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Year 6 Medicine > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

How is diabetes mellitus diagnosed?

A

Symptoms + 1 diabetes test result
No symptoms + 2 diabetes test results

Fasting >=7 mmol/L
HbA1c >=6.5%/ >=48mmol/L
OGTT >=11.1 mmol/L
Random >=11.1 mmol/L

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2
Q

What is impaired glucose tolerance?

A

random or OGTT >7.8 but <11.1

HbA1c 42-47

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3
Q

What is impared fasting glucose?

A

> 6.1 but <7.0

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4
Q

What are the symptoms of diabetes?

A

fatigue
polydipsia
polyuria

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5
Q

What are the complications of diabetes?

A 
microvascular and microvascular 
micro: 
retinopathy
nephropathy
neuropathy - gastroparesis (vag. nerve neuropathy), neuropathic pain, peripheral neuropathy

macro:
cerebrovascular disease
cardiovascular disease
peripheral vascular disease

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6
Q

Why does diabetic foot happen?

A

Secondary to peripheral artery disease -> intermittent claudication
and neuropathy -> charcot foot

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7
Q

How is diabetic foot screened for?

A

annually (at least)
ischaemia - palpate dorsalis pedis and posterior tibial
neuropathy - 10g monofilament test

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8
Q

how is diabetic nephropathy screened for?

A 
yearly ACr (albumin creatinine ratio)
1st - spot sample, if abnormal then use a morning sample
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9
Q

what is the first sign of diabetic nephropathy?

A

microalbuminuria

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10
Q

What is the management of diabetic nephropathy?

A

ACEi (protective in chronic but toxic in AKI)
Monitor eGFR: if drop >20% then stop ACEi
a small initial drop is expected

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11
Q

What may cause a falsely high HbA1c?

A

decreased destruction e.g. alcoholism, B12 deficiency, DA

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12
Q

What may cause a falsely low HbA1c?

A

SCD

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13
Q

How many times a day should BMs be monitored?

A

adult >=4x a day before meals and bed

child >=5x a day

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14
Q

What is the waking blood sugar target?

A

5-7mmol/L

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15
Q

What is blood sugar target at other points the day

A

4-7 mmol/L

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16
Q

How often is HbA1c monitored in T1DM?

A

Once every 3-6m

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17
Q

What is first line management of T1DM?

A

basal bolus regimen
Rapid = novo rapid/aspart
long acting = lantus/glargine

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18
Q

How should t1dm management be changed if the patient is sick?

A

continue normal insulin but increase monitoring to every 4 hours
may need to increase short acting insulin

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19
Q

What is 2nd line management of T1DM?

A

BD pre-mixed regimen (given at the start of breakfast and dinner, instead of TDS)
Intermediate + rapid acting
Intermediate + short acting

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20
Q

Give some examples of rapid acting insulin?

A

(Given at start of meal)
Novorapid (aspart)
Humalog (lispro)
Apidra (glulisine)

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21
Q

Give some examples of short acting insulin?

A

(Given 15-30 mins before meal)
Actrapid
Humulin S
FRII

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22
Q

Give some examples of intermediate acting insulin?

A

(Given OD/BD or as part of a mix)
Insulatard
Humulin I
Insuman basal

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23
Q

Give some examples of long acting insulin?

A

(Given OD)
Lantus (glargine)
Levemir (determir)
Tresiba (degludec)

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24
Q

What is a normal HbA1c?

A

20-42

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25
Q

When should conservative measures be initiated for T2DM?

A

If HbA1c >=42/ 6.0%

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26
Q

What HbA1c is pre-diabetes and how should it be managed?

A

42-48

refer to diabetes prevention programme

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27
Q

When should medical therapy be initiated for T2DM?

A

If Hba1c >=48 / 6.5%

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28
Q

What is medical management of T2DM

A

RF modification: aspirin, atorvastatin, anti HTN
1st line: metformin
2nd line: metformin + (sulphonylurea/thiazolidione/SGLT2/gliptin)
3rd line: triple therapy
4th: insulin
5th: metformin + sulphnylurea + GLP-1 analogue (exenatide)

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29
Q

When should dual therapy be initiated for T2DM?

A

If HbA1c rises to >58 mmol or >7.5%

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30
Q

What is target HbA1c in T2DM on single therapy?

A

48

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31
Q

What are the side effects of metformin?

A

appetite suppression, lactic acidosis, GI upset, reduced B12 absorption

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32
Q

What should be changed if GI upset on metformin?

A

switch from immediate release to modified release before trying new drugs

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33
Q

When is metformin contraindicated ?

A

eGFR <30
tissue hypoxia (MI, surgery)
alcohol abuse

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34
Q

What is T2DM HbA1c target on dual therapy?

A

53

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35
Q

Give some examples of sulphonylureas

A

gliclazide

glibenclamide

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36
Q

What are the side effects of suphonylureas?

A

weight gain
hypoglycaemia !!

