Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Fifth Year Medicine > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

Difference between proptosis and exophthalmos?

A

Exophthalmos is forward protrusion of eyeball related to Graves

Proptosis - forward protrusion related to any cause:
Malignancy
Inflammation
Traumatic

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

Signs of Cushing’s syndrome?

A

ACTH/cortisol

Moon face
Buffalo hump
Supraclavicular fat pads
Central obesity
Wasted limbs
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Signs of hyperandrogenism

A

Hirsutism
Temporal balding
Acne

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

What are the micro and macro problems of diabetes?

A

Micro:
Retinopathy
Nephropathy
Neuropathy

Macro:
Stroke
Renovascular disease
Limb ischaemia

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

What are the three ways diabetes may be diagnosed?

A
  1. Symptoms + 1 BM
  2. 2 BMs
  3. HbA1c ≥48 (6.5%)

BM: fasting ≥7 or random > 11

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

What signs indicate thyrotoxicosis?

A

Hair loss
Bulging eyes (proptosis/exophthalmus)
Onycholysis- nail separation from nail bed
Pretibial myxoedema

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

What measurements suggest impaired fasting glucose?

A

Fasting glucose of 6.1-7mmol/L

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

Impaired glucose tolerance is defined as?

A

Fasting plasma glucose

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

What HbA1c indicates prediabetes?

A

42-47mmol

6-6.4%

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

What is the target blood glucose if on metformin?

A

6.5%

48mmol

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

How is Atorvastin dosed differently depending on whether someone has a QRISK above 10% or has existing IHD?

A 
Primary prevention (QRISK)- 20mg
Secondary prevention (IHD)- 80mg
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What values after 2 hours indicate impaired glucose tolerance on an OGTT?

A

7.8-11mmol/L

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

Which drugs can cause diabetes mellitus?

A

Steroids
Anti-HIV drugs
Thiazides
Atypical antipsychotics

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

What features define metabolic syndrome?

A

Central obesity (BMI>30) with 2 of:
BP >130/85
Triglycerides >1.6
HDL 5.6 or diabetes

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

Functions of PTH?

A

In the kidney:
Increases Calcium reabsorption
Lowers Phosphate reabsorption
Vit D synthesis

Osteoclast activity

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

Vit D functions?

A

Acts mostly on the guts:
Calcium and phosphate reabsorption
Increases osteoclast activity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

How does tertiary hyperparathyroidism arise in CKD?

A

Failure of the kidney to activate vit D reduces Ca2+ absorption from the gut, chronic overproduction of hyperparathyroidism leads to it’s autonomous activation (tertiary hyperparathyroidism)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Patient has high PTH, but low Ca and high PO4 and short fourth and fifth metcarpals.
What’s the syndrome?

A

Pseudo-hypoparathyroidism

Target organs don’t react to PTH (due to genetic insensitivity) so kidney’s don’t absorb more calcium, low Ca drives PTH secretion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

In what circumstances does post-prandial hypoglycaemia typically occur?

IHX:

A

After bariatric surgery
In type 2 diabetics

IHx: prolonged Oral Glucose Tolerance Test

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Which endocrine tumour syndrome is insulinoma associated with?

A

Men1

Parathyroid tumours, pancreatic endocrine tumours, pituitary prolactinoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

IHx for suspected insulinoma?

A

Screening: Prolonged fast leads to high insulin (unusual) and low glucose

Suppression test: IV insulin and measure C-peptide (in normal people C peptide is suppressed by exogenous insulin)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

If you suspect hyperthyroidism is due to abuse of levothyroxine, what IHx can be used to confirm?

A

Low Serum thyroglobulin

- may be used to monitor carcinoma also

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Which illnesses warrant screening for thyroid dysfunction?

A 
Those with:
AF, hyperlipidaemia
DM, or type 1 DM in 1st trimester of pregnancy, or Addison's (yearly screen)
DHx: amiodarone or lithium
PMH: Down's, Turner's disease
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

IHx that is useful for detecting retrosternal goitre or ectopic thyroid tissue?

A

Isotope scan with 123-iodine or 99-technetium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What type of Ig antibodies occur in Grave’s disease?

A

IgG- TSH receptor antibodies

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

How do you test to differentiate a toxic multinodular goitre from a toxic adenoma in thyroid disease?

A

USS: cystic vs solid
+ fine needle aspiration in a multinodular goitre

Isotope scan: cold nodules (more likely to be malignant), hot nodules (more likely to be adenoma producing thyroid hormone)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

If a goitre is painful what does that make it likely to be?

