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Chem path Flashcards

1
Q

Osmolarity formula

A

2(Na + K) + urea + glucose

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2
Q

Units for osmolality and osmolarity

A 
Osmolality = mmol/kg
Osmolarity = mmol/l
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3
Q

Normal sodium range

A

135-145 mmol/l

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4
Q

Symptoms if sodium is <117 mmol/l

A

Coma -> death

Symptomatic = medical emergency
If compensated, rarely emergency, even if 110-120 and asymptomatic. More dangerous to correct too fast.

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5
Q

Causes of reported hyponatraemia if the serum osmolality is high, normal, and low.

A

High - glucose/mannitol infusion

Normal - spurious, drip arm sample, hyperlipidaemia

Low - true hyponatraemia

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6
Q

What is TURP syndrome?

A
  • Irrigation of bladder with Glycine 1.5% during transurethral resection of prostate
  • Absorption of fluids into prostatic venous sinuses
  • Hyponatraemia
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7
Q

Urinary sodium level if renal or non-renal cause of hyponatraemia (when hypo/hypervolaemic)

A

Renal >20 mmol/l

Non-renal <20 mmol/l

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8
Q

Urinary sodium in euvolaemic hyponatraemia

A

> 20 mmol/l

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9
Q

Causes of renal hypovolaemic hyponatraemia

A

Diuretics
Addison’s
Salt-losing nephropathies - kidney can’t reabsorb sodium, so water is lost too

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10
Q

Causes of non-renal hypovolaemic hyponatraemia

A

Vomiting
Diarrhoea
Excess sweating
Third spaces losses (ascites, burns)

Kidney holding onto sodium, so low urinary sodium, but still overall loss of sodium

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11
Q

Causes of euvolaemic hyponatraemia

A

SIADH - water retention, but not sodium retention (so high urinary sodium)
Severe hypothyroidism
Glucocorticoid deficiency

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12
Q

Normal range for serum osmolality

A

275-295 mmol/kg

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13
Q

Causes of renal hypervolaemic hyponatraemia

A

AKI

CKD

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14
Q

Causes of non-renal hypervolaemic hyponatraemia

A

Cardiac failiure
Cirrhosis
Inappropriate IV fluid

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15
Q

What is important to do before measuring urinary sodium in someone on diuretics?

A

Stop diuretics

Diuretics affect urinary sodium and not give accurate reflection of patient’s state

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16
Q

How does cirrhosis lead to hyponatraemia?

A
  • Poor breakdown of vasodilators (NO)
  • Low blood pressure
  • ADH release - water retention
  • Diluted sodium

(Similar in HF - but BNP/ANP are natriuretic (excretion of sodium) and thought to worsen hyponatraemia too)

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17
Q

Management of hypovolaemic hyponatraemia

A
  • Treat the cause e.g. antiemetics

* Supportive - replace fluid slowly, regularly check sodium

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18
Q

Management of euvolaemic hyponatraemia

A
  • SIADH - fluid restriction and treat the cause (demeclocycline and tolvaptan can induce state of diabetes insipidus)
  • Hypothyroidism - levothyroxine
  • Addison’s - hydrocortisone +/- fludrocortisone
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19
Q

Management of hypervolaemic hyponatraemia

A
  • Fluid restrict +/- diuresis

* Cirrhosis - specialist input

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20
Q

What can rapid correction of hyponatraemia lead to and how does it present?

How quickly should you correct sodium?

A

Central pontine myelinolysis
• Pseudobulbar palsy
• Paraparesis
• Locked-in syndrome

Aim to increase Na+ by no more than 8-10 mmol per 24 hours

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21
Q

How can surgery lead to hyponatraemia?

A

Overhydration with hypotonic IV fluids

Transient increase in ADH (water retention) due to stress of surgery i.e. SIADH

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22
Q

Diagnosis of SIADH

A 
Exclusion
• High urine osmolarity
• Clinically euvolaemic
• Normal 9am cortisol
• Normal TFTs
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23
Q

Most common malignancy and drugs causing SIADH

A
  • Malignancy - small cell lung cancer

* Drugs e.g. carbamazepine, SSRIs

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24
Q

How does tolvaptan work?

A

Reduces channel sensitivity to ADH in collecting duct

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25
Q

Causes of hypovolaemic hypernatraemia

A

Vomiting
Diarrhoea
Excessive sweating
Burns

Renal loss
• Loop diuretics
• Osmotic diuresis (glucose, mannitol)
• Diabetes insipidus - more likely euvolaemic

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26
Q

Causes of euvolaemic hypernatraemia

A

Respiratory (tachypnoea)
Skin (sweating, fever)
Renal (diabetes insipidus)

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27
Q

Causes of hypervolaemic hypernatraemia

A

Mineralocorticoid excess (Conn’s syndrome - too much sodium retention and potassium excretion)

Inappropriate saline

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28
Q

Management of hypernatraemia

A

Slow fluids - even saline, but this can cause initial rise in sodium before it falls

Encourage PO!

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29
Q

Urine : plasma osmalality ratio in diabetes inspidus and reason

A

< 2

Urine is dilute despite concentrated plasma

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30
Q

Types of diabetes inspidus and causes

A 
Cranial - lack of/no ADH
• Surgery
• Pituitary radiation
• Trauma
• Tumours
Nephrogenic
• Receptor insensitivity to ADH
• Inherited channelopathies
• Lithium
• Hypercalcaemia
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31
Q

Treatment of nephrogenic diabetes insipidus

A

Thiazide diuretics

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32
Q

What 3 things should be excluded in patients with diabetes inspidus first?

