

ALA Synthase deficiency

A

ALA synthase produces ALA (5-aminolaevulinic acid) from succinyl CoA + glycine).

*not a porphyria

Causes X-linked sideroblastic anaemia

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120
Q

Acute intermittent porphyria

what enzyme is defecient?

A

HMB synthase (hydroxymethylbilane)

aka

PBG deaminase (porphobilinogen deaminase)

-> buildup of ALA and PBG in serum and urine.

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121
Q

Acute intermittent porphyria

what inheritance?

A

autosomal dominant

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122
Q

What causes the neurovisceral symptoms in porphyria?

A

5-ALA

(5-aminolaevulinic acid)

is neurotoxic

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123
Q

what causes the skin lesions in porphyria?

A

porphyrins.

porphyrinogens become oxidised to porphyrins, which under light become activated porphyrins and oxygen.

porphorinogens are colourless while porphyrins are highly coloured.

also, porphyrinogens get oxidised in the circulation where there is high [O2] compared to in the cells where it is made.

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124
Q

Acute intermittent porphyria

symptoms

A

Auto dominant inheritance

HMB synthase deficiency

accumulation of PBG and ALA -> neurovisceral attacks

abdo pain, nausea and vomiting, tachycardia, HTN

constipation and urinary incontinence

hypoNa (SIADH)

seizures, psych distrubances

NO cutaneous manifestations

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125
Q

Treatment and Mx of acute intermittent porphyria

A

Avoid precipitating factors - adequate nutritional intake, avoid precipitant drugs, prompt treatment of infection/ illness

IV Carbohydrate + IV Haem Arginate (key tx)

  • inhibits ALA synthase, which turns off the pathway and reduces [ALA]
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126
Q

porphyria cutanea tarda

PCT

presentation

A

blistering

inherited/ acquired e.g. liver disease/ drugs

formation of vesicles on sun exposed areas of skin crusting, superficial scarring, pigmentation

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127
Q

PCT

porphyria cutanea tarda

which enzyme deficiency?

A

uroporphyrinogen decarboxylase deficiency

Ix: raised urinary uroporphyrins + coproporphyrins + increased ferritin

mx: avoid precipitants (alcohol, hepatic compromise)

128
Q

Presentation of homocystinuria?

A

Marfanoid habitus

Downward lens dislocation

mental retardation

heart rarely affected

recurrent thrombosis

129
Q

What is homocystinuria

A

auto recessive

Cystathione B-synthetase deficiency

-> accumulation of homocystine

130
Q

Mx of homocystinuria?

A

Some response to high-dose pyridoxine

131
Q

what is mutated in reticular dysgenesis (autosomal recessive severe SCID)

A

adenylate kinase 2 (AK2)

  • a mitochondrial enzyme metabolism enzyme
132
Q

mutation in AK2 + low neutrophils, lymphocytes, macrophages, platelets, requiring bone marrow transplantation

A

reticular dysgenesis

type of SCID

133
Q

what is mutated in Kostmann syndrome

A

HAX-1 (HCLS1 associated protein X-1)

134
Q

severe congenital neutropenia with HAX1 mutation

A

Kostmann syndrome

135
Q

Ix of Kostmann Syndrome?

A

PMN: absent

Adhesion molecules: normal

NBT/DHR: absent

Pus: none

136
Q

Mx of Kostmann syndrome?

A

G-CSF or BMT

137
Q

episodic neutropenia every 4-6 weeks, mutation in ELA2

A

cyclic neutropenia

138
Q

what is mutated in cyclic neutropenia

A

neutrophil elastase ELA-2

139
Q

what is the inheritance of cyclic neutropenia

A

autosomal dominant

140
Q

Mx of Cyclic neutropenia?

A

G-CSF

141
Q

recurrent infections, very high neutrophil counts in blood during infection, absence of pus formation, delayed umbilical cord separation.

