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Phase 4 > Metabolic Medicine > Flashcards

Metabolic Medicine Flashcards

1
Q

What are some causes of hyperkalemia?

A

acute kidney injury

drugs*: potassium sparing diuretics, ACE inhibitors, angiotensin 2 receptor blockers, spironolactone, ciclosporin, heparin**

metabolic acidosis

Addison’s disease

rhabdomyolysis

massive blood transfusion

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2
Q

What would you expect the K+ to be in DKA?

A

Low due to total body loss

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3
Q

When is hyponatraemia considered chronic?

A

> 48 hours
or
duration of symptoms are not known

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4
Q

What is the serious potential consequence of osmotic demyelination?

A

Locked in syndrome

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5
Q

How is Hyponatremia treated?

A

Mild cases/ usually associated with edematous fluid:

  • fluid restriction
  • diuretics - furosemide

Hypovolaemic
- 0.9% saline

Severe:
- hypertonic saline

SIADH:

  • fluid restriction
  • Saline
  • Tolvaptan - ADH receptor antagonist
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6
Q

when should calcium gluconate be given?

A

K+ >6.5

or ECG changes

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7
Q

What is the maximum rate K+Cl can be infused at?

A

20mmol/Hour

or

Max concentration of: 40mmol/L

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8
Q

List come causes of SIADH:

A

Small cell lung cancer

Subarachnoid bleed

Mycoplasma pneumonia

Meningitis

Drugs

  • carbamazepine
  • SSRI

Surgery

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9
Q

What are the symptoms of SIADH?

A

lethargy
headaches
dizziness

Postural Hypotension

ataxia
confusion
Seizures

Coma

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10
Q

How is hypernatremia investigated and treated?

A

Fluid status

Serum osmolality

Urine Na2+/ osmolarity

Treatment:
Acute - Dextrose 5%

Chronic: slow adjustment <10mmol daily
- fluids

Dehydration
- 0.9% saline

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11
Q

What are some etiologies for diabetes insipidus?

A

Cranial:

  • x-linked condition
  • Idiopathic (typically autoimmune)
  • Head injury
  • Craniopharyngioma
  • Infection
  • surgical

Nephrogenic:

  • Drugs - lithium
  • Receptor defect
  • Hypercalcaemia
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12
Q

What is the diagnostic investigation into Diabetes insipidus?

A

Water deprivation test / Desmopressin Stimulation test

Urine osmolarity measured

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13
Q

If someone had hypernatremia and underwent investigations into diabetes insipidus, and their results turned out to be primary polydipsia what would you expect the urine osmolality results to be?

A

Pre- desmopressin
- high osmolality (trying to reabsorb water)

Post desmopressin
- High osmolality (still trying to reabsorb water)

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14
Q

What things may give an artificially high K+ readying?

A

Contamination of K from EDTA tubes
- U&Es should be done first

Thrombocythemia
- K+ leaks out as the platelets try to clot

Delayed analysis
- K+ leaks out as cell decay

Poor venipuncture

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15
Q

How should severe hyponatremia be treated?

A

slow infusion of IV saline if >48 hours

Infusion of IV saline if <48 hours

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16
Q

What is the effect of hypokalemia on the heart?

A

Increased ventricular ectopics leadign to:

  • VT
  • VF
  • Torsade de point
  • decreases repolarisation inducing Early- after depolarisations
  • increase ventricular rate

U waves are seen

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17
Q

What is considered severe hypokalemia?

A

<2.5mmol

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18
Q

What drug can hypokalemia induce severe toxicity in?

A

Digoxin

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19
Q

What “malignancy” investigations should be done into hypercalcemia?

A

FBC
- Anaemia

Imaging

  • Bone scan
  • CXR
  • Neck US

Electrophoresis
- myeloma

Alkaline Phosphatase
- Bone mets

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20
Q

What is the management for severe Hypercalcaemia and what daily monitoring should be done?

A 
Dehydration 
Furosemide 
Bisphosphonates - Zoledronic acid 
\+/- 
Steroids (myeloma, sarcoidosis)

Daily Monitoring:

  • Ca2+
  • U&Es
  • Mg2+
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21
Q

Which drugs cause SIADH?

A

Cant Concentrate Serum Sodium

  • carbamazepine
  • cyclophosphamide
  • SSRIs
22
Q

What is first line treatment for hypercalcaemia?

A

IV fluid

23
Q

In dehydration what would you expect the haematocrit and serum haemoglobin to be?

A

Slightly raised

- relative polycythemia

24
Q

Which commonly used antithrombotic drug can cause a rise in K+?

A

Heparin

25
Q

List some causes of Hypocalcemia?