A

Diabetes mellitus
Hypokalaemia
Hypercalcaemia

These can cause resistance to ADH causing a ‘nephrogenic diabetes insipidus’

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33
Q

Diagnosis of diabetes insipidus and the meaning of different results

A

8 hour fluid deprivation test
• Normal - urine conc. >600 mOsmol/kg
• Primary polydipsia - urine conc. 400-600 (psychogenic, schizophrenia, cancer)
• Cranial - urine concentrates after desmopressin
• Nephrogenic - urine does not concentrate even after desmopressin

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34
Q

What is the primary intracellular cation and what is the normal blood range?

A

Potassium

3.5-5.5 mmol/l

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35
Q

Causes of hypokalaemia

A

GI loss

Renal loss
• hyperaldosterism (consider if high Na, low K)
• Thiazide and loop diuretics
• Osmotic diuresis

Redistribution into cells
• Insulin
• Beta-agonists
• Metabolic alkalosis (cells pump out H+, K+ goes in)

Rare causes
• Tubular acidosis
• Hypomagnesaemia

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36
Q

Outline renal tubular acidosis type 1, type 2, and type 4.

A

Type 1
• Most severe
• Distal failure of H+ excretion into renal lumen, subsequent acidosis and hypokalaemia (can’t be reabsorbed)

Type 2
• Milder
• Proximal failure to reabsorb bicarbonate
• Acidosis and hypokalaemia (increased flow rate to distal tubule, increased K excretion)

Type 4
• Aldosterone deficiency/resistance
• Acidosis and HYPERkalaemia

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37
Q

Features of hypokalaemia

A

Muscle weakness
Cardiac arrhythmias
Polyuria and polydipsia

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38
Q

Hypokalaemia treatment

A

oral SandoK

If lower than 3.0, consider IV potassium chloride

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39
Q

Why should IV potassium chloride not be administered >10mM/hr

A

Risk of arrhythmia

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40
Q

Causes of hyperkalaemia

A 
Excessive intake 
Transcellular movement
• Acidosis
Decreased excretion
• Acute renal failure
• Spironolactone
• Addison's
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41
Q

What should be considered when assessing for hyperkalaemia?

A
  • Repeat sampling - spurious result due to haemolysed blood
  • ECG
  • VBG - acidosis?
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42
Q

ECG changes associated with hyperkalaemia

A

Loss of P waves
Tall tented T waves
Widened QRS

ECG is “pulled apart” to create a ‘sine wave’ if left untreated

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43
Q

When should you treat hyperkalaemia

A

> 5.5 + ECG changes

> 6.5

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44
Q

Hyperkalaemia treatment

A
  1. 10ml 10% calcium gluconate (cardioprotection)
  2. 100ml 20% dextrose + 10U short-acting insulin e.g. actrapid
  3. Salbutamol adjunct
  4. Treat cause
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45
Q

When should you be careful with administration of IV calcium?

A

Patients on Digoxin

Cardiac monitoring as it can precipitate arrhythmias

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46
Q

Normal pH range

A

7.35 - 7.45

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47
Q

Normal CO2 range

A

4.7 - 6kPa

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48
Q

Normal bicarbonate range

A

22 - 30mmol/l

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49
Q

Normal O2 range

A

10 - 13kPa

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50
Q

Causes of metabolic acidosis

A

Elevated anion gap:
• Lactic acidosis e.g. in metformin OD
• Ketoacidosis e.g. DKA, alcoholic
• Toxins e.g. methanol

Intestinal fistula

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51
Q

Causes of respiratory acidosis

A

Pneumonia
COPD
Decreased ventilation e.g. morphine OD

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52
Q

Causes of metabolic alkalosis

A

Pyloric stenosis
Hypokalaemia
Diuretics

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53
Q

Causes of respiratory alkalosis

A

Mechnical ventilation
Panic attack
Aspirin OD (mixed with metabolic acidosis)

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54
Q

What is the anion gap, how do you calculate it, and what is the normal range?

A

Difference between cations and anions
Concentration of unmeasured anions
Almost all albumin

(Na + K) - (Cl + HCO3)

14 - 18mmol/l

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55
Q

What is the osmolar gap and normal range

A

Osmalality (measured) - Osmolarity (calculated)

Elevated - presence of abnormal/extra solutes e.g. alcohols, ketones, lactate

<10

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56
Q

When can AFP be elevated?

A
  • HCC
  • Testicular cancer
  • Pregnancy
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57
Q

What diagnosis does AST:ALT = 2 support?

A

Alcoholic hepatitis

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58
Q

What diagnosis does AST:ALT = 1 support?

A

Viral hepatitis

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59
Q

When is ALT raised?

A

When hepatocytes die - more sensitive than AST for hepatocyte damage

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60
Q

When is ALP raised?

A

Cholestasis (intra/extrahepatic)
Bone disease
Pregnancy

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61
Q

When is GGT raised and what can it confirm?

A

Chronic alcohol use
Bile duct disease
Metastasis

Confirms hepatic source of raised ALP

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62
Q

AST:ALT and GGT in NAFLD

A

AST:ALT < 1

Raised GGT

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63
Q

Is low or high albumin common in hospital patients?

