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Year 5: Pathology > Chem > Flashcards

Chem Flashcards

1
Q

SUMMARY CARD:

All relevant equations in Chem Path:
1. Osmolarity
2. Osmolar gap
3. Anion gap

A
  1. Osmolarity = 2(Na + K) + urea + glucose
  2. Osmolar gap = osmolality (measured) - osmolarity (calculated) (if < 10, then normal)
  3. Anion gap = (Na + K) - (Cl + HCO3) (normal range = 14-18)
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2
Q

SUMMARY CARD:

  • Where is fluid found in the body?
  • What is osmolality vs osmolarity?
  • BONUS: which ion is the largest contributor to osmolality?
A
  • 60-40-20 rule = 60% of total body weight is water (40% is intracellular, 20% extra cellular)
  • Osmolality = total number of particles in a solution measured with an osmometer; units are mmol/kg (AKA the mass of a solvent); normal range for serum osmolality is 275-279 mmol/kg
  • OsmolaRity = the volume in litRes of the solvement; units are mOsm/L

Omolality is more accurate, but osmolarity is easier to calculate!

NOTE: osmolality is more accurate because it uses mass of the solvent, which always stay the same, whereas volume expands with increasing temperatures

  • BONUS: Na+ is the biggest contributor to plasma osmolality
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3
Q

SUMMARY CARD:

Fluid balance equations:
1. Osmolarity equation
2. Osmolar gap equation
3. What does it mean to have a raised osmolar gap?

A
  1. Osmolarity = 2(Na + K) + urea + glucose
  2. Osmolality - osmolarity = < 10 (NORMAL)

If the osmolar gap is > 10, then there are other unmeasured ions in the sample –> SKALP:

  • Sugar: mannitol, sorbitol
  • Ketones
  • Alcohol: methanol, ethanol
  • Lipids (↑ triglycerides) / Lactate
  • Proteins: ↑ gammaglobulinaemia
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4
Q

SUMMARY CARD:

  • What is the normal range for plasma [Na+]?
  • How is Na+ regulated?
A

135-145 mmol/L

TWO ways to regulate Na+:

1. Blood volume: ↑ blood volume = atrial stretch = ANP (atrial natriuretic peptide) release = ↓ aldosterone release + ADH + renin = ↓ [Na+] in blood

2. Blood osmolality: ↑ blood osmolality = ↑ thirst + ADH release = ↓ [Na+] in blood

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5
Q

SUMMARY CARD:

  • What is mild vs severe hyponatraemia?
  • What are the Sx of hyponatraemia?
  • How do you define true vs pseudohyponatraemia and what are possible causes of each?
A
  • Mild hyponatraemia = 130-135 mmol/L; severe = < 125 mmol/L
  • Sx = N&V, confusion, muscle weakness/cramps, seizures, coma
  • Mx with IV 0.9% NaCl ONLY if symptomatic (or v. severe) hyponatraemia

Use OSMOLALITY to determine true vs pseudohyponatraemia

If LOW plasma osmolality, then TRUE hyponatraemia:

  • Assess volume status w/ clinical exam (e.g. BP, HR, oedema, cap refill) AND check urinary Na+ for cause
  • Hypovolaemic + urinary Na+ < 20 mmol/L = extra-renal causes e.g. D&V, burns, TURP syndrome (hypotonic irrigation absorbed through damaged prostate)
  • Hypovolaemic + urinary Na+ > 20 mmol/L = renal loss e.g. AKI/CKD, diuretics, Addison’s (can also be eu)
  • Euvolaemic = psychogenic polydipsia, SIADH, Addison’s (can also be hypo)
  • Hypervolaemic + urinary Na+ < 20 mmol/L = extra-renal e.g. HF, cirrhosis, nephrotic syndrome
  • Hypervolaemic + urinary Na+ > 20 mmol/L = renal failure

If NORMAL or HIGH plasma osmolality, then PSEUDO hyponatraemia:

  • May be caused by the sample coming from an arm with a drip in it OR due to other unmeasured ions e.g. mannitol, glucose (HHS) OR post-surgery (e.g. over hydration w/ IV fluids, or ↑ ADH release due to stress of the surgery)
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6
Q

SUMMARY CARD:

What are the steps to assessing the cause of hyponatraemia?

A
  • Step 1: assess plasma osmolality (true vs pseudo)
  • Step 2: assess volume status
  • Step 3: measure urinary sodium (extra-renal vs renal causes)
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7
Q

SUMMARY CARD:

What is the management for each of these?

A
  • If HYPOvoloaemic hyponatraemia: regardless of renal or extra-renal cause, Mx with IV 0.9% NaCl if symptomatic (or v. severe) hyponatraemia

If EUVOlaemic hyponatraemia:

  • Psychogenic polydipsia: if acute + symptomatic hyponatraemia = IV 0.9% saline; if chronic = fluid restriction + CBT (can consider furosemide)
  • Chronic hypothyroidism = levothyroxine
  • Addison’s (AKA adrenal insufficiency) = Hydrocortisone (glucocorticoid) +/- fludrocortisone (mineralocorticoid)
  • SIADH = demecocycline (check renal function first as it can cause NDI) OR tolvaptan
  • If HYPERvolaemic hyponatraemia: fluid restrict +/- diuresis (unless due to cirrhosis, then requires specialist input)
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8
Q

SUMMARY CARD:

For SIADH, what is / are the:

  1. Diagnostic criteria?
  2. Causes?
  3. Mx?
A

1. Diagnostic criteria = diagnosis of exclusion so NO adrenal/ thyroid / renal dysfunction, AND:

TRUE hyponatraemia (< 135) + LOW plasma osmolality + HIGH urine sodium (>20) + HIGH urine osmolality (>100)

SIADH = syndrome of inappropriate ADH secretion (not in response to a stimulus), which results in less water excreted in the urine

Ix require normal 9am cortisol, short synATCHen test and TFTs (as this is a diagnosis of exclusion)

2. Causes = Lung, Brain, Drugs:

  • Malignancy (ectopic ADH secretion): SCLC, pancreas, prostate, lymphoma
  • CNS disorders: infection, haemorrhage
  • Lungs: TB, pneumonia
  • Drugs: opiates, SSRIs, TCAs, carbamazepine, PPIs

3. Mx = acute vs chronic:

  • Acute: fluid restriction, if severe IV hypertonic saline +/- furosemide
  • Chronic: fluid restrict to 1L per day, demecocycline (check renal function first as it can cause NDI) or tolvaptan
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9
Q

SUMMARY CARD:

Why does cirrhosis cause hypervolaemic hyponatraemia?

BONUS: why does HF cause hypervolaemic hyponatraemia?

Due

A

Due to poor breakdown of vasodilators e.g. nitric oxide in the liver = ↓ BP = subsequent ↑ ADH release = ↑ water retention

BONUS: similar reason to cirrhosis –> ↓ cardiac output = subsequent ↑ ADH release = ↑ water retention

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10
Q

SUMMARY CARD:

What happens if Na+ is corrected too quickly (+Sx)?

What is the ideal rate of Na+ correction?

A

Central pontine myelinolysis

RF = malnourished alcoholic

  • Pseudobulbar palsy = indistinct speech, drooling, dysphagia, spastic tongue, brisk jaw jerk, dysarthria
  • Paraperesis = partial inability to move
  • Locked-in syndrome = body paralysis but consciousness and ability to move eyes are preserved

Ideally: do NOT increase Na+ by more than 8-10 mmol/L per 24hrs

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11
Q

DISEASE:

A patient is getting IV NaCl rehydration in their R arm following a night of binge drinking
They are currently asymptomatic

Their blood test shows Na+ of 123 mmol/L but high osmolality

Identify a possible cause of this result?

hint: nurse took blood from R arm

A

Low Na+ and ↑ osmolality = PSEUDOhyponatraemia

Sample was taken from drip arm –> caused dilution of the Na+

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12
Q

DISEASE:

28F - abdo pain + confusion + kussmaul breathing
PMH = T1DM
Ix = incidental hyponatraemia finding

What is a possible cause of this?

