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Year 3 > Block 34 Week 5 > Flashcards

Block 34 Week 5 Flashcards

1
Q

What is cushings caused by?

A
  • cause by prolonged exposure to excess of glucocorticoids
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2
Q

causes of cushings?

A
  • exogenous cause - use of glucocorticoids - the most common cause
  • endogenous - excess production of glucocorticoids by the body - very rare
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3
Q

cushings disease?

A
  • Cushing’s disease, which refers to cases caused by a pituitary adenoma, is responsible for the majority of endogenous cases.
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4
Q

ACTH dependent cushings?

A
  • ACTH dependent: cortisol excess is driven by ACTH, either from the pituitary or ectopic sources.
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5
Q

ACTH independent cushings?

A
  • ACTH independent: cortisol excess is independent of ACTH. Includes exogenous causes (consumption of cortisol) and adrenal lesions (adenomas, carcinomas).
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6
Q

HPA axis?

A
  • CRH from paraventricular nucleus of hypothalamus
  • ATCH from corticotrophs of AP
  • cortisol release from adrenal cortex
  • negative fedback on CRH and ACTH
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7
Q

ACTH excess is a feature of both?

A

ACTH excess is a feature of both Addison’s disease (primary adrenocortical insufficiency) and ACTH dependent Cushing’s syndrome - hyperpigmentation

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8
Q

what causes ACTH dep cushings?

A
  • due to the excess production of ACTH.
  • When exogenous causes are excluded, ACTH dependent causes are responsible for 80% of all Cushing’s syndrome.
  • Cushings disease involves excess ACTH.
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9
Q

ACTH dependent cushings - ectopic production?

A
  • Ectopic ACTH production: This may be seen as a paraneoplastic syndrome in lung cancers where malignant cells produce ACTH and are not subject to normal negative feedback mechanisms.
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10
Q

ACTH dependent cushings - ectopic CRH production?

A
  • Ectopic CRH production: Rarely CRH may be produced by malignant tissue resulting in increased ACTH and cortisol production.
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11
Q

ACTH independent cushings?

A
  • presence of normal ACTH production
  • endogenous administration
  • primary adrenal lesions
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12
Q

ACTH independent cushings - endogenous admin?

A
  • Endogenous administration: Prolonged exposure to exogenous glucocorticoids is the most common cause of Cushing’s syndrome. Results in suppression of CRH and ACTH.
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13
Q

ACTH independent cushings - primary adrenal lesions?

A
  • Primary adrenal lesions: tumours (adenomas, carcinomas and hyperplasia) may result in cortisol excess and suppression of CRH and ACTH.
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14
Q

symptoms of cushings syndrome

A
  • Tiredness
  • Depression
  • Weight gain
  • Easy bruising
  • Amenorrhoea
  • Reduced libido
  • Striae
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15
Q

signs of cushings syndrome

A
  • Acne
  • Moon facies
  • Plethora
  • Buffalo hump
  • Hypertension
  • Proximal muscle weakness
  • Hyperpigmentation(in ACTH dependent causes)*
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16
Q

definitive test in cushings?

A

dexamethasone suppression test

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17
Q

other tests used in cushings?

A
  • 24 hr urinary cotisol
  • midnight cortisol
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18
Q

24 hr urinary cortisol?

A
  • 24 hr urinary cortisol - often initial tests in suspected cushings syndrome
  • Three or more collections are usually needed.
  • Levels 3-4x normal are highly suggestive of Cushing’s syndrome.
  • creatinine levels need to be measured
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19
Q

midnight cortisol?

A
  • demonstrates loss of normal circadian pattern
  • Cortisol levels can be salivary or blood-based
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20
Q

low dose dexamethasone suppression tets?

A
  • dexamethasone given at 11pm and serum cortisol is then measured at 8am
  • In a normal individual, the administration of dexamethasone should suppress the morning rise in serum cortisol.
  • However, in patients with Cushing’s syndrome, there is a lack of suppression,
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21
Q

dexamethasone CRH test?

A
  • less commonly used
  • dexamethasone is given for a period following by administration of CRH
  • Serum cortisol (and ACTH) levels can then be measured.
  • It may help distinguish between Cushing’s and hypothalamus-pituitary-adrenal axis dysregulation
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22
Q

establishing cause of cushings - first test?

A
  • plasma ACTH is the first test done to find a cause
  • Suppressed / undetectable ACTH: Indicative of an ACTH independent cause of Cushing’s syndrome.
  • Raised / inappropriately normal ACTH: Suggestive of an ACTH dependent cause.
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23
Q

Imaging

first line for suspected ACTH independent cushings?

A
  • majority is caused by adrenal pathology
  • in patients with suspected ACTH independent Cushing’s syndrome a CT of the adrenal glands is normally the first line investigation.
  • Further tests may include MRI adrenal glands and PET/CT.
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24
Q

first line in ACTH dependent cushings?

A
  • high dose dexamethasone suppression test
  • Pituitary adenomas(Cushing’s disease): High levels of dexamethasone are able to suppress ACTH production.
  • Ectopic production: Despite high dose dexamethasone, ectopic tissues will not be suppressed and continue to produce ACTH.
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25
Q

ACTH dependent cushings - distinguishing causes?