A

Low

Acute illness, systemic inflammation and malnutrition lead to reduced albumin

Poor prognostic factor

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64
Q

How is clotting factor function measured?

A

INR

PT standardised for age and population

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65
Q

Is deranged clotting diagnostic of hepatocellular dysfunction on its own?

A

No

Other aetiologies e.g. warfarin, thrombophilia, DIC

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66
Q

Why is the measurement of clotting factors a better marker of acute liver function than albumin?

A

Shorter half life

Albumin has 20-day half life

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67
Q

Where is bilirubin ‘conjugated’?

A

Hepatocytes

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68
Q

How and where is conjugated bilirubin further metabolised?

A

Conjugated bilirubin -> urobilinogen (GI tract)

Some urobilinogen reabsorbed and excreted tin kidneys as urobilin

Rest of urobilinogen -> stercobilin

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69
Q

Causes of pre-hepatic jaundice

A

Haemolysis (increased bilirubin production)

Congestive heart failure (hepatic congestion)

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70
Q

Causes of hepatic jaundice

A

Liver failure
Gilbert syndrome
Hepatitis
PBC

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71
Q

Is conjugated or unconjugated bilirubin raised in hepatic jaundice?

A

Unconjugated

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72
Q

Causes of post-hepatic jaundice

A

Obstruction of biliary tree e.g. stones, mass (intra or extraluminal), inflammation

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73
Q

Is there urobilinogen in post-hepatic jaundice?

A

No

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74
Q

What is there a deficiency of in acute intermittent porphyria?

A

Hydroxymethylbilane (HMB) synthase

Autosomal dominant

(Build up of ALA and PBG)

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75
Q

Symptom groups of acute intermittent porphyria

A

Neuro-visceral

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76
Q

Diagnosis of acute intermittent porphyria

A

“Port wine urine” - oxidised over night

ALA and PBG in urine

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77
Q

Acute intermittent porphyria medication precipitatants

A

ALA synthase inducers (steroids, ethanol, barbiturates)

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78
Q

Treatment for acute intermittent porphyria

A

Avoid precipitating factors
Analgesia
IV carbohydrate / haem arginate

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79
Q

How does hereditary coproporphyria (HCP) and variegate porphyria (VP) present?

A

Neuro-visceral symptoms

Skin lesions

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80
Q

How does congenital erythropoietic porphyria (CEP), erythropoietic protoporphyria (EPP) and porphyria cutanea tarda (PCT) present?

A

All 3 are non-acute porphyrias - skin lesions

EPP - photosensitivity, burning, itching oedema following sun exposure. Non blistering. In children.

PCT - vesicles on sun exposed sites (cursting, pigmented)

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81
Q

What must be measured in erythropoietic protoporphyria (EPP)?

A

RBC protoporphyrin

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82
Q

Diagnosis of porphyria cutaena tarda (PCT)?

A

Increased urinary uroporphyrins and coproporphyrins
Increased ferritin
Microcytic anaemia

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83
Q

Which pituitary hormones does TRH stimulate?

A

TSH

Prolactin

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84
Q

Which pituitary hormone does dopamine stimulate?

A

Prolactin

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85
Q

What does the combined pituitary function test (CPFT) involve?

A

Administration of LHRH (GnRH), TRH and insulin

Measure pituitary hormones at 0, 30, 60, 90 and 120 mins

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86
Q

Contraindications and side effects of CPFT?

A

CI - IHD, epilepsy, untreated hypothyroidism

SE - hypoglycaemia, metallic taste with TRH

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87
Q

How do you interpret insulin tolerance in the CPFT?

A

Adequate cortisol and GH response

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88
Q

Describe the normal response in CPFT TRH tolerance test

A

Adequate TSH response, higher at 30mins than 60 mins

Raised prolactin

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89
Q

What does inadequate response to GnRH mean in CPFT?

A

Early indication of hypopituitarism

Not used to measure gonadotrophin deficiency - diagnosed on basal levels

Children should have no response of LH or FSH

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90
Q

Difference between pituitary micro and macroadenoma

A

Micro < 10mm, usually benign

Macro > 10mm, aggressive

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91
Q

How can a non-functioning adenoma increase prolactin levels and how is it treated?

A

Crush the stalk
Reduced blood flow
Lower dopamine inhibition
Increased prolactin

Small increase compared to prolactinoma

Surgical treatment - bromocriptine/cabergoline won’t work

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92
Q

What are the posterior pituitary hormones?

A

ADH

Oxytocin

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93
Q

What can a raised TSH and normal T4 suggest?

A

Treated hypothyroidism

Subclinical hypothyroidism

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94
Q

What can subclinical hyperthyroidism lead to?

