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Cardio > Biochemistry Thyroid > Flashcards

Biochemistry Thyroid Flashcards

1
Q

Thyroid Hormone

A

T3 is 5x more active as T4

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2
Q

T4 secretion

A

T3 secretion

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3
Q

T3 secretion

A

<20% secreted from thyroid, majority from peripheral de-iodination of T4.

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4
Q

3 proteins which bind thyroid hormone

A

Thyroid binding globulin (TBG)
Thyroid binding pre-albumin
Albumin

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5
Q

Bound T4 proportions

A
  • 99.98% of T4 is bound (70% TB, 20% TBPA, - 10% Alb
  • 99.7% T3 is bound
  • Only the free forms (unbound are active)
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6
Q 
Patient 1: serum results
T.S.H 60.0
Free T4 4.4
Free T3 ---
Clinical information: tired, weight gain

Diagnosis

A

1o hypothyroidism – impaired T4 production and loss of negative feedback

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7
Q

Primary Hypothyroidism: Biochemical Features

A

Raised TSH
Low Ft4
Ft3 – not helpful

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8
Q

Primary Hypothyroidism:Clinical Features

A 
Lethargy, tiredness
Weight gain
Cold intolerance
Coarsening of hair and skin 
Slow reflexes, hoarseness
Constipation
Menstrual abnormalities
Bradycardia
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9
Q 
Patient 2 →
T.S.H -10.0 (abnormal)
Free T4 – 13.2 (decreased slightly but not abnormal)
Free T3 ---
Clinical Information
Cold intolerance, constipation
Diagnosis
A

Compensated Hypothyroidism

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10
Q

Compensated Hypothyroidism: Biochemical Features

A

Raised TSH (4-15 min/L)
Low normal FT4
+ve Anti-thyroid peroxidase antibodies

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11
Q

Compensated Hypothyroidism: Wickham study

A

Management of this form of hypothyroidism is looking at the annual risk of overt hypothyroidism of TSH >6.0min/L and or TPOAb positive – thyroxine guidelines → TSH +10 even if T4 is low/normal.

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12
Q 
Patient 3 →
T.S.H – 10
Free T4 ---
Free T3 ---
Clinical information: On Thyroxine
Diagnosis
A

This patient requires increased dose to suppress TSH

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13
Q

Thyroxin Replacement → Aiming for levels of T.S.H and FT4 of

Ideal – adequate replacement

A

T.S.H – 2.0 (0.3-4.0)

Free T4 of 16.8 (10.0-24.0)

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14
Q

Thyroxin Replacement → Inadequate replacement – low dose or poor compliance

A

T.S.H – 20.0

Free T4 – 5.0

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15
Q

Thyroxin Replacement → Irregular compliance or recent change in dose (need to be on stable dose for 6 weeks)

A

T.S.H 12.0
Free T4 16.8

→ Under replaced but normal = adequate therefore need to take results after 6 weeks

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16
Q

Thyroxin Replacement → Adequate/over replacement increased risk AF (not normal to measure FT3)

A

T.S.H <0.02 (suppressed)
Free T4 – 23.0
Free T3 – 3.0

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17
Q

Thyroxin Replacement →Over replacement

A

T.S.H <0.02
Free T4 34.0
Free T 3 —

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18
Q

Thyroxin Replacement → Special situations

A

Patients with thyroid cancer on thyroxine

Some patients may be given T3 (deliberately supress TSH)

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19
Q

Thyroxin Replacement → Using T3 for replacement is difficult because

A
  • More potent
  • Increased risk
  • T0.5 shorter therefore management and dosing difficult
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20
Q 
Patient 4 →
T.S.H <0.02
Free T4 50.2
Free T3 22.0
Clinical Information: Weight loss, palpitations

Diagnosis

A

Thyrotoxicosis

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21
Q

Primary Hyper-thryoidism: Biochemical Features

A

Undetectable TSH
Raised FT4
Raised Ft3

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22
Q

Primary Hyper-thryoidism: Clinical Features

A 
Weight los
Heat intolerance
Palpitations
Agitation, tremor
Muscle Weakness
Diarrhoea
Thyroid eye disease
Menstrual abnormalities
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23
Q

Best discrimination of hyperthyroidism

A

FT3 then FT4

24
Q

T3 toxicoisis serum levels

A

T.S.H <0.02
Free T4 23.0
Free T3 12.0

25
Q

T3 toxicoisis diagnosis requires

A

Need FT3 measurement in patients with high normal – slight increased FT4

26
Q

Not Clear thyrotoxicosis

A

T.S.H <0.02 (low)
Free T3 23.0 (normal/high)
Free T4 6.8 (normal)

27
Q

Not Clear thyrotoxicosis management

A 
Recheck in recouple of months to confirm 
Remains suppressed (due to risks) then therefore confirm anti-thyroid treatment but evidence not 100% clear.
28
Q

Effects of non-thyroidal illness→

A

• Common in hospitalised patients
• Occurs in a variety of pathological conditions
• Pattern of results
o TSH low (may be increased in recovery phase)
o FT4/FT3 low or normal – metabolic response to illness
o Increased reverse T3 – metabolically inactive

→ Basal metabolism slowed down to protect body from illness.

