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MBChB4 > clinical biochem > Flashcards

clinical biochem Flashcards

1
Q

Features of hypokalaemia:

A

Muscle weakness
Hypotonia
Digoxin toxicity predisposition

U waves
Small / absent t waves
Prolonged PR and ST depression.

A/w acidosis or alkalosis.

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2
Q

Features of hyperkalaemia:

A

Tall tented t waves.
Small p waves
Widened QRS.

Associated with metabolic acidosis as H+ and K+ compete with eachother for exchange of Na+.

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3
Q

Features of hypocalcaemia:

A

Carpopedal spasm , tetany = numbness around mouth, seizures, prolonged QT.

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4
Q

Features of hypercalcaemia:

A

Bones, stones, groans, psychiatric moans + corneal calcification

Shortened QT on ECG
Hypertension

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5
Q

Causes of hyperkalaemia:

A

AKI
Drugs - Spiro, ACEi, ARB, ciclosporin, heparin
Metabolic acidosis
Addison’s
Rhabdomyolysis
Massive blood transfusion
RTA4

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6
Q

Causes of hypercalcaemia:

A

90% causes = primary hyperparathyroidism and malignancy.

Others:
Sarcoidosis
Acromegaly
Thyrotoxicosis
Addison’s

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7
Q

Features of hyponatraemia:

A

Headache
Muscle weakness
Confusion
Fatigue

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8
Q

Features of hypernatraemia:

A

Can be ‘normal’.
Symptoms increasing with severity:
Thirst.
Weakness, lethargy, irritability.
Ataxia, tremor.
Focal neuro deficit e.g. spasticity.
Coma and seizure

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9
Q

Causes of hypernatraemia:

A

Decreased water intake
Hypotonic fluid loss though sweat, GI
Renal disease:
- DI
- osmotic diuresis (hyperglycaemia, hyperkalaemia)
- nephropathy, myeloma, PKD, obstructive uropathy

Increased salt
- acute salt poisoning
- Mineralocorticoid excess - bp increase, potassium decrease, alkalosis
- Cushings (glucocorticoid increase)
- Ectopic ACTH

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10
Q

Explain SIADH:

A

ADH release is increased, meaning more water is retained, meaning there is intravascular fluid expansion leading to dilutional hyponatraemia.

ADh increases water reabsorption from the kidneys, and also decreases urine output. There is equal fluid distribution between all compartments so there are no fluid overload signs.

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11
Q

Causes of cranial vs nephrogenic diabetes insipidus:

A

Both present with polyuria, polydipsia, dehydration and postural hypotension.

Cranial = lack of ADH, at a hypothalamic / pituitary level.
Brain trauma, surgery, tumour, infection, genetic AD, Wolfram syndrome

Nephrogenic = lack of response to ADH in kidneys.
Lithium, mutations, hypokalaemia, hypercalcaemia, PKD

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12
Q

Investigations for acromegaly:

A

Serum IGF-1 levels is first line. (GH has diurnal variation so not diagnostic)

OGTT + serial GH measurements is used to confirm the diagnosis.

Pituitary MRI may show a pituitary tumour.

IGF-1 may also be used to monitor disease.

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13
Q

Features of hypomagnaesemia:

A

Features similar to hypocalcaemia inc tetany, paraesthesia, seizures, arrhtyhmias, decreased PTH secretion.

ECG features similar to hypokalaemia - U waves, small or absent P waves, prolonged PR and ST depression.

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14
Q

Features of hypermagnaesemia:

A

Hypotension, respiratory depression and cardiac arrest.
Widened QRS, increased t wave amplitude.

Uncommon, mostly occurs in renal failure after ingestion of magnesium containing drugs.
Also Addison’s or hypothyroidism.

IV calcium gluconate +/- furosemide.