A

Subacute de Quervain’s thyroiditis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Thyrotocosis Rx?

A

Propranolol

Carbimazole (titrated to TFTs) or carbimazole + levothyroxine
For 12-18 months

Carbimazole SE: agranulocytosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Main RF for eye involvement in Grave’s disease?

A

Smoking

Occurs in 25%-50% of those with Grave’s disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Rx for eye disease in Graves?

A

Mild- symptomatic (artificial tears, sunglasses etc)

Severe- methylprednisolone if opthalmoplegia or gross oedema

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Why do those with hashimoto’s get a goitre?

A

Lymphocytic and plasma cell infiltration of the thyroid, with autoantibodies against it

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

60 year old woman has high TSH and normal T3 and T4

Management?

A

Subclinical hypothyroidism:
Repeat in 2-4 months to check it’s persistent

Rx if symptomatic, TSH >10, thyroid autoantibodies, previous Graves
Or Rx trial for 6 months if TSH 4-10

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Which types of cancer may produce ectopic PTH?

A

Lung
Breast
Kidney

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Risk reducing Rx for patients with MEN-2 and test to determine if someone is applicable?

A

Test for ret-oncogene before age 3

Do a thyroidectomy (as 100% get medullary thyroid cancer- of the parafollicular C cells making calcitonin)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What are the 3 types of thyroid cancer?

A

70% papillary thyroid cancer (fingerlike)
15% follicular thyroid cancer
10% medullary thyroid cancer (parafollicular C cells- calcitonin)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

3 causes of primary hyperaldosteronism?

And Rx?

A
  1. Conn’s (solitary adenoma)- laparoscopic adrenalectomy + spironolactone 4 weeks pre-op
  2. Adrenocortical hyperplasia. Rx: aldosterone R antagonist (spironolactone or eplerenone)
  3. Rarely glucocorticoid-remediable aldosteronism, where ACTH controls aldosterone expression. Rx: dexamethasone
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Causes of secondary aldosteronism?

A

Due to high renin from reduced kidney perfusion:

Renal artery stenosis
Accelerated hypertension
Diuretics
CCF or hepatic failure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Features of Bartter’s syndrome:

A

Leaky sodium and chloride channel in the Loop of Henle means children become hypovolaemic, hypokalaemic and alkalotic (without much K+ to swap for Na+ they rely on H+ instead)

Rx: ACEi, K+ supplements, NSAIDs (reduces renal perfusion pressure)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

What type of cell forms phaeochromocytomas?

A

Sympathetic cells (chromaffin cells), often in the adrenal medulla

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

IHx for suspected phaeochromocytoma?

A

Plasma and 3x24 hour urines for:
Free metadrenaline + normetadrenaline

If borderline: clonidine supression test
Localising: MIBG chromaffin-seeking isotope

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Rx pre-op for phaeochromocytoma?

A

A blocker (phenoxybenzamine) then b-blocker if tachycardic/heart disease

Surgical removal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

A 30 year old woman with hypertension, low K+ that has been resistant to antihypertensives has her renin:angiotensin checked. Angiotensin is raised. What further tests are warranted?

A
  1. CT/MRI of adrenals
  2. Adrenal vein sampling

If no nodules, consider adrenal hyperplasia or glucocorticoid-remediable aldosteronism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Drug causes of gynaecomastia?

A 
Digoxin
Isoniazid
Spironolactone
Cimetidine
Oestrogen
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

CIs to phosphodiesterase 5? (Sildenafil)

A

CVS: unstable angina, concurrent nitrate use
MI 3 months ago, stroke 6 months ago
High BP, arrhythmia
Retina degeneration, renal or liver failure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Low FSH + LH, lack of smell and colour blind = which syndrome?

A

Kallman’s Syndrome:
Isolated lack of GnRH from the hypothalamus = secondary hypogonadism

NB lack of smell and colour blindness do not necessarily occur

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Rx of male hypogonadism?

A

Rx is for symptoms and to prevent osteoporosis:

Testosterone enanthate IM every 3 weeks

47
Q

2 hormones of the posterior pituitary?

A

ADH

GH

48
Q

Rx for short stature in childhood?

A

Somatotropin (synthetic GH)

49
Q

Child’s growth has dramatically halted in the last few months and they’ve been complaining of headache, thirst and visual changes. Most likely tumour cause?