A

leukocyte adhesion deficiency

142
Q

in leukocyte adhesion deficiency, what is the mutation/ deficiency?

A

CD18 deficiency.

CD11a/DC18 and CD11b/CD18 expressed on neutrophils regulate neutrophil adhesion and transmigration

143
Q

what receptors are involved in neutrophil adhesion and transmigration?

A

CD11a/ CD18
CD11b/CD18

144
Q

what complement proteins are involved in the classically pathway?

A

C1, C2, C4

145
Q

what is the main complement protein that is activated by the classical, alternative and lectin pathway?

A

C3

146
Q

Ix of Leukocyte Adhesion Deficiency?

A

PMN increased

Absent Adhesion molecules

147
Q

Nitroblue Tetrazolium test abnormal/ negative

A

chronic granulomatous disease

148
Q

in chronic granulomatous disease, what is deficient?

A

NADPH oxidase

149
Q

which complement protein is involved in the alternative pathway?

A

C3

C3 binds directly to
techoic acid on Gram + bacteria and to LPS on gram - bacteria

+ involves factors B, I, P

150
Q

Which complement proteins are involved in the lectin pathway?

A

C2 and C4

151
Q

mx of chronic granulomatous disease

A

IFN gamma

152
Q

dihydrorhodamine flow cytometry test abnormal / negative

A

chronic granulomatous disease

153
Q

chronic granulomatous disease presentation

A

susceptibility to bacteria esp catalase + bacteria.

(ie recurrent pneumonias + abscesses)

granuloma formation + lymphadenopathy + hepatosplenomegaly

154
Q

chronic granulomatous disease pathology

A

absent respiratory burst due to deficiency of one of the components of NADPH oxidase.

impaired killing if intracellular microorganisms and excessive inflammation with granuloma formation

155
Q

Ix of Chronic Granulomatous Disease?

A

Nitroblue Tetrazolium test abnormal + dihydrorhodamine flow cytometry test abnormal

156
Q

susceptibility to infection with mycobacteria (TB and atypical), BCG, Salmonella. What condition?

A

deficiency of IFNgamma/ IL12 and their receptors.

157
Q

what happens when one is deficient in early classical pathway? ie. C1/2/4

A

immune complexes fail to activate complement pathway -> increased susceptibility to infection

increased load of self-antigens

deposition of immune complexes which stimulated inflammation in skin, joints, kidneys e.g. SLE

158
Q

complement deficient - susceptibility to?

A

encapsulated bacteria

e.g. neisseria meningitidis,
strep pneumoniae, h influenza

159
Q

IL12/ IFNy

or receptor deficiency

  • what organisms are they susceptible to?
A

Mycobacteria and salmonella

BCG infection after vaccination

No granulomas

160
Q

what immune cells are vital for protection against viral infections and tumours?

A

NK cells and CD8 T cells

161
Q

4 month old, infections of all types, failure to thrive, persistent diarrhoea

A

SCID

162
Q

increased infection in patients who have another cause of immune impairment e.g. premature infant, HIV infection, chemotherapy, antibody deficiency

A

MBL deficiency

163
Q

DiGeorge’s syndrome

A

CATCH 22

Cardiac abnormalities (esp Tetralogy of Fallot)
Abnormal facies (low set ears, high forehead)
Thymic aplasia
Cleft palate
HypoCa/ HypoPTH

Chr22- deletion at 22q11.2

164
Q

Thymic aplasia - reduced numbers of T cells. which condition?

A

DiGeorge’s

165
Q

low T cells and NK cells, normal B cells, but low Igs.

A

X linked SCID

166
Q

Absent expression of MHC Class II molecules

A

Bare Lymphocyte Syndrome type II

167
Q

absent expression of MHC Class I molecules

A

Bare lymphocyte syndrome type I

168
Q

Bare lymphocyte Syndrome type II

A 
absent MHC Class II
-\> profound deficiency of CD4+ T cells
\+ failure to produce IgA/ IgG because no class switching

infections of all types.

may be associated with sclerosing cholangitis
FTT after 3 months

169
Q

In Bare Lymphocyte Syndrome Type II,

which cell populations are reduced?