Rarer:
SIADH
Hepatic dysfunction
BM suppression

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37
Q

What are sulphnylurea contraindications?

A

ketoacidosis

caution: high BMI, G6PDD

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38
Q

Give an example of a thiazolidione

A

pioglitazone

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39
Q

what are the side effects of thiazolidiones?

A

weight gain
abnormal LFTs
baldder cancer
osteoporosis

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40
Q

What are contraindications to thiazolidiones?

A 
HF
Bladder cancer (past/present)
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41
Q

Give an example of a gliptin?

A

sitagliptin

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42
Q

When are gliptins a good choice of second therapy?

A

when the patient is overweight

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43
Q

Contraindications to gliptins?

A

ketoacidosis

caution: eGFR <45

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44
Q

Give an example of an SGLT2 inhibitor?

A

empagliflozin

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45
Q

what are the side effects of SGLT2 inhibitors?

A

euglycaemic DKA, infections
fourniers gangrene
angioedema

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46
Q

SGLT2 inhibitors contraindications?

A

DKA,
eGFR <60 -> use gliclazide or sitagliptin instead

caution: UTI

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47
Q

When are SGLT2 inhibitors preferable?

A

encourage weight loss
improve cardiac outcomes
decrease admission rates of HF

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48
Q

Give some examples of triple therapy regimes for T2DM

A
  1. metformin + sulphonylurea + gliptin
  2. metformin + sulphonylurea + thiazolidione
  3. metformin + sulphonylurea/thiazolidione + SGLT2

2nd: insulin 1ml

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49
Q

When should a GLP-1 analogue be used?

A

if BMI>35 or if insulin unacceptable

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50
Q

What is MODY?

A

t2dm variant
<25yo
FHx (AD)
no ketosis

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51
Q

Ix MODY?

A

C-peptides

genetics

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52
Q

Mx MODY?

A

VERY SENSITIVE SULPHONYLUREAS

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53
Q

Types of MODY?

A

MODY2 (20%) - defective glucokinase
MODY3 (60%) - mutated HNF-1alpha, risk HCC
MODY5 (rare) - mutated HNF-1beta, liver cysts

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54
Q

What is LADA?

A

slowly progressive T1DM 20-50yo, no FHx
latent autoimmune diabetes in adults
ketones +ve

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55
Q

Ix for LADA?

A

GAD Abs, C peptide low

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56
Q

Mx of LADA?

A

oral hypoglycaemic -> insulin

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57
Q

What is the management of myxoedema coma?

A

yxoedema coma is a medical emergency requiring treatment with
IV thyroid replacement
IV fluid
IV corticosteroids (until the possibility of coexisting adrenal insufficiency has been excluded)
electrolyte imbalance correction
sometimes rewarming

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58
Q

What are some precipitating events of a thyroid storm?

A

thyroid or non-thyroidal surgery
trauma
infection
acute iodine load e.g. CT contrast media

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59
Q

what are the clinical features of thyroid storm?

A

fever > 38.5ºC
tachycardia
confusion and agitation - altered mental status
nausea and vomiting
hypertension
heart failure
abnormal liver function test - jaundice may be seen clinically

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60
Q

What is the management of thyroid storm?

A

symptomatic treatment e.g. paracetamol
treatment of underlying precipitating event
beta-blockers: typically IV propranolol
anti-thyroid drugs: e.g. methimazole or propylthiouracil
Lugol’s iodine
dexamethasone - e.g. 4mg IV qds - blocks the conversion of T4 to T3

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61
Q

what is subclinical hyperthyroidism?

A

TSH raised but T3, T4 normal

no obvious symptoms

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62
Q

What is the first line test for acromegaly?

A

serum IGF-1 level

if elevated then do OGTT

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63
Q

What are some causes of hypoglycaemia?

A

insulinoma - increased ratio of proinsulin to insulin
self-administration of insulin/sulphonylureas
liver failure
Addison’s disease
alcohol
nesidioblastosis - beta cell hyperplasia

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64
Q

What are some side effects of thyroxine?

A

hyperthyroidism: due to over treatment
reduced bone mineral density
worsening of angina
atrial fibrillation

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65
Q

What does thyroxine interact with?

A

iron, calcium carbonate

absorption of levothyroxine reduced, give at least 4 hours apart

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66
Q

Following a changes in thyroxine dose when should TFTs be checked?

A

after 8-12 w

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67
Q

How should the dose of thyroxine change for pregnant ladies?

A

omen with established hypothyroidism who become pregnant should have their dose increased ‘by at least 25-50 micrograms levothyroxine’* due to the increased demands of pregnancy. The TSH should be monitored carefully, aiming for a low-normal value

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68
Q

What are some common causes of hypothyroid?

A

Autoimmune (Hashimoto’s disease, atrophic)
Iodine deficiency
Thyroiditis (post-viral, post-partum)
Iatrogenic (thyroidectomy, radioiodine, drugs)

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69
Q

What is DKA?