A

Primary hypothyroidism

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95
Q

Findings in sick-euthyroid syndrome

A

Low T3 and T4 due to acute illness

TSH may start high then become low, or stay normal, TSH may transiently rise above normal during recovery

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96
Q

Causes of hyperthyroidism with high uptake on pertechnetate scan

A

Graves disease
• F > M (9:1)
• Anti-TSH receptor

Toxic multinodular goitre

Toxic adenoma
• Hot nodule

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97
Q

Causes of hyperthyroidism with low uptake on pertechnetate scan

A

Subacute De Quervains thyroiditis
• Self-limiting, post-viral
• Painful goitre
• Initially hyper, then hypothyroid

Postpartum thyroiditis
• Similar to De Quervain’s

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98
Q

Causes of autoimmune hypothyroidism

A

Primary atrophic
• Diffuse lymphocytic infiltration and atrophy
• No goitre - small

Hashimotos thyroiditis
• Plasma cell infiltration
• Elderly females
• Initial 'Hashitoxicosis'
• Anti-TPO/TG
• Hurthle cells and eosinophilic cytoplasm on histopathology
• Goitre
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99
Q

Non-autoimmune causes of hypothryoidism

A

Iodine deficience
Post-thyroidectomy/radioiodine
Drugs e.g. lithium, amiodarone

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100
Q

Medical treatement for hyperthyroidism

A

Symptomatic
• Beta-blockers
• Topical steroids for dermopathy
• Eye drops

Anti-thyroid
• Carbimazole (blocks TPO)

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101
Q

Non-medical treatment for hyperthyroidism

A

Radio-iodine
• Usually after medical has failed
• CI in pregnancy and lactating women

Surgical hemi/total

  1. Women intending to become pregnant in next 6 months
  2. Local compression e.g. oesophageal
  3. Cosmetic
  4. Suspected cancer
  5. co-hyperparathyroidism
  6. Refractory to med
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102
Q

What must patients be prior to thyroidectomy

A

Euthyroid

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103
Q

How does a thyroid storm present and how is it treated?

A

Shock, pyrexia, confusion, vomiting

HDU/ITU support
• Cooling
• High dose anti-thyroid meds
• Corticosteroids
• Circulatory and resp support
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104
Q

What is the most common thyroid neoplasm, its treatment, histological findings and prognosis?

A

Papillary

Surgery +/- radioiodine
Thyroxine to lower TSH

Psammoma body calcifications on histology

Very good prognosis (although cervical lymph node spread associated with recurrence)

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105
Q

What is the problem with follicular thyroid cancer?

A

Spreads early - blood -> liver / bone

cold nodules

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106
Q

What is a useful tumour marker for thyroid cancer?

A

Thyroglobulin

107
Q

Where does medullary thyroid cancer originate, what condition is it linked to and what does it produce?

A

Originates in parafollicular “C” cells

Linked to MEN2

Produces calcitonin

108
Q

What is a risk factor for thyroid lymphoma (majority non-Hodgkin B cell)?

A

Chronic Hashimotos / chronic lymphocitic thyroiditis

109
Q

Where do thyroid lymphomas originate?

A

MALT

110
Q

Prognosis in anaplastic thyroid cancer

A

Poor response to treatment

111
Q

What do the 3 forms of multiple endocrine neoplasias affect?

A

MEN1 (3Ps)
• Pituitary
• Pancreatic
• Parathyroid

MEN2a (2Ps, 1M)
• Parathyroid
• Phaeochromocytoma
• Medullary thyroid

MEN2b (1P, 2Ms)
• Phaeochromocytoma
• Medullary thyroid
• Mucocutaenous neuromas (and marfanoid)

112
Q

What is Cushing’s disease?

A

Excess ACTH caused by benign pituitary tumour

113
Q

What causes 10% and 5% of Cushing syndrome?

A

10% - adrenal tumour

5% - ectopic ACTH-producing tumour

114
Q

Investigations for Cushing’s syndrome

A

Want to see if cortisol can be suppressed

  1. Low dose dexamethasone (0.5mg) - fail to suppress cortisol in all cases
  2. High dose dexamethasone (2mg) - suppresses cortisol in pituitary tumour (Cushing’s disease)

Dose given every 6 hours for 48 hours

115
Q

Most common cause of Addison’s

A

TB (world)

Autoimmune (UK)

116
Q

Presentation of Addison’s

A

Postural hypertension
Skin pigmentation
Depression

High K+
Low Na+

117
Q

Investigation for Addison’s

A

Want to see if cortisol production is responding

Short synACTHen test

Normal is cortisol >550nm after 30mins

118
Q

Addison’s management

A

Treat hypotension

Hormone replacement
• Hydrocortisone/fludrocortisone if primary adrenal lesion

119
Q

What is Waterhouse-Friderichsen syndrome?

A

Adrenal gland failure due to bleeding

Caused by severe (meningococcal) bacterial infection

Septic, low BP, DIC, widespread purpura

120
Q

What is Conn’s syndrome and what is it caused by?

A

Primary aldosteronism - too much aldosterone

Adrenal tumour

121
Q

Signs of Conn’s

A

Uncontrollable hypertension

122
Q

Investigations for Conn’s

A

High Na+
Low K+

Aldosterone:Renin ratio raised

Raised aldosterone has negative feedback on renin

123
Q

Conn’s treatment

A

Aldosterone antagonists / potassium sparing diuretics e.g. spironolactone

124
Q

Causes of phaeochromocytoma

A

10% are…
MEN syndromes
Bilateral
Malignant

etc.

125
Q

Phaeochromocytoma investigation

A

24-hour urine collection for catecholamines, (nor)metanephrines, and creatinine

Plasma and serum measurements

126
Q

Phaeochromocytoma management

A
  1. Alpha-blocker e.g. phenoxybenzamine or doxazocin
  2. Beta-blocker
  3. Hydration
  4. Surgical excision of tumour when blood pressure controlled
127
Q

Phenytoin signs of toxicity

A

Ataxia and nystagmus

128
Q

Patient has just taken a medication, has xanthopsia (seeing yellow), arrhythmias, and heartblock. What is drug is he suffering toxicity to and what is the treatment?

A

Digoxin for arrhythmias

Treatment: digibind (immune Fab)

129
Q

Lithium toxicity treatment

A

Renal failure may need haemodialysis

130
Q

When do you need to be cautious of lithium toxicity?

A

Hyponatraemia - excretion impaired
Decreased renal function
Thiazide diuretics

131
Q

Gentamicin toxicity signs

A

Tinnitus, deafness, nystagmus, renal failure

132
Q

Theophyline indication and precipitators of toxicity

A

Indication: COPD and asthma (bronchodilator)

Precipitators: Erythromycin, cimetidine, phenytoin

133
Q

Normal calcium plasma range

A

2.2 - 2.6 mmol/l

134
Q

Why should we use corrected calcium and how do we calculate it?

A

50% of calcium bound to albumin, therefore measurement is affected by albumin

total calcium + 0.02(40-albumin)

135
Q

What does PTH do to calcium and how (3)?

A

Increases serum calcium

  • Increases 1a-hydroxylation of 25(OH)D3 (calcifediol) into active vitamin D (calcitriol)
  • Mobilises calcium from bone
  • Increases renal calcium reabsorption
136
Q

What is the role of calcitriol in calcium metabolism?

A

Increases calcium (and phosphate) absorption from the gut

Bone remodelling ?acts on both osteoblats and osteoclasts

137
Q

Primary hyperparathyroidism - primary defect and blood test levels

A

80% parathyroid adenoma

PTH - high/normal because of high calcium (inappropriately normal)
Calcium - high
Phosphate - low
Vitamin D - normal
ALP - high/normal
138
Q

Secondary hyperparathyroidism - primary defect and blood test levels

A

CKD
Low vitamin D
Leads to low calcium
Parathyroid hyperplasia

Also caused by vitamin D malabsorption

PTH - high
Calcium - low/normal after high PTH
Phosphate - high (not removed in CKD)
Vitamin D - low
ALP - high
139
Q

Tertiary hyperparathyroidism - primary defect and blood test levels

A

Secondary cause treated (e.g. renal transplant), but PTH still autonomously secreted

PTH - high
Calcium - high
Phosphate - Low 
Vitamin D - norma
ALP - high/normal

Similar to primary tests, but PTH is not normal and this progresses from secondary.

140
Q

Causes of hypoparathyroidism and blood test findings

A

DiGeorge syndrome, post-thyroid surgery

PTH - low
Calcium - low
Phosphate - high
Vitamin D - normal
ALP - low/normal
141
Q

Bloods in vitamin D deficiency / osteomalacia / rickets

A 
Vitamin D - low
Calcium - low (not absorbed)
Phospate - low (not absorbed)
PTH - high (because of low calcium)
ALP - high
142
Q

Paget’s disease bloods

A

High ALP

rest normal

143
Q

Osteoporosis bloods

A

All normal (could have high ALP from a fracture)

144
Q

Risk factors for osteomalacia

A 
Anticonvulsants
Phytic acid (food like chapatis) - vit D antagonist
Low sun exposure / vit D intake
145
Q

Management of osteoporosis

A

Reduce smoking and alcohol
Bisphosphonates
Vit D
Weight-bearing exercise

146
Q

Symptoms of hypercalcaemia

A 
Stones (renal)
Bones (pain)
Groans (psych)
Moans (abdo pain)
Polyuria
Muscle weakness
147
Q

Hypercalcaemia treatment

A
  1. Hydrate
  2. Bisphosphonates
  3. Correct cause e.g. chemo for cancer
148
Q

What can high calcium, high phosphate, and high ALP suggest in a patient with a cough / dyspnoae and how can this be treated?

A

Sarcoidosis

Steroids

149
Q

What is a brown tumour and where does it commonly present?

A

Hyperparathyroidism -> excess osteoclast activity -> bone lesion

Most commonly affects maxilla and mandible

Not a neoplasm

150
Q

How is DEXA Z-score different to T-score?

A

Age and sex adjusted

151
Q

DEXA T-score in osteoporosis and osteopaenia

A

Osteoporosis < -2.5

Osteopaenia -1 to -2.5

152
Q

Causes of hypocalcaemia

A

Artefact
• Hypoalbuminaemia

High phosphate
• CKD
• Hypoparathyroidism
• Pseudohypoparathyroidism - body doesn’t respond

Normal/low phosphate
• Osteomalacia
• Acute pancreatitis
• Overhydration

153
Q

Symptoms of hypocalcaemia

A

CATs go numb

Carpopedal spasm
Arrhythmia
Tetany (Trousseau’s - blood pressure above systolic -> carpal spasm. Chvostek’s - tapping inferior cheekbone -> facial spasm)

numb - perioral and acral paraesthesia

154
Q

Mild, CKD and severe hypocalcaemia treatment

A

Mild - SandoCal
CKD - alfacaldicol
Severe - 10% calcium gluconate IV, then calcium infusion as per trust

155
Q

Are most renal stone patients hyper, normo, or hypocalcaemic?