A

CD4

IgG, IgA

170
Q

tx of digeorge’s syndrome?

A

Thymus transplant

171
Q

in DiGeorge’s Syndrome, what cell populations are reduced?

A

CD4, CD8 T cells

IgG, IgA

172
Q

mutation in X linked SCID?

A

IL2R gamma chain mutation

(T cell- but B cells normal + IgM may be normal)

173
Q

mutation of auto recess SCID?

A

ADA deficiency

Adenosine Deaminase

-> everything T and B cells are low

174
Q

Hyper IgM syndrome aka

A

CD40L deficiency

175
Q

what gene is defective in Bruton’s X linked hypogammaglobulinaemia

A

B cell tyrosine kinase gene

(BTK gene)

176
Q

absence of mature B cells and no circulating Ig. Recurrent infections. Family history where brother is affected.

A

X linked Bruton’s hypogammaglobulinaemia

177
Q

recurrent respiratory tract and GI tract infections

A

selective IgA deficiency

178
Q

Selective IgA deficiency patients are at risk of what during blood transfusion?

A

anaphylaxis due to introduction of donor IgA

179
Q

High IgM, undetectable Ig G, Ig A, Ig E. Normal number circulating B cells.

failure of class switching due to T cell defect.

recurrent infections- e.g. h influenza, strep pneumo, pseudomonas, pneumocystis jiroveci

A

Hyper IgM syndrome

aka CD40L defciency

180
Q

what gene is mutated in Hyper IgM syndrome?

A

CD40 Ligand gene

(CD40L normally on T cell)

181
Q

Other than HIV, what other condition increases risk of pneumocystis jiroveci infection?

A

Hyper IgM syndrome

182
Q

What cell populations are reduced in Brutons hypogammaglobulinaemia?

A

B cells low

IgM/G/A all low

because pre-B cells cannot mature due to B cell tyrosine kinase deficiency

183
Q

what cell populations are reduced in Hyper IgM syndrome?

A

raised IgM

low Ig G/A

due to defective CD40 signalling - B cells cannot undergo class switch recombination and somatic hypermutation

184
Q

what condition is assoc w selective IgA deficiency?

A

Coeliac Disease

185
Q

no germinal centre development within lymph nodes and spleen. No class switching occurring.

A

Hyper IgM syndrome

186
Q

after an acute anaphylactic episode, how to confirm via ix?

A

measure serum mast cell tryptase (should return to baseline by 6h)

187
Q

first line test for allergy

A

skin prick (more sensitive and specific than blood tests)

188
Q

SLE associated with which complement deficiencies?

A

most common C2

C1q, C1r, C1s, C2 and C4 deficiency all seen in SLE

189
Q

Ix of Complement Dysfunction?

A

C3, C4 level

CH50: classical pathway

AP50: alternative pathway

if CH50 and AP50 both abnormal w normal C3/4 = final common pathway deficiency (C5-9)

190
Q

Presentation of B, I, P deficiency?

A

deficiency in alternative pathway

increased risk of infection w encapsulated bacteria

  • Meningococcus, pneumococcus, H influenzae

FHx of infection

Abnormal AP50

191
Q

presentation of C5-9 deficiency?

A

deficiency in terminal pathway -> inability to MAC (membrane attack complex)

increased risk of infection w encapsulated bacteria

  • Meningococcus, pneumococcus, H influenzae

FHx of infection

*CH50 and AP50 abnormal w normal C3,4

192
Q

presentation of common variable immune deficiency?