A

cushings disease: high levels of dexamethasone will suppres ACTH production

ectopic production: no ACTH suppression

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26
Q

other tests for a pituitary adenoma?

A
  • other tests: pituitary adenoma or malignancy - CTs and MRIs
  • Petrosal sinus sampling is an invasive test that may be used to help identify a microscopic pituitary adenoma
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27
Q

exogenous cushings management

A
  • gradual withdrawal from glucocorticoids
  • stopping could result in addisonian crisis
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28
Q

gold standard for managing cushings disease?

A
  • Transsphenoidal surgeryis the gold-standard for treatment of Cushing’s disease.
  • microadenomectomy
  • subtotal resections of the AP
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29
Q

medical management of cushings disease?

A

Metyrapone can be used, an inhibitor of 11β-hydroxylase, that leads to a reduction in cortisol synthesis.

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30
Q

Pituitary irradiation?

A
  • This may be used in children and young people w CD or those in whom surgical techniques have failed.
  • Effects are not immediate and takes around 6-12 months to have maximal effect.
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31
Q

adrenalectomy?

A
  • In those in who all other therapies for CS have failed bilateral adrenalectomy may be used.
  • This mandates lifelong glucocorticoid and mineralocorticoid replacement.
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32
Q

management of adrenal lesions ?

A
  • surgical resection
  • unilateral adrenal adnoma - curative tx
  • Following surgery patients will need a tapering course of exogenous steroids for a period of time as their endogenous CRH and ACTH will be suppressed.
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33
Q

Tx

Bilateral adrenal hyperplasia?

A

In patients with overt Cushing’s bilateral adrenalectomy may be offered. Following this patients require replacement of glucocorticoids and mineralocorticoids

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34
Q

causes of cushings syndrome - CAPE?

A
  • Cushings disease
  • Adrenal adenoma
  • paraneoplastic syndrome
  • Exogenous steroids
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35
Q

Skin pigmentation?

A
  • In a patient with Cushing’s syndrome, the pigmentation allows you to determine the cause as excess ACTH, either from Cushing’s disease or ectopic ACTH.
  • This sign is absent in an adrenal adenoma or exogenous steroids.
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36
Q

Lack of cortisol suppression in resp to dexamethasone suggests ?

A

cushings syndrome

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37
Q

dexamethasone suppression results

A

IMAGE

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38
Q

types of dexamethasone suppression test?

A
  • Low-dose overnight test(used as a screening test to exclude Cushing’s syndrome)
  • Low-dose 48-hour test(used in suspected Cushing’s syndrome)
  • High-dose 48-hour test(used to determine the cause in patients with confirmed Cushing’s syndrome)
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39
Q

bloods in CS?

A
  • Full blood countmay show ahigh white blood cell count
  • U&Esmay showlowpotassiumifanadrenal adenomais also secretingaldosterone
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40
Q

Findings causes

Other tests for cushinhs?

A
  • MRI brain for a pituitary adenoma
  • CT chest for small cell lung cancer
  • CT abdomen for adrenal tumours
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41
Q

what suggests syndrome of inappropriate ADH secretion?

A

The presence of euvolaemic hyponatraemia, with high urine osmolality (> 100 mOsm/kg) and high urine sodium (> 40 mmol/L),

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42
Q

cushings can cause?

A

DM

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43
Q

Sheehan syndrome?

A

Sheehan syndrome describes hypopituitarism caused by ischemic necrosis due to blood loss and hypovolaemic shock.

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44
Q

features of Sheehans syndrome?

A
  • agalactorrhoea
  • amenorrhoea
  • symptoms of hypothyroidism
  • symptoms of hypoadrenalism
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45
Q

Asherman’s syndrome?

A

Asherman’s syndrome, or intrauterine adhesions, may occur following dilation and curettage. This may prevent the endometrium responding to oestrogen as it normally would.

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46
Q

ABG in CS?

A

hypokalaemic metabolic alkalosis

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47
Q

Ectopic ACTH from lung cancer -

A

ACTH and cortisol remain high

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48
Q

high dose dexa test results?

A

A high dose of dexamethasone exerts negative feedback on pituitary neoplastic ACTH-producing cells (Cushing’s disease), but not on ectopic ACTH-producing cells or adrenal adenoma (Cushing’s syndrome).

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49
Q

Squamous cell carcinomas?

A
  • smokers
  • central location
  • raised calcium
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50
Q

small cell lung cancer?

A
  • smokers
  • ‘sentral’ location
  • syndromes - SIADH, ACTH
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51
Q

subacute thyroditis?

A

suggested by the tender goitre, hyperthyroidism and raised ESR. The globally reduced uptake on technetium thyroid scan is also typical

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52
Q

what can precipitate thyroid eye disease?

A

radioiodine therapy can precipitate thyroid eye disease but a majority of patients eventually require thyroxine replacement

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53
Q

CD results?

A

In Cushing’s disease, cortisol is not suppressed by low-dose dexamethasone but is suppressed by high-dose dexamethasone - problem at pituitary

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54
Q

hashimotos is associated w development of?

