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CSI 2 > tiredness > Flashcards

tiredness Flashcards

1
Q

what percentage of patients presenting with tiredness get a diagnosis?

A

66%

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2
Q

what percentage of patients with fatigue receive a diagnosis through blood tests?

A

less than 10%

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3
Q

what differentials are possible for fatigue?

A

anaemia (esp if heavy periods or pregnant)

sleep apnoea

hypothyroidism

coeliac disease

chronic fatigue syndrome

diabetes

glandular fever

depression

restless legs

anxiety

malignancy

vitamin D deficiency

heart failure

infection

lupus

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4
Q

what do the additional symptoms indicate?

A

weight gain, constipation, dry skin, feeling cold - hypothyroidism

family history - vitamin D deficiency, diabetes

CKD?

anaemia (vegetarian etc.) ?

infection?

haematological malignancy?

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5
Q

what can be excluded based on the history?

A

sleep apnoea

glandular fever - no feeling unwell

lupus

pregnancy

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6
Q

what blood tests would be ordered?

A

FBC

urea and electrolytes

vitamin D

thyroid function tests

HbA1c

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7
Q

what do the blood test results show?

A

TSH - 18 mU/L (0.2 - 5.5 mU/L) - high

fT4 - 1.2 pmol/L (10 - 24.5 pmol/L) - low

fT3 - 0.9 pmol/L (3.1 - 6.8 pmol/L) - low

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8
Q

what are the symptoms of hypothyroidism?

A

dry hair

loss of eyebrow hair

puffy face

enlarged thyroid

slow heartbeat

arthritis

cold intolerance

depression

dry skin

fatigue

forgetfulness

menstrual disorders

infertility

muscle aches

weight gain

constipation

brittle nails

hoarse voice

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9
Q

what is the mechanism by which fT4 and fT3 are low but TSH is high?

A

fT3 and 4 usually produce negative feedback to prevent pituitary from producing TRH and therefore TSH

low fT3 and 4, therefore increased TRH and TSH

(primary hypothyroidism)

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10
Q

what is the most common autoimmune reaction that causes hypothyroidism?

A

Hashimoto’s disease

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11
Q

what is the sequence of events that causes the immune system to attack the thyroid cells in Hashimoto’s disease?

A

thyroid usually produces TPO (thyroid peroxidase), used for production of thyroid hormones

MHC II and B7 proteins on APCs that are sensitive to TPO complement TCRs and CD28 proteins on T cells to activate it

TCRs and CD40s on T-cell interact with BCRs and CD40s on B-cells

B cells produce anti TPO antibodies

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12
Q

why don’t immune cells attack host cells?

A

PAMPs - pathogen associated molecular patterns, not found on human cells

  • peptidoglycan, lipopolysaccharide, lipoteichoic acid, mannan, flagella proteins etc.
  • allows eosinophils, basophils, neutrophils, macrophages and dendritic cells to recognise infected cells

normal healthy cells express MHC I receptors that mark it as ‘self’ - inhibitory receptors on surface of NK cells recognise MHC I, prevents it from killing

complementarity-determining regions (CDRs) are part of the variable chains in immunoglobulins (antibodies - generated by B-cells) and TCRs

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13
Q

how would a patient presenting with tiredness be approached?

A

75% of tiredness symptoms resolve within a month

67% of tiredness episodes triggered by life stresses

1 - must determine physical causes
- define type of tiredness (drowsiness, short of breath, weakness)

exertional tiredness - more likely to be physical

  • tiredness gets worse as they do something = worrying
  • tiredness gets better as they do something = not worrying

2 - why did patient present
- look for functional impairment (e.g. unable to make dinner for family)

3 - screen for red flags

  • lymphadenopathy
  • weight loss
  • specific malignancy features, focus on lung, breast, colon, upper GI, gynae
  • joint pains
  • focal neurology
  • infective symptoms - TB, glandular fever, Lyme

4 - explore psychosocial triggers

  • work
  • money
  • family
  • mood
  • drugs and alcohol

5 - examine patient

  • pulse
  • blood pressure
  • BMI

6 - plan

  • initial bloods: FBC (anaemia, iron deficiency, haematological malignancy), TFT, ESR (erythrocyte sediment rate - quicker fall = greater levels of inflammation, diagnose arthritis, endocarditis, Crohn’s disease, giant cell arteritis, polymyalgia rheumatica), glucose
  • even in non-anaemic menstruating women, treating low ferritin can improve tiredness symptoms
  • lymphomas often have normal total white cell count with abnormal differential in early stages

7 - manage persisting unexplained tiredness with normal initial bloods

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14
Q

what are some questions that someone with an underactive thyroid may ask?