A

Craniopharyngioma > hypopituitarism

Lack of ADH- thirst and frequency, lack of GH- short stature

50
Q

IHx for acromegaly?

A

If serum GH >0.4 and IGF-1 is raised

Oral glucose tolerance test (GH should normally reduce with higher glucose levels)

False +ve: anorexia, pregnancy, DM, liver/kidney disease

51
Q

What are somatotropin and somatostatin used as Rx for?

A

Somatotropin is synthetic GH used when there is deficiency

Somatostatin is GH-inhibiting hormone used in acromegaly (2nd line after surgery)

52
Q

How is serum osmolality measured?

A

2 x (Na + K) + urea + glucose

Normal is 285-295mOsmol/kg

53
Q

What urine to plasma osmolality ratio excludes significant diabetes insipidis?

A

2:1
As long as plasma osmolality is > 295
Shows urine is concentrating

54
Q

IHx for diabetes insipidis

A

Water deprivation test (providing urine output is >3L/d)

Stage 1: 8 hours
>3% weight loss + serum osmolality >300 at any point go to stage 2

Stage 2: Desmopressin (if concentrates = cranial DI)

55
Q

How is primary polydipsia differentiated with diabetes insipidis on water deprivation tests?

A

Primary polydipsia- urine concentrates but less than normal

DI- cranial or nephrogenic, urine doesn’t concentrate > 600

56
Q

What are the two main types of hypoglycaemia and the tests for them?

A
  1. Check drugs (diabetes, quinine, malnourished)
  2. Post-prandial (big influx of carbs causes large insulin release)- mixed meal test
    Fasting (more serious)- 72 hour fast

Check urine sulphonylurea for C-peptide (if taking artificial insulin it won’t have C-peptide)

57
Q

Which familial syndrome might be associated with insulinoma?

A

Men1- pancreas, parathyroid, pituitary

58
Q

Medical treatment of insulinoma?

A

Diazoxide
Hyperpolarises islet cells (acting the opposite way to sulphonylurea)

Or Octreotide (somatostatin blocks pancreatic hormone production)

59
Q

On which diabetes drug can you get a euglycaemic DKA?

Ie normal BMs

A

SGLT2s (dapagliflozin) makes you pee out glucose

60
Q

A patient has a high blood glucose, 1 unit of insulin will roughly reduce blood glucose by how many?

A

3

61
Q

How do you calculate serum osmolarity?

A

2 (sodium + potassium) + urea + glucose

62
Q

Patient has low sodium, what is the first step to find a diagnosis?

A

Check plasma osmolality:

Isotonic- lipids or proteins are masking true value so Na is not really low. Check on ABG machine instead.

Hypertonic- if given mannitol, high glucose/urea causes blood dilution

Hypotonic- what you expect with low Na, check fluid status next

63
Q

Low Na and hypovolaemic, causes?

A

Burns
Vomiting
Diuretics
Sepsis- 3rd space losses leads to intravascular depletion so increase ADH, more dilute sodium

64
Q

Low Na and euvolaemic, causes?

A

SIADH- more water kept than sodium
Psychogenic polydipsia
Addison’s
Beer Potomania- per litre of urine need enough solute/salts

65
Q

Low Na and hypervolaemic, causes?

A

Failures

66
Q

What is the difference between osmolality and tonicity?

A

Osmolality is an absolute concentration
Tonicity is a relative concentration that is more useful clinically, ie how is the RBC size affected by the concentration of fluid

67
Q

Per day, if someone has high sodium how much should you try and reduce the concentration?

A

6mmol/L change of Na per day

Otherwise demyelination may occur up to 6 days later

68
Q

Which two hormones if missing, means patient’s can’t pee out free water into urine so sodium drops?

A

Thyroid and cortisol (ie addison’s)

Mimics SIADH (ADH = like a bath plug)

69
Q

What two things have to be checked before diagnosing SIADH?

Low sodium, hypotonic serum, euvolaemic

A

ADH is like a plug in a bath with the tap running

  1. If they are on diuretics
  2. Cortisol or thyroid hormone levels
70
Q

Causes of SIADH?

Like putting a plug in the bath when the tap is running

A 
Post-op
Hypovolaemia- bleeding, dehydration
Drugs- opiates, SSRIs, CNS drugs, PPIs
Pulmonary disease- neoplastic (small cell lung cancer) or pneumonia
CNS disease
Tumours
71
Q

What are the two main types of hypoglycaemia and the tests for them?