A

bm>11
ketones >3
acidosis

rapid onset

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70
Q

Causes of DKA?

A

infection
alcohol
trauma
insulin missed

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71
Q

Ix DKA?

A 
U&E
ABG
ECG
BM
Ketones
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72
Q

Mx DKA?

A
  1. fluids (500 ml bolus over 15m if SBP <90 then 1L NaCl over 1h)
  2. Insulin 0.1U/kg/hr
  3. Potassium
  4. 10% dextrose when BM<15 100ml/hour
  5. VTE prophylaxis
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73
Q

How are fluids administered in DKA?

A 
1L over 1h
1L + kcl over 2h
1L + kcl over 2h
1L + kcl over 4h
1L + kcl over 4h
1L + kcl over 6h
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74
Q

What is a HHS?

A

t2dm
pH >7.3
osmolatiry >320 mOSM
BM >30mmol/L (massive hyperglycaemia non ketotic)

over a few days

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75
Q

Management of HHS?

A
  1. fluids - 3-6Lin 12h (1L 0.9% NaCl IV over 2h)
  2. monitor and avoid rapid correction Na
  3. Insulin 0.05u/kg/h sliding scale once BM stop dropping
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76
Q

what does rapid correction of Na in HHS causes?

A

osmotic demyelination syndrome

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77
Q

What are the types of thyroid cancer?

A 
PFMA 
Papillary
Follicular
Medullary 
Anaplastic
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78
Q

what is seen in medullary thyroid cancer?

A

raised calcitonin (PTH antagonist)

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79
Q

Investigations for thyroid neck lump?

A

TFTs
Technetium uptake scan
Auto Abs (anti-TPO, anti-TG)

<1cm do not investigate
>1cm USS+ FNA

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80
Q

Management of thyroid Ca?

A

hemi thyroidectomy (-/+total) + Iodine-131 to kill remaining cells
yearly follow up: if +ve administer more I-131:
- I-123 whole body scans
thyroglobulin measurements/calcitonin if medullary
Remission for 7y -> fully cured and discharged

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81
Q

What are some causes of hyperthyroidism?

A 
Graves (40-60%)
Toxic multinodular goitre (30-50%)
Single toxic adenoma (5%)
subacute thyroiditis/viral thyroiditis/de Quervains (hyper -> hypo)
Postpartum thyroiditis
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82
Q

What are some high uptake causes of hyperthyroidism?

A

Graves (40-60%)
Toxic multinodular goitre (30-50%)
Single toxic adenoma (5%)

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83
Q

What are some low uptake causes of hyperthyroidism?

A

subacute thyroiditis/viral thyroiditis/de Quervains (hyper -> hypo)
Postpartum thyroiditis

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84
Q

Features of Graves?

A

diffuse goitre
thyroid eye disease
thyroid acropatchy
pretibial myxoedema

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85
Q

Investigations for graves?

A

Anti TSH-R Abs (90%)
Anti-TPO Abs (75%)
increase homogenous radioactive uptake

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86
Q

Mx graves?

A
  1. propanolol (primary care), carbimazole (PTU 2nd line or pregnancy)
  2. radioiodine if unlikely remission with ATDs
  3. surgery - must be euthyroid
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87
Q

Types of treatment regime for Graves?

A

titration or block and replace

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88
Q

What is block and replace method?

A

6-9m fixed high dose carbimazole incl thyroxine

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89
Q

titration method for graves?

A

preferred method
12-18m dose on TFTs
reduce once euthyroid

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90
Q

what must be given to graves patients before surgery

A

must be euthyroid:

  1. thionamides (stop 10 days befre) or propanolol
  2. laryngoscopy (check vocal cords)
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91
Q

What can precipitate a thyroid storm?

A

surgery

radioiodine

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92
Q

S/S of thyroid storm?

A

hyperthermia, tachycardia, jaundice, altered GCS, cardiac (af, high output HF)

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93
Q

Mx thyroid storm?

A

IV Propanolol
thionamides (PTU)
hydrocortisone
Iodine (1-4 hours after ATDs)

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94
Q

Causes of primary hypothyroid?

A

Hashimoto (most common uK)
Reidels thyroiditis
Subacute/viral/de quervains
iodine deficiency (most common developing world)
Iatrogenic: post graves/ drugs (amiodarone, lithium)

95
Q

What is subclinical hypothyroid?

A

high TSH, T4 normal

no S/S

96
Q

When should subclinical hypothyroid be treated?

A

TSH>10

97
Q

Causes of secondary hypothyroid?

A

pituitary tumour

compressive lesion

98
Q

which drugs may cause hypothyroid?

A

amiodarone

lithium

99
Q

Mx of hypothyroid?

A

levothyroxine (50mcg, 25 in elderly) - check TFTs in 8-12w
aim for normal TSH
hypothyroid in pregnancy - increase T4 by 25-50

100
Q

Levothyroxine interactions?