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15
Q

Causes of secondary diabetes:

A
  1. cystic fibrosis
  2. haemochromatosis
  3. chronic pancreatitis
  4. PCOS
  5. Cushing’s
  6. Pancreatic cancer
  7. Glucagonoma

Some conditions result in insulin resistance (PCOS, Cushing’s) and need metformin to be treated.
Some result in loss of pancreatic function, i.e. low insulin so must be treated with insulin injections e.g. pancreatitis.

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16
Q

DKA protocol:

A

Isotonic saline
VRIII
Dextrose when glucose <14
Consider need for potassium replacement to prevent hypokalaemia

Resolution = pH >7.3, ketones <0.6, bicarb >15

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17
Q

Management of HHS:

A

IV 0.9% NaCl to restore circulating volume.
Insulin once glucose has plateaued on fluids.

+ VTE prophylaxis as hyperviscosity

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18
Q

DKA vs HHS features:

A

HHS usually older than DKA patients.

10-20% volume depletion in HHS compared to DKA

Days to weeks onset for HHS, hours to days for DKA

Endogenous insulin is usually present in HHS, but absnet in DKA.

Absent/mild ketoacidosis in HHS, can be severe in DKA

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19
Q

Addison’s investigation and management:

A

Short Synacthen test: plasma cortisol measured before and 30 mins after synacthen IM - in people with adrenal insufficiency, serum cortisol does not increase adequately, <500-550.
Adrenal autoantibodies can also be measured.

ACTH levels are high in Addison’s, but low in secondary causes.
Renin is high and aldosterone low in Addison’s.

Glucocorticoid and mineralocorticoid replacement required.
E.g. hydrocortisone + fludrocortisone
+ Give advice on sick days (normally double dose), injury or strenuous exercise dosing.
+ Vaccinations
+ Recognise symptoms of adrenal crisis

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20
Q

Metabolic syndrome criteria:

A

3/5 of:
1. low hdl levels
2. high ldl / triglyceride levels
3. large waist circumference
4. Hyperglycaemia
5. High blood pressure

Metabolic syndrome is a cluster of conditions thought to be caused by resistance to insulin. Common in patients who have central obesity.
T2DM is closely realted to metabolic syndrome, as it PCOS and NAFLD.
Albuminuria is often present.

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21
Q

Classes of T2DM drugs:

A

GPL1 agonist
Sulfonylurea
Metformin / Biguanide
SGLT2i
DPP4i / gliptin
Pioglitazone

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22
Q

GLP1 agonist:

A

3rd line drug
Increase insulin secretion and suppress glucagon secretion. Increase satiety and suppress appetite by slowing gastric emptying.

+ = weight loss, CV benefit, low hypo risk
- = GI side effects, injection

Contraindicated in pancreatic history or CKD4

23
Q

Sulfonylureas:

A

1st line if metformin is contraindicated or not tolerated.

  • = hypos, weight gain, frailty, no CV benefit

Close potassium channels on beta cells stimulating the release of stored insulin.

Work very quickly, compared to metformin which takes a few weeks.

24
Q

Metformin:

A

Biguanide, 1st line.
Reduces hepatic gluconeogenesis and decreases peripheral insulin sensitivity.

+ = weight control, CV benefit, low hypo risk
- = GI side effects

X in CKD4 / eGFR<30, due to small risk of lactic acidosis

25
Q

DPP4i / gliptins:

A

2nd line e.g. sitagliptin

Inhibit DPP4 and therefore enhance effect of endogenous incretins. Increases glucose mediated insulin secretion.

+ weight loss, low hyporisk, well tolerated
- variable efficacy

X in pancreatic history (like with GLP1-a)

26
Q

Pioglitazone:

A

3rd line, thiazolidinedione. Used rarely.

Increase sensitivity of fat , muscles and liver to endo/exogenous insulin
+ effective and low hypo risk
- = oedema , central adiposity and osteoporosis

X in bladder cancer, congestive heart failure

27
Q

Complications of diabetes:

A

Peripheral neuropathy
Autonomic neuropathy
Diabetic retinopathy
Foot disease

28
Q

Features of primary hypoaldosteronism:

A

Most common cause is bilateral idiopathic adrenal hyperplasia (60-70%).
+ Adrenal adenoma = Conn’s syndrome (20-30%).

