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Year 5 Pathology > Chem path > Flashcards

Chem path Flashcards

1
Q

Define hyponatraemia

A

Serum Na+ < 135mmol/L

most common electrolyte abnormality

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2
Q

Pathogenesis of hyponatraemia

A

Increased extracellular water due to excess ADH

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3
Q

How does ADH work?

A

Acts on V2 receptors on collecting duct cells in nephron

Leads to insertion of aquaporin-2 channels

Leads to water retention, increasing extracellular water

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4
Q

What stimulates ADH secretion?

A

Increased serum osmolality (detected by osmoreceptors, also leads to thirst)

Decreased blood volume/pressure (detected by baroreceptors)

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5
Q

First step in mx of pt with hyponatraemia

A

Volume status

  • hypovolaemic
  • euvolemic
  • hypervolemic
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6
Q

Compare clinical features of hypo and hypervolaemia

A

Hypo

  • tachycardic
  • postural hypotension
  • dry mucous membranes
  • reduced skin turgor
  • confusion/drowsiness
  • reduced urine output
  • LOW urine Na+ (<20)

Hyper

  • raised JVP
  • bibasal crackles
  • peripheral oedema
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7
Q

What is the most reliable clinical sign of hypovolaemia?

A

LOW urinary sodium (<20)

Shows the kidney is trying to retain fluid because in hypovolaemia, the body is low in salt AND water

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8
Q

What would alter interpretation of urine sodium?

A

Diuretic use

Urine can be checked 48hrs after stopping drug

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9
Q

Causes of hypovolaemic hyponatraemia

A

GI loss (vomiting and diarrhoea)
Diuretics
Salt losing nephropathy

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10
Q

Causes of euvolaemic hyponatraemia

A

Hypothyroidism
Adrenal insufficiency
SIADH

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11
Q

Causes of hypervolaemic hyponatraemia

A

Cardiac failure
Cirrhosis
Nephrotic syndrome/renal failure

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12
Q

How does SIADH lead to hyponatraemia?

A

SIADH describes a state where excess ADH is released

Results in excess retention of water and pt initially becomes hypervolaemic

However, expanded volume stimulates release of natriuretic peptides

Leads to natriuresis; loss of Na+ via urine and water follows

End volume status is euvolaemia w hyponatramia

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13
Q

Causes of SIADH

A

CNS pathology (tumour, abscess, stroke)
Lung pathology (small cell lung Ca, pneumothorax, PE, chest infection)
Drugs (SSRI, TCA, opiates, PPIs, carbamazepine)
Tumours
Surgery

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14
Q

How is SIADH diagnosed?

A

Diagnosis of exclusion

  • true hyponatraemia (<135)
  • low plasma/serum osmolality (<270)
  • high urine sodium (>20)
  • high urine osmolality (<100) due to natriuresis
  • no adrenal/thyroid/renal dysfunction so normal 9am cortisol and normal TFTs
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15
Q

Why do hypothyroid pts become hyponatraemic?

A

Hypothyroidism leads to reduced cardiac output due to reduced cardiac contractility

Detected by baroreceptors -> ADH release to correct BP

Increased water retention

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16
Q

Why do adrenal insufficient pts become hyponatraemic?

A

Adrenal insufficiency leads to low aldosterone and cortisol

Low aldosterone -> less salt and water retention in kidney

Low cortisol -> excess ADH release and water retention

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17
Q

What happens to urinary sodium in cardiac failure?

A

LOW

Secondary hyperaldosteronism occurs due to activation of renin-angiotensin-aldosterone system to keep BP high

Aldosterone promotes water and sodium retention in kidney

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18
Q

Treatment for hyponatraemia

A

Hypo
- volume replacement with 0.9% saline (NaCl)

Euvo/hyper

  • fluid restriction
  • treat underlying cause
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19
Q

Signs of severe hyponatraemia

A

Nausea and vomiting (<134)
Confusion (<131)
Seizures, non-cardiogenic pulmonary oedema (<125)
Coma (<117) and eventual death

expert help needed

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20
Q

Risks of sodium correction treatment

A

Central pontine myelinolysis if serum sodium corrected faster than 8-10mmol/L in first 24 hours

Water moves too quickly out of cells, affecting CNS gap junctions, inflammatory cells enter via compromised junctions -> osmotic demyelination

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21
Q

Signs of osmotic demyelination

A 
Quadriplegia
Dysarthria
Dysphagia
Seizures
Coma
Death

*manifest a few days after sodium corrected too quickly

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22
Q

What should you do if sodium is administered too quickly?

A

Lower Na+ using 5% dextrose

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23
Q

What drugs are used to treat SIADH?

A

If fluid restriction not enough

  1. Demeclocycline
    - reduce effect of ADH on collecting duct cells
    - monitor U&Es due to nephrotoxicity risk
  2. Tolvaptan
    - V2 receptor antagonist
    - expensive and associated w high risk in serum sodium
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24
Q

What causes hypernatraemia?

A

Hyper Na+ >145mmol/L
- raised urea, albumin and PCV

Caused by unreplaced water loss

  • GI loss
  • Sweat loss
  • Renal loss: osmotic diuresis, diabetes insipidus (reduced ADH release/action)

Typically in pts who don’t drink when dehydrated, i.e. elderly, children

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25
Q

What is approximate fluid balance in the body?

A

60-40-20
60% of total body weight = water
40% of body weight = intracellular
20% of body weigh = extracellular (needs salty water for cells to survive in)

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26
Q

Osmolality vs Osmolarity defintions

A

Osmolality
- total no. of particles in solution, measured with an osmometer (mmol/kg)

Osmolarity
- calculated (mmol/L)

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27
Q

Osmolarity equation

A

2(Na+ + K+) + urea + glucose

*anions will roughly equal cations thus cations doubled

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28
Q

What are the causes of hyponatraemia based on osmolality?

A

High osmolality
- glucose/mannitol infusion

Normal osmolality
- spurious result, drip arm sample, pseudohyponatraemia (hyperlipidaemia/paraproteinaemia)

Low osmolality
- true hyponatraemia

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29
Q

What is the difference in causes for hypovolaemic hyponatraemia based on urine sodium?

A

High urine Na+ (>20)

  • RENAL
  • diuretics, addison’s, salt-losing nephropathy
  • kidney fails to reabsorb sodium so water lost as well

Low urine Na+ (<20)

  • NON-RENAL
  • vomiting, diarrhoea, excess sweat
  • kidney doing best to hold onto Na
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30
Q

Signs of diabetes insipidus

A

Hypernatraemia (lethargy, thirst, irritability, confusion, coma, fits)
Clinically euvolaemic
Polyuria and polydipsia
Low urine osmolality (<2)

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31
Q

Ix for diabetes insipidus

A
  1. Serum glucose (exclude DM)
  2. Serum K+ (exclude hypokalaemia)
  3. Serum Ca2+ (exclude hypercalcaemia)
  4. Plasma and urine osmolality
  5. 8-hour water deprivation test; DIAGNOSTIC
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32
Q

How is the type of diabetes insipidus confirmed?

A

8-hour water deprivation test

Normal
- urine osmolality >600, can concentrate

Primary polydipsia
- urine concentrates less than normal

Cranial DI
- Urine osmolality increases >600 ONLY AFTER desmopressin

Nephrogenic DI
- no increase in urine osmolality even after desmopressin

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33
Q

Causes and treatment of diabetes insipidus

A

Cranial

  • lack/no ADH
  • surgery, trauma, craniopharyngioma, autoimmune hypohysitis
  • mx: desmopressin

Nephrogenic

  • insensitive to ADH
  • inherited, drugs (lithium, demeclocycline), hypokalaemia, hypercalcaemia
  • mx: thiazide diuretics
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34
Q

What are the three most important buffering systems in the body?

A

Bicarbonate (ECF< glomerular filtrate)
H+ + HCO3- /=/ H2CO3

Haemoglobin (red cells)
H+ + Hb- /=/ HHb

Phosphate (renal tubular fluid/intracellular)
H+ + HPO4- /=/ H2PO4

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35
Q

What is the main system H+ is excreted by the body?