A
  1. Check drugs (diabetes, quinine, malnourished)
  2. Post-prandial (big influx of carbs causes large insulin release)- mixed meal test
    Fasting (more serious)- 72 hour fast

Check urine sulphonylurea for C-peptide (if taking artificial insulin it won’t have C-peptide)

72
Q

Which familial syndrome might be associated with insulinoma?

A

Men1- pancreas, parathyroid, pituitary

73
Q

Medical treatment of insulinoma?

A

Diazoxide
Hyperpolarises islet cells (acting the opposite way to sulphonylurea)

Or Octreotide (somatostatin blocks pancreatic hormone production)

74
Q

On which diabetes drug can you get a euglycaemic DKA?

Ie normal BMs

A

SGLT2s (dapagliflozin) makes you pee out glucose

75
Q

A patient has a high blood glucose, 1 unit of insulin will roughly reduce blood glucose by how many?

A

3

76
Q

How do you calculate serum osmolarity?

A

2 (sodium + potassium) + urea + glucose

77
Q

Patient has low sodium, what is the first step to find a diagnosis?

A

Check plasma osmolality:

Isotonic- lipids or proteins are masking true value so Na is not really low. Check on ABG machine instead.

Hypertonic- if given mannitol, high glucose/urea causes blood dilution

Hypotonic- what you expect with low Na, check fluid status next

78
Q

Low Na and hypovolaemic, causes?

A

Burns
Vomiting
Diuretics
Sepsis- 3rd space losses leads to intravascular depletion so increase ADH, more dilute sodium

79
Q

Low Na and euvolaemic, causes?

A

SIADH- more water kept than sodium
Psychogenic polydipsia
Addison’s
Beer Potomania- per litre of urine need enough solute/salts

80
Q

Low Na and hypervolaemic, causes?

A

Failures

81
Q

What is the difference between osmolality and tonicity?

A

Osmolality is an absolute concentration
Tonicity is a relative concentration that is more useful clinically, ie how is the RBC size affected by the concentration of fluid

82
Q

Per day, if someone has high sodium how much should you try and reduce the concentration?

A

6mmol/L change of Na per day

Otherwise demyelination may occur up to 6 days later

83
Q

Which two hormones if missing, means patient’s can’t pee out free water into urine so sodium drops?

A

Thyroid and cortisol (ie addison’s)

Mimics SIADH (ADH = like a bath plug)

84
Q

What two things have to be checked before diagnosing SIADH?

Low sodium, hypotonic serum, euvolaemic

A

ADH is like a plug in a bath with the tap running

  1. If they are on diuretics
  2. Cortisol or thyroid hormone levels
85
Q

Causes of SIADH?

Like putting a plug in the bath when the tap is running

A 
Post-op
Hypovolaemia- bleeding, dehydration
Drugs- opiates, SSRIs, CNS drugs, PPIs
Pulmonary disease- neoplastic (small cell lung cancer) or pneumonia
CNS disease
Tumours
86
Q

What are the two types of auto-antibodies in thyroid disease identified by fluorescence?

A

Anti-Thyroid Peroxidase (TPO): against the membranes

Anti-Thyroglobulin: against the colloid in the middle of the circles.

87
Q

If a patient is dehydrated, what pattern of urea and creatinine would suggest this?

A

High urea compared to creatinine.

Urea is reabsorbed to try to rebalance electrolytes whereas creatinine is not

88
Q

What changes on bloods can indicate dehydration?

A

High urea, compared to creatinine
High albumin
High haematocrit (RBCs vs blood volume)

89
Q

Why is the anion gap needed?

A

Many lab tests do not measure every cation (+ve charge) or anion (-ve) in the blood, but plasma is neutral.
The unmeasured ions tend to be anions.

If acid has been added that is not measured on lab tests, ie ketoacids or lactate it will be buffered by HCO3, lowering concentration of this and increasing the anion gap

90
Q

How would bone mets look different to primary hyperparathyroidism on bloods?

A

Both cause high calcium
In mets the potassium would be normal or raised (as PO4 gets released from bone)
In primary hyperPTH potassium would be low or normal as PTH inhibits PO4 absorption from kidney (but note vit D increases phosphate absorption from intestine)

91
Q

Why is Po4 high in hypoparathyroidism?

A

Normally PTH prevents P04 reabsorption from the kidney, so if levels are low P04 will rise.

92
Q

Which two blood findings suggest excess alcohol intake?

A

Raised MCV and y-GT

93
Q

What happens to plasma and urine osmolality in diabetes insipidis?