A

MALT lymphoma

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55
Q

ABPi >1

A

An ABPI value of >1 can indicate vessel calcificaiton common in diabetes

Peripheral arterial disease will cause an ABPI value to be decreased, and a reduced ABPI is indicative of peripheral arterial disease

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56
Q

< 0.5 ABPI

A

<0.5 = severe arterial disease - PAD

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57
Q

ABPI 0.5-0.8 =

A

suggests presence of arterial disease or mixed arterial/venous disease - PAD or mixed PAD and PVD

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58
Q

ABPI > 1.3 =

A

> 1.3 = suggests presence of arterial calcification, such as in some people with diabetes, RA, systemic vasculitis, atherosclerotic disease and advanced chronic renal failure.

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59
Q

electrolytes abn in addisons?

A
  • hyponatreamia
  • hyperkalaemia
  • weight loss
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60
Q

what points to osteomalacia?

A
  • low calcium and phosphate
  • raised ALP
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61
Q

Sick euthyroid syndrome?

A
  • low T3/ T4 levels
  • inappropriately normal TSH
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62
Q

The first-line diagnostic test for Cushing’s syndrome is a

A

low dose dexamethasone suppression test

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63
Q

how does myxoedema coma present?

A

Myxoedema coma typically presents with confusion and hypothermia.

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64
Q

how does an addisonian crisis present?

A

Addisonian crises typically feature malaise, nausea and vomiting, abdominal pain, and muscle cramps and paraesthesia,

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65
Q

thyrotoxic storm presentation ?

A

A thyrotoxic storm is a complication of hyperthyroidism that features hyperthermia, tachycardia, vomiting, and agitation.

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66
Q

commonest cause of AD in the uK?

A

The commonest cause of Addison’s disease in the U.K is autoimmunity

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67
Q

AD electrolyte abn?

A

Addison’s disease causes a metabolic acidosis with a normal anion gap

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67
Q

TRUELove and witts criteria?

A

T - Temp > 37.8
R - Rate > 90
U - (Uh)naemia Hb < 105
E - ESR >3

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68
Q

first line for acute mesenteric ischaemia?

A

lactate levels

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69
Q

AF+ abdo pain ->

A

mesenteric ischaemia

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70
Q

features of IMA?

A
  • Acute
  • Painful
  • AF
    +- bloody stool
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71
Q

IC?

A
  • transient
  • not so painful
  • bloody diarhhea
  • no history of AF (especially in SBA)
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72
Q

Ix and Mx of IC?

A
  • do x ray = thumbprinting (especially splenic area)
  • less pain, transient = conservative
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73
Q

What does perinicous anaemia predispose to?

A

gastric carcinoma

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74
Q

if C diff doesn’t respond to first line vancomycin then

A

IfC. difficiledoes not respond to first-line vancomycin , oral fidaxomicin should be used next, except in life-threatening infections

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75
Q

barretts oesophagus inc risk of?

A
  • oesophageal adenocarcinoma
  • achalasia
  • risk of sq cell carcinoma of oesophagus
  • when found endoscopic intervention needs to be done
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76
Q

mesenteric ischaemia triad?

A

triad of CVD, high lactate and soft but tender abdomen

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77
Q

Subclinical hyperthyroidism is associated with?

A

atrial fibrillation, osteoporosis and possibly dementia

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78
Q

Hormones produced by pituitary?

A
  • Growth Hormone (GH)
  • Adrenocorticotropin (ACTH)
  • Thyrotropin (TSH)
  • Prolactin
  • FSH & LH
  • ADH
  • Oxytocin
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79
Q

hormones of pituitary

A
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80
Q

Cell types of pituitary?

A
  • somatotropes - 30-40%
  • corticotropes - 20%
  • thyrotropes
  • gonadotropes
  • lactotropes
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81
Q

most common cell type in the pituitary?

A

somatotropes

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82
Q

hypopituitarism - symptoms

A
  • Tiredness
  • Weight loss
  • Decreased libido
  • Increased sensitivity to cold
  • Loss of appetite
  • Infertility
  • Irregular periods
  • Loss of body or facial hair
  • Short stature
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83
Q

acromegaly presentation?

A
  • bitemporal hemianopia
  • sleep apnoea
  • poor dentition
  • poorly controlled T2DM, insulin resistance
  • HTN, cardiomyopathy, heart failure
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84
Q

screening test for acromegaly?

A
  • screening tests - IGF-1. random GH
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85
Q

confirmatory test of acromegaly?

A

GT test

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86
Q

other tests for acromegaly?

A
  • imaging MRI pituitary
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87
Q

Random GH level - acromegaly?

A
  • little value in diagosis
  • GH secretion is pulsatile
  • stimulated by a variety of factors like fasting exercise stress and sleep
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88
Q

IGF-1 measurement?

A
  • Long half-life
  • To assess GH secretion
  • Screen for acromegaly
  • Monitor response to treatment

First line test for acromegaly. OGTT is second line

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89
Q

What impacts IGF-1 levels?

A
  • IGF-1 concentrations vary with age
  • Starvation, obesity and diabetes mellitus IGF-1
  • pregnancy IGF-1
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90
Q

glucose tolerance test in acromegaly?