A

H+ excreted into renal tubules in return for Na+ absorption

Important for kidneys to excrete H+ and regenerate HCO3- to maintain bicarbonate buffering system (only works in short term as uses up HCO3- quickly)

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36
Q

How is HCO3- produced in the body?

A

From carbonic acid made from CO2 excreted by the lungs (product of metabolism)

CO2 + H2O /=/ H2CO3 /=/ H+ + HCO3-

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37
Q

What results do ABGs produce?

A

pO2 = partial pressure of oxygen
pCO2 = partial pressure of CO2
pH

Analyser does NOT directly measure bicarbonate; calculates it with equation

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38
Q

What may cause metabolic acidosis?

A

Increased H+ production (DKA, lactic acidosis)

Decreased H+ excretion (renal tubular acidosis, renal failure)

Bicarbonate loss (intestinal fistula)

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39
Q

How does the body compensate for metabolic acidosis?

A

Increases resp rate and blow off more CO2 in an attempt to reduce H+

Compensated metabolic acidosis should have a low pCO2

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40
Q

What may cause respiratory acidosis?

A

Lung pathology that leads to increased CO2

Decreased ventilation, poor lung perfusion, impaired gas exchange

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41
Q

How does the body compensate for respiratory acidosis?

A

Slightly increasing the bicarbonate concentration

Kidney scompensate by increasing H+ excretion and HCO3- regeneration but slower than respiratory compensation

May see elevated HCO3- and CO2 with normal H+ in compensated respiratory acidosis

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42
Q

What do you expect to see in patients with COPD in an ABG? (not an exacerbation)

A

Chronic respiratory acidosis with chronically high bicarbonate levels

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43
Q

What may cause metabolic alkalosis?

A

H+ loss (pyloric stenosis)

Hypokalaemia (K+ main transport agent for H+ exchange - Na/K/ATPase)

Ingestion of bicarbonate (overdose of antacids)

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44
Q

How does the body compensate for metabolic alkalosis?

A

If hypokalaemic, cannot excrete H+!!

Resp centre will become inhibited leading to a rise in pCO2 for H+ to return to normal

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45
Q

What may cause respiratory alkalosis?

A

Due to hyperventilation

Anxiety
Artificial ventilation or stimulation of resp centre (rare)
Pregnancy
Altitude

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46
Q

How does the body compensate for respiratory alkalosis?

A

May see with assisted ventilation - prolonged results in decreased renal H+ and decreased HCO3- generation

Compensation only occurs in chronic cases, H+ returns to normal but pCO2 and HCO3- remain low

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47
Q

Metabolic acidosis ABG

A

pH: LOW
pCO2: LOW
HCO3-: LOW

Immediate compsenation: hyperventilation

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48
Q

Metabolic alkalosis ABG

A

pH: HIGH
pCO2: HIGH
HCO3-: HIGH

Immediate compensation: hypoventilation

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49
Q

Respiratory acidosis ABG

A

pH: LOW
pCO2: HIGH
HCO3-: HIGH (renal delayed compensation)

*normal/high pCO2 worrying - ITU RV/vent support needed

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50
Q

Respiratory alkalosis ABG

A

pH: HIGH
pCO2: LOW
HCO3-: LOW (renal delayed compsensation)

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51
Q

Role of anion gap in ABGs

A

Elevated anion gap in metabolic acidosis, helps determine cause

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52
Q

Causes of metabolic acidosis with elevated anion gap

A

KULT

Ketoacidosis (DKA, alcoholic, starvation)
Uraemia (renal failure)
Lactic acidosis
Toxins (ethylene glycol, methanol, paraldehyde, salicylate)

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53
Q

What ABG changes may these drugs cause?

a) aspirin
b) salicylates
c) opioids
d) loop diuretics

A

a) Metabolic acidosis (high anion gap)
b) Respiratory alkalosis (brainstem stimulation)
c) Respiratory acidosis (T2 resp failure)
d) Metabolic alkalosis (K+ depletion)

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54
Q

Role of osmolar gap in ABGs

A

Helpful in differentiating caues of elevated anion gap metabolic acidosis

Elevation suggestive of presence of abnormal solute (alcohol, mannitol, ketones, lactate)

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55
Q

Which hormones regular potassium and where do they come from?

A

Angiotensin II

Aldosterone

*Angiotensinogen (liver) via renin -> angiotensin I via ACE in lungs -> angiotensin II STIMULATES aldosterone release (adrenals/zona glomerulosa)

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56
Q

What does aldosterone do?

A

Stimulate Na+ reabsorption (water retention) and K+ excretion

Acts on cortical collecting duct on mineralocorticoid receptor

Na+ channels increase on luminal membrane, more Na+ reabsorbed, lumen electronegative therefore K+ moves down electrogradient and SECRETED

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57
Q

What is normal serum concentration for K+?

A
  1. 5-5.0 mmol/L

* K+ most abundant intracellular cation*

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58
Q

ECG changes seen with hyperkalaemia

A

Loss of P waves
Tall, tented T waves
Broad QRS complexes (late change)

ECG is ‘pulled apart’ to create a ‘sine wave’ if severe/untreated

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59
Q

Mx of hyperkalaemia

A

Repeat sampling

  • may be spurious result due to haemolysis
  • repeat if >7

ECG
- check if any changes/arrhythmia

K+ >5.5 w ECG OR K+ >6.5 regardless of ECG triggers:

10ml of 10% calcium gluconate
- stabilise myocardium, prevent arrhythmia

100-200ml of 10-20% dextrose + 10 units of insulin

  • drive K+ into cells
  • dextrose avoid hypoglycaemia
  • note: 50ml 50% dextrose old mx, very irritant

Nebulised salbutamol
- drive K+ into cells

Consider calcium resonium 15g PO or 60g PR
- bind K+ in gut

Treat underlying cause

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60
Q

Causes of hyperkalaemia

A

Artefact
- spurious result due to haemolysis/EDTA contamination in FBC bottle

Renal impairment

  • renal failure as reduced GFR so reduced K+ secretion
  • happens late due to compensatory mechanisms

Reduced renin activity

  • RARE cause: type 4 renal tubular acidosis
  • NSAIDs

Drugs

  • ACEi -> less aldosterone
  • ARBs -> less angiotensin II, less aldosterone
  • spironolactone -> aldosterone antagonists

Low aldosterone

  • Addison’s (damaged adrenal cortex)
  • Type 4 renal tubular acidosis (low renin)

K+ release from cells

  • Rhabdomyolysis
  • Acidosis (high H+, K+ leaves cells to take H+ in to normalise pH and maintain gradient)
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61
Q

What care should be taken for patients on digoxin when administrating calcium?

A

Cardiac monitoring should be performed

IV Ca2+ can precipitate arrhythmias

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62
Q

Causes of hypokalaemia

A

GI loss
- D&V

Renal loss

  • Hyperaldosteronism (Conn’s), Cushing’s (excess cortisol) -> act on MR
  • Increased Na+ to distal nephron; drugs, Bartter/Gitelman syndromes
  • osmotic diuresis

Redistribution into cells

  • insulin
  • beta agonists
  • alkalosis; opposite mechanism of acidosis (H+ leave cell, K+ enters)

Rare

  • renal tubular acidosis type 1 and 2
  • hypomagnesaemia
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63
Q

Which drugs and syndromes cause hypokalaemia and why?

A

Loop diuretics + Bartter syndrome

  • blocks triple transporter (Na+/K+/Cl-) in ascending limb of loop of Henle
  • Na+ not absorbed loop of Henle so MORE deliver to distal nephron and K+ lost via voltage gradient in exchange

Thiazide diuretics + Gitelman syndrome

  • blocks Na+ and Cl- reabsorption in distal convoluting tubule
  • more Na+ delivered to distal nephron so K+ lost via voltage gradient in exchange
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64
Q

Clinical features of hypokalaemia

A

MAP

Muscle weakness
Arrhythmias
Polyuria and polydipsia (low K+ -> nephrogenic DI)

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65
Q

Screening ix to order if pt hypokalaemic + hypertensive

A

Aldosterone:renin ratio

  • 1o hyperaldosteronism; high ratio as renin supressed
  • think Conn’s
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66
Q

Can cardiac failure cause hypokalaemia?