29
Q

Causes of TSH suppression

A 
•	TNF
•	IL-1
•	Low TRH
•	Somatostatin
•	Glucocorticoids
Dopamine
30
Q

Amiodarone

A

→ hypo and hyperthyroidism (contains lots of iodine → long half-life (weeks) therefore can stop and wait to identify if its drug induced or has hypo/hyper primary.

31
Q

Etiological classification of Secondary Hypertension

A

Endocrine hypertension – primary aldosteronism

32
Q
  1. Endocrine hypertension
A

Primary aldosteronism, Phaeochromocytoma, Cushings syndrome, Adrenal

33
Q
  1. Renal Hypertension
A

Renal artery stenosis, renal parenchymal disease

34
Q
  1. Drug induced causes
A

OC, excess liquorice (mineral corticoids acts like aldosterone)

35
Q

Causes hypertension

A
  1. Endocrine hypertension
  2. Renal Hypertension
  3. Drug induced causes
  4. Co-arctation of the aorta
36
Q

Mineralocorticoid hypertension: Types

A
  1. Aldosterone-producing adenoma (APA) – 2/3 cases
  2. Bilateral idiopathic hyperplasia (IHA) – majority remainder (overproduction form both adrenals)
  3. Primary (unilateral) adrenal hyperplasia
  4. Aldosterone-producing adrenocortical carcinoma
  5. Familial hyperaldosteronism
37
Q

Mineralocorticoid hypertension: Familial hyperaldosteronism

A
  1. Glucocorticoid-remediable aldosteronism (FH type 1)

7. Familial APA or IHA (FH type II)

38
Q

Mineralocorticoid hypertension:Who should be screened

A 
Hypertension with hypokalaemia (Conn’s as increased Na+ = Reduced K+)
Particularly if sodium is high
60-70% of patients are normokalaemia
Resistant hypertension
Adrenal incidentalomma and hypertension
39
Q

Mineralocorticoid hypertension: How should they be screened?

A 
Plasma renin activity
Plasma aldosterone concentration
•	Morning blood sample in ambulant patient
•	Correct hypokaaemia (?)
•	Discontinue anti-hypertensives (?)
40
Q

Saline infusion test

A

Aldosterone secretion is not suppressed in response to an excessive salt and water load.

41
Q

Fludrocortisone suppression

A

Further sodium loading with a sodium retaining steroid will have no effect on plasma aldosterone because patients are in a salt retaining state.

42
Q

Interpretation both test:

A

Serum aldosterone >140 pmol/L at the end of the study confirms a diagnosis of Primary hyperaldosteronsim.

43
Q

Localisation of tumour

A

Selective venous catheterisation – 2 adrenals and look for v. difficult

Ct or MRI (nodules >7 mm, incidentalomas) = detection limit or not aldosterone producing.

44
Q

Calcium channel blockers

A

Decrease aldosterone, may increase PRA

Discontinue for 1 weeks

45
Q

Diuretics and vasodilators

A

Increase PRA and therefore aldosterone

46
Q

Beta Blockers

A

Decrease PRA and aldosterone

47
Q

ACE inhibitors

A

Prevent angiotensin II production, decrease aldosterone and increase PRA
Discontinue for 2 weeks

48
Q

Spironolacetone (aldosterone antagonist)

A

Variable effect depending on duration of treatment

Discontinue for 6 weeks

49
Q

Phaeochromocytomas: Incidence and important

A 
Rare tumour (<1% hypertnsives)
Potential to be lethal and for cure if diagnosed
50
Q

Phaeochromocytomas: Pathology (rule of 10’s)

A
  • Arises in chromaffin tissue of the sympathetic nervous sytem
  • Majority arise from the adrenal medulla, others from paraganglia at other sites (10%)
  • Most are benign (10% malignant)
  • Most are sporadic
  • Some familial (10%) – MEN type II and Von Hippel landau syndrome)
51
Q

Phaeochromocytomas:Who should be tested

A 
Hypertension (resistant, malignant, intra-operative, pregnancy)
•	Paroxysmal (45%)
•	Persistent (50%)
Headache
Diaphoresis or sweating, flushing attacks
Palpitations
Anxiety, feelings or impending doom
Pallor
Tremor

→ May associated with symptomatic episodes of an hour or less on a daily basis to once every few months.

52
Q

Phaeochromocytomas: Diagnostic problems

A

Poorly controlled BP may increase catecholamines by 50-100% (95% reference range therefore innapropriate)

53
Q

Phaeochromocytomas: Many medical disorders may increase catecholamine’s

A 
Surgery
Myocardial infarction
Diabetic ketoacidosis
Obstructive sleep apnoea
Stroke
Severe heart failure
54
Q

Phaeochromocytomas: 24-hour urine catecholamine or metabolites

A
  • Integral of overall production
  • Relatively high concentration
  • Relatively high stability (but needs 6M HCI)
  • One collection usually sufficient
55
Q

Phaeochromocytomas: Testing for Phaechromocytoma

A
  • Urine (see slides 106)

* Follow-up of initial positive urine test

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