A

why did I get an underactive thyroid?

will I get better?

do I need treatment?

what’s the best treatment for me?

will I need to have treatment for the rest of my life?

what are the side effects of treatment? how can I cope with them?

should I change what I eat?

what are the chances that someone else in my family will get an underactive thyroid?
does it run in families?

how will my treatment be managed if I wish to get pregnant?

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15
Q

what are the causes of an underactive thyroid?

A

autoimmune thyroid disease (most common cause) - usually Hashimoto’s thyroiditis

radioactive iodine treatment/surgery to correct hyperthyroidism/treat thyroid cancer

anti-thyroid drugs if given for an overactive thyroid disorder in too large a dose

medicines such as lithium (some mental health problems) and amiodarone (some heart problems)

some cough medicines containing large amounts of iodine can interfere with
thyroid function

some health foods taken in excess, e.g. kelp (seaweed)

malfunction of the pituitary gland

radiation for head and neck cancers (not common in the UK)

(congenital)

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16
Q

how is hypothyroidism diagnosed?

A

thyroid function test

underactive thyroid - high TSH, low fT4

if antibodies present, autoimmune

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17
Q

what can alter the results of a thyroid function test?

A

common illnesses can temporarily alter blood
test readings - need to rule out

some medicines (prescribed and over-the-counter) - tell doctor about any medication you are taking

sometimes hypothyroidism can develop after pregnancy and giving birth (temporary)

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18
Q

what is subclinical hypothyroidism?

A

level of hypothyroidism is slight

no obvious symptoms, can
only be detected by blood test (for another autoimmune disorder or if there is FHx of thyroid disorder)

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19
Q

what are the results for a blood test showing subclinical hypothyroidism?

A

slightly raised TSH, normal fT4

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20
Q

how is subclinical hypothyroidism dealt with?

A

regular thyroid function
test

consult your doctor if you notice any symptoms, as you may benefit from treatment

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21
Q

how is hypothyroidism treated?

A

levothyroxine prescribed

regular thyroid function tests (every 6-8 weeks), dose may be adjusted according to results

taken for life

22
Q

what do levothyroxine doses depend upon?

A

body weight

blood test results

23
Q

how does levothyroxine dose change in cases with severe hypothyroidism or with high risk of heart problems?

A

start low, increase dose

24
Q

when is levothyroxine taken?

A

in the morning, with water, on an empty stomach, at least half an hour
before eating and drinking anything

25
Q

what drugs can decrease levothyroxine absorption?

A

calcium

iron

cholesterol-lowering drugs (cholestyramine, colestipol)

multivitamin tablets

other drugs - check with pharmacist or doctor

26
Q

what should be done to counteract the effects of calcium, iron, cholesterol-lowering drugs and multivitamin tablets on levothyroxine absorption?

A

take levothyroxine at least 4 hrs apart from others

27
Q

why does grapefruit help increase levothyroxine absorption?

A

increases stomach acidity

28
Q

why does missing a dose of levothyroxine not matter very much?

A

reservoir of thyroxine

29
Q

when may levothyroxine tablets deteriorate?

A

exposed to extreme temperatures

30
Q

what is the correct dose of levothyroxine for a patient?

A

TSH in lower part of reference range

T4 towards the upper part or even slightly above reference
range

31
Q

what are the effects of an incorrect dose of levothyroxine?

A

too much levothyroxine - causes symptoms of
overactive thyroid

too little levothyroxine - underactive
thyroid symptoms not completely resolved

32
Q

what treatment should be given if complaints persist even with normal TSH levels?

A

combination therapy of levothyroxine and tri-iodothyronine (LT4 and LT3)

this is an experimental approach under the supervision of an accredited endocrinologist

(LT3 not always available on NHS)

33
Q

once stable, how is hypothyroidism managed?

A

annual blood test to check thyroid hormone levels

take tablets consistently every day; failure to do this can affect
blood test results and health

34
Q

what are the side effects of levothyroxine?

A

minimal

35
Q

why may people feel some differences between different brands of levothyroxine? (rare)

A

might
relate to differences in fillers and bulking agents between various brands

discuss with doctor to prescribe consistent brand

36
Q

what are the steps to take if planning a pregnancy while on levothyroxine?

A

let your doctor know, ideally have a blood test before
you conceive

increase dosage by 25-50mcg daily once pregnancy is confirmed to normalise thyroid function

have a thyroid function test

37
Q

what are the complications of pregnancy when taking levothyroxine?

A

risk only slightly higher than
normal

good chance of a successful pregnancy outcome

38
Q

how are thyroid problems associated with genetics?

A

thyroid problems often run in families

if family members are unwell they should be encouraged
to discuss with their own GP whether thyroid testing is warranted

39
Q

what are the risks of taking too much thyroxine?

A

atrial fibrillation

bones may get too thin (osteoporosis)

(doctor prescribes lowest possible dose to prevent)

40
Q

how does Hashimoto’s disease start to present?

A

thyroid gets infiltrated by white cells and slowly loses its function

usually enlarges but may not

may start with an over-active phase before becoming under-active

41
Q

what are the similarities between Graves’ disease and Hashimoto’s disease?

A

both forms of autoimmune thyroiditis - body’s defence mechanisms overact or respond dysfunctionally and cause damage to target tissues

can be triggered by stress factors and pregnancy

genetic predisposition

both may involve infiltration by white cells (lymphocytic infiltration), increased immunoglobulins within the gland, and increased blood levels of thyroid antibodies

42
Q

what is the relationship between Graves’ disease and Hashimoto’s disease?

A

each can change into the other

usually the over-active thyroid resulting from immune dysfunction that will revert to the under-active phase

43
Q

when may antibody levels decrease in hypothyroidism?

A

may diminish as hypothyroidism becomes established

treatment with thyroxine is given

44
Q

why may Hashimoto’s disease by missed?

A

undue reliance on blood tests

usually T4 (and maybe T3) is low, but may not be out of range - suggests poor thyroid hormone output

TSH normally rises in this situation, it may actually be normal, or even low

45
Q

why may TSH be normal or even low in Hashimoto’s disease, even though it should rise in normal cases of Hashimoto’s disease?

A

down-grading of HPG axis due to hypo-metabolism induced by low thyroid function (also applies to adrenal function, which can also be damaged by autoimmune disease)

hypothalamus responds poorly to low thyroid blood levels - may not produce a normal level of TRH

hypo-metabolism also adversely affects pituitary - may not properly respond to TRH, and therefore not produce a normal level of TSH

thyroid itself may be less responsive to TSH anyway (damaged by white cell infiltration and with damaged TSH receptors)

causes chain reaction of failure, beginning with the hypothalamus and extending to the pituitary

46
Q

if TSH is low (abnormal hypothyroid response, is usually high), what can confirm Hashimoto’s disease?

A

antibody test

usually quite conclusive

any level of thyroid antibodies suggests autoimmune processes at work

(note: as damage becomes chronic antibody levels may lessen)

47
Q

what are the 2 ways that autoimmune hypothyroidism may present?

A

goitrous autoimmune thyroiditis

atrophic autoimmune thyroiditis

48
Q

what are the features of goitrous autoimmune thyroiditis?

A

progressive infiltration of white cells enlarges thyroid

gland itself becomes a mass of fibrous tissue - follicular cells (where thyroid hormone is made) disappearing, enlarges into a goitre

49
Q

what effect does an increase in dietary iodine have on autoimmune thyroiditis?

A

worsens autoimmune thyroiditis

50
Q

what are the features of atrophic autoimmune thyroiditis?

A

(most common form)

results in thyroid gland shrinking with progressive loss of tissue

antibodies block thyroid TSH receptors so glandular tissue shrinks due to disuse

CSI 2 (6 decks)

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