A

ADH is like the bath plug, in this condition there is no ADH/bath plug but the taps are running so:
Salt gets deposited in the bath (high plasma osmolality)
Water runs down the plug hole (low urine osmolality)

94
Q

What is 5% dextrose useful for, hydration or fluid resuscitation?

A

Hydration- the sugar in the fluid gets quickly metabolised by the liver leaving pure water, the water will equilibrate into cells so little volume is left in the intravascular compartment to upkeep BP

95
Q

What volume of saline is appropriate for fluid resuscitation in the elderly or those with heart failure?

A

250mL

96
Q

In which scenarios should you consider increasing K+ replacement above the normal maintenance?

A

GI losses are rich in K+ so if someone has diarrhoea, vomiting or an NG tube

97
Q

Which other pathway does angiotensin converting enzyme input into?

A

It metabolises bradykinin, so ACEi lead to raised levels of bradykinin and might explain why some people get a cough

98
Q

What effect does ANP and BNP have on sodium in the kidney?

A

They reduce Na+ absorption from the DCT and inhibit renin (which means there’s less AT-II and thus aldosterone and therefore salt uptake)

99
Q

Name 4 causes of a metabolic acidosis with an increased anion gap:

A

More unmeasured anions= negatively charged (the acid donates it’s H+ to HC03- buffer, leaving behind it’s conjugate base)

  1. Lactic acid
  2. Urate (renal failure)
  3. Keto acids (diabetes or alcohol)
  4. Drugs (salicylates, methanol, metformin)
100
Q

Metabolic acidosis, anion gap 16

A

Normal anion gap:
If acidosis is caused by a loss of bicarbonate then chloride replaces it.
GI losses- diarrhoea, pancreatic fistula
Renal dysfunction- renal tubular acidosis type 1 or 2 (HCO3 loss)
Renal hypoaldosterone- Addison’s disease (Na absorption by aldosterone in DCT leads to H+ secretion), drugs (ACEi, diuretics)

101
Q

3 causes of metabolic alkalosis

A

Loss of acid:
GI- vomiting
Renal- K+ depletion from diuretics
Burns- unclear why

102
Q

In which conditions would respiratory acidosis prompt you to get an urgent ITU review?

A

CO2 is high, so it is a sign of exhaustion in
Asthma
Pneumonia
Pulmonary oedema

103
Q

How can tonicity/osmolality help to determine whether a low sodium is a true result?

A

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

Isotonic- pseudohyponatraemia from high lipids or proteins
Hypertonic- high glucose pushing sodium out of vessels
Hypotonic- consistent with low Na+

104
Q

If a patient is found to have a K+ of 6.7, what symptoms should you ask about?

A

Chest pain
Palpitations
Light headedness
Weakness

105
Q

Worrying ECG changes in hyperkalaemia?

A

Flattened P waves
Broad bizarre QRS
Upsweeping ST
Tall tented T’s

Also VF

106
Q

Causes of hyperkalaemia?

A

Drugs: ACEi, suxamethonium (nAChR inhibitor anaesthetics), K+ sparing diuretics
Kidney: renal failure, metabolic acidosis, Addison’s
Cell destruction: Rhabdomyolysis, massive blood transfusion, burns

107
Q

Digoxin toxicity is made worse by which metabolite abnormality?

A

Hypokalaemia

(As digoxin inhibits myocardial Na/K/ATPase, increasing Na in cell and preventing Na/Ca exchanger)
Na/K/ATPase pumps Na out of cell, Na/Ca exchanger allows sodium in

108
Q

ECG changes that are a worry in cases of hypokalaemia?

A

Everything is down or sluggish
Small/inverted T waves
Long PR
Depressed ST

Only up is that U wave!

109
Q

Which metabolic imbalance is hard to correct until Mg levels have normalised?

A

Hypokalaemia

110
Q

Endocrine causes of hypokalaemia?

A

Conns (aldosteronism- high BP)

Cushing’s

111
Q

Which food can cause hypokalaemia?

A

Liquorice

112
Q

Management of asymptomatic patient with K+ of 2.6mmol, no ECG changes?

A 
If mild (>2.5, asymptomatic)
Oral K+ supplements like Sando-K
113
Q

What is the fastest that K+ can be given if severe hypokalaemia (<2.5mmol ± dangerous symptoms)?

A

No more than 20mmol/hour

Not more concentrated than 40mmol per litre

Fifth Year Medicine (32 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions