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Chem Path Flashcards

1
Q

Normal pH range

A

7.35 - 7.45

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2
Q

Normal PCO2

A

4.7 - 6kPa

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3
Q

Normal Bicarbonate

A

22 - 30 mmol/L

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4
Q

Normal PO2

A

10 - 13 kPa

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5
Q

Blood gas results in Metabolic Acidosis
pH
HCO3
CO2

A

pH LOW
HCO3 LOW
CO2 normal or LOW in compensation

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6
Q

Causes of Metabolic Acidosis (4)

A
  1. DKA - increased H+ production
  2. Renal tubular - decreased H+ excretion
  3. Intestinal fistula - decreased HCO3
  4. Lactate build up
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7
Q

Blood gas results in Respiratory Acidosis
pH
HCO3
CO2

A

pH LOW
HCO3 normal or HIGH in compensation
CO2 HIGH

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8
Q

Causes of Respiratory Acidosis (4)

A
  1. Impaired gas exchange e.g. pneumonia, COPD
  2. Poor perfusion
  3. Decreased ventilation e.g. head injury
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9
Q

Blood gas results in Metabolic Alkalosis
pH
HCO3
CO2

A

pH HIGH
HCO3 HIGH
CO2 normal/High

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10
Q

Causes of Metabolic Alkalosis (3)

A
  1. D&V
  2. Pyloric stenosis - babies vomit up all their stomach acid
  3. hypokalaemia
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11
Q

Blood gas results in Respiratory Alkalosis
pH
HCO3
CO2

A

pH HIGH
HCO3 normal/LOW
CO2 LOW

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12
Q

Causes of Respiratory Alkalosis (2)

A
  1. Mechanical ventilation

2. Hyperventilating/Panic attack - blow off all your CO2

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13
Q

Why look at the PO2?

A

Gives an indication of lung function, and tissue oxygenation

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14
Q 
What's the problem?
pH		6. 90			(7.35-7.45)
H+		126	nmol/l	(35-46)
pCO2	3.0	kPa		(4.7-6.0)
pO2		 24.0	kPa		(10.0-13.3) 
Bicarbonate 6	mmol/l	(22-30)
A

Metabolic Acidosis with partial respiratory compensation

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15
Q 
What's the problem?
pH		7. 55			(7.35-7.45)
H+		28	nmol/l	(35-46)
pCO2	8.2	kPa		(4.7-6.0)
pO2		10.0	kPa		(10.0-13.3) 
Bicarbonate  51	mmol/l	(22-30)
A

Metabolic Alkalosis with partial respiratory compensation

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16
Q 
What's the problem?
pH		7. 55			(7.35-7.45)
H+		28	nmol/l	(35-46)
pCO2	3.0	kPa		(4.7-6.0)
pO2		 14.4	kPa		(10.0-13.3) 
Bicarbonate  20	mmol/l	(22-30)
A

Respiratory Alkalosis

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17
Q

What’s the problem?

72 year old man
Long history of chronic obstructive airways disease
On diuretics for cardiac failure
Potassium 2.6 mmol/l (3.5-5.5)

pH		7. 41			(7.35-7.45)
H+		39	nmol/l	(35-46)
pCO2	10.4	kPa		(4.7-6.0)
pO2		 7.8	kPa		(10.0-13.3) 
Bicarbonate 47	mmol/l	(22-30)

Which?
Normal
Metabolic Acidosis
Respiratory Acidosis
Metabolic Alkalosis
Respiratory Alkalosis
Mixed metabolic acidosis and respiratory acidosis
Mixed metabolic alkalosis and respiratory alkalosis
Mixed metabolic alkalosis and respiratory acidosis
Mixed metabolic acidosis and respiratory alkalosis

A

Mixed metabolic alkalosis and respiratory acidosis

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18
Q 
A young woman was admitted to hospital 8 hours after she had taken an overdose of aspirin. 
Arterial blood:
pH		  7. 46		(7.35-7.45)
H+		35	nmol/l	(35-46)
pCO2	  2.0	kPa		(4.7-6.0)
pO2		17.8	kPa		(10.0-13.3) 
Bicarbonate 10	mmol/l	(22-30)

Normal
Metabolic Acidosis
Respiratory Acidosis
Metabolic Alkalosis
Respiratory Alkalosis
Mixed metabolic acidosis and respiratory acidosis
Mixed metabolic alkalosis and respiratory alkalosis
Mixed metabolic alkalosis and respiratory acidosis
Mixed metabolic acidosis and respiratory alkalosis

A

Mixed metabolic acidosis and respiratory alkalosis

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19
Q 
Arterial blood:
pH		  6. 93		(7.35-7.45)
H+		116	nmol/l	(35-46)
pCO2	  9.7	kPa		(4.7-6.0)
pO2		65.8	kPa		(10.0-13.3) 
Bicarbonate 15 mmol/l	(22-30)

Normal
Metabolic Acidosis
Respiratory Acidosis
Metabolic Alkalosis
Respiratory Alkalosis
Mixed metabolic acidosis and respiratory acidosis
Mixed metabolic alkalosis and respiratory alkalosis
Mixed metabolic alkalosis and respiratory acidosis
Mixed metabolic acidosis and respiratory alkalosis

A

Mixed metabolic alkalosis and respiratory acidosis

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20
Q

How to calculate the anion gap?

Normal range?

A

(Na+ + K+) - (Cl- + HCO3)

14 - 18mmol/L

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21
Q

Causes of raised anion gap metabolic acidosis?

a) Endogenous (3)
b) Exogenous (MUD PILES)

A

a) DKA
Lactic acidosis
Starvation

b)
Methanol
Uraemia
Drugs

Paracetamol 
Insecticides
Lithium 
Ethanol
Salicylates (aspirin)
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22
Q

How to measure Osmolality?

A

2(Na + K) + urea + glucose

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23
Q

How to measure the osmolar gap?

A

Measure Osmolality - Calculated Osmolarity

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24
Q

What’s the normal osmolar gap?

A
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25
Q

What could cause an increased osmolar gap?

A

extra solute present in the plasma e.g. ethanol, methanol

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26
Q

What is Osmolality? Units?

A

Measured total number of particles present in a solution mmol/kg

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27
Q

What is Osmolarity? Units?

A

Calculated total number of particles present in a solution mmol/L

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28
Q

Normal range for serum osmolality?

A

275 - 295 mmol/kg

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29
Q

Normal range for sodium?

A

135 - 145 mmol/L

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30
Q

Pathogenesis of HYPOnatraemia?

A

increased extracellular water, dilutionary effect

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31
Q

Level of severe HYPOnatraemia?

A
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32
Q

Signs of HYPOnatraemia? (4)

A
  1. nausea and vomiting
  2. confusion
  3. seizures
  4. coma
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33
Q

In true HYPOnatraemia will the osmolality be high or low?

A

LOW

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34
Q

Clinical features of HYPOvolaemia? (7)

A
  1. low BP
  2. tachycardia
  3. postural hypotension
  4. reduced skin turgor
  5. dry mucous membranes
  6. confusion/drowsiness
  7. reduced urine output
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35
Q

Clinical signs of HYPERvolaemia? (3)

A
  1. raised JVP
  2. bibasal crackles
  3. peripheral oedema
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36
Q

Classification of hyponatraemia (3)

A
  1. HYPERvolaemic
  2. EUvolaemic
  3. HYPOvolaemic
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37
Q

Causes of HYPERvolaemic HYPOnatraemia? (3)

A
  1. Heart failure
  2. Cirrhosis
  3. NephrOtic syndrome
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38
Q

Causes of HYPOvolaemic HYPOnatraemia? (3)

A
  1. D&V
  2. diuretics
  3. salt losing nephropathy
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39
Q

Causes of SIADH? (4)

A
  1. CNS - trauma, inflammation, abscess
  2. Lung - pneumonia, abscess, small cell lung Ca
  3. Malignancies - lymphoma, Ewing’s sarcoma, lung, GI, GU
  4. Drugs - SSRI, TCA, PPI, opiates, amitriptyline
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40
Q

Diagnostic test for SIADH?

A

Short SynACTHen test

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41
Q

How would you treat a HYPOvolaemic HYPOnatraemic patient?

A

Replace with 0.9% N.Saline

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42
Q

How would you treat a HYPERvolaemic HYPOnatraemic patient?

A

Fluid restrict and treat underlying cause

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43
Q

What must you NOT do when correcting sodium?

why?

A

Serum Na must NOT be corrected > 12 mmol/L in the first 24 hours
Risk of osmotic demyelination (central pontine myelionlysis)

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44
Q

What are the effects of central pontine myelionlysis?

A
  1. quadriplegia
  2. pseudobulbar palsy
  3. seizures
  4. coma
  5. death
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45
Q

Drugs used to treat SIADH? (2)

A
  1. Vaptans

2. Demeclocyline

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46
Q

What are the two main stimuli for ADH secretion?

a. Reduced bld volume & reduced serum osmolality
b. Increased bld volume & increased serum osmolality
c. Increased bld volume & reduced serum osmolality
d. Reduced bld volume & increased serum osmolality

A

d. Reduced bld volume &; increased serum osmolality

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47
Q

Causes of hyponatraemia post-surgery? (2)

A
  1. dilutionary due to over hydration with hypotonic IV fluids
  2. transient increase in ADH due to stress of surgery
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48
Q

Clinically HYPERnatraemic?

A

> 145mmol/L

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49
Q

Causes of HYPOvolaemic HYPERnatraemia?

  • GI
  • Skin
  • Renal
A

GI - vomiting, diarrhoea
Skin - excessive sweating, burns
Renal - loop diuretics, osmotic diuresis

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50
Q

Causes of EUvolaemic HYPERnatraemia?

  • resp
  • skin
  • renal
A
  • resp - tachypnoea
  • skin - excessive sweating, fever
  • renal - DI
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51
Q

Causes of HYPERvolaemic HYPERnatraemia? (2)

A
  1. Hypertonic saline

2. Conn’s syndrome - mineralocorticoid syndrome

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52
Q

Signs of HYPERnatraemia? (6)

A
  1. lethargy
  2. thirst
  3. irritability
  4. confusion
  5. coma
  6. fits
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53
Q

What investigations would you order in a patient with suspected diabetes insipidus?

a. Serum glucose (exclude diabetes mellitus)
b. Serum potassium (exclude hypokalaemia)
c. Serum calcium (exclude hypercalcaemia)
d. Plasma & urine osmolality
e. Water deprivation test

A

e. Water deprivation test

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54
Q

Symptoms of DI? (2)

A

polyuria

polydipsia

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55
Q

Types of DI?