A

Pt is presenting w/ DKA = ↑ ketones –> lowers water potential of blood = high osmolality, therefore it appears they have hyponatraemia (AKA pseudohyponatraemia)

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13
Q

DISEASE:

Post-surgical pt complains of N&V + cramping in his legs
He was given IV fluids during his surgery
Ix = Na+ of 122 mmol/L

Identify a possible cause of this result?
(BONUS: Mx?)

A

(Hypervolaemic) hyponatraemia (AKA pseudohypoatraemia) can occur post surgery due to overhydration with IV fluid during the surgery

As the pt is symptomatic with severe hyponatraemia (< 125), Mx = IV 3% NaCl (hypertonic) + furosemide

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14
Q

DISEASE:

35M = extensive burns following a workplace accident
He complains of weakness and confusion

Ix = hyponatremia w/ Na+ 125 mmol/L

What type of hyponatraemia is this?
(Bonus: Mx for ↓Na+?)

A

Hypovolaemic hyponatraemia due to fluid loss via burns

Mx = fluid replacement w/ IV NaCl

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15
Q

DISEASE:

65M - underwent transurethral resection of the prostate for BPH

Post-op, he develops hyponatremia (Na+ 128 mmol/L)

What is this syndrome called and why does it occur?

A

TURP (transurethral resection of the prostate) syndrome

Fluids absorbed during irrigation in TURP through damaged prostate = hyponatraemia

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16
Q

DISEASE:

26F - 5kg weight loss, muscle weakness, hyperpigmented palms of hands
Does not appear clinically dehydrated

U&Es = ↓Na+, ↑K+

  1. Diagnosis?
  2. Ix?
  3. Mx?
  4. BONUS: how is an addisonian crisis managed?
A
  1. Addison's disease (AKA adrenal insufficiency) –> causes hypo/eu volaemic hyponatraemia due to lack of aldosterone release
  2. Ix:
  • 9AM cortisol = low
  • Short synACTHen test –> serum cortisol fails to double at 30 mins indicates adrenal failure (normal = sufficient increase in cortisol)
  1. Long-term Mx = replacement of glucocorticoids with hydrocortisone (3x/day) and mineralocorticoids with fludrocortisone

BONUS:

  • Addisonian crisis = hypotensive shock, usually precipitated by infection / surgery
  • MEDICAL EMERGENCY –> Mx = rapid IV fluid rehydration w/ 1l 0.9% normal saline over 1 hour + 50 mL of 5% dextrose to correct hypoglycaemia + IV/IM 200 mg hydrocortisone bolus + Tx of underlying cause
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17
Q

DISEASE:

60M - ascites + lower limb oedema
PMH - alcohol misuse

Bloods: ↑elevated liver enzymes, ↓Na+

What is this type of hyponatraemia?
BONUS: what is the cause?

A

Hypervolaemic hyponatraemia due to cirrhosis / liver failure

Liver fails to break down vasodilators e.g. NO = ↓BP = ↑ ADH release = hypervolaemic hyponatraemia

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18
Q

DISEASE:

55M - severe D&V following street food/takeaway –> given IV NaCl
Now: quadriparesis, indistinct speech, dysphagia
PMH: poor diet + alcohol misuse

What is the diagnosis?
What are the RFs?

A

Central pontine myelinolysis due to rapid correction of Na+

Sx = pseudobulbar palsy (indistinct speech, dysphagia), paresis, etc.

RFs = malnourished alcoholics

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19
Q

DISEASE:

70F - brought in by LAS from carehome following 2 hours of muscle weakness and confusion
No FLAWS

Ix = Na+ 126 mmol/L and plasma osmolality < 100

What is the diagnosis?
BONUS: Mx?

HINT: euvolaemic hyponatraemia

A

Psychogenic polydipsia = euvolaemic hyponatraemia

RFs = carehome, elderly pt

Acute Mx = IV 0.9% saline as pt is symptomatic
Chronic MX = fluid restriction

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20
Q

DISEASE:

57M - cough + crackles in R lung bases
Tachycardic, temp 38.8°C

Ix = low Na+, normal urea

What is the cause of the low Na+?

A

SIADH - can be caused by pneumonia

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21
Q

SUMMARY CARD:

  • What is mild vs clinically significant hypernatraemia?
  • What are the Sx of hypernatraemia?
A
  • Hypernatraemia is Na+ >145 mmol/L; it is clinically significant if Na+ > 148 mmol/L
  • Sx = thirst, confusion, irritability, ataxia + seizures, coma
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22
Q

SUMMARY CARD:

What are the steps to identifying the cause of hypernatraemia?

A

Assess volume status, then assess urinary Na+

  1. HYPOvolaemic hypernatraemia + LOW urinary Na+: GI losses (D&V if water>electrolytes lost), skin losses (sweating, burns)
  2. HYPOvolaemic hypernatraemia + HIGH urinary Na+: loop diuretics, osmotic diuresis (e.g. uncontrolled DM, glucose, mannitol following initial hyponatraemia), DI
  3. EUVOlaemic hypernatraemia: tachypnoea, skin (sweating, fever), DI
  4. HYPERvolaemic hypernatraemia: Conn’s syndrome, inappropriate hypertonic saline
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23
Q

SUMMARY CARD:

  • What are the TWO types of DI (+ Sx)?
  • Ix?
  • Mx?
A

Nephrogenic vs Cranial diabetes insipidus

Sx = lethargy, thirst, irritability, confusion, coma, fits –> due to ↑Na+
Clinically EUVOLAEMIC, but DILUTE urine

CDI = lack of/ no ADH production

  • Causes = surgery, trauma, craniopharyngioma, autoimmune hypophysitis (from CTLA-4 ipilimumab)
  • Mx = desmopressin

NDI = receptor defect leads to insensitivity to ADH

  • Causes = drugs (e.g. lithium, demecocycline)
  • Mx = thiazide diuretics

Ix:

  • Check electrolytes to rule out other causes
  • Plasma (normal / high) + urine osmolality (LOW)

8-hour water deprivation test:
* If urine to plasma (U:P) osmolality ratio > 2, then it’s normal (normal concentration ability)
* If urine osmolality increases after administration of desmopressin –> CDI
* If urine osmolality does not change after administration of desmopressin –> NDI

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24
Q

SUMMARY CARD:

What is the general management of hypernatraemia?

A
  1. Drink more water
  2. SLOW IV fluids as usually hypovolaemic cause (can use saline, dextrose or Hartmann’s)
  3. Try IV dextrose if no improvement (1L/ 6hrs)

MEASURE urine output + plasma Na+ to guide Mx

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25
Q

DISEASE:

45F - severe D&V following BBQ
Ix = Na+ 150 mmol/L, low urinary Na+

What is the type of hypernatraemia?
BONUS: Mx?

A

Hypovolaemic hypernatraemia due to water>electrolyte losses in D&V

Mx = encourage oral fluid intake (if not possible, slow IV fluids)

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26
Q

DISEASE:

60M - irritable + thirsty
PMH cirrhosis (on furosemide)
Ix = ↑Na+, ↑ urinary Na+

What type of hypernatraemia is this?