A

Two things happening

  1. 2o hyperaldosteronism due to excess activation of RAAS -> increase K+ excretion
  2. Renal hypoperfusion meaning reduced GFR -> reduce K+ excretion

Therefore net clinical effect may not be hypokalaemia; difficult to predict K+ levels in these patients

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67
Q

Can cardiac failure cause hyponatraemia?

A

Low cardiac output -> baroreceptors detected -> stimulate ADH -> retains water -> dilutes osmolality -> hyponatraemia

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68
Q

Mx of hypokalaemia

A

K+ 3.0-3.5

  • oral KCl (2 SandoK tablets for 48 horus)
  • re-check level

K+ <3.0

  • IV KCl
  • max. rate 10mmol/hour
  • highly irritant

Treat underlying cause

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69
Q

How can renal tubular acidosis affect K+?

A

Type 1

  • most severe
  • distal failure of H+ excretion and subsequent acidosis
  • HYPOKALAEMIA

Type 2

  • milder
  • failure to reabsorb HCO3- leads to acidosis
  • HYPOKALAEMIA

Type 3 irrelevant lol

Type 4
- leads to acidosis HOWEVER aldosterone deficiency/resistance so HYPERKALAEMIA

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70
Q

A 67-year-old man was started on Bendroflumethiazide for hypertension 2 weeks ago. He has had diarrhoea and vomiting for two days. He has dry mucous membranes and reduced skin turgor.

  • Sodium: 129 mmol/l
  • Potassium: 3.5 mmol/l
  • Urea: 8.0 mmol/l
  • Creatinine: 100 micromoles/l

Mx plan?

A

This patient is showing signs of hypovolaemia. He is also hyponatraemic. Causes of hypovolaemic hyponatraemia include D&V, diuretics and salt-losing nephropathy.

Treatment: 0.9% sodium chloride.

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71
Q

A 57-year-old woman has breathlessness, worsened on lying flat. Her past medical history includes an NSTEMI. She is taking ramipril, bisoprolol, aspiring and simvastatin. She has an elevated JVP, Bibasal crackles and bilateral leg oedema.

  • Sodium: 128 mmol/l
  • Potassium: 4.5 mmol/l
  • Urea: 8.0 mmol/l
  • Creatinine: 100 micromoles/l

Mx plan?

A

o Increased urea can suggest reduced GFR aka renal impairment

o Reduced urea can suggest alcoholism

This patient is showing signs of hypervolaemia (clinically). Causes of hypervolaemic hyponatraemia include cardiac failure (likely here), cirrhosis and nephrotic syndrome.

Treatment: fluid restriction, treat the underlying cause.

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72
Q

A 55-year-old man has jaundice. He has a past history of excessive alcohol intake. He has multiple spider naevi, shifting dullness and splenomegaly.

  • Sodium: 122 mmol/l
  • Potassium: 3.5 mmol/l
  • Urea: 2.0 mmol/l
  • Creatinine: 80 micromoles/l

Mx plan?

A

The diagnosis is cirrhosis. Cirrhosis can cause hyponatraemia due to a release in excess nitric oxide. Portal hypertension is associated with a systemic vasodilation due to release of NO – the resulting reduced blood pressure is detected, causing a release in ADH.

Treatment: fluid restriction, treat the underlying cause.

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73
Q

A 40-year-old woman presents with fatigue, weight gain, dry skin and cold intolerance. On examination, she looks pale.

  • Sodium: 130 mmol/l
  • Potassium: 4.2 mmol/l
  • Urea: 5.0 mmol/l
  • Creatinine: 65 micromoles/l

Next ix and mx?

A

This sounds like a diagnosis of hypothyroidism. Reduced cardiac contractility results in a reduced blood pressure, which is sensed by baroreceptors. There is a subsequent release in ADH, and more water absorbed (and hyponatraemia). The patient is euvolaemic. We need to check TFTS.

Treatment: Treat the underlying cause (thyroxine replacement)

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74
Q

A 45-year-old woman presents with dizziness and nausea. On examination, she looks tanned and has postural hypotension.

  • Sodium: 128 mmol/l
  • Potassium: 5.5 mmol/l
  • Urea: 9.0 mmol/l
  • Creatinine: 110 micromoles/l

Next ix and mx?

A

This sounds like adrenal insufficiency; hyponatraemia and hyperkalaemia make us think of hypoadrenalism. The patient is euvolaemic. We should perform a short synACTHen test (in a healthy person, cortisol will shoot up, but in adrenal insufficiency, it won’t).

Treatment: Hydrocortisone and Fludrocortisone (both glucocorticoid and mineralocorticoid replacement).

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75
Q

A 62-year-old man has chest pain, cough and weight loss. He looks cachectic. He has a 30-pack year smoking history.

  • Sodium: 125 mmol/l
  • Potassium: 3.5 mmol/l
  • Urea: 7.0 mmol/l
  • Creatinine: 85 micromoles/l

Next ix?

A

This sounds like a potential case of lung cancer; the patient may have SIADH as a result (excess ADH released ectopically and inappropriately from the lung tumour). The patient will be euvolaemic. The next thing to do is check plasma and urine osmolality (plasma osmolality low, urine osmolality high). The diagnosis of SIADH:

  • No hypovolaemia
  • No hypothyroidism
  • No adrenal insufficiency
  • Reduced plasma osmolality AND increased urine osmolality (>100)

Causes of SIADH include CNS pathology, lung pathology, drugs (SSRI, TCA, opiates, PPIs), tumours and surgery.

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76
Q

A 20-year-old man presents with polyuria and polydipsia. On examination, he has bitemporal hemianopia.

  • Sodium: 150 mmol/l
  • Potassium: 4.0 mmol/l
  • Urea: 5.0 mmol/l
  • Creatinine: 70 micromoles/l

Next ix?

A

This patient has hypernatraemia. Causes of hypernatraemia include unreplaced water loss (GI losses, sweat loss, renal losses e.g. osmotic diuresis, reduced ADH release/action) in association with the patient not being able to control water intake (children, elderly).

Investigations for suspected diabetes insipidus:

  • Serum glucose (exclude diabetes mellitus)
  • Serum potassium (exclude hypokalaemia)
  • Serum calcium (exclude hypercalcaemia)
  • Plasma and urine osmolality
  • Water deprivation test
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77
Q

A 65-year-old man with type 2 diabetes mellitus and hypertension presents malaise and drowsiness. He is on a basal bolus insulin regimen, ramipril, amlodipine, simvastatin and aspirin.

  • Sodium: 125 mmol/l
  • Potassium: 6.5 mmol/l
  • Urea: 18.0 mmol/l
  • Creatinine: 250 micromoles/l

Mx plan?

A

This patient is hyperkalaemic. They are on ACE inhibitors. The creatinine and urea are also very high, which prompts us to think that the hyperkalaemia is being caused by renal failure (reduced GFR and reduced filtration). We would advise the patient to hold off of Ramipril (less ACE à less aldosterone à less potassium excretion).

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78
Q

A 50-year-old man is referred with hypertension, that has been difficult to control despite maximum doses of amlodipine, ramipril and bisoprolol.

  • Sodium: 140 mmol/l
  • Potassium: 3.0 mmol/l
  • Urea: 4.0 mmol/l
  • Creatinine: 70 micromoles/l

Next step?

A

The hypernatraemia and hypokalaemia prompt us to want to measure the aldosterone:renin ratio.

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79
Q

What is a porphyria?

A

Group of disorders caused by deficiencies in enzymes of haem biosynthetic pathway

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80
Q

Why is haem vital for erythroid and liver cells?