A

Normocalcaemic

156
Q

Causes of renal stones

A

Hyperoxaluria - increased intake, absorption

Hypercalciuria - increased intake, renal leak

157
Q

Most common constituents of renal stones

A
  1. Calcium - mixed (45%)
  2. Calcium oxalate (35%)
  3. Triple phosphate “struvite” (10%)
158
Q

Constituents of radiolucent renal stones on x-ray

A

Uric acid
Cysteine

The rest are radioopaque

159
Q

What are very high serum amylase levels a sign of?

A

Acute pancreatitis (>10x upper limit)

160
Q

Physiological and pathological causes of raised creatine kinase

A

Physiological
• Afro-Caribbean

Pathological
• Duchenne Muscular Dystophy
• MI
• Rhabdomyolysis
• Statin related myopathy
161
Q

How is statin related myopathy treated?

A

Cessation of statin (reversible)

162
Q

Where is ALP found?

A

Liver, bone, intestine, placenta

163
Q

Physiological causes of raised ALP

A
  • 3rd trimester of pregnancy

* Childhood growth spurt

164
Q

Marker of heart failure and why this is

A

BNP (>400 sensitive for HF, <100 specific for no HF)

Released in response to ventricular stretch

NT-proBNP more sensitive

165
Q

What marker is useful to detect reinfarction of the myocardium?

A

CK-MB

Rapid decrease so you know if it was recent when high

166
Q

Troponin I/T is a myocardial injury biomarker. When should it be measured? How long does it remain elevated?

A

6 and 12 hours post onset of chest pain

Remains elevated for 3 - 10 days

167
Q

Patient has HDL deficiency on tests and ABCA1 transporter deficiency. What clinical signs would you expect to see? What is the name of this disease?

A

Cholesterol ester deposition in organs
• Hepatosplenogemaly
• Enlarged orange/yellow tonsils

Tangier disease

168
Q

What is the least dense lipoprotein?

A

Chylomicron

169
Q

Role of PCSK9 and anti-PCSK9 mAb

A

Binding and degradation of LDL receptors

LDL receptors remove LDL from extracellular fluid, but PCSK9 slows this

Anti-PCSK9 mAb stops this, increasing LDLR and decreasing LDL levels

170
Q

Lipoprotein (a) is a risk factor for cardiovascular disease. What can be used to lower this?

A

Nicotinic acid (niacin)

171
Q

Hyperlipidaemia management

A
  1. Conservative
  2. Statins - HMG-CoA reductase inhibitor, reduces intrinsic synthesis of cholesterol in liver

Less often - ezetimibe used (block NPC1L1)

172
Q

Obesity medical management

A

No meds safely proven for sustained weight loss

Orlistat (gut lipase inhibitor) used. SE - profound flatus and diarrhoea

Rimonabant (cannabinoid antagonist) - trialled and discontinued due to increase risk of suicide

173
Q

Obesity surgical management

A

Bariatric surgery BMI >40 or >30 with obesity-associated comorbidity

174
Q

‘Overweight’ BMI

A

25-30

175
Q

Retinol (vit A) deficiency and excess effects

A

Deficiency
• Colour blindness

Excess
• Exfoliation
• Hepatitis

176
Q

Cholecalciferol excess effects

A

Hypercalcaemia

177
Q 
Anaemia
Neuropathy
Decreased reflexes
Decreased coordination
Effects of which vitamin deficiency?
A

Tocopherol (vit E)

178
Q

Phytomenadione (vit K) defiency effects

A

Defective clotting

179
Q

What do you test to decide whether vitamin K needs to be given?

A

Prothrombin time

180
Q

Which vitamins are fat soluble?

A

A D E K

181
Q

Thiamine (B1) deficiency effects

A

Beri-beri (wet - oedema, HF. dry - neuro sx)
Neuropathy
Wernicke encephalopathy

182
Q

Test for thiamine deficiency

A

Erythrocyte transketolase

183
Q

Riboflavin (B2) deficiency effects

A

Glossitis

Mucosal damage

184
Q

Test for riboflavin deficiency

A

Erythrocyte glutathione reductase

185
Q

Pyridoxine (B6) deficiency and excess effects

A

Deficiency
• Dermatitis
• Anaemia

Excess
• Neuropathy

186
Q

During what therapy should pyridoxine be supplemented?

A

Isoniazid, as it inhibits metabolic actions of pyridoxine

187
Q

Test for long term pyridoxine status

A

Erythrocyte AST activation

188
Q

Cobalamin (B12) deficiency effect

A

Pernicious anaemia

189
Q

Ascorbate (vit C) deficiency and excess effects

A

Deficiency

• Scurvy (poor dentition, slow healing wounds, petechiae)

190
Q

Folate (B9) deficiency effects

A

Megaloblastic anaemia

Neural tube defect

191
Q

Niacin (B3) deficiency effects

A 
Pellagra
• Dementia
• Dermatitis
• Diarrhoea
• Death if untreated
192
Q

Iron excess effects, particularly in males

A

Haemochromatosis
• Deposition of iron in testes
• Hypogonadism
• Decreased libido

Also associated with DM and cirrhosis

193
Q

Iodine deficiency effects

A

Goitre

Hypothyroid

194
Q

Zinc deficiency effects

A

Dermatitis

195
Q

Copper deficiency and excess effects

A

Deficiency
• Anaemia

Excess
• Wilson’s disease

196
Q

Test for high copper in blood

A

High urine and blood free copper

Low ceruloplasmin

197
Q

Fluoride deficiency and excess effects

A

Deficiency
• Dental caries (tooth decay)

Excess
• Fluorosis

198
Q

What vitamin deficiencies are the following conditions associated with:
• Crohns
• Coeliac
• Pancreatic insufficiency

A

All ADEK, and..