A

Give T4 at least 4 hours before:
Iron
calcium carbonate

try to take thryoxine 1h before foood/other meds in general

101
Q

what are the S/S of a myoxedema coma?

A

hypothermia
hyporeflexia
bradycardia
seizures

102
Q

What is a myxoedema coma?

A

Myxedema coma is an extreme complication of hypothyroidism in which patients exhibit multiple organ abnormalities and progressive mental deterioration

103
Q

Mx of myxoedema coma?

A

IV thyroxine
IV hydrocortisone
IV fluids

104
Q

Causes of addisonian crisis?

A
  1. sepsis/surgery
  2. adrenal haemorrhage
  3. steroid withdrawal

autoimmune, TB

105
Q

Management of addisonian crisis?

A

Initial:

  1. IM hydrocortisone (100mgSTAT)
  2. IV fluid bolus (0.9% saline >90sbp) +/-glucose

Continuing:
IV fluids
IV/IMhydrocortisone, convert to PO dexamethasone after 72h

Patient education:

  1. do not miss doses
  2. medic alert bracelet
  3. given hydrocortisone for injection in case of crisis
  4. discuss how to adjust dose in illness (double glucocorticoid, fludro stays same)
106
Q

What is addisons?

A

mineralocorticoid and glucocorticoid deficiency

107
Q

What are S/S addisons?

A

postural hypotension
skin pigmentation
lethargy
depression

108
Q

what electrolyte disturbances are seen in addisons?

A

raised K

low NA and glucose

109
Q

Addisons Ix?

A
  1. 9am cortisol if high (>500 unlikely addisons),<500 do synacthen
  2. SynACTHen test - cortisol should at least double or primary insufficiency
  3. plasma cortisol at 30/60 min
110
Q

What is cushings?

A

XS cortisol

111
Q

what are the causes of cushings?

A

endogenous:
Pituitary tumour ‘Cushing’s disease’ - 85%
Adrenal tumour (10%)
Ectopic ACTH producing tumour (5%)-SCLC

exogenous:
Iatrogenic steroid use - majority

112
Q

What is pseudo-cushings?

A

mimics cushings - often ETOH XS or depression
causes false +ve dex suppression or 24h urinary free cortisol
use insulin stress test to differentiate

113
Q

How do you screen/confirm cushings?

A
  1. 11pm salivary cortisol - if low not cushings AND/OR
  2. LDDST - 1mg dex at 11pm, measure cort before 9am
    in cushings cortisol will not be suppressed

confirm:
inferior petrosal sinus sampling
distinguishes pituitary from ectopic ACTH

114
Q

Mx cushings?

A
  1. pituitary adenoma -> surgery
  2. adrenal mass -> adrenalectomy +/-steroid replacement
  3. ectopic -> ketoconazole, meyrapone, mifepristone
115
Q

what is Nelsons syndrome?

A

removal of adrenal leads pituitary enlargement (hypopituitarism by compressing stalk) and +++ACTH (pigmentation)

116
Q

What is Conn’s syndrome?

A

primary hyperaldosteronism

tumour of Zona G

117
Q

What biochemical abnormalities are seen in conns?

A

high Na
Low K
uncontrollable HTN
Raised Aldo:renin ratio

118
Q

S/S of conns?

A

refractory hypertension

hypokalaemia

119
Q

Ix conns?

A

plasma aldo/renin ratio

HR-CT and adrenal vein sampling (uni vs bilateral)

120
Q

Mx conns?

A

solitary - spironolactone/surgery

bilateral/elderly - spironolactone/eplerenone only

121
Q

Differentials for conns and how would you assess this?

A

renal artery stenosis
Conn’s (ARR high, high aldosterone, low renin)
Renal artery stenosis (ARR normal, high aldosterone, high renin)

122
Q

prevalence of pituitary adenoma?

A

10% but most asymptomatic

123
Q

classification of pituitary adenomas?

A

micro: <1cm
macro: >1cm

hormonal status
secretory/functioning
non-secretory/non functioning

124
Q

Differentials for pituitary adenoma?

A 
pituitary hyperplasia
brain mets
vascular malformation e.g. aneurysm
lymphoma
craniopharynioma
meningioma
hypophysitis
125
Q

S/S pituitary adenoma?

A
  1. XS hormones
    men: prolactinoma -> impotence, low libido, galactorrhea
    women: infertility, low libido, amenorrhoea, galactorrhea, osteoporosis
  2. headaches
  3. bitemporal hemianopia
  4. hypopituitarism
126
Q

investigations for prolactinoma?

A

bloods: GH, prolactin, ACTH, FH, LSH, TFTs
visual field testing
MRI brain with contrast

127
Q

investigations for acromegaly?

A

serum IGF-1 then OGTT

MRI brain with contrast

128
Q

Management of prolactinoma?