A

Creates cytochrome, needed for electron transfer chain in mitochondria

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81
Q

What is one of the key enzymes in the haem synthesis pathway?

A

ALA synthase (aminolevulinic acid)

Starts of pathway by generated 5-ALA from succinyl CoA + glycine

The rest of the pathway relies on enzymes to change 5-ALA into haem

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82
Q

How may porphyrias be classified?

A

Site of enzyme deficiency

  • erythroid
  • hepatic

Clinical presentation

  • acute = neurovisceral
  • non-acute cutaneous
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83
Q

What causes neurovisceral signs in porphyrias?

A

Accumulation of 5-ALA

Typically acute presentation

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84
Q

What causes cutaneous signs in porphyrias?

A

Porphyrin precursors accumulate in skin, become oxidised into porphyrins then into toxic, activated porphyrins by UV light that can cause blistering/non-blistering skin lesions

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85
Q

Porphyrinogens vs porphyrins

A

Porphyrinogens

  • RAISED in porphyria; precursor to porphyrins
  • colourless as no double bond
  • unstable so will readily oxidise when sample reaches lab

Porphyrins

  • highly coloured as double bonds present
  • will show up as deep red/purple when urine sample left to oxidise (porphyrinogens -> porphyrins)
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86
Q

Name the acute porphyrias and the enzymes affected

A

Acute porphyria:

  • PBG synthase/ALA dehydratase deficiency
  • RARE

Acute intermittent porphyria:
- HMB synthase/PBG deaminase deficiency

Acute porphyrias w skin lesions:
- hereditary coproporphyria (HCP) due to coproporphyrinogen oxidase deficiency

  • variegate porphyria (VCP) due to protoporphyrinogen oxidase deficiency
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87
Q

How can you differentiate between the acute prophyrias?

A

AIP: NO skin lesions
HCP and VP: skin lesions

Send urine sample - PBG raise in ALL three

Check total porphyrins in urine (protect from light) and stool sample

  • HIGH in HCP and VP
  • not high in AIP
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88
Q

Name the non-acute porphyrias and the enzymes affected

A

Porphyria cutaenea tarda (most common)
- uroporphyrinogen decarboxylase deficiency

Erythropoietic protoporphyria
- ferrochetelase deficiency

Congenital erythropoietic porphyria
- uroporphyrinogen III synthase deficiency

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89
Q

Which porphyrias are associated with myelodysplastic syndromes?

A

Erythropoietic porphyria

Congenital erythropoietic porphyria

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90
Q

Which sx are seen in acute porphyrias and in which ones?

A

Neurovisceral:

  • Painful abdomen
  • Seizures
  • Peripheral neuropathy
  • Psychosis
  • Port urine
  • Muscle weakness
  • Constipation
  • Urinary incontinence

=> AIP, HCP, VP

Skin lesions:

  • blistering
  • skin fragility
  • affects back of hands and back of neck (sun exposed)

=> HCP, VP

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91
Q

Mx of acute porphyrias

A

Conservative

  • avoid precipitating factors (infection, pre-empt if surgery, ALA synthase inducers)
  • adequate nutrition and analgesia

Acute attack

  • treat underlying infection/illness
  • IV haem arginate
  • IV carbohydrate
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92
Q

Which sx are seen in non-acute porphyrias and in which ones?

A

NO neurovisceral, ONLY skin lesions

PCT

  • vesicles on sun-exposed areas
  • skin crusting
  • superficial scarring and pigmentation

EPP + CEP

  • NON-blistering
  • photosensitivity; burning, itching, oedema after sun exposure
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93
Q

Mx of non-acute porphyrias

A

PCT

  • avoid precipitants (alcohol, liver disease)
  • chloroquine

EPP, CEP
- avoid sun exposure

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94
Q

How do you differentiate between the cutaenous porphyrias?

A

PCT

  • increased urinary uroporphyrins and coproporphyrins
  • increased ferritin
  • abnormal LFTs

EPP
- RBC protoporphyrin levels elevated

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95
Q

What carcinogen can trigger PCT-like syndrome?

A

Hexachlorobenzene

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96
Q

What would you expect to see in urine sample if AIP vs PCT?

A

AIP
- Increased urinary porphobilinogen and aminolaevulinic acid

PCT
- increased urinary uroporphyrins and coproporpyrins

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97
Q

Why may you see hyponatraemia associated with AIP?

A

Due to SIADH

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98
Q

Which LFTs are indicative of liver cell damage?

A 
ALT
AST
ALP (alk phos)
GGT
Bilirubin
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99
Q

Which LFTs are indicative of synthetic function?

A

Clotting (INR)
Albumin
Glucose

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100
Q

What is the best marker of liver function in acute liver injury?

A

Prothrombin time

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101
Q

LFT shows ALT and AST > 1000

Ddx?

A

Acute viral hepatitis
Toxin i.e. paracetamol
Ischaemic hit

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102
Q

What would you suspect with the following LFT findings?

a) AST:ALT 2:1
b) AST:ALT 1:1
c) ALT > AST
d) ALT + AST > 1000

A

a) EtOH liver disease
b) viral hepatitis
c) chronic liver disease
d) acute viral hep, paracetamol OD, ischaemic hit

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103
Q

What LFTs would you see in a cholestatic/obstructive picture?

A

Raised GGT and ALP

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104
Q

Why may you see an isolated raised ALP?

A

Physiological
- pregnancy, childhood

Bone issues
- x5 = Paget’s, osteomalacia
-

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105
Q

Why is ALP normal in myeloma?

A

Plasma cells suppress osteoblasts

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106
Q

Which conditions may you see low albumin in?

A 
Chronic liver disease
Malnutrition
Protein-losing enteropathy
Nephrotic syndrome
Sepsis (3rd spacing)
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107
Q

Which conditions may you see low urea in?

A

Severe liver disease
Malnutrition
Pregnancy

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108
Q

Which conditions may you see raised urea (x10) in?

A

Upper GI bleed
Large protein meal
Dehydration
AKI

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109
Q

What clinical findings would you expect to see in prehepatic jaundice?

A

Normal/increased

  • unconjugated bilirubin
  • urobilinogen

Normal

  • urine colour
  • stool colour
  • AST/ALT
  • ALP

Splenomegaly present

Absent

  • conjugated bilirubin
  • urine bilirubin
  • conjugated bilirubin in urine
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110
Q

What clinical findings would you expect to see in hepatic jaundice?

A

Increased

  • conjugated bilirubin (in urine)
  • unconjugated bilirubin
  • urobilinogen (in urine)
  • AST/ALT
  • ALP (could be normal)

Urine colour dark

Stool colour normal/pale

Splenomegaly present

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111
Q

What clinical findings would you expect to see in post-hepatic jaundice?

A

Increased

  • conjugated bilirubin (in urine)
  • ALP
  • AST/ALT
  • urine bilirubin present

Urine colour dark

Stool colour pale

Absent

  • splenomegaly
  • urobilinogen (or decreased)
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112
Q

Why don’t you get urine bilirubin in prehepatic jaundice?

A

Uncojugated BR from haem breakdown by macrophages in spleen are tightly bound to albumin thus unable to pass through glomerulus

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113
Q

Why do you get dark urine and pale stools in post-hepatic jaundice?

A

Increase in urobilinogen/conjugated BR (lots absorbed by blood), pale stool = low levels of stercobilinogen + dark urine

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114
Q

Hepatomegaly with a smooth margin is indicative of which conditions?

A

Viral hepatitis
Biliary tract obstruction
Hepatic congestion secondary to HF (Budd Chiari)

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115
Q

Hepatomegaly with a craggy border is indicative of which conditions?

A

Hepatic metastatic disease
Polycystic disease
Cirrhosis (shrinks)

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116
Q

Causes of prehepatic jaundice

A
  1. Haemolytic anaemia
  2. Ineffective erythropoiesis i.e. thalassaemia
  3. Congestive cardiac failure
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117
Q

Causes of hepatic jaundice

A
  1. Hepatocellular dysfunction (viral, alcohol hep)

2. Impaired conjugation, BR excretion, BR uptake (Gilbert syndrome, Crigler Najjar syndrome)

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118
Q

Causes of post-hepatic jaundice

A

Obstruction of biliary tree
1. Intraluminal (stones, strictures)

  1. Luminal (mass/neoplasm, inflammation - PSC, PBC)
  2. Extra-luminal (Ca pancreas, cholangio Ca)
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119
Q

What are common problems in LBW babies?

A

Respiratory distress syndrome
Retinopathy of prematurity (due to oxygen hypertoxicity)
Intraventricular haemorrhage
Patent ductus arteriosus
Necrotising enterocolitis (inflammation bowel wall - necrosis + perforation)

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120
Q

What is NEC?

A

Necrotising enterocolitis

  • inflammation of bowel wall progressing to necrosis and perforation
  • bloody stools
  • abdominal distention
  • intramural air (pneumatosis intestinalis) on X ray
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121
Q

Compare newborn renal function to adults

A

Low GFR for surface area

Less reabsorption as short proximal tubule

Reduced concentrating ability as short loops of Henle and distal collecting ducts

Persistent sodium loss due to distal tubule being relatively aldosterone-insensitive

122
Q

Why do newborns have a high insensible water loss?

A

High surface area to body weight ratio

Skin blood flow increased

Metabolic/respiratory rate higher than adults

Transepidermal fluid loss (skin not as good barrier/skin not keratinised in prems)

123
Q

When would you see hypernatraemia in a baby?

A

Common in first two weeks of term baby/common prems

Associated with dehydration or overly concentrated milk formula

124
Q

When would you see hyponatraemia in a baby?

A

Relatively rare

Causes include

  • excessive intake > total body water (first 4-5 days life)
  • loss of Na loss due to immature tubular function in pts on diuresis (after 4-5 days life)
  • factitious (hyperglycaemia)
  • congenital adrenal hyperplasia (21-hydroxylase deficiency)
125
Q

Clinical features of congenital adrenal hyperplasia when presenting as a child

A

Hyponatraemia/hyperkalaemia with volume depletion

Hypoglycaemia (lack of cortisol)

Ambiguous genitalia in perceived female neonates
- believed male neonates more likely to present w salt-losing crisis

Growth acceleration due to excess androgens (rare complaint in children)

126
Q

What presentation of jaundice is always pathological in a neonate?

A

Jaundice <24 hours of life

  • acute haemolysis
  • sepsis

Jaundice > 2 weeks of life
- hepatobiliary failure

Conjugated hyperbilirubinemia at any stage of infancy

  • biliary atresia
  • ascending cholangitis in TPN
127
Q

Typical changes seen in hepatic markers due to pre hepatic jaundice

A 
Unconjugated BR: ++
Conjugated BR: normal
ALT/AST: normal
ALP: normal/++
GGT: normal/++
128
Q

Typical changes seen in hepatic markers due to hepatic jaundice

A 
Unconjugated BR: normal
Conjugated BR: ++
ALT/AST: ++
ALP: +
GGT: +
129
Q

Typical changes seen in hepatic markers due to post hepatic jaundice

A 
Unconjugated BR: normal
Conjugated BR: ++
ALT/AST: +
ALP: ++
GGT: ++
130
Q

Fat soluble vitamins

A

A, D, E, K

131
Q

Water soluble vitamins

A

B1, B2, B3, B6, B12, C, folate

132
Q

Vit A deficiency results in

A

Colour blindness

133
Q

Vit A excess results in

A

Exfoliation

Hepatitis

134
Q

Vit D deficiency results in

A

Osteomalacia

Rickets

135
Q

Vit D excess results in

A

Hypercalcaemia

136
Q

Vit E deficiency results in

A

Anaemia/neuropathy

?Malignancy/IHD

137
Q

Vit K deficiency results in

A

Defective clotting

138
Q

How do you test for fat soluble vitamin levels?

A

A, D, E = serum

K = PTT

139
Q

What are the other names for the following vitamins?

a) B1
b) B2
c) B3
d) B6
e) B12

A

a) thiamine
b) riboflavin
c) niacin
d) pyridoxine
e) cobalamin

140
Q

B1 deficiency results in

A

Beri-beri
Neuropathy
Wernicke’s

141
Q

B2 deficiency results in

A

Glossitis

142
Q

B3 deficiency results in

A

Pellagra (3Ds)

  • dementia
  • dermatitis
  • diarrhoea
143
Q

B6 deficiency result sin

A

Dermatitis

Anaemia

144
Q

B12 deficiency results in

A

Pernicious anaemia

145
Q

B6 excess results in

A

Neuropathy

146
Q

Vit C deficiency results in

A

Scurvy

147
Q

Vit C excess results in

A

Renal stones

148
Q

Folate deficiency results in

A

Megaloblastic anaemia

Neural tube defects

149
Q

How do you test for water soluble vitamin levels?

A 
B1 = RBC transketolase
B2 = RBC glutathione reductase
B6 = RBC AST activation
B12 = serum B12
Vit C = plasma levels
Folate = RBC folate
150
Q

Iron deficiency results in

A

Hypochromic anaemia

151
Q

Iodine deficiency results in

A

Goitre

Hypothyroidism

152
Q

Zinc deficiency results in

A

Dermatitis

153
Q

Copper deficiency results in

A

Anaemia

154
Q

Fluoride deficiency results in

A

Dental caries

155
Q

Copper excess results in

A

Wilson’s disease

156
Q

Fluoride excess results in

A

Fluorosis

157
Q

What are caeruloplasmin levels in Wilson’s disease?

A

Low

- caeruloplasmin is a copper-binding protein so all used up in Wilson’s

158
Q

What deficiencies are seen in Crohn’s?

A

ADEK
B12
Foalte
Calcium, phosphate, magnesium, zinc deranged if high output/chronic diarrhoea

159
Q

What deficiencies are seen in coeliac?

A

Iron
ADEK
B1
B6

160
Q

What deficiencies are seen in chronic liver disease?

A 
ADEK
B12
Selenium
Magnesium 
Zinc
Folate
161
Q

What is seen in chronic kidney disease?

A

Protein energy wasting syndrome

162
Q

What deficiencies are seen in pancreatic insufficiency?

A

ADEK

163
Q

Causes of hyperinsulinaemic hypoglycaemia

A

Insulin overdose
Sulfonylurea excess
Insulinoma
Anorexia nervosa

164
Q

Causes of hypoinsulinaemic hypoglycaemia with +ve ketones

A 
Alcohol binge with no food
Pituitary insufficiency 
Addison's 
Liver failure
Anorexia nervosa
165
Q

Causes of hypoinsulinaemic hypoglycaemia with -ve ketones

A

Non pancreatic neoplasms

  • fibrosarcomata
  • fibromata
166
Q

Triad of hypoglycaemia

A

Low glucose (varies for different patient populations)

Symptoms (adrenergic, neuroglycopenic, but could be no symptoms)

Relief of symptoms on administration of glucose

167
Q

Sx seen in hypoglycaemia

A

Adrenergic: tremors, palpitations, sweating, hunger

Neuroglycopaenic: somnolence, confusion, incoordination, seizures, coma

Asymptomatic in individuals who have frequent hypos

168
Q

Hyperglycaemic hypoglycaemic with low C-peptide

What is this a result of?

A

Exogenous insulin overdose

  • patient education to ensure correct insulin delivery method
  • may have been intentional so consider psych review
169
Q

What is seen in non-islet tumour hypoglycaemia?

A

Low glucose, insulin, C-peptide, FFA and ketones

Result of paraneoplastic syndrome secreting IGF-2, binding to IGF-1 and insulin receptor

170
Q

Drugs that cause hypoglycaemia

A

Oral hypoglycaemics

  • sulphonylureas
  • GLP-1 agents

Insulin

Other drugs

  • beta-blockers
  • salicylates
  • alcohol (inhibits lipolysis)
171
Q

Calicum range

A

2.2-2.6 mmol/l

172
Q

Which two hormones are involved with calcium metabolism?

A

PTH

Calcitriol (1, 24 (OH)2D)

173
Q

What does PTH do?

A

Increases tubular 1-alpha hydroxylation of vit D (25(OH)D)

Mobilises calcium from bone

Increases renal calcium reabsorption

Increases renal phosphate excretion (phosphate trashing hormone)

174
Q

What does calcitriol do?

A

Increases calcium and phosphate absorption from the gut

Bone remodelling

175
Q

Primary hyperparathyroidism causes

A

Parathyroid nodule (80%)
Hyperplasia and multiple adenomas (15%)
Carcinomas (0.5%)
MEN1 and MEN2

176
Q

Secondary hyperparathryoidism causes

A

CKD

Vit D deficiency

177
Q

Tertiary hyperparathryoidism causes

A

Prolonged secondary hyperPTHism causing unregulat secretion of PTH
Kidney transplant

178
Q

Hypoparathyroidism causes

A 
Postsurgical (most common) 
Postradiation
Autoimmune
Iron deposition in people with thalassaemia
Hypo/hypermagnaseamia
PseduohypoPTH (resistant to PTH) 
DiGeorge Syndrome
179
Q 
Calcium: high
Phosphate: low
PTH: high/normal
ALP: high/normal
Vit D: normal

Dx?

A

Primary hyperparathyroidism

=> intrinsic problem with parathyroid gland causing increased PTH

180
Q 
Calcium: low/normal
Phosphate: high
PTH: high
ALP: high
Vit D: normal

Dx?

A

Secondary hyperparathyroidism

=> stimulation of parathyroid gland to produce more PTH

181
Q 
Calcium: high
Phosphate: low
PTH: high/normal
ALP: high/normal
Vit D: normal

Dx?

A

Tertiary hyperparathyroidism

=> autonomous PTH secretion

182
Q 
Calcium: low
Phosphate: high
PTH: low
ALP: low/normal
Vit D: normal

Dx?

A

Hypoparathyroidism

183
Q 
Calcium: low
Phosphate: low
PTH: high
ALP: high
Vit D: low

Dx?

A

Osteomalacia/Ricket’s in children

184
Q 
Calcium: normal
Phosphate: normal
PTH: normal
ALP: high
Vit D: normal

Dx?

A

Paget’s disease

=> re-modelling of bone, very rare

185
Q 
Calcium: normal
Phosphate: normal
PTH: normal
ALP: normal
Vit D: normal

Dx if pt has bone pain?

A

Osteoporosis

=> bone loss as result of wear and tear

186
Q

Risk factors for Vit D deficiency

A

Lack of sunlight
Dark skin
Dietary changes
Gut malabsorption (i.e. coeliac)

187
Q

Hypercalcaemia definition

A

> /= 2.6 mmol/L

188
Q

Hypercalcaemia sx

A

Stones (renal)

Bones (pain)

Groans (psych)

Moans (abdo pain)
- constipation

Polyuria
- it is an osmotic diuretic

Neuro

  • muscle weakness
  • confusion
  • seizures
  • coma
189
Q

Hypercalcaemia treatment

A

Double check it is genuine result (repeat if in doubt)

Rehydrate, fluids!

Bisphosphonates IV

  • zolendronic acid
  • pamidronate

Treat the underlying cause (check PTH levels)

190
Q

Causes of hypercalcaemia

A 
Dehydration
Hyperparathyroidism 
Cancer
Sarcoidosis 
Milk alkali syndrome 
Thyrotoxicosis 
Hypervitaminosis D
191
Q

What can PTH tell us about the cause of hypercalcaemia?

A

Appropriate response

  • PTH suppressed
  • malignancy most likely
  • sarcoid, vit D excess, thyrotoxicosis, milk alkali syndrome

Inappropriate response

  • PTH not suppressed (raised/normal)
  • primary hyperparathyroidism most likely
  • familial hypocalciuric hypercalcaemia (rare)
192
Q

Hypocalcaemia sx

A

Increased reflexes

Stridor

Perioral paraesthesia

Chvostek’s sign (twitching when you tap face)

Trousseau’s sign (carpopedal spasm with BP cuff)

193
Q

Why does malignancy result in hypercalcaemia?

A

Ectopic PTH-related peptide released by tumour
- squamous cell lung cancer

Bone mets resulting in local bone osteolysis
- breast cancer

Haematological malignancy releases cytokines causing bone breakdown
- myeloma

194
Q

Hypocalcaemia treatment

A

Repeat result and adjust for albumin (corrected calcium) to confirm if unsure

Symptomatic or Ca2+ < 1.875 mmol/L
-> 10% calcium gluconate IV

Asx/chronic/milk

  • Oral calcium supplementation (not at mealtime); SandoCal
  • vit D if low PTH or vit D
195
Q

Hypocalcaemia causes with high phosphate

A

High phosphate

  • CKD
  • hypoparathyroidism
  • post thyroid surgery
  • pseudohypoparathyroidism
  • hypomagnesaemia
196
Q

Hypocalcaemia misreading due to

A

Artefact

- hypoalbuminaemia

197
Q

Hypocalcaemia causes with low phosphate

A

Low phosphate

  • osteomalacia
  • acute pancreatitis
  • overhydration
  • respiratory alkalosis (decreased ionised/active Ca2+)
198
Q

Risk factors for renal stones

A

Dehydration
Abnormal urine pH (meat intake, renal tubular acidosis)
Increased excretion of stone constituents
Urine infection
Anatomical abnormalities

199
Q

Renal stones that are radio-opaque

A

Calcium mixed
Calcium oxalate
Calcium phosphate
Triple phosphate “Struvite” (staghorn appearance)

200
Q

Renal stones that are radiolucent

A

Uric acid

Cysteine

201
Q

Preventative mx of renal stones

A 
Good hydration
Reduce oxalate intake
Maintain normal Ca intake
Thiazide-induced hypocalciuria 
Citrate to alkalinise urine
202
Q

Ix for recurrent renal stones

A

Serum: Cr, bicarb, Ca, phosphate, urate, PTH
Stone analysis
Spot urine: pH, MCS, amino acids, albumin
24 hr urine: volumte (>2.5l), Ca, oxalate, urate, citrate

203
Q

Best measure of kidney function

A

Glomerular filtration rate
= 120ml/hr
= age-related decline approx. 1ml/hr/yr

204
Q

What does the presence of proteinuria on dipstick suggest?

A

Abnormal excretion of protein (usually albumin) due to leaky glomeruli or inability of tubules to reabsorb protein

205
Q

What are the key differences between AKI and CKD?

A

AKI

  • abrupt decline in GFR
  • potentially reversible
  • treatment targeted to precise diagnosis and reversal of disease

CKD

  • longstanding decline in GFR
  • irreversible
  • treatment targeted to prevention of complications of CKD and limitation of progression
206
Q

What do we measure to assess severity of an AKI?

A

Serum creatinine

Urine output

207
Q

What makes a good marker for GFR?

A

Clearance of marker = GFR if:

  • not bound to serum proteins
  • freely filtered by glomerulus
  • not secreted/reabsorbed by tubular cells
208
Q

What GFR marker do we use in clinical practice?

A

Creatinine

  • endogenous marker
  • higher in muscular individuals as by-product of muscle turnover
  • important to know baseline to FOLLOW TREND
209
Q

Define AKI

A
  1. Rise in serum Cr over 26 within 48 hours
  2. 50% or greater rise in serum Cr known or presumed to have occurred within the past 7 days
  3. Fall in urine output to less than 0.5ml/kg/hour for more than 6 hours
210
Q

Indications for emergency dialysis

A

A E I O U

  1. Acidosis
  2. Electrolyte disturbance (refractory hyperkalaemia)
  3. Intoxication (lithium, aspirin)
  4. Overload (pulmonary oedema)
  5. Uraemic encephalopathy
211
Q

CKD Staging

A

Stage 1
- kidney damage with normal GFR (90+)

Stage 2
- Mild GFR (60-89)

Stage 3
- Moderate GFR (30-59)

Stage 4
- Severe GFR (15-29)

Stage 5
- End-stage kidney failure (< 15/dialysis)

212
Q

Common causes of CKD

A 
Diabetes
Atherosclerotic renal disease
Hypertension
Chronic glomerulonephritis
Infective or obstructive uropathy
Polycystic kidney disease
213
Q

Complications of CDK

A

Failing homeostatic function
- acidosis, hyperkalaemia

Failing hormonal function
- anaemia (no EPO), renal bone disease (low vit D)

CVD
- vascular calcification, uraemic cardiomyopathy

Uraemia and death

214
Q

How is haemodialysis done?

A

Tunneled central line (Tessio line)
OR
Arteriovenous fistula

215
Q

How is peritoneal dialysis done?

A

Via a Tenckoff catherer where peritoneum used as dialysis membrane

216
Q

Aldosterone action

A

Sodium IN

Potassium OUT

217
Q

What do the following hypothalamic hormones trigger production of in the pituitary?

a) GHRH
b) GnRH
c) TRH
d) Dopamine
e) CRH

A

a) GH
b) LH/FSH
c) TSH, prolactin
d) Prolactin
e) ACTH
* remember this is hypothalamo-pituitary axis

218
Q

Contraindications of combined pituitary function test

A

Ischaemic heart disease

Epilepsy

Untreated hypothyroidism (impairs GH and cortisol response)

219
Q

Side effects of combined pituitary function test

A

Adrenergic effects of hypoglycaemia
- sweating, palpitations, LOC. convulsions (RARE)

Metallic taste in mouth, flushing and nausea

220
Q

What is in combined pituitary function test?

A

LHRH (GnRH), TRH and insulin

221
Q

Pituitary tumour classifications

A

Microadenoma < 10mm (usually benign)

Macroadenoma > 10mm (aggressive bb)

Non-functioning adenoma (crushes stalk…)

222
Q

What visual changes may you see with a pituitary adenoma?

A

Bitemporal hemianopia due to optic chiasm compression

223
Q

Macroprolactinaemia

A

> 5000 miu/l prolactin lol

224
Q

Mx of prolactinoma

A

1st line:
Replacement
- hydrocortisone, T4, oestrogen, GH
- DA antagonists (cabergoline, bromocriptine)

2nd line:
Transphenoidal excision

225
Q

Mx of non-functioning pituitary adenoma

A

Cabergoline/bromocriptine

  • watch and wait if asx
  • if no sx just leave it alone bb
226
Q

Diagnosis of acromegaly

A

OGTT (gold standard)
IGF-1

Signs: high glucose, Ca, phosphate

227
Q

Mx of acromegaly

A
  1. Transphenoidal surgery
  2. Pituitary radiotherapy if surgery fails
  3. Cabergoline
  4. Octreotide - somatostatin analogue (expensive bad boi and cannot stop once started)
  5. GH antagonist - pegvisomant
228
Q

High TSH
Low T4

Diagnosis?

A

Hypothyroidism

  • atrophic
  • Hashimoto’s
  • subacute (De Quervain’s)
  • postparum
  • Riedal thyroiditis
229
Q

High TSH
Normal T4

Diagnosis?

A

Treated hypothyroidism or subclinical hypothyroidism

  • look out for associated hypercholesterolaemia seen in hypothyroid pts
230
Q

High TSH
High T4

Diagnosis?

A

TSH secreting tumour

Thyroid hormone resistance

231
Q

Low TSH
High T4/3

Diagnosis?

A

Hyperthyroidism

  • Grave’s
  • toxic multinodular goitre (Plummer’s)
  • toxic adenoma
  • drugs (thyroxine, amiodarone)
  • ectopic (trophoblastic tumour, struma ovarii)
232
Q

Low TSH
Normal T4/3

Diagnosis?

A

Subclinical hyperthyroidism

- may progress to 1o hypothyroidism if pt is anti-TPO antibody +ve

233
Q

Low TSH
Low T4

Diagnosis?

A

Secondary hypothyroidism

- hypothalamic/pituitary disorder

234
Q

High TSH followed by low TSH
Low T3/4

Diagnosis?

A

Sick euthyroidism with any severe illness

- body shuts down metabolism as thyroid gland reduced output

235
Q

Normal TSH
Abnormal T4

Diagnosis?

A

?Assay interference

Changes in TBG

Amiodarone

236
Q

Hyperthyroid tx

A

Sx relief

  • beta blockers
  • topical steroids for dermopathy
  • eye drops in Graves

Medical
- carbimazole (agranulocytosis risk, rashes common)

Radio-iodine

  • risk of permanent hypothyroidism
  • CI in pregnancy and lactating women

Surgical
- hemi/total thyroidectomy

237
Q

Indications for surgical thyroidectomy

A

Women intending to become pregnant in next 6/12
Local compression 2o to thyroid goitre (oesophageal/tracheal)
Cosmetic
Suspected cancer
Co-existing hyperparathyroidism
Refractory to medical tx

238
Q

Thyroid storm tx

A 
HDU/ITU support
Cooling required
High dose anty-thyroid medication
Corticosteroids
Circulatory and respiratory support
239
Q

How could a pt present in thyroid storm?

A

Shock
Pyrexia
Confusion
Vomiting

240
Q

anti-TSH receptor abs

Which thyroid problem?

A

Graves disease

- hyper, high uptake on isotope (Tc99)

241
Q

anti-TPO/TG abs

Which thyroid problem?

A

Hashimotos thyroiditis

242
Q

Hurthle cells

What’s wrong with thyroid?

A

Hashimotos thyroiditis

243
Q

Higher risk of thyroid neoplasm

A 
Solitary
Solid
Young
Male
Cold nodules
244
Q

Psammoma bodies and empty-appearing nuclei with central clearing

Which thyroid neoplasia?

A

Papillary

  • women
  • associated with irradiation
  • good prognosis

empty nuclei = Orphan Annie eyes

245
Q

What do follicular thyroid neoplasias spread to first?

A

Blood&raquo_space; lungs, bone, liver, breast, adrenals

246
Q

Parafollicular C cells secreting calcitonin

Which thyroid neoplasia?

A

Medullary

- sporadic 80%, MEN2 20% cases

247
Q

What should you screen for with medullary thyroid neoplasia?

A

Phaeochromocytoma

- MEN2 mutation

248
Q

What is MALToma associated with?

A

Chronic Hashimoto’s

249
Q

Undifferentiated follicular, large pleomorphic giant cells with spindle cells

Which thyroid neoplasia?

A

Anaplastic

  • elderly
  • die within a year :(
250
Q

MEN1 disorders

A

Pituitary
Pancreatic (insulinoma)
Parathyroid (hyper)
*3Ps

251
Q

MEN2a disorders

A

Parathyroid
Phaeochromocytoma
Medullary thyroid
*2Ps, 1M

252
Q

MEN2b disorders

A

Phaeochromocytoma
Medullary thyroid
Mucocutaneous neuromas (& marfanoid)
*1P, 2Ms

253
Q 
High K+
Low Na+
Low glucose
90/50 BP upon standing
Skin pigmentation noted in mouth

What ix would confirm diagnosis?

A

SynACTHen test

- Addison’s

254
Q 
High K+
Low Na+
Low glucose
90/50 BP upon standing
Skin pigmentation noted in mouth

What tx needed?

A

Hydrocortisone and fludrocortisone if primary adrenal lesion present
- Addison’s

255
Q

Ix for Cushing’s

A

Overnight dexamethasone suppression test
OR
24hr urinary free cortisol

Ideal now is inferior pituitary petrosal sinus sampling however not always available

256
Q

ACTH dependent Cushing’s

A 
Pituitary tumour (Cushing's disease x)
Ectopic ACTH-producing tumour (small cell Ca, carcinoid tumour)
257
Q

ACTH independent Cushing’s

A

Adrenal adenoma/cancer
Adrenal nodular hyperplasia
Iatrogenic steroid use lol

258
Q

Low K+
High Na+
156/100 BP not responding to tx

What ix would confirm diagnosis?

A

Aldosterone:renin ratio

- RAISED in Conn’s

259
Q

Low K+
High Na+
156/100 BP not responding to tx

What tx needed?

A

Aldosterone antagonists/K+ sparing diuretics for Conn’s

  • spironolactone
  • eplerenone
  • amiloride
260
Q

Phaeo tx

A
  1. Alpha blockade
  2. Beta blockade
  3. Surgery when BP well controlled
261
Q

Phaeo ix

A

Plasma and 24h urinary metadrenaline measurement/catecholamines & VMA (metabolite of adrenaline)

262
Q

Phenytoin toxicity

A

Ataxia

Nystagmus

263
Q

Digoxin toxicity

A

Arrhythmias
Heart block
Confusion
Xanthopsia

264
Q

Lithium toxicity

A 
Tremor (early)
Lethargy
Fits
Arrhythmia
Renal failure
265
Q

Aminoglycosides toxicity

A

Tinnitus
Deafness
Nystagmus
Renal failure

266
Q

Theophylline and aminophylline toxicity

A

Arrhythmias
Convulsions
Anxiety
Tremor

267
Q

Which enzymes are raised in acute pancreatitis?

A

Amylase (>10x upper limit normal)

Lipase (>3 upper reference)

268
Q

Pathological raised levels of CK

A

Duchenne Muscular Dystrophy
Myocardial infarction
Rhabdomyolysis
Statin related myopathy

269
Q

How do we differentiate ALP raised due to bone of liver problems?

A

We can differentiate liver from bone ALP either by seeing if there is a rise in gamma-GT (liver ALP
rises with this), by performing electrophoresis, or by ordering a bone-specific assay of ALP

270
Q

Physiological causes of raised ALP

A

Pregnancy (3rd trimester)

Childhood (during growth spurt)

271
Q

Pathological causes of raised ALP

A

> 5x ULN

  • Bone = Paget’s, osteomalacia
  • Liver = cholestasis, cirrhosis

<5x ULN

  • Bone = tumours, fractures, osteomyelitis
  • Liver = infiltrative disease, hepatitis
272
Q

When is BNP released?

A

In response to ventricular stretch

Highly sensitive for heart failure when levels > 400

Highly specific for excluding HF when levels < 100

273
Q

What is troponin?

A

Myocardial injury biomarker

NOT an enzyme b

274
Q

When is troponin measured for MI?

A

Measure at 6 hours then 12 hours post onset of pain

Remains elevated for 3-10 days

275
Q

When is troponin raised?

A 
Coronary spasm
Coronary dissection
PCI
Myocarditis
PE
HF
Cardiomyopathies
Sepsis
Cardiac surgery 
Chest trauma
Defibrillation
276
Q

Types of lipoprotein metabolism disorders

A

Primary hypercholesteraemia

Primary hypertriglyceridaemia

Primary mixed hyperlipidaemia

Hypolipidaemia

277
Q

How do statins work?

A

HMG-CoA reductase inhibitor

  • reduces intrinsic synthesis of cholesterol in lover
  • SE: myopathy, rhabdomyolysis, fatigue
278
Q

Lipoproteins in order of density

A

Chylomicron < FFA < VLDL < IDL < LDL < HDL

279
Q

What does Guthrie blood spot test for at 6 days of age?

A

Phenylketonuria, congenital hypothyroidism, cystic fibrosis, sickle cell disease, MCAD (medium
chain acylCoA dehydrogenase) deficiency

*The newborn screening programme measures chemicals in the blood spot, it doesn’t
involve any genetics. An abnormal chemical level doesn’t always mean that there is a
genetic disorder!

280
Q

What does specificity mean?

A

Probability that someone without the disease will correctly test negative
o TN/(FP+TN)
o 85 people without CF in total, and 80 actually test negative. Specificity is 80/85=94%

281
Q

What does sensitivity mean?

A

Probability that someone with the disease will correctly test positive
o TP/(TP+FN)
o 100 people with CF in total, and 90 actually test positive. Sensitivity is 90/100=90%

282
Q

What does positive predictive value mean?

A

Probability that someone who tests positive actually has the disease
o TP/(TP+FP)
o 95 people tested positive, of which 90 had the disease. PPV=90/95=95%

283
Q

What does negative predictive value mean?

A

Probability that someone who tests negative actually doesn’t have the disease
o TN/(TN+FN)
o 90 people tested negative, of which 80 didn’t have the disease, NPV=80/90=89%

284
Q

Metabolic conditions that result in accumulation of toxins

A

Organic acidaemias
- propionic acideamia

Urea cycle disorders

Aminoacidopathies

  • PKU
  • Maple syrup urine disease
285
Q

Metabolic conditions that result in reduced energy stores

A

Glycogen storage disorders
- Von Gierke;s

Galactossaemia

Fatty acid oxidation disorders
- MCADD

286
Q

Metabolic conditions that result in large molecule synthethesis

A

Peroxisomal disorders

Glycosylation disorders

287
Q

Metabolic conditions that result in defects in large molecule metabolism

A

Lysosomal disorders

- Tay Sachs disease

288
Q

Metabolic conditions that affect the mitochondria

A

MELAS
Kearn’s
Sayre
POEMS

289
Q

Diabetes mellitus type 2 diagnosis

A

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

290
Q

IGTT > 7.8 but < 11.1

Diagnosis?

A

Impaired glucose tolerance

291
Q

Fasting glucose > 6.1 but < 7.0

Diagnosis?

A

Impaired fasting glucose

292
Q

DKA criteria

A

pH < 7.3, Plasma Glucose >11mM, Blood Ketones>3mM (2+ in urine).
Rapid onset
Medical emergency

293
Q

DKA presentation

A

Symptoms: confusion, Kussmaul breathing, abdominal pain, nausea, vomiting

Precipitants include infection, surgery, missed insulin doses, trauma

294
Q

DKA mx

A

A-E, senior help

Fluid = 0.9% saline

Insulin = AFTER fluids, ensure K+ fine, 0.1u/kg/h fixed rate

Early senior review +/- ITU involvement

Monitor glucose and K+ hourly

Catheter to monitor UO

295
Q

HHS criteria

A

pH > 7.3, Osmolarity > 320mOsm, Blood Glucose > 30mM

HHS develops over few days

Patients present acutely unwell with confusion and clinical dehydration

296
Q

HHS mx

A

A-E

Fluids = 0.9% saline over 1hr

IV insulin = only if > 1 mmol/L ketones, 0.05u/kg/hr fixed rate

Monitor = serial U&Es, glucose reading

297
Q

When is DKA resolved?

A

When ketones < 0.6 and pH > 7.3

298
Q

Causes of a raised anion gap metabolic acidosis

A

G: Glycols (ethylene glycol and propylene glycol) [overdose]
O: Oxoproline [chronic paracetamol use, usually malnourished women]
L: L-lactate [sepsis]
D: D-lactate [short bowel syndrome]
M: Methanol [overdose]
A: Aspirin [overdose. Initially causes respiratory alkalosis but in moderate/severe overdose causes metabolic acidosis]
R: Renal failure
K: Ketoacidosis [DKA, alcoholic, starvation

299
Q

Causes of a normal anion gap metabolic acidosis

A

Addison’s disease
Bicarbonate loss (diarrhoea, laxative abuse, Renal Tubular Acidosis)
Chloride gain (Sodium Chloride 0.9% infusion)
Drugs (acetazolamide)

300
Q

An unexplained metabolic acidosis (usually in the context of overdose) with a raised anion and raised osmolar gap could be caused by?

A

Glycol, ethanol, mannitol or methanol poisoning

Year 5 Pathology (6 decks)

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