Crohns
• B12 (terminal ileal disease)
• Folate (methotrexate therapy)
• Calcium, phosphate, magnesium, zinc

Coeliac
• Iron
• Thiamine
• Vitamin B6

199
Q

When is the neonatal blood spot screening performed and how does it determine the presence of the following conditions?
• Phenylketonuria
• Congenital hypothyroidism
• Cytstic fibrosis
• Medium chain acylCoA dehydrogenase deficiency

A

5-9 days

Phenylketonuria
• Phenylalanine levels

Congenital hypothyroidism
• TSH levels

Cystic fibrosis
• Immune reactive trypsin levels
• If positive, DNA mutation detection

MCADD
• Acylcarnitine levels

200
Q

What effect does phenylketonuria have on development?

A

Intellectual disability, IQ < 50
Severe behaviour problems
Severe epilepsy

201
Q

How can MCADD lead to sudden unexpected infant death?

A

Hypoglycaemia

202
Q

How many newborns does phenylketonuria occur in?

A

1 in 10,000

203
Q

What is the PPV of TSH levels in congenital hypothyroidism (Guthrie)?

A

60-70%

204
Q

How many newborns does CF occur in?

A

1 in 2500

205
Q

How many newborns does MCADD occur in?

A

1 in 10,000

206
Q 
Lens dislocation
Mental retardation
Thromboembolism
Fair skin
Eczema
Brittle hair
These are all features of which condition?
A

Homocystinuria

207
Q

What is specificity?

A

Probability that someone without the disease correctly tests negative

The percentage of people without the disease that test negative against a total of people that are actually negative

208
Q

What is sensitivity?

A

Probability that someone with the disease correctly tests positive

The percentage of people with the disease that test positive against a total of people that are actually positive

209
Q

What is positive predictive value?

A

Probability that someone who tests positive actually has the disease

The percentage of people that have the disease against the number of all people that tested positive (whether they had the disease or not)

210
Q

What is negative predictive value?

A

Probability that someone who tests negative actually doesn’t have the disease

The percentage of people that don’t have the disease against all people that tested negative (whether they had the disease or not)

211
Q

What enzyme deficiencies can lead to accumulation of toxins (group 1)?

A
  • Organic acidaemia e.g. Isovaleric acidaemia, Reye’s syndrome
  • Urea cycle disorders e.g. ornithine transcarbamylase deficiency
  • Aminoacidopathies e.g. PKU and maple-syrup urine disease
212
Q

Clinical features of organic acidaemia and treatment

A
  • Metabolic acidosis - ketoacidodic comas, cerebral abnormalities
  • Funny smell
  • High ammonia
  • High anion gap

Treat with low protein diet

213
Q

Reye’s syndrome cause and presentation

A

Aspirin, valproate, anti-emetics

Liver and brain swelling

214
Q

Urea cycle disorder: what is high? what is seen on abg? and treatment

A
  • High ammonia
  • Respiratory alkalosis

Treat with low protein diet, sodium benzoate / dialaysis for ammonia removal

215
Q 
• High phenylalanine
• Blue eyes  and fair skin
• Retardation
• Sweaty feet (maple-syrup)
Condition
A

Aminoacidopathy

216
Q

Which metabolic disorders lead to reduced enegy stores (group 2)?

A
  • Glycogen storage disorders e.g. Von Gierke’s
  • Galactossaemia
  • Fatty acid oxidation disorders e.g. MCADD
217
Q

Treatment of glycogen storage disorders

A

Regular carbohydrates

218
Q

Key features of galactossaemia, testing, and treatment

A
  • Cataracts (high Gal-1 phosphate levels)
  • Sepsis
  • Hypoglycaemia
  • Hepatomegaly

Test with urine reducing agents
Treat with low lactose diet

219
Q

Key features of fatty acid oxidation disorders, testing, and treatment

A
  • Hypoglycaemia
  • Low ketones

High blood acylcarnitine
Treat with regular carbohydrates

220
Q

Examples of metabolic disorders that lead to dysmorphic large molecule synthesis (group 3)

A
  • Peroxisomal disorders (can’t catabolise long fatty acids or make bile acids)
  • Glycosylation disroders
221
Q

Key features of peroxisomal disorders

A
  • Retinopathy

* Hypotonia

222
Q

Key features and testing of glycosylation disorders

A
  • Retardation
  • Nipple inversion

Serum transferrin

223
Q

Give an example of a lysosomal metabolic disorder leads to defects in large molecule metabolism (group 4) and lipid accumulation in neurones

A

Tay Sachs disease

224
Q

Testing of lysosomal disorders

A

Urine mucooligopolysaccharide and WBC enzyme levels

225
Q

Examples of mitochondrial (group 5) disorders

A

MELAS
Kearn’s Sayre
Barth syndrome

226
Q

Key features and testing of mitochondrial disorders

A

MELAS - the name: mitochondrial encephalopathy, lactic acidosis, stroke-like epidoses
Kearn’s Sayre - retinopathy, deafness, ataxia
Barth - cardiomyopathy, neutropaenia

High lactate and CK after fasting
Muscle biopsy diagnostic

227
Q

Diagnosis of diabetes mellitus

A 
2 of, or typical symptoms + 1 of:
• Fasting glucose > 7
• Random glucose > 11.1
• OGTT > 11.1
• HbA1C > 48 (NICE recommendation)
228
Q

What does random/OGTT of > 7.8 or < 11.1 mean?

A

Impaired glucose tolerance

229
Q

What does fastin glucose > 6.1 but < 7.0 mean?

A

Impaired fasting glucose

230
Q

Hyperosmolar hyperglycaemic state (HHS) criteria

A

pH > 7.3
Osmolarity >320
Blood glucose > 30

231
Q

How do HHS patients present?

A

Confusion and clinical dehydration

Develops over few days

232
Q

HHS management

A

Fluid replacement
Potassium supplement
Insulin

233
Q

DKA management

A

VBG (or ABG in resp function concerns
Fluids (add KCl if potassium low), front load replacement, maintence/taper off
Insulin

234
Q

When is DKA resolved?

A

Ketones < 0.6

pH > 7.3

235
Q

What causes hypoinsulinaemic hypoglycaemia?

A 
\+ve ketones
• alcohol binge, no food
• pituitary insufficiency
• Addison's 
• liver failure
• strenuous exercise
• premature neonate

-ve ketones
• non-pancreatic neoplasms (fibrosarcomata, fibromata)
• metabolic disorder in neonate

236
Q

By what age do you have a functional maturity of glomerular filtration rate

A

2 years

237
Q

Why do children have less kidney reaborption and concentrating ability than adults?

A

Reabsorption - short proximal tubule

Concentration - short loops of Henle and collecting duct

238
Q

Why do children have persistant kidney sodium loss?

A

Relatively aldosterone-insensitive distal tubule

239
Q

How is water lost in children a lot more than it is as an adult?

A

Transepidermal
• Increased skin blood flow
• High surface area to body weight ratio
• High metabolic/resp rate

240
Q

How can bones be affected in premature babies?

A

Osteopaenia of prematurity
• Not enough calcium and phosphate

(high ALP)

241
Q

When can hypernatraemia be common in babies?

A

First 2 weeks of life

242
Q

What can cause hyponatraemia in neonates?

A

First 4-5 days
• Excess water intake
• SIADH secondary to infection or intraventricular haemorrhage

After first 4-5 days
• Immature tubular function in patients on diuresis (sodium loss)

Hyperglycaemia (normal but appears low)
Congenital adrenal hyperplasia

243
Q

How does congenital adrenal hyperplasia present?

A

21-hydroxylase deficiency
Low cortisol and aldosterone
High 17-hydroxyprogesterone
High androgens

Ambiguous genitalia in females
Salt wasting crisis in males
Growth acceleration

244
Q

Neonatal jaundice bilirubin threshold for phototherapy and exchange for term and premature babies

A

Term
• Photo - 350
• Exchange - 450

Premature
• Photo - 120
• Exchange - 230

245
Q

Gold standard measure of GFR

A

Inulin (difficult to test so research only)

246
Q

Better marker than creatinine for renal function

A

cystatin C - produced by all nucleated cells

247
Q

What is the problem of the MDRD equation in estimating the GFR with creatinine?

A

May underestimate GFR if young + above average weight

248
Q

First line investigation for upper UTI obstruction e.g. kidney stones

A

CT KUB

249
Q

Which investigation is good at looking at anatomical defects of the urinary system and how it is working in children?

A

IV urogram

250
Q

AKI definition

A

Rise in creatinine > 26.5 or 1.5x (3x if severe) baseline, in 48 hours

or

Urine output < 0.5mls/kg/hr but bladder and prostate pathology may cause this too

251
Q

Causes of pre-renal AKI

A 
NSAIDs
ACEi
Diuretics
Hypotension
Shock
Sepsis
252
Q

Indications for dialysis as an emergency

A 
AEIOU
• Acidosis (metabolic)
• Electrolyte disturbance
• Intoxication e.g. lithium, aspirin
• Overload
• Uraemic encephalopathy
253
Q

Does urea or creatinine increase more in AKI and CKD?

A

AKI - urea

CKD - creatinine

254
Q

GFR in stage 1-5 CKD (kidney damage with normal GFR, mild, moderate, severe, end-stage)

A
  1. > 90
  2. > 60
  3. > 30
  4. > 15
  5. <15
255
Q

2 causes of CKD

A

Diabetes (common to see high K+ in CKD)

Hypertension

256
Q

Is AKI and CKD reversible

A

AKI is reversible, CKD isn’t

257
Q

Treatment of acidosis in CKD

A

oral sodium bicarbonate

258
Q

Most important complication of CKD that leads to death

A

Uraemic cardiomyopathy - LV hypertrophy, calcified plaques

259
Q

Homeostatic function effects of CKD

A

acidosis, hyperkalaemia

260
Q

Hormonal effects of CKD

A

anaemia (loss of EPO)

renal bone disease (low vit D)

261
Q

How can haemodialysis be done and how often?

A

Tunneled central line (Tessio line) or arteriovenous fistulae

3x a week

262
Q

Pertinoeal dialysis deliver medium

A

Tenckoff catheter

263
Q

Incision and location for kidney transplant

A

Rutherford Morrison incision (hockey stick scar)

Right iliac fossa

Path (5 decks)

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