A
  • Baseline GH level
  • Ingestion of 75g oral glucose
  • GH measured at 30, 60, 90 and 120 mins
  • Failure to suppress GH levels to < 1ug/L
  • Paradoxical rise
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91
Q

Tx options for acromegaly

A
  • surgery
  • radiotherapy
  • medical
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92
Q

CS image showing symptoms

A
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93
Q

most common cause of CS

A

exogenous steroids

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94
Q

epidemiology of CS?

A
  • female to male incidence is 1.5
  • peak age of incidence: 25-40
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95
Q

Effects of glucocorticoids?

A
  1. Increase glucose production
  2. Inhibit protein synthesis
  3. Increase protein breakdown
  4. Stimulate lipolysis
  5. Immunologic and inflammatory responses
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96
Q

important signs in cushings

A
  • Spontaneous ecchymoses
  • Purple striae
  • Proximal myopathy
  • Osteoporosis
  • Hypokalemia
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97
Q

HPT axis?

A
  • hypo: TRH
  • AP: TSH
  • thyroid: T4 and T3
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98
Q

HPA axis?

A
  • hypo: CRH
  • AP: ACTH
  • adrenals: cortisol releasse
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99
Q

Cross talk between HPA and HPT?

A
  • The pituitary-thyroid and pituitary-adrenal axes exhibit cross-talk and mutual regulation, with hormones from one axis influencing the function and secretion of hormones in the other axis.
  • For example, cortisol can modulate thyroid hormone metabolism and activity, while thyroid hormones can affect adrenal steroidogenesis and cortisol metabolism.
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100
Q

how pituitary affects individuals clinically?

A

hormonal imbalances, vision changes, menstrual irregularities, infertility, growth abn, life threatening adrenal insufficiency

101
Q

how adrenal diseases affect ppl clinically?

A

fatigue, weakness, weight changes, mood disturbances, blood pressure fluctuations, electrolyte imbalances, and metabolic disturbances. In severe cases, adrenal crises can occur, posing immediate danger to life.

102
Q

how thyroid disease affect ppl clinically?

A

affecting metabolism, energy levels, mood, heart rate, weight, and reproductive health. If left untreated, these conditions can lead to complications such as heart disease, infertility, or thyroid storm (in hyperthyroidism)

103
Q

social impacts of endocrine disorders?

A
  • work and productivity: fatigue, mood changes, cognitive impairment
  • QOL
  • financial burden - Managing these chronic conditions often requires regular medical appointments, medications, and sometimes surgical interventions, which can lead to financial strain due to healthcare costs and lost income.
104
Q

visible symptoms of some endocrine disorders?

A
  • The visible symptoms of some endocrine disorders, such as weight changes or mood swings, may lead to stigma or misunderstanding from others. Additionally, living with a chronic illness can contribute to feelings of anxiety, depression, or isolation.
105
Q

initial Ix of thyroid disease?

A
  • TFTs
  • imaging such as US for further evaluation of nodules
106
Q

Ix for adrenal disease?

A
  • cortisol levels
  • ACTh stimulation test
  • aldosterone and renin levels
  • DHEA-S levels
107
Q

Ix of pituitary disease?

A
  • ACTH
  • GH
  • TSH
  • LH
  • FSH
  • prolactin levels
108
Q

imaging in endocrine disorders?

A
  • MRI: with contrast is the preferred imaging modality for evaluating pituitary gland structure
  • CT scan if MTI CI
  • visual field testing - pituitary tumour can compress optic chiasm -> visual disturbances
109
Q

PP produces?

A
  • 2 hormones: oxytocin and ADH - periventricular and supraoptic nuclei.
  • ADH is produced by the hypothalamus and stored by PP
110
Q

ADH?

A
  • inc water permeability and reabs in CDs
  • increases total peripheral resistance
111
Q

SIADH?

A
  • excessive ADH secretion
  • e.g. SCLC
  • Continual ADH production occurs independent of serum osmolality, leading to abnormally low serum sodium levels (dilutional hyponatreamia) , highly osmolar urine and high urinary sodium levels.
112
Q

Causes of SIADH?

A
  • SIADH has a variety of causes, including brain injury, malignancy, drugs, infection, and hypothyroidism.
113
Q

Risk of SIADH after ?

A
  • paticular risk in transsphenoidal pituitary surgery (which is done for cushings disease)
114
Q

Sx of SIADH?

A
  • Headache
  • Confusion
  • Lethargy
  • Anorexia
115
Q

signs of SIADH?

A
  • Seizures
  • Reduced GCS
  • Coma
  • Myoclonus
  • Ataxia
  • Hyporeflexia
  • Asterixis
116
Q

Ix results in SIADH?

A
  • renal function - hyponatreamia
  • low serum osmolarity
  • urine osmolarity- high above 100
  • high urine sodium
117
Q

Clinical signs of acromegaly

118
Q

DI?

A
  • Diabetes insipidus is characterised by the passage of vast volumes of dilute urine.
  • deficiency/ resistance to ADH
  • In some cases, as much as 20 litres of urine can be produced in 24 hours, leading to rapid dehydration and potentially death.
119
Q

What are the causes of neurogenic DI?