A

recurrent bacterial infections:

  • bronchiectasis
  • sinusitis

usually chronic lung disease + GI infections

Autoimmune disease

Granulomatous disease

193
Q

What cell populations are decreased in Common variable immune deficiency

A

Low Ig G and Ig A

cause is poorly understood

Tx usually lifelong Ig replacement therapy

194
Q

X-linked recessive disease

eczema, thrombocytopenia, immunodeficiency and bloody diarrhoea

A

Wiskott-Aldrich Syndrome

195
Q

what gene mutation is implicated in Wiskott-Aldrich?

A

X-linked

WASP gene mutation

196
Q

Features of Wiskott-Aldrich Syndrome?

A

eczema

thrombocytopenia

immunodeficiency

raised Ig E

197
Q

what immunoglobulins are low/ raised in Wiskott-Aldrich Syndrome?

A

Ig A and Ig E are raised

Ig M is low

Ig G: may be normal, raised, low

198
Q

Where is the mutation in X linked SCID?

A

Mutation of gamma chain of IL2 receptor on chromosome Xq13.1

199
Q

Very low or absent T and NK cell numbers, Normal or increased B cell numbers but low Igs

A

X linked SCID

200
Q

what is deficient in auto recessive SCID?

A 
Adenosine deaminase (ADA) deficiency
-\> accumulation of precursors are toxic to lymphocytes.
201
Q

mx of auto recessive SCID?

A

PEG-ADA enzyme replacement therapy

202
Q

how does the IL12-IFNy network usually work?

A

Infected macrophages produce IL12 -> IL12 induces T cells to produce IFNy -> IFNy stimulates macrophages to produce TNF and activates NADPH oxidase.

203
Q

B cell differentiation involves which ligands?

A

CD40-CD40L interaction

204
Q

site of T cell maturation?

A

Thymus

205
Q

site of B cell maturation?

A

Bone marrow

206
Q

secondary lymphoid organs?

A

Spleen, LNs, MALT

207
Q

brutons agammaglobulinaemia mx?

A

IVIG

208
Q

main cytokine responsible for fibrosis seen in CREST syndrome?

A

TGF-beta.

stimulates collagen production by fibroblasts.

209
Q

rheumatoid arthritis
how does it affect the complement pathway?

A

high CH50.
complement factors are acute phase proteins and a high CH50 indicates acute or chronic inflammation.

210
Q

type 2 autoimmune hepatitis- what autoantibody?

A

anti-LKM-1.
anti liver/ kidney microsomal-1 antibody

211
Q

what three sites are classically affected in hereditary angio-oedema?

A

upper airway, subcutaneous tissues and abdo organs (diarrhoea/ abdo pain).

212
Q

magnesium deficiency can lead to hypo….?

A

hypoCa, hypoK, hypoPTH

213
Q

before a transplant, what medication would you give to induce the patient?

A

suppress T cell response
e.g. anti-CD25 Basiliximub or anti-CD52 Alemtuzumab or OKT3 (muromonab)/ Anti-thymocyte globulin

214
Q

calcineurin inhibitor with side effects of nephrotoxicity, neurotoxicity, HTN, dysmorphic features and gum hypertrophy

A

cyclosporin

215
Q

calcineurin inhibitor with side effects of nephrotoxicity, neurotoxicity, HTN and is diabetogenic

A

tacrolimus

216
Q

what are calcineurin inhibitors indicated in?

A

transplant rejection prophylaxis by reducing T cell activation and proliferation

217
Q

calcineurin inhibitors?

A

tacrolimus and cyclosporin

calcineurin normally activates IL-2. -> calcineurin inhibitors reduce T cell activation and proliferation

218
Q

what is the most sensitive specific in pernicious anaemia?

A

anti parietal cells antibody

219
Q

mixed connective tissue disease
antibody?

A

anti-U1RNP antibody (speckled pattern)

220
Q

presentation of hereditary angioedema?