A
  1. medical (bromocriptine, cabergoline)

2. surgical - transsphenoidal hypophysectomy

129
Q

Management of acromegaly?

A
  1. surgery (transsphenoidal hypophysectomy)
  2. Somatostatin analogue (octreotide -> bromocriptine, cabergoline)
  3. pegvisomant (GH-antagonist)
  4. radiotherapy
130
Q

Complications of acromegaly?

A

HTN
Diabetes (>10%)
Cardiomyopathy
Colorectal Ca

131
Q

MEN1 gene and features?

A

MEN1 gene (PPP)
pituitary adenoma
parathyroid hyperplasia
pancreatic tumour

132
Q

MEN2A gene and features?

A

RET oncogene (PMP)
parathyroid hyperplasia
medullary thyroid carcinoma
pheochromocytoma

133
Q

MEN2B gene and features?

A 
RET oncogene (MMMP)
Mucosal neuromas
marfanoid body habitus
medullary thyroid carcinoma
phaeochromocytoa
134
Q

How to calculate serum osmolality?

A

2(Na + K) + urea + glucose

135
Q

Complications of HHS?

A

Seizures
cerebral oedema
contral pontine myelinolysis

136
Q

Which thyroid condition causes a tender goitre?

A

De Quervains thyroiditis

137
Q

What is seen in sulphonylurea OD?

A

Hyperinsulinaemia

High C peptides

138
Q

What are the causes of hyperaldosteronism?

A

conns (adrenal adenoma)
bilateral idiopathic adrenal hyperplasia (70%)
unilateral idiopathic adrenal hyperplasia

139
Q

What are the features of GI autonomic neuropathy?

A

complication diabetes
Gastroparesis
- symptoms include erratic blood glucose control, bloating and vomiting
- management options include metoclopramide, domperidone or erythromycin (prokinetic agents)

Chronic diarrhoea
- often occurs at night

Gastro-oesophageal reflux disease
- caused by decreased lower esophageal sphincter (LES) pressure

140
Q

Side effects of thyroxine therapy?

A

hyperthyroidism: due to over treatment
reduced bone mineral density
worsening of angina
atrial fibrillation

141
Q

what are the diabetes sick day rules?

A

If a patient is on insulin, they must not stop it due to the risk of diabetic ketoacidosis. They should continue their normal insulin regime but ensure that they are checking their blood sugars frequently

142
Q

When should you refer for surgery in primary hyperparathyroid?

A
  • Polydipsia, polyuria or constipation.
  • Osteoporosis, fragility fracture or nephrolithiasis.
  • Albumin-adjusted serum calcium is ≥ 2.85 mmol/L.
143
Q

What are the causes of primary hyperparathyroid?

A

80%: solitary adenoma
15%: hyperplasia
4%: multiple adenoma
1%: carcinoma

144
Q

what do investigations in primary hyperparathyroid show?

A

raised calcium, low phosphate
PTH may be raised or (inappropriately, given the raised calcium) normal
technetium-MIBI subtraction scan
pepperpot skull is a characteristic X-ray finding of hyperparathyroidism

145
Q

Mx primary hyperparathyroid?

A
  • the definitive management is total parathyroidectomy
  • conservative management may be offered if the calcium level is less than 0.25 mmol/L above the upper limit of normal AND the patient is > 50 years
    AND there is no evidence of end-organ damage
  • patients not suitable for surgery may be treated with cinacalcet, a calcimimetic
146
Q

S/s of primary hyperparathyroid?

A 
'bones, stones, abdominal groans and psychic moans':
polydipsia, polyuria
depression
anorexia, nausea, constipation
peptic ulceration
pancreatitis
bone pain/fracture
renal stones
hypertension
147
Q

what electrolyte abnormalities would be seen in cushings on ABG?

A

hypokalaemic metabolic alkalosis

Impaired glucose tolerance

148
Q

What are the biochemical abnormalities in congenital adrenal hyperplasia?

A

Increased plasma 17-hydroxyprogesterone levels
Increased plasma 21-deoxycortisol levels
Increased urinary adrenocorticosteroid metabolites

149
Q

what is the inheritance patterns of congenital adrenal hyperplasia?

A

autosomal recessive

150
Q

what are the main causes of hypernatraemia?

A

Increase in sodium:

  • dietary high intake
  • medical high intake (saline, sodium bicarb)
  • conns/ bilateral adrenal hyperplasia
  • renal artery stenosis

loss of water:

  • diabetes inspidus
  • osmotic diuresis
  • GI loss
  • sweat loss
151
Q

what are some causes of nephrogenic DI?

A

Hypercalcaemia
hyperkalaemia
lithium
sickle cell anaemia

152
Q

investigations for hypernatraemia?