A
  • Mutations in vasopressin gene
  • Malignancy: pituitary adenomas, craniopharyngiomas/metastases
  • Trauma
  • Infection: Meningitis
  • Vascular: Sheehan’s Syndrome
120
Q

Other causes of central/ neurogenic DI?

A
  • Sarcoidosis (formation of granulomas in the pituitary gland)
  • Haemochromatosis (deposition of iron in the hypothalamus and pituitary gland)
121
Q

When does nephrogenic DI occur?

A

when ADH cannot bind to their receptors in the kidney.

122
Q

causes of nephrogenic DI?

A
  • Mutations in ADH receptor gene or aquaporin-2 gene
  • Metabolic: hypercalcaemia, hyperglycaemia, hypokalaemia
  • Drugs
  • Chronic renal disease
  • Amyloidosis
123
Q

Acquired causes of nephrogenic DI?

A
  • lithium
  • hypercalacemia
  • hypokalaemia
  • instrinic renal disease
  • post obst uropathy
124
Q

Clinical features of DI reflect the inability to concentrate urine. The classic symptoms are:

A
  • Polyuria
  • Polydipsia
  • Nocturia
  • produces very large amounts of dilute urine
125
Q

DI - signs of dehydration?

A
  • dehydration - dry membranes, prolonged cap refill, hypotension
126
Q

Ix of DI?

A
  • Water deprivation test
  • urine analysis
  • desmopressin challenge test
127
Q

DI - Water dep test?

A

In central DI, urine osmolality remains low despite dehydration, whereas in nephrogenic DI, urine osmolality increases following administration of exogenous ADH (desmopressin acetate)

128
Q

urine analysis?

A
  • urine analysis: In patients with DI, urinalysis typically reveals low urine osmolality (< 300 mOsm/kg) despite hypernatremia and plasma hyperosmolality.
129
Q

Desmopressin challenge test?

A

In patients with central DI, desmopressin typically results in a significant increase in urine osmolality.

130
Q

bloods for DI?

A
  • FBC
  • Renal function(check for renal impairment and hypokalaemia)
  • Plasma osmolality
  • Plasma glucose
  • HbA1c
  • Bone profile(check calcium)
131
Q

urine tests for DI?

A
  • 24-hr urine collection
  • Urine specific gravity
  • Urine osmolality
132
Q

central/ neurogenic DI Mx?

A

Desmopressin

133
Q

risk of using desmopressin?

A
  • water retention -> hyponatreamia
  • can occur as the synthetic ADH is not suppressible as ADH would be in normal physiology when plasma osmolality
134
Q

nephrogenic DI Mx?

A
  • diuretics - thiazide
  • desmopressin in non hereditary forms of nephrogenic DI
135
Q

most common cause of hypopituitarism?

A
  • compression of the pituitary gland bynon-secretory pituitary macroadenoma (most common)
136
Q

other causes of hypopituitarism?

A
  • pituitary apoplexy
  • Sheehan’s syndrome: postpartum pituitary necrosis secondary to a postpartum haemorrhage
  • hypothalamic tumours e.g. craniopharyngioma
  • trauma
  • iatrogenic irradiation
  • infiltrative e.g. hemochromatosis, sarcoidosis
137
Q

hypopit - ACTH deficiency?

A
  • tiredness
  • postural hypotension
138
Q

hypopit - LH/ FSH deficiency?

A
  • amenorrhoea
  • infertility
  • loss of libido
  • low TSH
  • feeling cold
  • constipation
139
Q

hypopit - low prolactin?

A
  • problems with lactation
140
Q

hypopit - features of the underlying cause?

A
  • pituriary macroadenoma → bitemporal hemianopia
  • pituitary apoplexy → sudden, severe headache
141
Q

Mx of hypopit?

A
  • treatment of any underlying cause (e.g. surgical removal of pituitary macroadenoma)
  • replacement of deficient hormones
142
Q

what is acromegaly caused by?

A
  • acromegaly is caused by an excess of GH production related to a pituitary adenoma
143
Q

how does acromegaly present?

A
  • tends to present with macrognathia, frontal bossing and enlargement of hands and feet.
  • Presentation may also be related to the aetiology - e.g. mass effect of a pituitary adenoma resulting in visual field defects and headache.
144
Q

acromegaly is assoc w systemic conditions like?

145
Q

GH/ somatotropin is released by?

A

somatotropic cells of the AP

146
Q

GH release pathway?

A
  • Growth hormone releasing hormone (GHRH) is released from the arcuate nucleus of the hypothalamus.
  • At the AP GH is released
  • this stimulates release of IGF-1
147
Q

GH secretion is?

A

pulsatile, IGF-1 has more stable levels

148
Q

IGF-1?

A
  • produced and released by the liver
  • This axis features negative feedback, in which IGF-1 and GH release leads to the inhibition of GHRH and stimulation of somatostatin release.
149
Q

What accounts for over 90% of cases of acromegaly?

A

pituitary adenomas - Growth hormone secreting somatotroph adenomas are the commonest cause of acromegaly.

150
Q

gigantism?