A

Hypoparathyroidism
- autoimmune/ thyroidectomy

CKD

Low vitamin D

Hypomagnesemia

Acute pancreatitis

Celiac disease
- unable to absorb

Crohn’s

Tumour lysis syndrome

26
Q

What are two classical signs seen in hypocalcemia:

A

Trousseau’s sign
- inflating cuff causing hand to cramp

Chvostek’s sign
- taping facial nerve triggers facial twitch

27
Q

What is the management for hypocalcemia?

A

Mild:

  • calcium supplements
  • Mg2+

CKD:

  • phosphate binders
  • Mg2+ correction
  • Vitamin D supplementation

Severe:

  • Calcium gluconate
  • Mg correction
28
Q

What are some common causes to hypomagnesemia?

A

Deficiency in diet

Diuretic use

Reduced G.I absorption

Pancreatitis

29
Q

How is hypomagnesemia treated?

A

Mg2+ infusion with glucose

30
Q

What do the bloods show in primary hyperparathyroidism?

A

High PTH
High Ca2+
Low PO4-

31
Q

What do the bloods show in secondary hyperparathyroidism?

A

High PTH
Low/ normal Ca2+
High PO4-

32
Q

What are the causes of hypokalemia?

A

Transcellular shit:

  • Beta agonists (salbutamol)
  • Alkalosis

G.I loses
- Diarrhea

Mineralocorticoid stimulation

  • Conn’s syndrome
  • Cushing’s disease

Drugs:
- Loop diuretics

33
Q

For mild hypokalemia (>2.5) what drug can be given?

A

Sando K

34
Q

What are the signs and symptoms of hyperkalemia?

A 
lethargy 
Mental slowness 
Muscle weakness
Palpitation
Chest pain
35
Q

What is the dose of calcium gluconate given in hyperkalemia?

A

10% in 10ml over 10mins

36
Q

What medications can push K+ up?

A

ACE inhbiitors
ARBs
Aldosteronism antagonists

37
Q

What things need to be excluded for SIADH?

A

Abnormal Cortisol

TFTs

38
Q

What are the common medications that cause Hyponatremia?

A

Omprzole
SSRIs
Carbamazepine

39
Q

What affect can calcium have in the G.I other than constipation?

A

Calcium can promote gastrin release causing peptic ulcers

40
Q

What changes radiologically are seen with hyperparathyroidism?

A

Subperiosteal bone resorption

Pepperpot skull

Acroosteolysis
- reabsorption of the distal phalanges

41
Q

What is the effective of hypercalamia on blood pressure?

A

Increased the diastolic pressure due to arterial contraction

42
Q

What are the investigations into hyperparathyroidism?

A

Bloods:

  • corrected calcium
  • PTH

Orifices:
- Calcium

X-rays:
Head and bones
- subperiosteal erosion
- Pepper pot skull

Special tests:

  • Technetium Sestamibi radionuclide scan
  • localisation of adenoma
43
Q

What are the typical lab findings for secondary hyperparathyroidism?

A

Normal to Low Calcium
High Phosphate

*phosphate is high because the kidney is unable to effectively secrete the phosphate away.

Ca2+ is normal to low because it was low in first place and this is correcting it, plus large amounts of PO4- inhibit its reabsorption

44
Q

What are the indications for surgery in primary hyperthyroidism?

A 
<50 years 
Calcium >3 
Severe Neurological symptoms 
Nephrolithiasis
Reduced Bone density
45
Q

What is one of the most common causes of dilutional hyponatremia?

A

Post operative

- excessive fluid resuscitation

46
Q

What is the maximum the fluid osmolality can be changed?

A

10-12mmol/L in 24 hours

2mmol/L an hour

47
Q

Which drug is a ADH receptor antagonist?

A

Tolvaptan

48
Q

What deposits of calcium may be seen?

A

Chondrocalcinosis

Corneal calcification

49
Q

What is the major complication following parathyroid surgery, and what can be done to minimise it and how is it followed up?

A

Hypocalcaemia is the major complication

Monitored before and after the surgery.

those at high risk can be given supplemental calcium dn vitamin D before hand.

50
Q

What are the signs and symptoms of hypokalamia?

A

Weakness
Intestinal Ileus
Cramps
Tetany

51
Q

What must be ruled out in order for there to be SIADH, and why?

A

Need to rule out hypothalamic-pituitary axis defects.

  • remember that adrenal insufficiency can give a similar picture with the severe hyponatremia
52
Q

With results of an extremely high PTH, with moderately raised calcium - what type of PTH is this?

A

Teitrary

It causes massively raised PTH level

Phase 4 (49 decks)

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