A

Hypovolaemic hypernatraemia due to loop diuretic use

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27
Q

DISEASE:

40F - polyuria + polydipsia
no signs of dehydration or fluid overload

Ix = ↑Na+, low urinary Na+

water deprivation test shows U:P < 2

What to administer next + what the different results mean (+Mx)?

A

Administer desmopressin

CDI = responsive, concentrates urine –> Mx = desmopressin

NDI = unresponsive, urine conc remains the same –> Mx = thiazide diuretic e.g. indapamide, bendroflumethiazide

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28
Q

DISEASE:

56M - confusion, irritability
PMH - poorly controlled hypertension despite trialing several different Tx
U&Es: ↑Na+, ↓ K+
Urinalysis: ↑K+

  • What is the diagnosis?
  • Ix?
  • Mx?
A
  • Conn's syndrome = primary hyperaldosteronism (most commonly caused by adrenal hyperplasia)
  • Ix = aldosterone:renin ratio (HIGH)
  • Mx = spironolactone (potassium-sparing diuretic - aldosterone antagonist)
  • Long-term Mx = laparoscopic adrenalectomy (if malignant or unresponsive to medical therapy)
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29
Q

SUMMARY CARD:

  • What is the normal range for [K+]?
  • Where is K+ normally found?
A

3.5-5.0 mmol/L

It is mostly only an intracellular cation (only 2% found extracellularly)

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30
Q

SUMMARY CARD:

  • What is mild vs severe hypokalaemia and their Mx?
  • Sx of hypokalaemia (+ findings on ECG)?
A

Hypokalaemia, < 3.5mmol/L, is caused by either a depletion of K+ or due to a shift of K+ into cells

Moderate hypokalaemia = 3.0-3.5 mmol/L –> Mx is oral KCl (2 SandoK tablets TDS for 48hrs) then recheck serum K+

Severe hypokalaemia = < 3.0mmol/L (↑ risk of cardiac arrest) –> Mx = IV KCl (max rate of 10 mmol/hr or else ↑ risk of arrhythmia)

Clinical features (everything is SLOW): hypotonia, hyporeflexia, paralytic ileus, muscle weakness, cardiac arrhythmias

On ECG: flat/inverted t-waves, prominent u-waves, prolonged PR interval + ST depression

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31
Q

SUMMARY CARD

What are some causes for hypokalaemia?

A

Hypokalaemia causes that result in ALKALOSIS:

  • GI loss: D&V
  • Renal loss: hyperaldosteronism (suspect if ↑BP, ↑Na+, ↓K+), loop & thiazide diuretics

NOTE: loop diuretics block Na+/K+/Cl- transporter = reduced reabsorption of all 3
NOTE: Normally, in the CD, Na+ reabsorption is exchanges for K+ excretion –> thiazide diuretics block Na+ reabsorption earlier in the nephron so more Na+ reaches the CD, so more Na+ is reabsorbed as more K+ is excreted out

  • Redistribution into cells e.g. insulin, salbubtamol, refeeding syndrome
  • Mg2+ deficiency (because Mg2+ deficiency can cause ↑K+ wasting) –> Mx = Mg2+ replacement alongside KCl

Hypokalaemia causes that result in ACIDOSIS:

  • Renal tubular acidosis types 1 & 2
  • Type 1 = most severe; distal failure of H+ excretion and subsequent acidosis + ↓K+ (failed H+/K+ pump)
  • Type 2 = milder, proximal failure to reabsorb bicarbonate –> leads to acidosis + ↓K+
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32
Q

SUMMARY CARD:

  • What is hyperkalaemia?
  • What are some Sx of hyperkalaemia (+ ECG changes)?
  • Mx?
A
  • [K+] > 5.0 mmol/L, either caused by reduced excretion or release of intracellular K+
  • Sx = weakness, paralysis, paraesthesia
  • ECG changes: small / loss of p waves, tall tented T waves, widened QRS complex

Initiate Mx if: K+ >5.5 w/ ECG changes OR K+ > 6.5 regardless of ECG changes

  • 10mls 10% calcium gluconate over 10 minutes – cardioprotective (it doesn’t do anything to the K+)
  • IV insulin w/ dextrose
  • Nebulised salbutamol as an adjunct
  • Consider calcium resonium (K+ binders - binds to K+ in the gut) 15g PO or 30g PR
  • NOTE: cardiac monitoring for those on Digoxin as IV calcium can precipitate arrhythmias

NOTE: if K+ sample > 7 mmol/L and asymptomatic –> redo sample (may be raised due to haemolysis in the sample)

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33
Q

SUMMARY CARD:

What are some causes of hyperkalaemia?

A

Hyperkalaemia can be caused by excessive intake, release of intracellular K+, OR decreased excretion

Excessive intake:

  • Oral / parenteral
  • Blood transfusion

Transcellular movement ICF>ECF:

  • Acidosis (due to H+/K+ cotransporter)
  • Insulin shortage (i.e. DKA)
  • Tissue damage e.g. rhabdomyolysis

Decreased excretion:

  • Acute renal failure
  • Drugs e.g. spironolactone (K+ sparing diuretic, NSAIDs, ACEi, ARBs
  • Addison's disease (↓Na+, ↑K+)
  • Type 4 renal tubular acidosis (aldosterone deficiency or resistance leads to ↓Na+, ↑K+)

OR may be due to artefact e.g. haemolysis of the sample

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34
Q

DISEASE:

60M - muscle weakness, hypotonia, hyporeflexia
ECG: flat t-waves + u-waves, PR prolongation
U&Es: K+ 3.2 mmol/L

PMH: recently started indapimide

  • Cause of this electrolyte abnormality?
  • Mx?
A

hypokalaemia due to thiazide diuretic (i.e. indapimide)

If K+ 3.0-3.5 mmol/L, Mx = oral KCl (2 SandoK tablets TDS for 48hrs) then recheck serum K+

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35
Q

DISEASE:

70F - muscle weakness
PMH: HF
currently on furosemide, dose recently increased

  • What is the most likely electrolyte abnormality?
  • Assuming it caused a severe electrolyte abnormality, what is the Mx?
A

Hypokalaemia due to loop diuretic

If severe hypokalaemia (< 3.0mmol/L) –> ↑ risk of cardiac arrest, therefore Mx = IV KCl (max rate of 10 mmol/hr or else ↑ risk of arrhythmia)

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36
Q

DISEASE:

55M - muscle weakness + tingling
PMH: alcohol misuse and poor diet presents
K+ 3.2 mmol/L

What other electrolyte abnormality should be screened for?

A

Check for Mg2+ deficiency

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37
Q

DISEASE:

What is the difference in [K+] between type 1+2 RTA and Type 4 RTA?

A

Type 1 (failure of H+ excretion) + 2 (failure of bicarb reabsorption) = acidosis & hypokalaemia

Type 4 = hyperkalaemia (due to aldosterone deficiency / resistance)

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38
Q

DISEASE:

72M - found after a fall
complaints of severe muscle pain + dark urine

Ix = K+ 6.6 mmol/L, elevated Cr

  • Cause of hyperkalaemia?
  • Mx?
A

Rhabdomyolysis –> long lie = breakdown of muscle tissue = release of intracellular K+

Mx for [K+] >6.5 mmol/L:
* 10mls 10% calcium gluconate over 10 minutes – cardioprotective (it doesn’t do anything to the K+)
* IV insulin w/ dextrose
* Nebulised salbutamol as an adjunct
* Consider calcium resonium (K+ binders - binds to K+ in the gut) 15g PO or 30g PR

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39
Q

DISEASE:

65F - muscle weakness + tingling, nausea
PMH: HF –> treated with spironolactone
Ix = 5.7 mmol/L

  • Reason for hyperkalaemia?
  • Important Ix?
A

Spironolactone (K+ sparing diuretic) can cause hyperkalaemia

Important to do ECG –> may show tall t waves + absent p-waves (warrants immediate Mx)

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40
Q

SUMMARY CARD:

What are the steps to interpreting acid-base balance on a blood gas?