A

excess GH secretion in childhood prior to fusion of the epiphyseal growth plates

151
Q

other causes of acromegaly (rare)

A
  • Ectopic release of GH: May be seen in neuroendocrine tumours.
  • Ectopic release of GHRH: Related to tumours including carcinoid and small cell lung cancer
  • Excess hypothalamic release of GHRH: Related to hypothalamic tumours.
152
Q

acromegaly tends to have a

A

insidious onset

153
Q

CF of acromegaly - GH excess?

A
  • Acromegaly leads to enlargement of hands, feet, lips and nose.
  • Examination should look for wide spaced teeth, prognathism (large forehead) and frontal bossing.(protrusion of lower jaw)
154
Q

acromegaly - men?

A

may be deepening of voice

155
Q

syndrome associated w acromegaly?

A

Carpal tunnel

156
Q

CFs of acromegaly - mass effects?

A
  • macroadenomas can lead to this
  • headaches common
  • visual changes - pressure on the optic chiasm -> bilateral hemianopia
157
Q

acromegaly - macroadenomas can impair pituitary function ->

A
  • In women menstrual dysfunction is seen, ED in men
  • In up to 30% of patients concomitant hyperprolactinaemia is seen.
158
Q

features of hyperprolactinaemia?

A
  • galactorrhea
  • dysmenorrhoea
  • hypogonadism
  • infertility
159
Q

GH and IGF-1 excess can lead to:

A
  • inc CV disease - HTN, cardiomyopathy, HF
  • insulin resistance -> T2DM
  • obstructive sleep apnoea
  • organomegaly - heart, liver, lungs, prostate and kidneys
  • CRC and diverticulosis - inc risk
  • thyroid enlargement & inc incidence of thyroid cancer
  • headache - mass effect or result of GH excess
160
Q

diagnosis of acromegaly?

A
  • IGF1 levels
  • high - confirms diagnosis -> image
  • equivocal: carry out oral glucose tolerance test
160
Q

acromegaly inc risk of?

A
  • T2D
  • OSA
  • CRC & diverticulosis
  • thyroid cancer
161
Q

Oral GTT in acromegaly?

A
  • Serum GH can be measured before and after glucose stimulation.
  • In healthy individuals, GH release is suppressed following the administration of exogenous glucose.
  • In patients with acromegaly, GH levels are unsuppressed.
162
Q

pituitary MRI in acromegaly?

A
  • Images pituitary - adenoma?
  • Rarely other causes may be found including hypothalamus tumours and pituitary carcinoma.
163
Q

further Ix of acromegaly - GHRH levels?

A

Elevated levels indicate excess production from a hypothalamus tumour or ectopic source.

164
Q

CT CAP in acromegaly?

A

Used to look for evidence of tumours that may lead to acromegaly through GH or GHRH production (e.g. small cell lung cancer, carcinoid).

165
Q

what is the first line in acromegaly?

A
  • transphenoidal surgery
  • microadenomas tend to have better results than macroadenomas
166
Q

transphenoidal surgery?

A
  • CD and acromegaly
167
Q

when are medical therapies used for acro?

A

Medical treatments may be used in patients who are not operative candidates or where surgery fails to achieve biochemical cure.

168
Q

Mx of acro - octerotide?

A
  • Somatostatin analogs(e.g. Octreotide): given as a monthly injection it reduces the release of GH and may cause shrinkage of tumours.
169
Q

Acro Mx - GH antagonists?

A
  • Growth hormone antagonists(e.g. Pegvisomant): given as daily injection, lowers IGF-1 levels.
170
Q

Acro Mx - dopamine agonists?

A

(e.g. Bromocriptine): can reduce the release of GH, though they are only effective for a small proportion. Advantage is they can be given as a tablet.

171
Q

radiotherapy in acro??

A
  • where surgery and medical management fails
  • rarely used as primary therapy
  • The biochemical response to radiotherapy can be slow, taking years.
172
Q

why is radiotherapy for acro avoided in reproductive age grs?

A
  • Risks include the development hypopituitarism; therefore, it is generally avoided in those of reproductive age.
173
Q

cancer screening w acro?

A
  • inc risk of thyroid and CRC
  • CRC screening from age 40
174
Q

patients w acro presenting w ? should be referred on a 2 week wait pathway

A

palpable nodularities

175
Q

prognosis of acro?

A
  • inc mortality
  • inc risk of OSA and CV complications
176
Q

Diastolic murmur + AF → ?

A

mitral stenosis

177
Q

How does lymphoma present?

A
  • incidental raised WBC
  • lymphadenopathy - usually painless, neck or groin
  • sweats - drenching sweats, often at night
  • weight loss
  • splenomegaly
178
Q

pruitis is especially seen in

A

Hodgkins lymphoma

179
Q

Sx of myeloid disorders?

A
  • weight loss
  • fatigue - anemia, non specific
  • splenomegaly - feelings of fullness in abd, left upper quadrant pain, early satiety
  • intermittent fevers
180
Q

Features of BM failure?

A
  • tiredness
  • bruising
  • infections - pneumocytis jiveroki with hodgkins lymphoma
  • anemia - MCV may be raised
  • neutropenia
  • thrombocytopenia
181
Q

which infection can occur paticularly w hodgkins lymphoma?

A

pneumocystis jiveroki

182
Q

bone pains?

A
  • bone pains - myeloma usually but any haem malignancy
183
Q

other features of BM failure?