A
  • serum glucose (exclude DM/osmotic diuresis)
  • serum K (exclude hypokalaemia/nephrogenic)
  • serum calcium (exclude hypercalcaemia/nephrogenic)
  • plasma and urine osmolality (exclude hyperaldosteronism)
  • water deprivation test
153
Q

What is the management of hypernatraemia

A

treat underlying cause
correct water deficit -> 5% dextrose
correct ECF vol depletion 0.9% saline
serial Na+ measurements -> every 4-6h

154
Q

What are the complications of hypernatraemia?

A

rapid hypernatraemia correction -> cerebral oedema

rapid hyponatraemia correction -> central pontine myelinolysis

155
Q

What is seen in the plasma/urine osmolality in hyperaldosteronism?

A

high plasma osmolality

low urine osmolality

156
Q

What is the best indicator of hypovolaemia?

A

low urine Na (<20)

157
Q

What are some causes of hyponatraemia in a hypervolaemic patient?

A

cardiac failure- ADH release
cirrhosis- ADH release
renal failure

158
Q

What are some causes of hyponatraemia in a euvolaemic patient?

A

psychogenic polydipsia
SIADH
Hypothyroid
Adrenal insufficiency

159
Q

what are some causes of SIADH?

A

CNS pathology - stroke, haemorrhage, tumour
Lung pathology - pneumonia (legionella), pneumothorax
Drugs - SSRI, TCA, PPI, carbamazepine, sulphonylureas, vincristine, cyclophosphamide
Tumours
Surgery

160
Q

What are some causes of hyponatraemia in a hypovolaemic patient?

A

diarrhoea
vomiting
diuretics

161
Q

Investigations for euvolaemic hyponatraemia?

A

hypothyroid -TFTs
adrenal insufficiency -short synACTHen
SIADH - plasma osmolarity and urine osmolarity

162
Q

What is seen in the plasma/urine osmolality in SIADH?

A

low plasma osmolality (<275), plasma Na <135

high urine osmolality (>100),urine Na>30

163
Q

Management of hyponatraemia?

A 
hypovolaemic -> slow 0.9% saline
euvolaemic/hypervolaemic -> fluid restrict (<800ml/day)+ treat cause
severely hyponatraemic (<120) -> slow 3% saline
164
Q

Management of SIADH?

A

Democlocycline - induce nephrogenic DI
monitor U&E
vaptans (v2 Receptor antagonist)

165
Q

S/S of central pontine myelinolysis?

A 
quadriplegia
dysarthria
dysphagia
seixures
coma
death
166
Q

Causes of hyperkalaemia?

A 
reduced GFR
reduced renin
ACEi
ARBs
Addisons
Aldosterone antagonists (spiro)
Heparins
tacrolimus
potassium release from cells*
167
Q

what can cause K release from cells?

A

acidosis

rhabdomyolysis

168
Q

management of hyperkalaemia?

A 
10ml 10% calcium gluconate
120ml 20% dextrose
10 units insulin
nebuliser salbutamol
treat underlying cause
169
Q

What is seen on ECG with hyperkalaemia?

A 
peaked T wave (early)
broad QRS
flat P wave
Prolonged PR (brady)
Sine wave
170
Q

what are the general symptoms of hyperkalaemia?

A

muscle weakness/cramps
lethargy, fatigue, paraesthesia
palpitations

171
Q

What are the causes of hypokalaemia?

A 
GRRR
GI losses (diarrhoea>vomiting)
Renal losses (loop/thiazides, MR XS)
Redistribution
Rare causes - RTA t1,2, hypomagnesaemia
172
Q

What causes K+ to shift into cells

A

insulin
beta agonists
alkalosis

173
Q

What are the clinical features of hypokalaemia?

A

muscle weakness
cardiac arrhythmia
polyuria and polydipsia

174
Q

What ECG changes are seen in hypokalaemia?

A

ST depression, flat T waves, U waves

175
Q

what is the management of mild/moderate/asymptomatic hypokalaemia?

A

K+ 2.5-3.5

oral KCl - 2 SanoK tablets TDS

176
Q

what is the management of severe/symptomatic hypokalaemia?

A

K+ <2.5 mmol/L
IV KCl - 3x 1L 0.9% saline + 40 mmol/KCL over 24h
Cardiac monitoring

177
Q

Which cancer is hashimoto associated with?

A

MALT lymphoma

178
Q

What is thyroid acropachy?

A

digital clubbing
soft tissue swelling of the hands and feet
periosteal new bone formation

179
Q

which hormones are reduced in the stress response/surgery?

A

Insulin
Testosterone
Oestrogen

180
Q

What are some causes of hyperparathyroid?

A

solitary adenoma (80%)
hyperplasia (15%)
multiple myeloma (4%)
carcinoma (1%)

181
Q

What is parathyroid solitary adenoma associated with?

A

hypertension

182
Q

what is parathyroid hyperplasia associated with?

A

MEN I, MEN II

183
Q

What are the S/S of hypercalcaemia?