HYPERTENSION + HYPOKALAEMIA (muscle weakness), + metabolic alkalosis.

Hypokalaemia is more common with Conn’s syndrome.

29
Q

Symptoms of Addison’s:

A

Lethargy, weakness, anorexia, n+v, weight loss, salt craving
Hyperpigmentation in palmar creases (Addison’s specific) due to production of MSH alongside ACTH.
Vitiligo
Loss of pubic hair in women
Hypotension
Hypoglycaemia
Crisis: collapse, shock, pyrexia

30
Q

Hypokalaemia causes; acidosis or alkalosis?

A

Acidosis: diarrhoea, RTA, acetazolamide, partially treated DKA

Alkalosis: vomiting, loop + thiazide diuretics, Cushing’s, Conn’s

31
Q

Hypokalaemia causes; raised BP or normal?

A

Normal BP: diuretics, GI loss, RTAI+II

Raised BP: Conn’s, Cushing’s, Liddle’s, 11-Bhydroxylase deficinecy (rare cause of CAH)

32
Q

3 mechanisms of increased calcium in malignancy:

A

PTHrP secretion from e.g. squamous cell lung cancer.

Bone mets releasing calcium.

Myeloma releases cytokines that increase osteoclast activity.

33
Q

Hypercalcaemia causes a PTH drop - what is the normal function of PTH (4)?

A
  1. Calcium mobilisation from bones
  2. Increases renal calcium absorption
  3. Increases renal phosphate excretion
  4. increases formation of 1-25hydroxy..
34
Q

Causes of hypocalcaemia:

A

‘CHARM’
CKD
Hyperparathyroidism + hyperparathyroidism
Acute pancreatitis
Rhabdo early stages
Magnesium deficiency

+ massive blood transfusion
+ vitamin D deficiency / osteomalacia

35
Q

Causes of SIADH:

A

Split into malignancy, neuro, drugs, infection and others:

Malignancy: small cell lung cancer, pancreas, prostate

Neuro: SAH, SDH, meningitis, encephalitis, stroke, abscess

Drugs: SSRIs, PPIs, Antiepileptics e.g. carbamazepine + S.V, ACEi, diuretics

Infection: TB, pneumonia

Other inc porphyria

36
Q

Treatment of hypovolaemic hyponatraemia:

A

IV 0.9% NaCl
Stop diuretics

37
Q

Treatment of euvolaemic hyponatraemia:

A

Treat underlying cause.
Stop culprit medications.

If SIADH:
1. Slow correction, at risk of Central pontine myelinosis:
2. Fluid restrict to 1L per day.
3. Demeclocycline reduces tubule sensitivity to ADH.
4. ADH receptor antagonists e.g. Tolvaptan

38
Q

Treatment of hypervolaemic hyponatraemia:

A

Treat underlying cause.
Restrict sodium and water.
Continue diuretics.

39
Q

Causes of hypertonic hyponatraemia:

A

Post-TURP
Hyperglycacaemia
Mannitol

40
Q

Causes of isotonic hyponatraemia:

A

Hyperlipidaemia
Paraprotein increase

41
Q

Investigation and management of Diabetes Insipidus:

A

Investigate = low urine osmolality, normal or high serum osmolality, >3L urine per day.
WATER DEPRIVATION TEST:
Avoid fluids for 8 hours.
Measure urine osmolality after 8 hours, and if low give desmopressin, and measure 2-4 hours post this.
If urine osmolality is low after desmopressin = nephrogenic. High = cranial.
(If urine osmolality is high after initial water deprivation, rule out DI).