A
  • osteolytic lesions - inhibition of osteoblasts
  • localised/ generalised pain
  • malignancies that cause expansion of the bone marrow can cause diffuse bone pain
  • e.g. myelofibrosis, acute leukemias
184
Q

why can haem malignancies cause gout?

A
  • high cell turnover
  • assoc w myelofibrosis and myeloproliferative disorders
185
Q

paraneoplastic features of haem maligancies?

A
  • skin rashes
  • vasculitis
  • arthropathy
  • immune cytopenias
186
Q

red flags of haem cancer?

A
  • painless lymphadenopathy
  • weight loss
  • night sweats
187
Q

causes

Anaemia - Reduced Hb and reduced MCV ?

A
  • Iron deficiency
  • Thalassaemias and haemoglobinopathies
  • Lead poisoning
  • Sideroblastic anaemias
  • Anaemia chronic disease (but this is mostly normocytic)
188
Q

Anaemia - normal MCV?

A
  • Anaemia chronic disease
  • Acute blood loss
  • Bone marrow failure syndromes
  • Malignant infiltration
  • Mixed haematinic deficiencies
  • Haemolysis
189
Q

Inc MCV anaemia?

A
  • Megalobalstic anaemias
  • Liver disease
  • Alcohol
  • Hypothyroidism
  • Myelodysplasia
  • Malignant infiltration
  • Haemolysis
190
Q

Causes of decreased red cell production ?

A
  • iron def
  • megaloblastic anemia
  • haemoglobinopathies
  • anemia of chronic disease
  • anemia renal disease
  • BM failure
191
Q

relative anaemias?

A
  • preg
  • dilutional
192
Q

inc ref cell production?

A
  • Hereditary causes
  • Membrane defects
  • Enzymopathies
  • Haemoglobinopathies
193
Q

acquired causes of anaemia?

A
  • Acute blood loss
  • Haemolytic disorders (immune and non-immune).
  • Hypersplenism
194
Q

IDA profile?

A
  • ferritin low
  • iron low
  • transferrin high
  • transferrin saturation low
195
Q

haemachromatosis profile?

A
  • high ferritin and iron
  • low transferrin
  • high transferrin sat
196
Q

AOCD profile?

A
  • ferritin is normal/ high
  • iron low
  • transferrin low
  • transferiin sat low
197
Q

IDA vs AOCD?

A
  • transferrin is high in IDA but low in AOCD
198
Q

Haemolytic anaemia?

A
  • ferritin is high
  • iron high
  • transferrin sat: low
  • transferrin: normal/ low
199
Q

megaloblastic anaemia?

A
  • B12 and folate deficiency.
  • Raised bilirubin and lactate dehydrogenase (LDH) due to ineffective erythropoiesis.
200
Q

AOCD causes ?% of anaemias over 65?

201
Q

AOCD involves?

A
  • MCV normal/ low
  • non-progressive anemia
  • B12/Folate/Ferritin normal.
  • Iron/transferrin/transferrin saturation low.
  • Main differential myelodysplasic syndromes.
202
Q

profile of haemolytic anaemia?

A
  • macrocytic anaemia
  • reticulocytosis
  • rasied LDH and bilirubin
  • polychromasia
203
Q

inherited causes of haemolytic anaemia - red cell defects?

A
  • Hereditary spherocytosis
  • Hereditary elliptocytosis
204
Q

inherited causes of haem anaemia - hb abn?

A
  • Thalassaemias
  • Sickle cell anaemia
205
Q

inherited causes of haem anaemia - metabolic defects?

A
  • Glucose-6-phosphate dehydrogenase deficiency
  • pyruvate kinase fef
206
Q

IDA slide

207
Q

Megaloblastic anaemia histology

208
Q

drug indused haemolysis histology

209
Q

IDA appearance on histology?

A
  • washed out
  • pale center - halo look
  • small red cells, microcytic hyperchromic anemia
210
Q

Megaloblastic anaemia appearance?

A
  • large
  • oval appearance of RBC - oval macroytes
  • red cell precursors - normocytes
  • abn WBC - hypersegmented neutrophil
211
Q

comps of megaloblastic anaemia?

A
  • subacute degen of the SC -> demylination -> paraperesis
212
Q

hereditary spherocytosis - appearance

A
  • circ dense red cells w no central pallor
  • spherical shape instead of biconcave
213
Q

histology of myeloma?

A
  • malignant plasma cells
  • Monoclonal immunoglobulin (M band)
214
Q

myeloma features?

A

1.Renal dysfunction, hypercalcaemia, bone damage, anaemia.
2.>1 bone lesion on whole body MRI/CT/PET-CT.
3.Free light chain ratio >100.
4. >60% plasma cells in bone marrow.

215
Q

myeloma tends to present in which age gr?

A

70s normally

216
Q

presentation of myeloma?

A
  • pain from osteolytic bone lesions
  • renal issues
  • anemia
  • bone problems
  • infections
  • amyloidosis
217
Q

blood film of myeloma?

A
  • rouleax formation
  • Increased levels of abnormal plasma cells in the blood can cause red blood cells to stick together, forming stacks known as rouleaux formation.
  • This can appear as linear stacks of red blood cells on the blood film.
218
Q

lab features of myeloma?