A 
bones
stones
abdominal groans
psychic moans
polydipsia and polyuria
HTN, corneal calcification, short QT
184
Q

What are some S/S of hypocalcaemia

A 
paraesthesia
muscle cramps
spasms
Long WT
Low Mg (required for PTH)
185
Q

what are the investigations for hyperparathyroid/hypercalcaemia?

A

PTH may be raised or inappropriately normal
Technetium MIBI subtraction scan
XR -> pepper pot skull
ALP- raised pagets

186
Q

What are some causes primary hyperparathyroidism?

A

85% solitary adenoma

187
Q

What are some causes of secondary hyperparathyroidism?

A

chronic renal failure
vitamin D deficiency
parathyroid hyperplasia

188
Q

what are some causes of tertiary hyperparathyroid?

A

ESRF

189
Q

what is the management of hypercalcaemia?

A

conservative if ca<2.85 AND patient >50yo AND no evidence organ damage

initially IV fluids (3-4L/day) and bisphosphonates
definitive: total parathyroidectomy
cinacalcet if unsuitable for surgery

190
Q

primary hyperparathyroid indications for surgery?

A 
elevated serum Ca >1mg/dL above normal
Hypercalciuria >400mg/day
Creatinine clearance <30% compared with normal
life threatening hypercalcaemia
Nephrolithiasis
Age <50
Neuromuscular symptoms
Reduction in bone mineral density >2.5SD below peak bone mass
191
Q

secondary hyperparathyroid indications for surgery?

A

usually managed medically but:
bone pain
persistent pruritis
soft tissue calcifications

192
Q

tertiary hyperparathyroid indications for surgery?

A

allow 12 months to elapse following renal transplant as many cases will resolve

193
Q

what are some causes of hypocalcemia?

A

vit D defieincy
renal failure
hypoparathyroid: surgical, autoimmune, MG deficiency

194
Q

What lab values are seen in primary hyperparathyroid?

A

PTH high
Ca high
Phosphate low
Vitamin D normal/low

195
Q

What lab values are seen in secondary hyperparathyroid?

A

PTH high
Ca normal/low
phosphate high/norm
vitamin D very low

196
Q

what are the actions of PTH?

A
  1. Ca release from bones
  2. kidneys absorb calcium and decrease excretion
  3. inactive vit D -> active -> small intestine absorbs Ca
197
Q

What lab values are seen in tertiary hyperparathyroid?

A

PTH high high
Ca high
PO high
Vit D low normal

198
Q

What are the types/progression of multiple myeloma ?

A
  1. MGUS
  2. Smouldering myeloma
  3. Multiple myeloma
  4. Bcell leukaemia
199
Q

What are the features of MGUS?

A

No crab s/s
monoclonal serum protein <30g/L
BM plasma cells <10%
Annual risk of progression to MM 1-2%

200
Q

What are the features of Smouldering myeloma?

A

no CRAB s/s
monoclonal serum protein >=30g/L
bm plasma cells >=10%
annual risk of progression to MM 10%

201
Q

what are the S/S of multiple myeloma

A 
back pain
fatigue
osteoporosis and pathological fractures
abnormality on routine lab test
acute renal failure
pneumonia 
paralysis and cord compression 
recurrent infections
amyloidosis: macroglossia, carpal tunnel neuropathy, hyperviscosity
CRAB
202
Q

What is CRAB MM?

A

Calcium elecated
Renal impairement
Anaemia -watch out for MM in anaemia Qs
Bone lesion/pain

203
Q

What are the investigations for multiple myeloma?

A

serum/urine electrophoresis (monoclonal gammopathy/bence jones), IgG/A
FBC, U&E, bone profile, blood film (rouleaux)
WBLD-CT/mri (whole body CT/mri)
bone marrow aspirate and biopsy (>=10% BM plasma cells)
XR (rain drop skull)
Immunophenotyping

204
Q

Positive immunophenotyping MM?

A 
CD38
CD138
CD56/58
monotypic cytoplasmic Ig
Light chain restriction (kappa or lambda +ve)
205
Q

negative immunophenotyping MM?

A

CD19
CD20
Surface Ig

206
Q

Management of multiple myeloma?

A

Induction: thalidomide/bortezomib + dexamethasone

Bone disease: bisphosphonates + analgesia

207
Q

what are the S/S of referring syndrome?

A 
rhabdomyolysis
low rr
arrhythmias
shock
seizures
coma
208
Q

What is the Mx of referring syndrome?

A

phosphate supplementation

209
Q

What is the aetiology of refeeding syndrome

A

Starvation -> catabolic state of low insulin and fat -> depletes intracellular PO
Refeeding -> rise in insulin -> intracellular shift of PO -> hypophosphataemia

210
Q

what are some causes of hypercalcaemia?

A 
sarcoid
vitamin D
acromegaly
thyrotoxicosis
addisons
211
Q

what are some common causes of polyuria?

A 
diuretics, caffeine, ETOH
DM
lithium
HF
hypercalcaemia
DI
212
Q

Investigations for polyuria?