A

attacks may be precipitated by alcohol, exercise, stress

recurrent angioedema but urticaria + not itchy:

skin

oropharynx -> asphyxia (laryngeal oedema)

GIT - nausea, vomiting, diarrhoea, abdo pain

+ve Family history

Normal C1/3 but low C2 and C4

221
Q

Hereditary angioedema aka?

A

C1 esterase deficiency

222
Q

Diagnosis of Hereditary angioedema?

A

C1 inhibitor - quantitatively low in type 1 (85%)

C1 inhibitor - functionally deficient in type 1 (15%)

C4 (low)

223
Q

features of infections in immune deficiency?

A

2 major or 1 major + recurrent minor infections in 1 year

unusual organisms

unusual sites

unresponsive to oral abx

chronic infections

early structural damage

224
Q

May be history of anxiety

‘lump in the throat’
Symptoms are often intermittent and relieved by swallowing

Swallowing of saliva is often more difficult.
Usually painless - the presence of pain should warrant further investigation for organic causes

A

Globus pharyngis (also known as globus hystericus)

225
Q

liver impairment is possible due to statins.

How often should LFTs be measured?

A

at baseline, 3 months and 12 months

tx should be discontinued if serum transaminase conc rise to and persist at 3x the Upper limit

226
Q
A

The whole colon, without skip lesions, is affected by an irregular mucosa with loss of normal haustral markings.

ulcerative colitis

Barium enema shows:

loss of haustrations

superficial ulceration, ‘pseudopolyps’

long standing disease: colon is narrow and short -‘lead pipe colon’

227
Q

what does barium enema of Ulcerative colitis show?

A

loss of haustrations

superficial ulceration, ‘pseudopolyps’

long standing disease: colon is narrow and short -‘lead pipe colon’

228
Q

apart from antibiotics, what medications increases risk of c difficile infection?

A

PPI e.g. omeprazole

229
Q

1st line long term mx of TIA?

A

Clopidogrel 75 mg daily

2nd: aspirin + modified release dipyridamole if C not tolerated

aspirin if both C and D not tolerated

modified release dipyridamole if C and A not tolerated

230
Q

immediate antithrombotic tx in TIA?

A

aspirin 300mg

unless

  1. pt has a bleeding disorder/ taking anticoag -> immediate admission for imaging to exclude haemorrhage
  2. pt alr taking low dose aspirin -> cont dose until reviewed by specialist
  3. aspirin contraindicated
231
Q

which anti emetic is contraindicated in Parkinson’s disease?

A

Metoclopramide - dopamine antagonist

used for nausea, GORD

SE: oculogyric crisis, hyperprolactinaemia, tardive dyskinesia, parkinsonism

232
Q
A

depigmented Ash leaf spots which flouresce under UV light

Tuberous Sclerosis

233
Q
A

Shagreen patches:

roughed patches of skin over lumbar spine

Tuberous sclerosis

234
Q
A

adenoma sebaceum (angiofibromas): butterfly distribution over nose

Tuberous Sclerosis

235
Q
A

fibromata beneath nails (subungual fibromata)

painless, slow-growing tumor seen in the nail apparatus

-> tuberous sclerosis

236
Q

neuro features of tuberous sclerosis?

A

developmental delay

epilepsy (infantile spasms or partial)

intellectual impairment

237
Q

Teratogenic features of phenytoin?

A

assoc w cleft palate and congenital heart disease

238
Q

what AED is assoc w peripheral neuropathy as a side effect?

A

Phenytoin

239
Q

if pt is symptomatic (ie polyuria/ polydipsia), what else do you need to diagnose pt w Diabetes Mellitus?

A

fasting glucose greater than or equal to 7.0 mmol/l (or HbA1c >48mmol)

random glucose greater than or equal to 11.1 mmol/l (or after 75g oral glucose tolerance test)

240
Q

what investigation would be most useful initially to differentiate between irritable bowel syndrome (IBS) and inflammatory bowel disease (IBD) in primary care?

A

Faecal calprotectin

released in the bowel in the presence of inflammation

A positive result does not indicate definite IBD but patients should be referred on to secondary care for further investigation.

241
Q

Ix that should be done for IBS?

A

FBC, ESR, CRP and coeliac screen (TTG)

242
Q

Treatment of asymptomatic hyperuricaemia?

A

none

just conservative

Lifestyle changes (less red meat, alcohol and sugar) can reduce uric acid levels

243
Q

Ix of Lyme Disease?

A

Lyme disease can be diagnosed clinically if erythema migrans is present

enzyme-linked immunosorbent assay (ELISA) antibodies to Borrelia burgdorferi are the first-line test

if this test is positive or equivocal then an immunoblot test for Lyme disease should be done

244
Q

Mx of disseminated Lyme disease?

A

ceftriaxone

245
Q

1st line drug in mx of ocular myasthenia gravis?

A

Pyridostigmine (anticholinesterase)

+/- prednisolone

246
Q

alternative mx of wilson’s disease?

A

trientine hydrochloride is an alternative chelating agent which may become first-line treatment in the future

247
Q

young person w liver and neurological disease?

A

Wilsons disease

liver: hepatitis, cirrhosis
neurological: basal ganglia degeneration, speech, behavioural and psychiatric problems are often the first manifestations. Also: asterixis, chorea, dementia

248
Q

tx of choice for smoking cessation in pregnancy?

if smoking cessation without nicotine replacement fails.

A

nicotine replacement patch

varenicline and bupropion are contraindicated

249
Q

what is TIBC measuring?

A

TIBC is a measure of available binding sites on transferrin. If there is a lot of iron, these sites are taken up so there is less capacity to bind more, hence TIBC is low in iron overload.

TIBC high in Fe deficiency

250
Q

Ix to screen for haemochromatosis?

A

general population: transferrin saturation is considered the most useful marker.

testing family members: genetic testing for HFE mutation

251
Q

joint xrays in Haemochromatosis characteristically show?

A

chondrocalcinosis

252
Q

features of Orf?

A

Orf is a viral skin disease spready to humans by handling infected sheep and goats e.g. farmers, sheep shearers, vets

  • caused by a parapoxvirus

small, red, itchy or painful lump (lesion) that usually appears on the fingers, hands, forearms or face after an incubation period of 3 to 5 days

lesion -> pustule or blister

+ fever, fatigue, LNpathy

253
Q
A

Calcaneal Spur on XR

-> common in plantar fasciitis

254
Q

If QRISK score is high (>10%), what tx?

A

Statins indicated

255
Q

Posterior vs anterior hip dislocation?

A

90% of hip dislocations are posterior

posterior: limb flexed, adducted, internally rotated

(may be assoc w sciatic n palsy)

Anterior: limb externally rotated w mild flexion and abduction

256
Q

1st Ix of pancreatic cancer?

A

Abdo US

257
Q

what abx medication may cause yellow skin?

A

Co-amoxiclav

-> may cause cholestatic jaundice

258
Q

what medication is associated with seeing yellow tinge around lights?

A

Digoxin assoc w xanthopsia (yellow tinge on white objects)

259
Q

Mx of stable angina?

A

GTN sublingual for rapid relief of symptoms

1st line regular tx: BB (bisoprolol, atenolol) or CCB (verapamil)

260
Q

most likely histological type of renal cell cancer?

A

clear cell

261
Q

airway mx of choice if GCS<8?

A

cuffed endotracheal tube

262
Q

teratoma/ germ cell tumours

tumour markerS?

A

AFP

BHCG

263
Q

what muscle group is overused in medial vs lateral epicondylitis?

A

medial: flexor compartment
lateral: extensor compartment

264
Q

what is sildenafil?

A

used to treat erectile dysfunction and pulmonary hypertension

MOA: phosphodiesterase (PDE5) inhibitor

265
Q

what vein is compressed in Budd-Chiari?

