Chem path 13 - Diabetes CPC Flashcards

1
Q

What are the units for Hba1c and what is the cut off for diabetes?

A

mmol/mol, for a diagnosis of diabetes the Hba1c needs to be above 48mmol/mol (6.5%)

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

What is the normal value for Hba1c (non-diabetics)?

A

<42mmol/mol

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

WHat is the cut off for WHOLE fasted-blood in diabetics?

A

> /=6.1mmol/L

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

o 48yo unconscious, presented February 2002
o Acutely unwell a few days, vomiting, polyuria, polydipsia, SOB and dehydrated
o PMHx: appendicectomy, osteoporosis, poorly controlled HTN
o DHx: amlodipine 10mg, atenolol 100mg
o O/E: obese, dehydrated, BP 80/40

What is the cause of this woman’s unconsciousness and what investigation would you do next?

A

Hypotension

ABG

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

What are some causes of metabolic alkalosis?

A

H+ loss (i.e. vomiting)
Hypokalaemia (hypokalaemic alkalosis is a thing)
Ingestion of bicarbonate (i.e. lots of rennie in peptic uclers)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What will a high HCO3- do to CO2 levels?

A

It will slightly raise them due to a shift in the equilibrium and NOT as a form of compensation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What effect does metabolic alkalosis have on ventilation and why is the extent of respiratory compensation limited in metabolic alkalosis?

A

Metabolic alkalosis will inhibit ventilation so this will drive CO2 up further however the extent of compensation is limited because ventilation needs to remain sufficient to maintain good O2 levels so there is relatively little resp compensation for met alk.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

How do you calculate osmolality?

A

2(Na+K) + U + G

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

How do you calculate the anion gap?

A

Na + K - Cl - HCO3-

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

How can the anion gap help you distinguish whether the cause is DKA or not?

A

DKA fuels a high anion gap through excess ketones

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is the link between hypokalaemia and alkalosis?

A

Hypokalaemia causes alkalosis and alkalosis causes hypokalaemia, need to figure out which came first

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

How does a low ECF K+ cause alkalosis?

A

Causes a drive of H+ in to cells (instead of K+)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

How does an alkalosis cause hypokalaemia?

A

Causes a drive of K+ in to cells (instead of H+)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What are the 4 main causes of hypokalaemia?

A

GI loss, renal loss, redistribution in to cells and rare causes (GRRR)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Name some causes of renal losses of K+

A

Mineralocorticoid excess e.g. hyperaldosteronism/Conn’s, Cushing’s

Increased Na+ delivered to DCT

Osmotic diuresis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Name some causes of redistribution of potassium in to cells

A

Insulin/insulinomas
Beta agonists
Alkalosis

17
Q

What are some rare causes of hypokalaemia?

A

Renal tubular acidosis types 1 and 2
Hypomagnesaemia - low magnesium means you will be unable to bring back up a low K+ so you have to correct the mg2+ before you can correct the K+

18
Q

Explain the mechanism of renal potassium losses when excess Na+ reaches the DCT

A

Triple or co-transporter is blocked –> less Na+ is reabsorbed in the ascending LOH –> more reaches DCT.
More Na+ is absorbed in the DCT –> electronegative nephron which results in a loss of K+ down the electrochemical gradient through ROMK channels

19
Q

Which drug class blocks the triple and co-transporter (Na+/Cl-), respectively?

A

Triple transporter: Loop diuretics

Co-transporter: Thiazides

20
Q

Summarise the pathophysiology of hypokalaemia and alkalosis

A

Lack of extracellular K+ for exchange with Na+ –> Increased H+ entering cells and an extracellular alkalosis.
Lack of intracellular K+ –> increased excretion of H+ in exchange for sodium and the production of an acidic urine and generation of bicarbonate

21
Q

Name 3 endogenous causes of CUshing’s syndrome

A

Pituitary adenoma
Adrenal tumour
Ectopic ACTH

22
Q

What test is now done to assess for pituitary or ectopic cause of cushing’s instead of high dose dexamethasone suppression test?

A

IPSS (a high dose suppression test would have suppressed cortisol if pituitary cause but not ectopic, if adrenal cause then the ACTh would have been suppressed anyway)

23
Q

How does ectopic ACTH cause hypokalaemia?

A

Such high doses of cortisol overpowers MR receptors which has an aldosterone-like effect and causes K+ loss

24
Q

What are causes of ectopic ACTH?

A
Lung cancer (SCLC)
Other cancers
25
Q

Why do you do a repeat CXR in patients with pneumonia?

A

To ensure there isn’t an endobronchial lesion remaining

26
Q

This patient, who initially presented with hypotension and has Cuhsing’s, should be hypertensive but why are they not?

A

she was severely dehydrated (presented with glycosuria)

27
Q

How would you manage this severely dehydrated and hypokalaemic patient?

A

Rehydrate cautiously to prevent central pontine myelinolysis
And replace K+ cautiously as too much K+ at once can result in asystole

28
Q

This same patient comes back anuric with an elevated creatinine, given her PMH, what are the two possible causes of this presentaiton?

A

ATN (Dehydration) or chronic renal failure (diabetes)

29
Q

If you are anuric, at what rate will your creatinine rise?

A

It will rise by ~100/day

30
Q

What is the most effective investigation to differentiate between the two possible differentials?

A

Renal biopsy

31
Q

How would you manage if ATN and if diabetic glomerular kidney disease?

A

ATN: 3 weeks of dialysis then they will recover
Diabetic: life long dialysis

32
Q

What will be seen on renal biopsy of pt with ATN?

A

Tubules necrosed but glomeruli intact

33
Q

UMN vs LMN lesion signs

A

UMN

  • Spastic paresis- increased tone
  • Hyperreflexia
  • Babinski +ve
  • No atrophy
  • No fasciculations
  • Reduced power

LMN

  • Flaccid paresis - HYPOTONIA
  • Severe atrophy
  • Hyporeflexia
  • Babinski -ve
  • Fasciculations
  • Reduced power