A

1. pH

  • Low = acidosis
  • High = alkalosis

2. CO2

  • acidosis + ↑CO2 = respiratory acidosis
  • acidosis + ↓CO2 = partially compensated metabolic acidosis
  • alkalosis + ↑CO2 = partially compensated metabolic alkalosis

3. HCO3-

  • alkalosis + ↑ HCO3- = metabolic alkalosis
  • alkalosis + ↓HCO3- = partially compensated respiratory alkalosis
  • acidosis + ↓HCO3- = partially compensated respiratory acidosis

4. Consider compensation:

  • normal pH = fully compensated
  • abnormal pH = partial compensation
41
Q

SUMMARY CARD:

  • What is an anion gap?
  • What is the equation to calculate anion gap?
  • What does a raised anion gap mean?
A

The anion gap helps determine the concentration of unmeasured ions in the plasma as it is the difference between the [principal cations] and [principal anions]

As the anion gap is largely controlled by albumin, beware of hypoalbuminaemia

(Na + K) - (Cl + HCO3) = anion gap

Normal range = 14-18 mmol/L

It is also useful to determine gas results that are 50/50 e.g. pH 7.5 (high), pCO2 2.0 (low), pO2 11 (normal), HCO3 12 (low) - is this resp alk w/ met comp or met alk w/ resp comp?

Mneumonic for RAISED anion gap (i.e. due to unmeasured ions) - KULT:
* Ketoacidosis (DKA, alcoholic, starvation)
* Uraemia (renal failure)
* Lactic acidosis (RARE SE of metformin)
* Toxins (ethylene glycol AKA antifreeze, methanol, salicylate, paraldehyde)

NOTE: salicylate (aspirin) poisoning can cause respiratory alkalosis FIRST, followed by metabolic acidosis

42
Q

SUMMARY CARD:

What are some causes of metabolic acidosis?

How is metabolic acidosis compensated?

A

Causes of metabolic acidosis can be split into normal VS raised anion gap

NORMAL anion gap (14-18 mmol/L):

  • Diarrhoea (loss of HCO3- in small bowel)
  • Acetazolamide (CA inhibitor)
  • Pancreatic stoma (loss of HCO3-)
  • Addison’s disease (↓Na+, ↑K+ –> K+/H+ cotransporter)
  • Renal tubular acidosis (due to decreased H+ excretion)
  • Ammonium chloride ingestion (found in batteries)

RAISED anion gap (>18 mmol/L):

  • Ketones (alcohol, DKA, starvation)
  • Lactic acid (sepsis, shock, ischaemia, rare SE of metformin)
  • Ethanol
  • Aspirin (starts w/ resp alk, before met acidosis)
  • Biguanides (metformin –> causes lactic acidosis)
  • Ethylene glucol
  • Uraemia

Compensation = hyperventilation

43
Q

SUMMARY CARD:

What is renal tubular acidosis and the 4 different types?

BONUS: what is Fanconi syndrome?

hint: RTA = met acidosis; fanconi = failure of PCT resorption

A

NOTE: majority of HCO3- is absorbed in PCT

  • Type 1 (Distal RTA) = SEVERE, due to alpha intercalated failure to secrete H+ and resorb K+ leads to profound metabolic acidosis + hypokalaemia + renal stones
  • Type 2 (Proximal RTA) = moderate, failure of proximal tubular cells to reabsorb HCO3- leads to metabolic acidosis + hypokalaemia
  • Type 3: mixture of types 1 + 2
  • Type 4: adrenal failure (aldosterone deficiency or resistance) leads to ↓Na+, ↑K+, mild reduction in serum pH

Fanconi syndrome = complete failure of PCT kidney reabsorption

Sx of Fanconi = glycosuria, failure to thrive, Type 2 renal tubular acidosis, hypokalaemia, proteinuria + hyperuricosuria

Causes of Fanconi:

  • Wilson’s (also associated with T1 RTA)
  • Tetracyclines
  • MM
  • Lead poisoning
44
Q

SUMMARY CARD:

What are some causes of metabolic alkalosis?

How is it compensated?

A
  • Vomiting e.g. pyloric stenosis, bulimia (H+ loss)
  • Loop diuretics (K+ depletion –> H+/K+ pump)
  • ↓K+
  • Conn’s (hyperaldosteronism = ↓K+)
  • Antacid use
  • Burns

Compensation = hypoventilation

45
Q

SUMMARY CARD:

What are some causes of respiratory acidosis?

How is it compensated?

A
  • Hypoventilation (Type 2 resp failure)
  • Acute / chronic lung disease (e.g. acute asthma attack, COPD)

NOTE: COPD causes chronic respiratory acidosis; pink puffers (AKA breathlessness) + blue bloaters (AKA no longer breathless) –> maintain pO2 88-92% as CO2 is a driver for ventilation

  • Opioids
  • Sedatives
  • Neuromuscular weakness

NOTE: normal / high pCO2 is worrying as it may signal exhaustion –> v. important to ventilate!

Compensation: renal retention of HCO3-

46
Q

SUMMARY CARD:

What is the difference between Type 1 and Type 2 respiratory failure?

A

Type 1: normal pCO2 but low pO2

Causes of Type 1:
* Reduced ventilation and normal perfusion (e.g. pneumonia, pulmonary oedema, bronchoconstriction)
* Reduced perfusion with normal ventilation (e.g. pulmonary embolism)

Type 2: low pO2 AND high pCO2 –> occurs due to HYPOventilation

  • COPD (acute exacerbation)
  • Reduced compliance of the lung tissue/chest wall e.g. pneumonia, rib fractures, obesity
  • Reduced strength of the respiratory muscles e.g. GBS, NMD
  • Reduced respiratory drive e.g. opioids, sedatives
47
Q

SUMMARY CARD:

What are some causes of respiratory alkalosis?

How is it compensated?

A
  • Hyperventilation e.g. anxiety
  • High altitude (hypoxaemia)
  • Salicylate poisoning (first resp alk, followed by met acidosis)

Compensation = reduced renal HCO3- reabsorption

48
Q

DISEASE:

28F - found to be persistently acidotic and hypokalaemic

2 months ago had right loin pain, was treated for sepsis (not gynae related)

Currently, no FLAWS but acidotic + low K+

  • Diagnosis?
A

Renal tubular acidosis Type 1 - due to triad of renal stones + metabolic acidosis + ↓K+

NOTE: type 2 does not present with renal stones as it is milder

49
Q

DISEASE:

15F - panic attack

What acid-base imbalance is expected?