Cranial –> desmopressin and monitor sodium

Nephrogenic –> lots of water, high dose desmopressin, thiazide diuretics, NSAIDs

42
Q

Correction of sodium derangement cautions:

A

Don’t correct either hyper or hypo too fast as can have severe complications.

Correction of hypernatraemia too fast can cause CEREBRAL OEDEMA, which can lead to brain herniation. 10mmol/day correction rate.

Correction of hyponatraemia can cause CENTRAL PONTINE MYELINOSIS. This is secondary to astrocyte apoptosis. Same correction rate as above.
Symptoms include dysarthria, coma, locked in syndrome, para/quadraplegia, seizures and confusion. Symptoms are irreversible.

43
Q

Complications of acromegaly:

A

Colorectal cancer
Cardiomyopathy
Hypertension
Diabetes in >10%, impaired glucose tolerance

44
Q

Treatment of hypomagnaesemia:

A

<0.4 or tetany, arrhythmia or seizure = IV magnesium replacement.

> 0.4 = oral magnesium salts, caution diarrhoea

45
Q

Hypercalcaemia management:

A

Rehydration with saline
Bisphosphonates
Calcitonin?
Steroids?
Loop diuretics if patient cannot tolerate aggressive fluid rehydration.

46
Q

Hypocalcaemia replacement:

A

Severe = Sx / <1.9 IV calcium gluconate, 10, 10, 10 + ECG monitoring + underlying cause addressed.

Mild = 1.9-2.2, asx = calcichew oral replacement.
If vitD deficient, commence vit D replacemtn, load with cholecalciferol.
Check for hypomagnesaemia as well.

47
Q

When to replace potassium?

A

<2.5 or symptomatic with cardiac arrhytmias = IV KCl not exceeding rate 10mmol/hr, in NaCl or 5% glucose.

2.5-3.5 = oral KCl replacement

48
Q

Treatment of hyperkalaemia:

A
  1. identify and treat underlying cause
  2. plasma k+ 5.5-6.5 = oral calcium resonium, monitor daily until <5.5
  3. plasma k+ >6.5 OR cardiac arrhythmias = 30mmol calcium gluconate IV + insulin bolus in IV glucose / dextrose (moves K+ into cells)
    +/- nebulised salbutamol, which is a beta agonist
    +/- sodium bicarb ? in acidotic renal patients.
49
Q

Complications of DKA:

A

Gastric stasis
Thromboembolism
Cerebral oedema, hypokalaemia, hypoglycaemic = iatrogenic
Arrhythmias due to hyperkaleamia or hypo
ARDS
AKI

50
Q

Other causes of hypoadrenalism:

A

Primary = TB, mets, meningococcal septicaemia, HIV, antiphospholipid syndrome

Secondary = pituitary disorders, exogenous glucocorticoid therapy

51
Q

Addison’s disease + severe intercurrent illness e.g. vomiting, persistent diarrhoea:

A

Take emergency IM injection of hydrocortisone and seek immediate medical advice.

52
Q

Precipitants of an adrenal crisis:

A

Sepsis or surgery causing an acute exacerbation of chronic Addison’s

Adrenal haemorrhage e.g. Waterhouse Friderichsen syndrome

Steroid withdrawal

Management = 100mg hydrocortisone IM or IV. Continue every 5 hours until stable, No fludrocortisone is required as high dose hydrocortisone exerts weak mineralocorticoid action.

53
Q

Pathway for prescribing in T2DM:

A

1st line = metformin, or SU, (+SGLT2i if BMI >30 or CV disease

2nd line = SGLT2i, SU, DPP4i, Pioglitazone

3rd line = 3rd agent from 2nd line, GLP-1 agonist, Insulin

54
Q

Mechanism of exogenous insulin in T2DM:

A

Increases glucose uptake and utilisation in skeletal muscles.
Reduces hepatic gluconeogenesis.
Increases glycogenesis.
Decreases lipolysis.

  • weight gain, hypo risk, injections

MBChB4 (15 decks)

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