A

Hepatic vein thrombosis

e.g. Polycythaemia Rubra vera, Pregnancy

/ compression

266
Q

what nerve is affected in herpes zoster ophthalmicus?

A

Trigeminal nerve V1 - ophthalmic branch

267
Q

e.g.s of non sedating antihistamines?

A

cetirizine

268
Q

features of typical angina?

A
  1. constricting discomfort in the front of the chest, or in the neck, shoulders, jaw or arms
  2. precipitated by physical exertion
  3. relieved by rest or GTN in ~5 minutes

all 3= typical angina

2 = atypical angina

0/1 = non anginal chest pain

269
Q

Ix of Stable Angina?

A

1st line: CT coronary angio

2nd: Non-invasive functional imaging
- MPS (myocardial perfusion scintigraphy) w SPECT
- stress echo
- MR imaging

3rd line: invasive coronary angio

270
Q

High CK and K after giving Abx

what abx?

what condition?

A

trimethoprim

in CKD

271
Q

Young pt on chemo, which drug may cause heart failure?

A

Doxorubicin

272
Q

worldwide commonest cause of IDA?

A

Hookworm infection

273
Q

Mx of SIADH?

A

fluid restrict

274
Q

mx of acute exacerbation of COPD who does not require admission?

A
  1. Increase doses/ freq of use of SABA
  2. oral corticosteroids 30mg OD 7-14d if SOB interferes w daily activities
  3. Oral Abx: amoxicillin, or doxycycline or clarithromycin
275
Q

abx for acute pyelonephritis?

A

1st line: cefalexin, or co-amoxiclav or trimpethoprim or cipro

if pregnant: cefalexin

276
Q

what is Caplan’s syndrome?

A

rheumatoid arthritis, pneumoconiosis and pulmonary rheumatoid nodules

277
Q

Anion gap formula?

A

Na+ + K+- Cl- -HCO3-

usually 10-18

278
Q

DKA insulin therapy?

A

fixed rate insulin infusion (0.1u/kg/h) + continue long acting insulin

279
Q

Mx of Orthostatic hypotension?

A

education and lifestyle measures such as adequate hydration and salt intake

discontinuation of vasoactive drugs e.g. nitrates, antihypertensives, neuroleptic agents or dopaminergic drugs

if symptoms persist, consider compression garments, fludrocortisone, midodrine, counter-pressure manoeuvres, and head-up tilt sleeping

280
Q

features of acute liver failure?

A

hepatic encephalopathy + jaundice + coagulopathy (raised PT time)

+ hypoalbuminaemia

renal failure common (hepatorenal syndrome)

281
Q

features of Kartagener’s syndrome?

A

aka primary ciliary dyskinesia

  • > immotile cilia
  • dextrocardia or complete situs inversus
  • bronchiectasis
  • recurrent sinusitis
  • subfertility (secondary to diminshed sperm motility and defective ciliary action in fallopian tubes)
282
Q

What type of malignancy is most assoc w Acanthosis nigricans?

A

GI carcinoma

283
Q

How much morphine to prescribe a palliative care patient?

A

to begin: opioid-naive pts can be started on oral morphine, 5-10mg every 4 h.

Once a 24h requirement is established: dose can be given as modified release preparation in 2 divided doses

+ 1/6 of total daily morphine dose should be given PRN for breakthrough pain

ie. if pt needs 60mg,

give 30mg of modified release morphine BD + 10mg total daily dose of morphine for breakthrough pain

284
Q

mx of dermatitis herpetiformis in coeliac?

A

tx underlying cause- gluten free food

dapsone can reduce symptoms of itching

285
Q

mx of pyoderma gangrenosum?

A

high dose oral prednisolone which are gradually redeuced as lesions heal

+ application of non-adherent dressings

286
Q

Mx of Lyme Disease assoc w cardiac or neurological complications?