A

Resp alkalosis

50
Q

DISEASE:

In general, what pH imbalance is associated with:
* hypokalaemia
* hyperkalaemia

A
  1. ↓K+ = alkalosis due to H+/K+ pump (H+ exchanged to pump out K+)
  2. ↑K+ = acidosis due to H+/K+ pump (H+ pumped out to drive K+ into cells)
51
Q

DISEASE

24F - appears unwell + dehydrated
PMH: T1DM

pH 7.20
BE -12
Na 155mmol/L
K 5mmol/L
Cl 115mmol/L
HCO3 20mmol/L
Glucose 27mmol/L
Lactate 2mmol/L

Urea (15mmol/L)
Serum osmolarity which is 365mmol/L

  • What is the anion responsible for the patient’s metabolic acidosis?
A

always calculate anion gap in metabolic acidosis to differentiate between different causes

Anion gap = (Na + K) - (Cl + HCO3) = 25 (RAISED)

Therefore, due to PMH of T1DM, most likely unmeasured ion is ketones

52
Q

DISEASE:

30F - BP 84/36, 3/7 hx of productive cough and fevers

PMH: coeliac disease

pH 7.21
BE -12
Na 131mmol/L
K 6mmol/L
Cl 109mmol/L
HCO3 12mmol/L
Glucose 3mmol/L
Lactate 2mmol/L
Urea (6mmol/L) and serum osmolarity which is 290mmol/L. Inflammatory markers are normal.

  • What is the serum osmolarity?
  • And anion gap?
  • What condition is responsible for of her metabolic acidosis?
A

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

So, the pt’s serum osmolarity = 289 mmol/L

Anion gap = (Na + K) - (Cl + HCO3) = 16 (normal)

Diagnosis: Addison's disease –> due to normal anion gap +↓Na+ and ↑K+ (causes acidosis due to H+/K+ cotransporter)

53
Q

DISEASE:

Inadequate function of the proximal renal tubules

TRIAD of glucosuria + hypophosphatemia + hyperuricosuria

  • Diagnosis?
A

Fanconi syndrome = complete failure of PCT kidney reabsorption

54
Q

DISEASE:

21F - overdose of medication, N&V and ringing in ears
PMH: EUPD

pH 7.5
pCO2 low
HCO3- low

  • What has she most likely overdosed on?
A

Aspirin (salicylate)

Causes resp alk followed by met acidosis

55
Q

DISEASE:

76M - acute COPD exacerbation

Arterial blood gas shows:

pH 7.30 (7.35-7.45)

PaCO2 9 kPa (4.7-6.0 kPa)

PaO2 10 kPa (11-13 kPa on 21% FiO2)

HCO3- 38 mmol/L (22-26 mEq/L)

  • What type of respiratory failure does he have?
  • How would you describe this patient’s acid base disturbance?
A
  • Type 2 respiratory failure (low pO2 AND high pCO2)
  • Partially compensated respiratory acidosis / chronic respiratory acidosis
56
Q

DISEASE:

1 week old male infant w/ projectile vomiting after feeds
Vomit is milky + nonbilious
Still hungry after feeds
O/E: small mass in epigastrium

  • What is the diagnosis?
  • What acid base disturbance would you expect?
A

pyloric stenosis
metabolic alkalosis (due to loss of H+)

57
Q

DISEASE:

3M - concerns about failure to thrive

PMH: rickets and is on appropriate calcium and vitamin D replacement

Blood tests show him to be hypokalaemic.

Urine dip shows the presence of protein and glucose. The pH of the urine is 8.6 (alkaline). There are no ketones in his blood.

  • Diagnosis?
A

Fanconi syndrome - complete failure of PCT

Sx of Fanconi = glycosuria, failure to thrive, Type 2 renal tubular acidosis, hypokalaemia, proteinuria + hyperuricosuria

58
Q

DISEASE:

53F - sudden sharp chest pain
Recently returned from Australia

ABG:

pH 7.49 (NR 7.35-7.45)

PaO2 8.7 kPa (NR: 11-13 kPa on 21% FiO2)

PaCO2 3.1 kPa (NR: 4.7-6.0 kPa)

HCO3- 23 mmol/L (NR 22-26 mEq/L)

How would you describe this patient’s acid base disturbance?

A

pulmonary embolism

respiratory alkalosis with partial compensation

59
Q

SUMMARY CARD:

Which hormones from the hypothalamus stimulate hormone release from the pituitary?

GnRH, TRH, dopamine, CRH

A

Hypothalamus and ANTERIOR PITUITARY (AP) hormones:

  • GnRH and somatostatin from hypothalamus stimulates somatotrophs in AP = somatotrophin (AKA growth hormone) release
  • GnRH from hypothalamus stimulates gonadotrophs in AP = gonadotrophin (AKA LH + FSH) release
  • CRH from hypothalamus stimulates corticotrophs = ACTH release
  • TRH from hypothalamus stimulates thyrotrophs = TSH release AND prolactin release
  • Dopamine from hypothalamus INHIBITS lactotrophs = inhibits prolactin

NOTE: GnRH = Gonadotropin hormone-releasing hormone; CRH = Corticotropin-releasing hormone; TRH = Thyrotropin-releasing hormone; ACTH = adrenocorticotropic hormone

POSTERIOR pituitary hormones:

  • Oxytocin
  • Vasopressin
60
Q

SUMMARY CARD:

What is hypopituitarism?

What is the mainstay investigation for hypopituitarism?

Combined pituitary function test

A

Hypopituitarism = deficiency in 1 or more hormones by the pituitary gland due to e.g. pituitary tumours, traumatic brain injury (TBI), or autoimmune conditions

Combined pituitary function test: used to assess hypopituitarism

Procedure:

  1. Patient fasts overnight, IV access established, and weight recorded
  2. Mix insulin dose (0.15 units/kg; to stimulate GH and ACTH), TRH 200mcg (to stimulate TSH and prolactin), LHRH 100mcg (AKA GnRH, to stimulate LH/FSH) in a 5ml syringe and administer IV
  3. Bloods taken for basal thyroxine, glucose, cortisol, GH, LH, FSH, TSH, and prolactin every 30 minutes for 1 hour
  4. Replace hydrocortisone, T4, estrogen, and GH if needed urgently

Interpretation of results:

1. Insulin Tolerance Test: Hypoglycemia (< 2.2mmol/L) triggers ↑ACTH and ↑GH. Adequate cortisol response is >170 nmol/l. Adequate GH response is >6mcg/L

2. Thyrotrophin Releasing Hormone Test: Triggers ↑TSH and ↑Prolactin. Normal result is TSH rise to >5 mU/l. Hyperthyroidism shows suppressed TSH, while hypothyroidism shows an exaggerated response.

3. Gonadotrophin Releasing Hormone Test: Triggers ↑LH/FSH. Normal peaks can occur at 30 or 60 minutes. Inadequate response may indicate hypopituitarism. Diagnosis of gonadotrophin deficiency is based on basal levels.

NOTE: contraindications to CPF test = ischaemic heart disease, epilepsy, untreated hypothyroidism (as it impairs GH + cortisol response)

61
Q

SUMMARY CARD:

What are some causes (+ Sx + Mx) of hypopituitarism?

A

Causes:

  • Malignancy e.g. pituitary adenoma, craniopharyngioma
  • Infection e.g. TB (Mx = RIPE), syphilis (Mx = abx)
  • Infiltration e.g. sarcoidosis, lymphoma
  • Iatrogenic e.g. surgical / trauma / radiation
  • Infarct e.g. Sheehan’s or apoplexy

S&S:

  • Generic Sx = lethargy, weight gain, ↓ BP, hair loss, myalgia
  • ↓ sex hormones = impotence, ↓ libido, amenorrhoea
  • ↓ ACTH = Addisonian crisis
  • ↓ TSH = myxoedema coma

Ix:

  • 9AM cortisol, TFTs, testosterone/oestrogen
  • CPFT
  • Imaging

Mx = replacement of hormones:

  • ↓ ACTH = Addison’s –> hydrocortisone +/- fludrocortisone
  • ↓ TSH = secondary hypothyroidism –> thyroxine replacement
  • ↓ LH/FSH = replace sex hormones (testosterone/oestrogen)
62
Q

SUMMARY CARD:

What are the features of these pituitary tumours:

  1. Microadenoma
  2. Macroadenoma
  3. Prolactinoma
  4. Non-functioning pituitary adenoma
  5. Acromegaly
A

Pituitary tumours can produce any combination of the pituitary hormones or be non-secreting

1. Microadenoma:

  • < 10mm, usually benign
  • MORE likely to be functional e.g.:
  • GH secreting presents w/ Sx of acromegaly, diabetes, HF, HTN; leading cause of death is HF
  • Prolactin secreting presents with Sx of galactorrhoea, gynaecomastia, amenorrhoea, impotence

2. Macroadenoma:

  • > 10mm
  • Can be non-functional or prolactinoma
  • Compression of optic chiasm = bitemporal hemianopia

3. Prolactinoma:

  • Macroprolactinoma >5000 miu/L
  • Moderate elevation (1000-5000) = microprolactinoma
  • Mx = dopamine agonists e.g. cabergoline, bromocriptine

4. Nonfunctioning pituitary adenoma:

  • Prolactin up to 5000
  • Mx = watch and wait if no Sx

5. Acromegaly:

  • ↑GH, ↑prolactin
  • Initial Ix = IGF-1 (↑ in acromegaly)
  • OGTT w/ GH (75mg glucose) = GOLD STANDARD → >2 mU/L = acromegaly; < 2 = normal
  • Mx = trans-sphenoidal surgery, 2nd line = octreotide (somatostatin analogue – inhibits GH release), pegvisomant – GH receptor antagonist, cabergoline (DA agonist)
63
Q

DISEASE:

Which of the following results from a Combined Pituitary Function Test (CPFT) would be consistent with a diagnosis of hypopituitarism?

a) Elevated cortisol and GH levels after insulin administration
b) Elevated TSH and prolactin levels after TRH administration
c) Low cortisol and GH levels after insulin administration
d) Elevated LH and FSH levels after GnRH administration
e) Elevated TSH levels after TRH administration

A

c) Low cortisol and GH levels after insulin administration (hypoglycaemia SHOULD trigger ACTH and GH release!)

64
Q

DISEASE:

A patient with hypopituitarism shows low levels of LH, FSH, and testosterone. Which biochemical test would you perform next to confirm the diagnosis?

A

GnRH stimulation test (that should trigger a ↑LH/FSH)

65
Q

DISEASE:

28F - amenorrhea, galactorrhea + visual disturbances
Prolactin >6000
MRI reveals a 12 mm pituitary mass

  • What is the most likely diagnosis?
  • BONUS: what is the Mx?
A

Prolactinoma

Mx = cabergoline, definitive = transphenoidal surgery

66
Q

DISEASE:

Which initial test is most appropriate for a patient with suspected acromegaly due to a pituitary tumour?

A

IGF-1 (raised)

67
Q

DISEASE:

55F - pituitary tumour presents with high blood pressure, diabetes, and weight gain

  • What hormone is being secreted?
A

Cushing’s disease - ACTH secretion causing hypercortisolism

68
Q

SUMMARY CARD:

What is the hypothalamo-pituitary-thyroid axis?

How is thyroxine synthesised?

A

HPT axis:

  • Hypothalamus detects low plasma thyroxine → releases thyrotropin releasing hormone (TRH) → stimulates anterior pituitary to release thyroid-stimulating hormone / thyrotropin (TSH) → stimulates thyroid gland to release T3/T4
  • T3/T4 has a negative feedback mechanism on the hypothalamus and pituitary (suppresses TRH and TSH production respectively)
  • NOTE: T3 is the active form, T4 is converted to T3 in the liver and muscle cells

Thyroxine synthesis:

  • Iodide –thyroid peroxidase–> Iodine
  • Iodine enters the colloid and iodinates tyrosine residues on thyroglobulin forming monoiodotyrosine (MIT) + diiodotyrosine (DIT)
  • These go on to form T3 (triiodothyronine) and T4 (thyroxine)
  • Then T4 converted to T3 in the periphery
  • NOTE: perchlorate controls whole process
69
Q

SUMMARY CARD:

Features of the following hypothyroid conditions (RFs, Sx, Ix, + Mx):

Primary hypothyroidism:

  1. Iodine deficiency
  2. Hashimoto’s thyroiditis
  3. Primary atrophic hypothyroidism
  4. Subacute thyroiditis (AKA De Quervains)
  5. Riedel’s thyroiditis
  6. Drug-induced

Secondary hypothyroidism:

  1. Post-partum (Sheehan’s)
  2. Pituitary apoplexy / adenoma / surgery

Other:

  1. Subclinical hypothyroidism
  2. Sick euthyroid
  3. Treated hypothyroidism
A

S&S of hypothyroidism = weight gain, cold intolerance, depression, dry skin, hair loss, fatigue, constipation, bradycardia

Ix = TSH + T3/T4 (2 sets of bloods 3 months apart)

Mx = levothyroxine replacement (6 weekly checks until stable TSH)

If myxoedema coma (e.g. hypothermia < 35.5°C, bradycardia) → MEDICAL emergency = IV T3+T4 AND glucocorticoids e.g. IV hydrocortisone until adrenal insufficiency is excluded

Primary hypothyroidism - generally ↓T4 ↑TSH:

  • Severe iodine deficiency = most COMMON CAUSE of hypothyroidism worldwide
  • Autoimmune thyroiditis = most common cause in the developed world / UK
  • Primary strophic hypothyroidism = diffuse lymphocytic infiltration causes atropy → SMALL goitre; associated w/ other AI conditions e.g. pernicious anaemia, vitiligo
  • Hashimoto's thyroiditis = anti-thyroid peroxidase Abs or anti-thyroglobulin Abs, diffuse goitre, ↑risk of developing NHL
  • Subacute = post-viral infection → damaged thyroid follicles initially spill thyroxine into the blood (hyperthyroid) then become hypothyroid as follicles heal (self-limiting, 6-8 weeks)
  • Riedel's thyroiditis = dense fibrosis replaces normal thyroid parenchyma → painless, woody thyroid
  • Drug-induced = antithyroid drugs, lithium, amiodarone
  • NOTE: amiodarone can cause hyper or hypothyroidism as it damaged thyroid cells (hypo) but also contains iodine (hyper)

Primary hypothyroidism - generally ↓TSH ↓T4:

  • Causes include: pituitary apoplexy, pituitary tumour, transphenoidal surgery, post-partum (Sheehan’s)

Other:

  • Subclinical hypothyroidism = NORMAL T3/T4 but ↑ TSH
  • Sick euthyroid = occurs w/ any severe illness as body shuts down metabolism to conserve energy so ↓ T3/T4 , normal TSH
  • Treated hypothyroidism can present similarly to subclinical hypothyroidism = NORMAL T3/T4 but ↑TSH
70
Q

SUMMARY CARD:

How is thyroid function affected in pregnancy?

What is neonatal hypothyroidism?

A
  • hCG has an analogous structure to TSH, rise in hCG in first trimester → free T4 slight increase
  • TBG levels increase in pregnancy and later in pregnancy, hCG levels drop → T4 levels drop and TSH rises slightly

Neonatal hypothyroidism:

  • Diagnosed as part of Guthrie test (48-72hrs in)
  • NOTE: do not want to diagnose too early because if you measure too early the TSH might be erroneously high due to maternal TSH in the blood
  • If not diagnosed and treated w/ levothyroxine within the first four weeks, it causes irreversible cognitive impairment
71
Q

SUMMARY CARD:

Features of the following hyperthyroid conditions (RFs, Ix, Mx):

Primary hyperthyroidism:

  1. Graves’ disease
  2. Solitary toxic nodule
  3. Plummer’s (toxic multinodular)
  4. Subacute thyroiditis (AKA De Quervains)
  5. Drug-induced
  6. Ectopic
  7. Post-partum

Secondary hyperthyroidism:

  1. TSH secreting tumour
  2. Thyroid hormone resistance

Other:

  1. Subclinical hyperthyroidism
A

S&S of hyperthyroidism = weight loss, heat intolerance, irritability, difficulty sleeping

Ix = TSH + T3/T4

Mx = Carbimazole (either titrate, or block and replace w/ levothyroxine); radio-iodine therapy (CI: pregnancy / breastfeeding); thyroidectomy

If thyroid storm (e.g. hyperthermia > 41°C, tachycardia) → MEDICAL emergency = IV propylthiouracil + IV hydrocortisone (+ Lugol solution)

Primary hyperthyroidism - generally ↑T4 ↓TSH:

  • Graves' disease = anti-TSH-R antibodies; Sx triad of thyroid acropachy, pretibial myxoedema + exophthalmos; diffuse goitre w/ high uptake on technetium scan
  • Single or multi- toxic nodules = patchy technetium scan uptake; Mx = radioiodine
  • Subacute = post-viral infection → damaged thyroid follicles initially spill thyroxine into the blood
  • Drug-induced e.g. thyroxine, amiodarone
  • Ectopic e.g.trophoblastic tumour, struma ovarii
  • Post-partum (damaged thyroid follicles spill T3/T4 into the blood)

Secondary hyperthyroidism - generally ↑TSH ↑T3/T4:

  • TSH secreting tumour or thyroid hormone reisstance

Other:

  • Subclinical hyperthyroidism = NORMAL T3/T4 but ↓ TSH
72
Q

SUMMARY CARD:

What are some features of the following types of thyroid cancer:

  1. Papillary
  2. Follicular
  3. Medullary
  4. Anaplastic
  5. MALT lymphoma (due to Hashimoto’s)
A
  • May present as solitary painless nodule (hard + immovable)
  • Usually non-functioning

1. Papillary

  • Most common (70%) + best prognosis
  • RF = exposure to ionising radiation during childhood
  • Psammoma bodies + Orphan Annie nuclei
  • Mx = total thyroidectomy (TT) +/- radioiodine (to wipe out last survivors) + levothyroxine
  • Monitor thyroglobulin for recurrence

2. Follicular adenocarcinoma

  • 2nd most common (20%)
  • RF = low dietary iodine
  • Vascular invasion (can spread easily)
  • Mx = total thyroidectomy + radioiodine
  • NOTE: Hurthle cell = rare variant of follicular thyroid cancer

3. Medullary

  • Arise from c-cells found in the thyroid medulla
  • C-cells that produce calcitonin (tumour marker), linked to MEN2
  • Causes diarrhoea + flushing of the skin

4. Anaplastic

  • Most undifferentiated + poor prognosis
  • Elderly
  • Rapid growth
  • Giant and spindle shaped cells + pleomorphic giant cells

5. MALT lymphoma (due to Hashimoto’s)

  • Chronic Hashimoto’s = lymphocytic proliferation = MALT lymphoma
73
Q

SUMMARY CARD:

What are the Multiple Endocrine Neoplasia (MEN) syndromes?

A

MEN1 (3Ps): Pituitary adenoma, Pancreatic (e.g. insulinoma) + Parathyroid hyperplasia

MEN2A (2Ps, 1M): Parathyroid hyperplasia, Phaeochromocytoma, Medullary thyroid cancer

MEN2B (1P, 3Ms): Phaeochromocytoma, Medullary thyroid cancer, Mucocutaneous neuromas (& Marfanoid)

74
Q

DISEASE:

What is the most common cause of hypothyroidism worldwide vs UK?

A

Iodine deficiency vs autoimmune (e.g. Hashimoto’s)

75
Q

DISEASE:

45F - diffuse goiter and anti-thyroid peroxidase antibodies
Bloods: ↓T4, ↑TSH

Diagnosis?

A

Hashimoto’s thyroiditis

76
Q

DISEASE:

Which laboratory finding is indicative of subclinical hypothyroidism?

If subclinical hypothyroidism is found on a blood test - what is the next step in management?

T4 and TSH

A

Normal T4 and T3 with elevated TSH

Repeat TSH + T3/T4 levels in 6 weeks (only treat if symptomatic)

77
Q

DISEASE:

23M - bradycardia, hypothermia, and altered mental status
Bloods = low T3, T4, and elevated TSH

  • What is the diagnosis?
  • Mx?
A

Myxoedema coma

Mx = IV T3+T4 AND glucocorticoids e.g IV hydrocortisone until adrenal insufficiency is excluded

78
Q

DISEASE:

What is the initial management for a patient presenting with a thyroid storm?

A

IV hydrocortisone and IV propylthiouracil

79
Q

DISEASE:

60M - solitary, painless thyroid nodule
USS = solid, hypoechoic mass with microcalcifications
Fine-needle aspiration biopsy = psammoma bodies

  • Diagnosis?
A

Papillary thyroid carcinoma

80
Q

DISEASE:

Which type of thyroid cancer is associated with MEN2 syndrome and elevated calcitonin levels?

A

Medullary thyroid cancer

81
Q

SUMMARY CARD:

What hormones are produced by the adrenals and what are their roles?

A

Mnemonic: GFR + sweeter as you go down

Cortex:

Zona glomerulosa = aldosterone (mineralocorticoid; retains Na+, excretes K+)
Zona fasciculata = cortisol (glucocorticoid; diurnal, sleep wake cycle)
Zona reticularis = DHEA (precursor to sex steroids = androgens + oestrogen)

Medulla: (nor)adrenaline (AKA catecholamines)

82
Q

SUMMARY CARD:

What are features of the following adrenal conditions:

Zona glomerulosa (aldosterone):

  1. Addison’s disease (adrenal insufficiency)
  2. Conn’s syndrome (hyperaldosteronism)
A

1. Addison’s disease (adrenal insufficiency)

  • Causes: autoimmune (primary cause in Europe), TB (primary causes worldwide)
  • Sx = tan skin (POMC → ACTH + MSH), lethargy, depression
  • Bloods = ↓Na+, ↑K+
  • 9AM cortisol >350 excludes Addison’s
  • Short synACTHen test → serum cortisol < double at 30 mins indicates Addison’s
  • Serum ACTH: ↑ = primary, ↓ = secondary
  • Hormone replacement w/ hydrocortisone (glucocorticoid) +/- fludrocortisone (mineralocorticoid)
  • NOTE: double steroid dose on sick days
  • Addisonian crisis = hypotensice shock, ↑HR, hypothermic, ↓Na+, ↑K+, ↑urea → Mx = IV fluids 0.9% NaCl + 50ml dextrose if hypoglycaemic + IM 200mg hydrocortisone bolus

2. Conn’s syndrome (hyperaldosteronism):

  • Adrenal hyperplasia = most common cause
  • Sx = treatment resistant HTN
  • Bloods: ↑Na+, ↓K+
  • ↑ Aldosterone:renin ratio (renin suppressed due to high levels of aldosterone)
  • Aldosterone antagonists & K+ sparing diuretics
  • If >4cm, consider surgical excision
83
Q

SUMMARY CARD:

What are features of the following adrenal conditions:

Zona fasciculata (cortisol):

  1. Cushing’s syndrome (hypercortisolism)
  2. ACTH deficiency
A

1. Cushing’s syndrome (hypercortisolism):

  • Causes = ACTH dependent e.g. Cushing’s disease (pituitary tumour, most common) or ectopic (SCLC); OR ACTH-independent e.g. adrenal adenoma, adrenal hyperplasia or iatrogenic steroid use
  • Sx = moon face, central obesity, striae, acne, HTN, diabetes, proximal myopathy, hirsutism, bruising
  • Bloods: ↑ 9AM cortisol
  • Low dose dexamethasone test fails to suppress cortisol levels
  • Inferior pituitary petrosal sinus sampling (IPPSS): ↑ ACTH = Cushing’s disease; ↓ = ectopic
  • MRI /CT of pituitary
  • Mx = treat underlying disease

2. ACTH deficiency:

  • Causes = pituitary tumours / surgery, Sheehan’s, etc.
  • NOTE: increases sensitivity to insulin
  • Sx = fatigue, weakness, weight loss, hypotension, hypoglycemia, nausea, vomiting, decreased libido, and amenorrhea in women
  • Bloods: ↓ ACTH, ↓ cortisol
  • Combined pituitary function test to identify hypopituitarism
  • Mx = hormone replacement e.g. hydrocortisone
84
Q

SUMMARY CARD:

What are features of the following adrenal conditions:

Zona reticularis (DHEA):

  1. CAH
A
  • Most common cause = 21-alpha hydroxylase deficiency
  • In neonates = ambiguous genitalia in females, salt-wasting crisis (vomiting, dehydration, electrolyte imbalances)
  • In children = precocious puberty, rapid growth, early skeletal maturation
  • Blood tests = ↑ 17-hydroxyprogesterone, ↓ cortisol levels, ↑ ACTH
  • Hormone replacement = hydrocortisone (glucocorticoid suppresses ACTH) +/- fludrocortisone
  • Genital recontructive surgery in females
85
Q

SUMMARY CARD:

What are features of the following adrenal conditions:

Medulla (adrenaline):

  1. Phaeochromocytoma
A
  • Causes = adrenal medulla tumour, periperhal neural tumour
  • Triad of Sx = headaches + HTN + hyperhidrosis
  • Arrhythmias
  • Plasma metanephrines + 24hr urinary catecholamines / metanephrines
  • Mx = alpha-blockade first (e.g. phenoxybenzamine FIRST ~ 2 week; to prevent unopposed vasoconstriction), THEN beta blockade (e.g. propranolol)
  • Surgical Mx when BP well-controlled

LONG NOTE: Alpha receptors are found in the blood vessels and when activated cause vasoconstriction, so an alpha blockade stops vasoconstriction. Beta receptors are found in the heart and when activated increases HR, so a beta blockade reduced HR. If a the beta blockade is given FIRST, then the reduction in HR will cause the body to automatically vasoconstrict to preserve the BP, and the alpha blockade then won’t work.

86
Q

DISEASE:

40F - fatigue, depression + tan skin
Bloods = decreased sodium and increased potassium levels

Diagnosis?
Ix to confirm the diagnosis?

A

Addison’s disease

Short synACTHen test fails to double cortisol levels

87
Q

DISEASE:

What is the primary cause of Addison’s disease in Europe vs worldwide?

A

autoimmune vs TB

88
Q

DISEASE:

What is the most common cause of primary hyperaldosteronism?

A

Adrenal hyperplasia

89
Q

DISEASE:

30M - paroxysmal episodes of headaches, hypertension + hyperhidrosis

Diagnosis?
Mx?

A

Phaeochromocytoma

Mx = alpha-blockade first (e.g. phenoxybenzamine FIRST ~ 2 week; to prevent unopposed vasoconstriction), THEN beta blockade (e.g. propranolol)
Surgical Mx when BP well-controlled

90
Q

DISEASE:

Which condition is characterised by increased plasma metanephrines and 24-hour urinary catecholamines/metanephrines

A

Phaeochromocytoma

91
Q

DISEASE:

Which enzyme deficiency is the most common cause of congenital adrenal hyperplasia?

A

21-alpha hydroxylase

92
Q

DISEASE:

55F - weight gain, central obesity, striae, + proximal muscle weakness

Most likely hormone imbalance?

A

Cushing’s syndrome - high cortisol

93
Q

DISEASE:

What is the primary cause of ACTH deficiency?

A

pituitary adenoma

94
Q

DISEASE:

What is a potential complication of untreated congenital adrenal hyperplasia (CAH) in neonates?

A

Adrenal (AKA addisonian) crisis

95
Q

SUMMARY CARD:

What is the renin angiotensin aldosterone system (RAAS)?

What conditions affect aldosterone?

A

Angiotensinogen —renin—> angiotensin 1 —ACE—> angiotensin 2

Angiotensin 2 acts on receptors in the adrenal glomerulosa to stimulate aldosterone release

LOW aldosterone (↑ K+):

  • Addison’s disease
  • ACE inhibitors (as angiotensin isn’t formed to act on the adrenals)
  • ARBs (as they block the receptors in the adrenals so angiotensin 2 can’t act on them)
  • RTA type 4 (is like adrenal failure, presents like Addison’s)
  • K+ sparing diuretics e.g. spironolactone
  • Diabetes insipidus (i.e. vasopressin insufficiency / resistance)

HIGH aldosterone (↓ K+):

  • Conn’s syndrome
  • RTA type 1 (affects DCT)
  • Guitelman’s syndrome (Affects DCT)
  • RTA type 2 (affects PCT)
  • Fanconi syndrome (RTA type 2 plus syndrome)
  • Loop diuretics e.g. furosemide
  • Barter’s syndrome (like if you took lots of loop diuretics)
96
Q

SUMMARY CARD:

What is GFR?

What markers can be used for eGFR?

glomerular filtration rate

A

Marker of renal function
Normal = 120ml/min

3 criteria to use a marker as an estimate of GFR:
* Freely filtered
* Not bound to plasma proteins + not reabsorbed
* Inulin = GOLD-STANDARD but needs IV steady state infusion so not used
* Cockcroft-Gault equation for creatinine and eGFR uses age, sex and weight
* MDRD equation used for creatinine and eGFR uses age, sex and ethnicity

97
Q

SUMMARY CARD:

What is AKI?

What are the indications for dialysis in AKI?

A

AKI:

  • >26 rise in serum Cr within 48hrs
  • OR >50% rise in serum Cr in past 7 days
  • OR fall in urine output < 0.5 mL/kg/hr for >6hrs

Dialysis Indication = AEIOU:

  • Acidosis
  • Electrolyte Disturbance
  • Intoxication i.e. w/ lithium
  • Overload w/ fluids i.e. pulmonary oedema
  • Uraemic encephalopathy
98
Q

SUMMARY CARD:

What is CKD (+ its causes)?

What are the stages of CKD and how is it managed?

A

Causes of CKD = diabetes, atherosclerosis, HTN, chronic glomerulonephritis, infection / obstructive uropathy, PCKD

CKD can lead to: acidosis + hyperkaelaemia, anaemia due to loss of EPO synthesis + renal bone disease (secondary hyperparathyroidism)

Use the eGFR clock for CKD staging

Renal replacement therapy:

  • Haemodialysis (Tessio Line or AV fistula) = done 3x a week
  • OR peritoneal dialysis (Tenckoff Catheter, can be done at home)
  • Renal transplant is usually to the right iliac fossa and the surgical scar is the Rutherford Morrison Scar (Hockey Stick scar in RIF)
99
Q

SUMMARY CARD:

A

Year 5: Pathology (7 decks)

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