A

–Raised calcium
–Raised urea & creatinine
–Raised total protein

219
Q

prognostic protein in myeloma?

A

beta-2 microglobulin

220
Q

what is usually elevayed in myeloma?

A
  • ESR and plasma viscosity
  • bone marrow has inc plasma cells
221
Q

what else is seen in myeloma- bands

A
  • M band in serum.
  • M band in urine (BJP).
  • Serum free light chains.
222
Q

abn in myeloma?

A
  • immunoelectrophoresis - marked immune paresis
  • most cases produce IgG
223
Q

what is diagnostic of myeloma?

A
  • if more than 10% of WBC in the marrow are plasma cells -> diagnostic of myeloma
224
Q

myeloma bone lesions?

A
  • myeloma bone lesions won’t show up on a radionucleotide bone scan
  • other lesions e.g. met breast cancer will bc theyre hypermetabolic
  • in myeloma these are areas of reduced bone density so won’t show
225
Q

Tx of myeloma?

A

*Solitary plasmacytomas radiotherapy.
*MGUS and asymptomatic Myeloma (chains of <100) do not require therapy.

226
Q

myeloma bone disease?

A

bisphophonates

227
Q

Myeloma - for patients under 70?

A
  • Thalidomide/lenalidomide/bortezomib containing combination therapy.
  • autologous stem cell transplant with high dose Melphalan.
  • Bisphosphonate for myeloma-bone disease.
228
Q

genetics of sickle cell?

A
  • recessive - 2 copies of the defective hb gene needed - 2x HbS
  • chromosome 11 for beta chains
  • 1 hbs gene: sickle cell trait
229
Q

thalassemias vs haemoglobinpathies?

A
  • decreased production of alpha or beta chains - thalassemias
  • mutant variant of these chains - haemaglobinopathies
230
Q

normal vs Hbs?

A
  • normal: HbA
  • Hbs: 2 abn beta chains
231
Q

sickle cell trait?

A
  • sickle cell trait offers protection against malaria bc sickle cells are less suitable for malaria parasites
  • sickle cell is endemic in sub saharan africa and areas of the middle east
232
Q

SCA -large risk of ?

233
Q

why is sepsis high risk in SCA?

A
  • Underlying immune dysfunction related to hyposplenism.
  • Mainly encapsulated bacteria.
  • Highest risk under the age of 5 years.
234
Q

Reducing sepsis risk in SCA?

A
  • Role of pneumococcal vaccination and prophylactic penicillin in children w SCA
235
Q

painful vaso-occlusive crisis?

A
  • reccurent episodes of bone pain
  • often in thighs, arms, ribs, pelvis, spine
  • children are more affected in small bones of the hands and feet
236
Q

Sickle cell crises can be triggered by?

A
  • crises can be triggered by stress or infection
  • exposure to cold
  • Mx: rest/ rehydration
  • simple analgesia
237
Q

SCA - acute chest syndrome?

A
  • serious comp
  • children or adults
  • history of painful crisis in ribs w assoc inc breathlessness
238
Q

SCA - AC syndrome - chest XR?

A
  • hypoxemic - abn chest XR - infiltrates in lungs can be seen
239
Q

Mx of acute chest syndrome?

A
  • analgesia for pain
  • red cell exchange for hypoxia - aims to reduce HbS levels down to less than 30%
240
Q

leg ulceration w SCA?

A
  • vasoocclusion of small vessels
  • over medial and lateral malleolus
  • can be chronic and recurrent
241
Q

SCA comps - vascular?

A
  • children and adults
  • stenosis of ICA due to hyperplasia
242
Q

screening w SCA?

A
  • All children w sickle cell should be screened for ICA stenosis using transcranial dopplers
  • if found, transfusion required
243
Q

MX of stroke w SCA?

A

hypertransfusion - reg transfusion of red cells to suppress HbS

244
Q

SCA - anaemic crisis?

A
  • can suddenly worsen
  • infection w parovirus can cause an aplastic crisis
  • in young children there can be splenic sequestration in which blood pools
245
Q

Hb levels on a FBC?

A
  • low levels - anemia
  • high levels - dehydration, polycythemia vera
246
Q

WBC on a FBC?

A
  • leukopenia - bone marrow disorders, viral infections
  • leukocytosis - infections, inflammation, leukemia
247
Q

Platelet count on FBC?

A
  • thrombocytopenia
  • thrombocytosis - inflammation, infection, bone marrow disorder
248
Q

MCV on FBC

A
  • Low MCV indicates microcytic anemia, often due to iron deficiency.
  • High MCV suggests macrocytic anemia, commonly caused by vitamin B12 or folate deficiency, alcohol
249
Q

Bone marrow aspiration?

A
  • bone marrow aspiration and biopsy provides direct observation of RBC precursors
  • The presence of abnormal maturation (dyspoiesis) of blood cells and the amount, distribution, and cellular pattern of iron content can be assessed
  • only done when: anemia is unexplained, more than one cell lineage abn - a.g. anemia and leukopenia, suspected primary bone marrow disorder e.g. leukemia

Year 3 (45 decks)

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