A

IV ceftriaxone or cefotaxime

287
Q

1st line ix for Lyme Disease?

A

ELISA antibodies to Borrelia burgdoferi

288
Q

what are the preferred opioids in patients with chronic kidney disease.?

A

Alfentanil, buprenorphine and fentanyl

289
Q

Mx of cerebral abscess caused by streptococcal or anaerobic infections?

A

IV cefuroxime and metronidazole

290
Q

Mx of Cerebral abscess caused by staphylococcal infection?

A

IV flucloxacillin with cefuroxime

291
Q

what NOAC is most preferred in pts with CKD?

A

Apixaban

292
Q

What is the single most important factor in determining whether cryoprecipitate should be given?

A

low fibrinogen level

293
Q
A
294
Q

features of legionella?

A

dry cough

relative bradycardia

lymphopenia

hypoNa

deranged LFTs

pleural effusion

295
Q

HAART usually involvs?

A

2 NRTIs

+

protease inhibitor or NNRTI

296
Q

e.g.s of entry inhibitors

CCR5 receptor antagonists?

A

maraviroc, enfuvirtide

prevent HIV-1 from entering and infecting immune cells by blocking CCR5 cell-surface receptor

297
Q

e.g.s of Nucleoside reverse transcriptase inhibitors?

A

Zidovudine, Abacavir, Lamivudine, Emtricitabine, Tenofovir

298
Q

e.g.s of NNRTIs?

A

efavirenz, nevirapine

299
Q

e.g.s of protease inhibitors?

A

-navir

indinavir, ritonavir

300
Q

e.g. of integrase inhibitors

A

-gravir

Raltegravir, dolutegravir

301
Q

maintenance fluid requirements for adults based on weight?

A

25-30ml / kg/ day of water

ie. 80kg patient - 2L of water

302
Q

fluid requirements of children?

A

100mL / 24 hr/ kg (0-10kg)

then 50 mL/24h /kg (11-20 kg)

then 20 mL per kg after

303
Q

1st line tx in MODY

A

HNF1A type

Sulphonylureas e.g. gliclazides

304
Q

urea breath test

  • what may decrease the accuracy?
A

No abx in past 4 wks

no PPIs in past 2 wks

305
Q

preferred method of acces for haemodialysis?

A

AV fistulas

306
Q

VTE prophylaxis after elective hip replacement?

A

LMWH for 28d

or

LMWH for 10d then aspirin for 28d

or

Rivaroxaban

307
Q

VTE prophylaxis after elective knee surgery?

A

LMWH for 14d

or

Aspirin for 14 d

or

Rivaroxaban

308
Q

VTE prophylaxis for fragility fractures of the pelvis, hip and proximal femur?

A

LMWH or fondaparinux

continue until pt no longer has significantly reduced mobility

309
Q

SEs of hydroxychloroquine?

A

bulls eye retinopathy- may result in severe and permanent visual loss

-> baseline opthal examination + monitor annually

310
Q

allergy to sulfasalazine may also mean allergy to??

A

aspirin or sulphonamides

311
Q

abx prophylaxis for meningococcal meningitis?

A

oral ciprofloxacin

312
Q

terminal cancer, pt suffering from bowel colic?

A

add hyoscine butylbromide to syringe driver

313
Q

terminal ca- what to add to syringe driver to reduce resp secretions?

A

hyoscine hydrobromide

314
Q

mx of intractable hiccups in palliative care??

A

chlorpromazine

or haloperidol/ gabapentin

315
Q

features of anticholinergic symptoms?

A

Blind as a bat (dilated pupils)

Red as a beet (vasodilation/flushing)

Hot as a hare (hyperthermia)

Dry as a bone (dry skin)

Mad as a hatter (hallucinations/agitation)

“Bloated as a toad”; ileus, urinary retention

And the heart runs alone (tachycardia)

Medicine (16 decks)

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