A

Bloods: U&E, glucose, paired serum and urine osmolarity, serum calcium
- U&E (exclude hypokalaemia/nephrogenic DI)
- Calcium (exclude hypercalcaemia/nephrogenic DI)
- Glucose (exclude DM - osmotic diuresis)
- osmolality (hyperaldosteronism)
Special: water deprivation test
Other: lithium levels

213
Q

What is fibromusclar dysplasia?

A

an idiopathic non inflammatory disorder of the arteries encompassing two subtypes: focal and non-focal.

214
Q

where does fibromusclar dysplasia affect?

A

renal and cervical arteries

215
Q

what are some S/S of FMD?

A

Renal artery FMD: resistant HTN (74%), abdominal bruits, unilateral small kidney, renal artery stenosis
Cervical artery FMD: chronic migraines (70%), pulsatile tinnitus

216
Q

Investigations for FMD?

A

Gold standard = CTA, catheter angiography (+MRA head)

Bloods (lipids, autoantibodies, ESR)

217
Q

what is the management of FMD?

A

C: Stop smoking
M: antiplatelets (clopidogrel)
anti HTN (ACEi or ARB)
S: surgical stenting (renal, cervical, iliac arteries)

218
Q

What are the causes of Vitamin B12 deficiency ?

A

autoimmune
atrophic gastritis (2nd to H.Pylori)
gastrectomy
malnutrition

219
Q

S/S of B12 deficiency?

A

Anaemia
neurological (peripheral neuropathy, SCDC, amnesia, poor concentration)
Glossitis
Mild jaundice

220
Q

Investigations for B12 def?

A

FBC (macrocytic anaemia, hypersegmented neuts)
Vitamin B12 (<200nh/L)
Antibodies: anti IF AB [low sensitivity, high specificity]
anti parietal cell AB [high sensitivity, low specificity]

221
Q

Management of B12 def ?

A

cyanocobalamin PO or IM; hydroxycobalamin IM

Symptomatic:
mild/mod: PO/IM vit B12
severe: referral to neurology +/- haem, IM vit B12 x3/week for 2 WEEKS -> 3monthly injection

222
Q

What are some causes of hypomagnesaemia?

A 
Drugs (diuretics, PPI)
Diarrhoea (IBD)
Hypokalaemia, hypocalcaemia
TPN
etch
metabolic disorder (Gitelman's, barters)
223
Q

S/S hypomagnesaemia?

A 
Similar to hypocalcaemia
Paraesthesia, seizures, decreased PTH secretion -> hypocalcaemia
tetany
arrhythmias
ECG features similar to hypokalaemia
Exacerbates digoxin toxicity
224
Q

What is the management of hypomagnesaemia?

A

<0.4mmol/L: IV MgSO4 (40 mmol over 24 h)

>0.4 mmol/L: PO Mg2+ salts (10-20 mmol PO OD)

225
Q

How does orlistat work

A

pancreatic lipase inhibitor

226
Q

Who should orlistat be prescribed to?

A

BMI of 28 kg/m^2 or more with associated risk factors, or
BMI of 30 kg/m^2 or more
continued weight loss e.g. 5% at 3 months
orlistat is normally used for < 1 year

227
Q

what are the complications of DKA?

A

gastric stasis
thromboembolism
arrhythmias secondary to hyperkalaemia/iatrogenic hypokalaemia
iatrogenic due to incorrect fluid therapy: cerebral oedema*, hypokalaemia, hypoglycaemia
acute respiratory distress syndrome
acute kidney injury

228
Q

Why does Nelson’s syndrome occur?

A

Nelson’s syndrome occurs due to rapid enlargement of a pituitary corticotroph adenoma (ACTH producing adenoma) that occurs after the removal of both adrenal glands

  • Raised ACTH
  • Raised MSH and hyperpigmentation
229
Q

what are the types of autoimmune polyendocrine syndromes?

A

type 1: autosomal recessive, addisons, candidiasis, hypoparathyroid
type 2: Schmidt syndrome
polygenic
addisons, thyroid (hypothyroid or Graves), T1DM

230
Q

what is schmidt syndrome ?

A 
type 2 autoimmune polyendocrine syndromes
polygenic
addisons
thyroid (hypothyroid or graves)
T1DM
231
Q

What are the features of carcinoid tumours?

A

flushing (often earliest symptom)
diarrhoea
bronchospasm
hypotension
right heart valvular stenosis (left heart can be affected in bronchial carcinoid)
other molecules such as ACTH and GHRH may also be secreted resulting in, for example, Cushing’s syndrome
pellagra can rarely develop as dietary tryptophan is diverted to serotonin by the tumour

232
Q

Ix carcinoid tumours?

A

urinary 5-HIAA (serotonin)

plasma chromogranin A y

233
Q

Mx carcinoid tumours?

A

somatostatin analogues e.g. octreotide

diarrhoea: cyproheptadine may help

Year 6 Medicine (18 decks)

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