A
  1. Cranial - lack of ADH

2. Nephrogenic - insensitivity to ADH

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56
Q

Causes of cranial DI? (3)

A
  1. head trauma
  2. tumour
  3. surgery
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57
Q

How does cranial DI respond to desmopressin?

A

ability to concentrate urine

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58
Q

What is Psychogenic Primary Polydipsia?

- response to 8 hr fluid deprivation test?

A

common in mentally ill patients, institutionalised patients
continuous feeling of thirst, will seek fluids from any source possible

able to concentrate urine

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59
Q

Cause of EUvolaemic HYPOnatraemia? (3)

A
  1. hypothyroidism
  2. SIADH
  3. adrenal insufficiency
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60
Q

Normal range of potassium?

A

3.5 - 5.5mmol/L

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61
Q

What hormones are involved in potassium homeostasis? (2)

A
  1. Aldosterone

2. Angiotensin II

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62
Q

ECG change associated with HYPERkalaemis?

A

Peaked T waves

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63
Q

Causes of HYPERkalaemia? (7)

A
  1. excessive intake
  2. acidosis
  3. insulin shortage
  4. rhabdomyolysis
  5. Addison’s disease
  6. reduced GFR - renal/cardiac failure
  7. drugs
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64
Q

Drugs that can cause HYPERkalaemia? (4)

A
  • ACEi, ARB, NSAIDs, K+ sparring diuretics
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65
Q

Clinical features of HYPOkalaemia? (3)

A
  1. muscle weakness
  2. cardiac arrhythmias
  3. polyuria/polydipsia
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66
Q

Causes of HYPOkalaemia? (7)

A
  1. Hyperaldosterism Conn’s syndrome
  2. GI loss
  3. Renal loss
  4. ostmotic diuresis
  5. insulin
  6. beta agonists - salbutamol
  7. alkalosis
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67
Q

Hyperkalaemia is a side-effect of which of the following drugs?

a. Furosemide
b. Bendroflumethiazide
c. Salbutamol
d. Ramipril

A

c. Salbutamol

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68
Q

Hypokalaemia is a side-effect of which of the following drugs?

a. Spironolactone
b. Indomethacin
c. Perindopril
d. Furosemide

A

d. Furosemide

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69
Q

Normal Calcium range

A

2.2 - 2.6 mmol/L

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70
Q

What happens in response to low calcium? (4)

A 
1. Parathyroids release PTH 
PTH acts at...
1. Bone - increased calcium resorption 
2. Kidney - increases Ca reabsorption
- increases PO4 excretion
- increases 1a(OH)ase 
- increases VitD3
3. GI - increases Ca absorption 
- increases VitD3 absorption
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71
Q

Enzyme required for rate limiting step in activation of 25-hydroxycholecalciferol to 1,25-dihydroxycholecalciferol (VitD3)? Where?

A

1-alpha-hydroxylase

kidney

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72
Q

Hormones that control Calcium homeostasis?

A
  1. PTH

2. Calcitriol

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73
Q

In what condition is 1alpha-hydroxylase secreted in the lung?

A

Sarcoidosis

Causes an increase in Ca2+

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74
Q

Enzyme required to convert cholecalciferol to 25-hydroxycholecalciferol? Where?

A

25-hydroxylase

Liver

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75
Q

Where is the majority of calcium within the body?

A

Skeleton (99%)

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76
Q

What percentage of plasma calcium is bound to albumin?

A

50%

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77
Q

In sepsis, when albumin is low, what can happen to calcium levels?

A

low calcium

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78
Q

Effects of Vitamin D3? (3)

A
  1. increased calcium absorption from gut
  2. increased phosphate absorption from gut
  3. bone remodelling
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79
Q

Vitamin D3 deficiency in children?

A

Ricket’s

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80
Q

Vitamin D3 deficiency in adults?

A

Osteomalacia

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81
Q

What happens to Ca/PO4/ALP/PTH in Vit D deficiency?

A 
Low VitD3 
Low Ca
Low PO4
High PTH
High ALP
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82
Q

Clinical features of Osteomalacia? (3)

Pathonogmonic?

A
  1. Boen pain
  2. myalgia
  3. increased risk of fractures

Looser’s zones

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83
Q

Clinical features of Ricket’s? (4)

A
  1. bowing of bones
  2. widened epiphyses at the wrist
  3. costochondral swelling
  4. myopathy
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84
Q

Causes of Osteomalacia? (4)

A
  1. renal failure
  2. lack of sunlight
  3. chappati’s
  4. anticonvulsants (sodium valproate) breakdown Vit D3
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85
Q

What is Osteoporosis?

A

Loss of bone density, associated with age

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86
Q

What happens to Ca/PO4/ALP/PTH in Osteoporosis?

A

All normal

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87
Q

Clinical features of Osteoporosis? (3)

A
  1. increased liklihood of fractures
  2. Typical NOF
  3. Typical Colle’s
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88
Q

Diagnosis of Osteoporosis?

Osteopenia?

A

DEXA scan

T

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89
Q

Risk factors associated with Osteoporosis?

A
  1. Age
  2. Childhood illness, failure to reach peak bone density
  3. Early menopause
  4. sedentery lifestyle
  5. smoking
  6. alcohol
  7. low BMI
  8. endocrine - Cushings, hyperprolactinaemia, thyrotoxicosis
  9. steroids
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90
Q

Treatment of Osteoporosis?

A

Bisphosphonates e.g. Alendronate

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91
Q

Symptoms of HYPOcalcaemia? (3)

Signs (2)

A
  1. perioral parasthesiae
  2. carpopedal spasm
  3. neuromuscular excitability
  4. Trousseau’s
  5. Chvostek’s
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Perfectly
92
Q

What is Trousseau’s sign?

A

flexion of wrist & metacarpal joints and adduction on fingers when BP cuff is applied
due to hypocalcemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
93
Q

What is Chvostek’s sign?

A

twitch of facial nerve when masseter at the angle of the jaw is tapped
due to hypocalcemia

How well did you know this?
1
Not at all
2
3
4
5
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94
Q

What happens in response to high calcium?

example

A

Parathyroids release less PTH

e.g. in malignancy, when there is a high calcium, PTH is suppressed

95
Q

What’s the commonest cause of hypercalcemia?

A

primary hyperparathyroidism

96
Q

Causes of primary hyperparathyroidism (3)

Most common?

A
  1. parathyroid adenoma
  2. parathyroids hyperplasia
  3. parathyroid carcinoma

adenoma (80%)

97
Q

Association with parathyroid hyperplasia?

A

MEN1

98
Q

Clinical features of HYPERcalcaemia? (6)

A 
Bones - pain 
Groans - psychogenic 
Moans - abdominal pain - constipation, pancreatitis
Stones - renal
polyuria
muscle weakness
99
Q

Types of hypercalcaemia in malignancy? (3)

A
  1. Humoral hypercalcaemia due to atopic secretion of PTHrP e.g. small cell lung cancer
  2. Metastases to the bone e.g. breast
  3. Haematological malignancies e.g. myeloma
100
Q

What happens to Ca/PO4/ALP/PTH in Myeloma?

A

HIGH Ca
HIGH PO4
Normal ALP
Normal PTH

101
Q

What happens to Ca/PO4/ALP/PTH in Bone metastasis?

A

HIGH Ca
LOW PO4
HIGH ALP
Normal PTH

102
Q

What causes secondary hyperparathyroidism?

How?

A

CKD causing renal osteodystrophy
Damaged kidney doesn’t produced sufficient 1alpha-hydroxylase to activate VitD3 therefore calcium falls
A fall in Calcium causes an increase in PTH

103
Q

What is tertiary hyperparathyroidism?

A

When after sustained time of hyperparathyroidism, PTH is then secreted excessively causings an elevated Ca2+

104
Q

What happens to Ca/PO4/ALP/PTH in secondary hyperparathyrodism?

A

LOW Ca
HIGH PO4
HIGH PTH
HIGH ALP

105
Q

What happens to Ca/PO4/ALP/PTH in tertiary hyperparathyroidism?

A

HIGH Ca
LOW PO4
Norm/high ALP
HIGH PTH

106
Q

What is Paget’s disease?

A

remodelling of the bone with both increase osteoblast & osteoclast activity

107
Q

Clinical features of Paget’s Disease? (8)

A
  1. bone pain
  2. bone warmth
  3. bone deformation
  4. increased risk of fracture
  5. enlarged skull
  6. deafness
  7. blindness
  8. increased risk of malignancy
  9. increased cardiac output
108
Q

What happens to Ca/PO4/ALP/PTH in Paget’s Disease?

A

Norm Ca
Norm PO4
HIGH ALP
Norm PTH

109
Q

Which has the lowest calcium?

a. Primary hyperparathyroidism
b. Secondary hyperparathyroidism
c. Osteoporosis
d. Pagets disease of the bone
e. Breast cancer

A

b. Secondary hyperparathyroidism

110
Q

What causes HYPOparathyroidism?

a) primary
b) secondary

A

a) Di George syndrome - due to malfunction parathyroid glands
b) post-thyroidectomy

111
Q

What happens to Ca/PO4/ALP/PTH in HYPOparathyroidism?

A

LOW Ca
HIGH PO4
Norm ALP
LOW PTH

112
Q

Risk factors for developing renal stones (5)

A
  1. dehydration
  2. abnormal pH of urine
  3. urine infection
  4. renal tubular acidosis
  5. anatomical abnormalities
113
Q

Most common type of renal stone? X-ray appearance?

A

Mixed - radio-opaque

114
Q

Type of renal stones that are radiolucent?

A

Uric acid, cysteine

115
Q

Type of renal stones formed due to UTI?

A

Staghorn - triple phosphate “struvite”

116
Q

Enzyme raised in acute pancreatitis?

A

amylase

117
Q

Marker of muscle damage?

A

creatine kinase

118
Q

Pathological causes of raised CK? (4)

A
  1. Duchenne’s Muscular dystrophy
  2. MI
  3. Rhabdomyolysis
  4. Statin related myopathy
119
Q

Causes for ALP to be raised? (4)

A

Increased activity in…

  1. Liver
  2. Bone
  3. Intestine
  4. Placenta
120
Q

Physiological causes of raised ALP? (2)

A
  1. Pregnancy

2. Childhood growth spurt

121
Q

Pathological causes of raised ALP?

a) Bone (6)
b) Liver (4)

A 
a) metastasis
osteomyelitis
osteomalacia
Pagets
fractures
tumours

b) hepatitis
cirrhosis
cholestasis
tumours

122
Q

Marker of myocardial injury?

A

Troponin

123
Q

When do you measure Troponin?

A

6 hrs
12 hrs
post-onset of chest pain

remains elevated fro 3 - 10 days

124
Q

Diagnostic Criteria for MI?

A

Rise in Troponin and gradual fall with at least one of the following symptoms

  1. ischaemic symptoms
  2. pathologic Q waves of ECG
  3. ECG changes
  4. coronary artery intervention
125
Q

Markers of liver cell damage (5)

A 
AST
ALT
ALP
GGT
Bilirubin
126
Q

Marker of liver function (3)

A

Glucose
Clotting
Albumin

127
Q

Marker elevated in chronic alcohol disease?

A

GGT

128
Q

When are AST/ALT raised?

A

when hepatocytes die

129
Q

What’s the AST:ALT in alcoholic liver disease?

A

2:1

130
Q

What’s the AST:ALT in viral liver disease?

A
131
Q

Which marker is elevated in cholestasis?

A

ALP

132
Q

What are porphyrias?

What cell types? (2)

A

a group of disorders due to a deficiency in enzymes in the make up of Haem
causing a build up of toxic haem precursors

  1. hepatic
  2. erythroid
133
Q

Types of porphyrias? (3)

A
  1. build up of Aminolaevulinic Acid (ALA)
  2. build up of Porphobilinogen (PBG)
  3. build up of Porphrinogens
134
Q

Areas affected by Porphyrias?

a) build up of ALA/PBG
b) build up of porphrinogens

A
  1. neuro-visceral

2. skin

135
Q

Colour of

a) porphrinogens
b) porphyrins

A

a) colourless

b) highly coloured

136
Q

What is Acute Intermittent Porphyria?
inheritance
enzyme deficiency
build up of? (2)

A

Autosomal dominant
Hydroxymethylbilane synthase (HMB synthase)
1. ALA
2. PBG

137
Q

Overall area affected in Acute Intermittent Porphyria?
Symptoms (10)
Signs

A
  1. N&V
  2. abdo pain
  3. confusion
  4. psych disturbances
  5. seizures
  6. tachycardia
  7. hypertension
  8. muscle weakness
  9. constipation
  10. urinary incontinence

Port wine urine

138
Q

Precipitating factors of Acute Intermittent Porphyria? (5)

A

ALA synthase inhibitors

  1. steroids
  2. ethanol
  3. barbiturates
  4. stress - surgery/infection
  5. reduced calorie intake
139
Q

Hereditary Coproporphyria

  • inheritance
  • build up of
  • symptoms
  • what skin lesion?
A

autosomal dominant
porphyrins
neurovisceral and skin lesions
blistering and skin fragility

140
Q

Variegate Porphyria

  • inheritance
  • build up of
  • symptoms
  • what skin lesion?
A

autosomal dominant
porphyrins
neurovisceral and skin lesions
blistering and skin fragility

141
Q

Non-acute porphyrias? (3)

  • area affected?
  • symptoms (3)
  • precipitating factor
A
  1. Congenital Erythopoietic Porphyria
  2. Erythropoietic Protoporphyria
  3. Porphyria Cutanea Tarda

skin lesions

  1. photsensitivity
  2. itching
  3. burning

sun exposure

142
Q

Treatment of acute porphyrias? (2)

A
  1. IV carbohydrate

2. Haem arginate

143
Q 
During acute porphyria, the most useful sample to send is…?
Blood
CSF
Urine
Muscle biopsy
Stool
Skin biopsy
A

Urine

144
Q

Cutaneous erythema without blisters or bullae, most likely indicates

a. Erythropoietic protoporphyria
b. Congenital erythropoietic porphyria
c. Acute intermittent porphyria

A

a. Erythropoietic protoporphyria

145
Q

What occurs first in response to hypoglycaemia?

a. Suppression of insulin
b. Release of glucagon
c. Release of adrenaline
d. Release of cortisol

A

a. Suppression of insulin

146
Q

Causes of hyperinsulinaemic hypoglycaemia? (3)

A
  1. iatrogenic insulin
  2. sulfonylurea excess
  3. insulinoma
147
Q

What is C-peptide?

a. is the cleavage product of insulin
b. is secreted in equimolar amounts to insulin
c. has a half-life of 2 hours
d. interferes with insulin measurement

A

b. is secreted in equimolar amounts to insulin

148
Q

Half life of Insulin?

Half life of C peptide?

A

4 - 6 mins

30 mins

149
Q

Causes of hypoinsulinaemic hypoglycaemia with positive ketones? (4)

A
  1. alcohol binge with no food
  2. pituitary insufficiency
  3. addison’s
  4. liver failure
150
Q

Causes of hypoinsulinaemic hypoglycaemia with negative ketones?

A

non pancreatic neoplams e.g. fibrosarcomata

151
Q 
20 year old female, BMI 17 kg/m2
Lanugo hair noted
Finger prick glucose – 3.8mmol/L
Routine bloods taken
Doctor rung by lab 1 hr later as plasma glucose 2.6 mmol/L

a. Undertakes strenuous exercise regularly
b. Insulinoma
c. Anorexic with poor liver glycogen stores
d. Laxative abuse

A

c. Anorexic with poor liver glycogen stores

152
Q

What would the insulin and C-peptide result be if they had been measured ?

a. Low insulin, low C-peptide
b. Low insulin, high C-peptide
c. High Insulin, lowC-peptide
d. High insulin, high C-peptide

A

a. Low insulin, low C-peptide

153
Q

What is beta-hydroxybutyrate?

a. End product of insulin metabolism
b. A free fatty acid
c. A triglyceride
d. A ketone body
e. A component of artificial nutrition

A

d. A ketone body

154
Q

45 year old lady brought in fitting. Recurrently seen GP in previous months due to weight gain and increased appetite
Husband reports personality change in last few months.

Glucose 1.9 mmol/L
Insulin 35 mu/L
C-peptide 1000 pmol/L
Urine sulponylurea drug screen negative

What is the diagnosis?

a. Insulinoma
b. Cushings syndrome
c. Addison’s disease
d. Sulphonylurea excess
e. Need more information

A

a. Insulinoma

155
Q

Associated with insulinoma?

A

MEN1

156
Q

What is Non-islet tumour hypoglycaemia?

- lab results (5)

A 
tumour that causes a paraneoplastic syndrome when IG-2 is secreted and binds to IGF-1 and insulin receptors 
everything low
LOW glucose
LOW Insulin 
LOW C-peptide
LOW FFAs
LOW ketones
157
Q 
Diagnosis of DM 
Fasting glucose 
OGTT
Random glucose 
HbA1C
A

Fasting glucose > 7
OGTT > 11.1
Random glucose > 11.1
HbA1C > 48

158
Q

Phenytoin

  • signs of toxicity (2)
  • inication
  • interactions
  • treatment of toxicity
A
  1. Ataxia
  2. Nystagmus
    - seizures
    - at high levels, liver becomes saturated and there is a surge in blood levels
    - omit/reduce dose
159
Q

Digoxin

  • indication
  • signs of toxicity (4)
  • interactions
  • treatment of toxicity
A
  • arrhythmias
    1. Arrhythmias
    2. Heart block
    3. Confusion
    4. Xanthopsia - seeing yellow
  • levels can increase with hypokalaemia, so reduce dose in elderly/renal failure
  • Digibind
160
Q

Lithium

  • indication
  • signs of toxicity (5)
  • interactions
  • treatment of toxicity
A

Bipolar disorder

  1. Tremor
  2. Lethargy
  3. Fits
  4. Arrhythmias
  5. Renal failure
    - excretion impaired by hyponatraemia, low renal function and diuretics
    - renal failure may need dialysis
161
Q

Gentamicin

  • indication
  • signs of toxicity (4)
  • interactions
  • treatment of toxicity
A
  • uncontrolled infection
    1. Tinnitus
    2. Deafness
    3. Nystagmus
    4. Renal failure
  • mostly use single daily dosing
  • omit or reduce dose
162
Q

Theophylline

  • indication
  • signs of toxicity (4)
  • interactions
  • treatment of toxicity
A
  • Asthma
    1. Arrhythmias
    2. Anxiety
    3. Tremor
    4. Convulsions
  • level can be increased by erythromycin, phenytoin, cimetidine
  • omit/reduce dose
163
Q

Vitamin A deficiency

A

Night blindness

164
Q

Vitamin D deficiency (2)

A
  1. Osteomalacia

2. Rickets

165
Q

Which steroid is made in the zona fasciculata of the adrenal gland?

A

Cortisol

166
Q

Which steroid is made in the zona glomerulosa of the adrenal gland?

A

Aldosterone

167
Q

Which steroid is made in the zona reticularis of the adrenal gland?

A

Cortisol and sex hormones

168
Q

Where are the catecholamines made in the adrenal gland?

A

medulla

169
Q 
31 year old presents with profound tiredness.
Acutely unwell a few days.
Vomiting
Na: 125,  K: 6.5,  U 10, Glucose 2.9mM.
FT4  50mU/l
What does this TSH suggest?
A. A TSH producing pituitary adenoma
B. Graves disease
C. A toxic thyroid nodule 
D. Primary hypothyroidism
E. de Quervain’s (viral) thyroiditis.
A

D. Primary hypothyroidism

170
Q

Cushing’s syndrome

  • excess what?
  • causes (3)
  • diagnostic test
  • diagnostic test suggestive of pituitary adenoma
A

ACTH

  1. pituitary adenoma
  2. ACTH secreting tumour
  3. iatrogenic steroid use
    - Low dose Dexamethasone
    - High dose Dexamethasone
171
Q

Clinical features of Cushing’s? (12)

A 
truncal weight gain
moon facies
thin skin - easy bruising, striae
hirsuitism 
acne
depression & psychosis 
insomnia
oligomenorrhoea
proximal myopathy 
DM 
osteoporosis
172
Q

Addison’s syndrome

  • deficiency in what? (2)
  • causes (5)
  • diagnostic test
A 
Cortisol and Aldosterone 
1. autoimmune
2. TB
3. adrenal tumour deposits 
4. adrenal haemorrhage
5. amyloidosis 
Short SynACTHen test (cortisol will fail to rise)
173
Q

Clinical features of Addison’s? (9)

Lab findings in Addison’s? (3)

A 
weight loss
fatigue
depression
vomiting 
diarrhoea 
postural hypotension
pigmentation 
vitiligo 
adrenal cortex atrophy

low sodium
high potassium
low glucose

174
Q

Why does increased pigmentation of the palmar creases occur in Addison’s?

A

High ACTH -> high POMC cleavage -> high alpha-MSH -> increased pigmentation of buccal, palmar, scars

175
Q

Treatment of Addison’s? (2)

A
  1. Hydrocortisone to replace cortisol

2. Fludrocortisone to replace Aldosterone

176
Q

Conn’s syndrome

  • excess what?
  • causes
  • diagnostic test?
A

Aldosterone
Adrenal tumour of zona glomerulosa
Renin:Aldosterone ratio

177
Q

Clinical features of Conn’s (3)

A

uncontrollable hypertension
high sodium
low potassium

178
Q

Treatment of Conn’s (2)

A
  1. Spironolactone (ARB) before surgery

2. Surgery to remove tumour

179
Q

Phaeochromocytoma

  • excess what
  • causes
  • diagnostic test
A

Adrenaline/NA
adrenal tumour of the medulla
24hr urinary catecholamines

180
Q

Clinical features of Phaeochromocytoma (11)

A 
hypertension 
tachycardia
panic sensation 
nervousness
clammy 
pale
arrhythmias
headache 
sweating 
CNS exciteability
seizures
181
Q

Treatment of Phaeo? (5)

A
  1. fluid resuscitation
  2. 24 hour urinary catecholamine collection
  3. alpha blockade preparation to prevent hypovolaemic crisis
  4. beta blockade to tachycardia ++
  5. surgery
182
Q

Hypertensive 33 year old.
Na 147, K 2.8, U 4.0. Glucose 4.0 mM
Plasma aldosterone raised.
Plasma renin suppressed.

Diagnosis?

A

Primary hyperaldosteronism

Conn’s

183
Q

A 30-year-old woman complains of galactorrhoea and amenorrhoea. A CT scan of her pituitary shows a large (2cm) macroadenoma.

What complication of a large pituitary tumour should you examine for?

A

Bitemporal hemianopia

184
Q

A 30-year-old woman complains of galactorrhoea and amenorrhoea. A CT scan of her pituitary shows a large (2cm) macroadenoma.
Her prolactin level comes back at 30,000 (normal

A

C. Prolactinoma

185
Q

Clinical features of Prolactinoma? (9)

A 
galactorrhoea
oligomenorrhoea
amenorrhoea
infertility
reduced libido 
osteoporosis
headaches
pituitary insufficiency 
bitemporal hemianopia
186
Q

Diagnosis of prolactinoma? (2)

A
  1. Prolactin > 2000mU

2. MRI pituitary

187
Q

Management of prolactinomas? (2)

A
  1. DA agonists e.g. Bromocriptine, Cabergoline

2. Surgery

188
Q

Side effects of Bromocriptine? (5)

A
  1. N&V
  2. cramps
  3. psychomotor excitation
  4. dykinesias
  5. postural hypotension
189
Q

Combined Pituitary Function Test (CPFT) - what is it for?

A

Assesment of the function of the anterior pituitary

a) when suspecting a tumour
b) following tumour surgery

190
Q

What is involved in CPFT? (3)

A
  1. Insulin tolerance Test - adequate GH
  2. TRH Test - thyroid pathology
  3. GRH Test - indication of hypopituitarism
191
Q

Laron dwarfism

  • inheritance
  • what
A

autosomal recessive

variant of GH receptor in insensitive to GH

192
Q

Endocrine Related short stature

  • diagnosis (2)
  • risks associated with GH therapy (3)
A
  1. Insulin tolerance test
  2. growth charts
  3. risk of leukaemia
  4. antibody resistance
  5. headaches
193
Q

Types of DI? (3)

A
  1. Central/Cranial/Neurogenic - failure to produce ADH
  2. Nephrogenic - failure to respond to ADH
  3. Dispogenic - failure to initiate thirst drive due to damage to hypothalamus
194
Q

Target tissues of thyroid hormone? (9)

A
  1. Endo - GnRH, Prolaction secretion
  2. CNS
  3. SNS - increases response to NA/Adrenaline
  4. Bone
  5. CVS - increases contractility, increase HR
  6. Skeletal muscle - increases muscular contraction
  7. Liver - increases gluconeogeneis, glycogenolysis, cholesterol synthesis
  8. Haematopoetic - increases EPO
  9. GI - increases gut motility
195
Q

HYPOthyroidism

  • what
  • who
  • causes (4)
  • lab results
A 
destruction/atrophy of thyroid gland
F>M
1. autoimmune - antibodies destroy thyroid gland
2. transient due to viral infection
3. iodine deficiency
4. drug induced e.g. lithium, amiodarone

HIGH TSH
LOW T3/T4

196
Q

Causes of secondary HYPOthyroidism? (4)

- lab results

A
  1. post-thyroidectomy
  2. post pituitary surgery
  3. Radioiodine
  4. Drug induced

LOW TSH LOW T3/T4

197
Q

Hashimotos Thyroiditis

  • what
  • who
  • clinical features
  • association
A

Autoimmune hypothyroidism causing plasma cell infiltration
elderly women
goitre present
initial “hashitoxicosis”

198
Q

Treatment of HYPOthyroidism?

A

Replacement with Levothyroxine (T4)

199
Q

Clinical Features of HYPOthyroidism (10)

A
  1. low metabolic rate
  2. reduced appetite
  3. weight gain
  4. low HR
  5. constipation
  6. lethargy
  7. increased sensitivity to cold
  8. slow speech
  9. thickened skin
  10. brittle nails and hair
200
Q

HYPERthyroidism

  • what
  • who
  • causes (4)
  • lab results
A 
increased level of thyroid hormone 
F>M
1. Grave's
2. Multinodular goitre
3. Toxic adenoma
4. DeQuervain's Thyroiditis
5. Post-partum thyroiditis

LOW TSH HIGH T3/T4

201
Q

Clinical Features of HYPERthryoidism (10)

A 
increased metabolic rate 
increased appetitie
weight loss
exopthalamus/lid lag 
increased HR
diarrhoea
tremor
low tolerance to heat 
agitation
sweating
202
Q

What is De Quervain’s thyroiditis?

Symptoms (3)

A

Self-limiting post-viral thyrotoxicosis

  1. painful goitre
  2. malaise
  3. fever
203
Q

What is Grave’s disease?

A

Tsh stimulating antibodies cause an increase in TSH

204
Q

What is Plummer’s disease?

- associations (2)

A

toxic multi-nodular goitre

  1. AF
  2. heart failure
205
Q

Which thyroid conditions have high uptake on radioisotope scan? (3)

A
  1. Grave’s
  2. Plummer’s/Toxic Multi-nodular goitre
  3. Solitary toxic adenoma
206
Q

Complication of hypothyroidism during pregnancy?

A

Neonatal cretinism - elevated TSH LOWT3/T4 -> mental retardation, growth arrest, deafness, immature body proportions

207
Q

Treatment of high uptake HYPERthyroidism?(3)

A
  1. Beta blockers
  2. Carbimazole/Propylthiouracil to block TSH
  3. Surgery
208
Q

Thyroid Neoplasms (4)

A
  1. Papillary
  2. Medullary
  3. Follicular
  4. Aplastic
209
Q

Papillary Thyroid Carcinoma

  • who
  • associations (2)
  • treatment
A

F>M aged 30-40years
1. MEN-1
2. BRAF mutations
Surgery and radioiodine

210
Q

Follicular Thyroid Carcinoma

  • who
  • associations (2)
A
  • F>M middle aged
    1. aggressive
    2. mets to lung & bone
211
Q

Medullary Thryoid Carcinoma

- associations (2)

A
  1. MEN-2

2. Produces calcitonin - lowers calcium

212
Q

Aplastic thyroid Carcinoma

A

very aggressive
p53 mutation
elderly population

213
Q

Vitamin A deficiency

A

Nigh blindness

214
Q

Vitamin D deficiency (2)

A
  1. Osteomalacia

2. Rickets

215
Q

Vitamin E deficiency (Tocophenol) (2)

A
  1. Anaemia

2. Neuropathy

216
Q

Vitamin K deficiency

- investigation

A

Clotting defective

PTT

217
Q

Thiamin deficiency B1 (3)

A
  1. Bert Beri
  2. Neuropathy
  3. Wernicke’s encephalopathy
218
Q

Vitamin B2

A

Glossitis

219
Q

Vitamin B6 Pyridoxine (2)

A
  1. Dermatitis

2. Anaemia

220
Q

Vitamin B12

A

Pernicious anaemia

221
Q

Vitamin C

A

Scurvy

222
Q

Folate deficiency (2)

A
  1. Megaloblastic anaemia

2. Neural tube defects

223
Q

Vitamin B3 Niacin (3)

A

Pellagra 1. Dementia

  1. Dermatitis
  2. Diarrhoea
224
Q

Iron deficiency

A

Hypochromic anaemia

225
Q

Iodine deficiency (2)

A
  1. Goitre

2. Hypothyroid

226
Q

Zinc deficiency

A

Dermatitis

227
Q

Copper deficiency

A

Anaemia

228
Q

Fluoride deficiency

A

Dental caries

229
Q

Phenylketonuria PKU

  • what
  • screening test
  • outcomes
  • management
A
  • phenylalanine hydroxyl are deficiency causes a build up of phenylalanine
  • Guthrie test
  • progressive developmental delay and mental retardation
  • dietary avoidance of phenylalanine
230
Q

Congenital hypothyroidism

  • what
  • screening test
  • presentation (5)
  • results (2)
  • management
A
  • dysgenesis of thyroid gland, can be due to iodine deficiency or maternal carbimazole
  • Guthrie test
  • baby has 1. Poor feeding
    2. Somnolence
    3. Reduced crying
    4. Lethargy
    5. Constipation
  • high TSH low T4
  • L-thyroxine replacement
231
Q

Cystic Fibrosis

  • mutation
  • outcome
  • affected organs (5)
  • screening test
A
  • CFTR
  • viscous secretions which can cause ductal blockages
    1. Respiratory tract
    2. Pancreas
    3. Biliary tract
    4. Liver
    5. Kidney
  • Guthrie test
232
Q

Medium Chain AcylCoA Dehydrogenase Deficiency MCADD

  • what
  • inheritance pattern
  • risks (3)
  • screening
  • management
A
  • Inherited disorder if fatty acid metabolism, unable to produced ketones -> hypoglycaemia and hypoketouria
    1. Stress
    2. Illness
    3. Exercise
  • Guthrie test
  • avoid fasting, cannot feed >every 8 hours about in first year of life, >10 hours thereafter
233
Q

What does the Guthrie Test screen for? (5)

A 
Must Heel Prick Small Child
MCADD
Congenital hypothyroidism
PKU
Sickle cell
CF

Pathology (7 decks)

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