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Endocrinology > Pathology > Flashcards

Pathology Flashcards

1
Q

What is Cushing’s syndrome

A

An excess of cortisol

Can have many origins

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2
Q

What are some of the potential causes of Cushing’s syndrome

A

Pituitary - caused by tumour in corticotroph cells (usually microadenomas)
Adrenal - caused by adrenal adenoma/carcinoma
Ectopic - some lung, thymus and pancreas cancers etc produce ACTH
Exogenous steroids - excess drug intake
Alcohol and depression

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3
Q

What are the symptoms of Cushing’s syndrome

A 
Cushingoid faces - moon-like, fat 
Acne
Hirsutism
Abdominal striae and central obesity
Interscapular and  supraclavicular fat pads- buffalo hump 
Proximal myopathy - wasting, thin limbs
Osteoporosis
Hypertension
Impaired glucose tolerance - DM 
Thin skin - easy bruising
Psychosis - euphoria or depression 
Thirst and polyuria
Immunosuppression  - prone to infection
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4
Q

What can cause cervical lymphadenopathy

A

infective, malignancy or haematological (leukaemia/lymphoma)

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5
Q

What is the most accurate way to diagnose cervical lymphadenopathy

A

Aspiration

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6
Q

What symptoms may be associated with cervical lymphadenopathy

A

Systemic symptoms: fever, weight loss, sweats

Specific symptoms: hoarseness, cough, dyspnoea

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7
Q

What is a dermoid cyst

A

Rare congenital cysts

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8
Q

Describe the presentation of a cystic hygroma

A

posterior triangle
Seen in kids (usually first year of life)
Can be large and cause pressure symptoms
Can be filled with lymph

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9
Q

Where would you find a branchial cyst

A

upper anterior triangle

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10
Q

What is a pituitary adenoma

A

Derived from cells of the anterior pituitary
Relatively common
Either sporadic or associated with MEN1 (multiple endocrine neoplasia syndromes )
Further classified by cell type/ hormone produced
Large ones can cause local mass effects such as visual defects

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11
Q

Describe the effect of a tumour that secretes prolactin

A

Most common functional pituitary adenoma - prolactinoma

Leads to infertility, amenorrhea, galactorrhea, gynaecomastia and lack of libido (late presentation)
May also present with structural effects

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12
Q

Describe the effect of a tumour that secretes growth hormone

A

Second most common type of functional tumour
Causes increase in insulin like growth factor which stimulates growth of bone, cartilage and connective tissue
Can lead to diabetes, hypertension and carpal tunnel name
Get gigantism or acromegaly

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13
Q

Describe the effect of a tumour that secretes ACTH

A

Causes Cushing’s disease
Usually caused by a micro-adenoma
Causes bilateral adrenocortical hyperplasia

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14
Q

What is a craniopharyngioma

A

Derived from remnants of Rathke’s pouch
Type of internal cranial tumour
Slow growing, often cystic and may calcify
Can arise in the vicinity of the pituitary

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15
Q

What are the symptoms of a craniopharyngioma

A

Headaches and visual disturbances

Children may have growth retardation

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16
Q

Describe diabetes insipidus

A

Caused by a lack of ADH function
Can be central - due to ADH deficiency
Can be caused by trauma, tumours, inflammatory disorders

Can be nephrogenic due to renal resistance to ADH

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17
Q

What causes SIADH

A

An excess of ADH

Many causes:

  • Ectopic production of ADH – paraneoplastic syndrome from cancer
  • CNS infections
  • Intracranial bleeds
  • ADH analogues like desmopressin or drugs which stimulate its action (SSRIs)
  • Idiopathic or hereditary
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18
Q

What can cause adrenal hyperfunction

A

Hyperplasia
Adenoma
Carcinoma

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19
Q

What can cause adrenal hypofunction

A

Acute - Waterhouse-Friderichsen

Chronic - Addison’s disease

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20
Q

Describe congenital adrenocortical hypoplasia

A

Group of autosomal recessive disorders
Caused by deficiency/ lack of enzyme required for steroid biosynthesis
This blocks other pathways and leads to increased androgen production
Baby girls with this will present with ambiguous genitalia
Reduced cortisol stimulates ACTH release and cortical hyperplasia

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21
Q

Describe acquired adrenocortical hyperplasia

A

Caused by endogenous ACTH production
Can be a pituitary adenoma (Cushing’s) or ectopic ACTH production (e.g. SC lung cancer)
Leads to bilateral adrenal enlargement

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22
Q

What are adrenogenital syndromes

A

Defects in enzymes in the production of adrenal hormones lead to accumulation of precursors which can then be diverted to other endpoints – e.g. produce testosterone instead of cortisol

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23
Q

Which age group tends to be affected by adrenocortical tumours

A

Mainly adults

Can affect younger patients - Li-Fraumeni syndrome

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24
Q

How do adrenocortical tumours present

A

Incidental finding (radiology, autopsy)
Hormonal effects
Mass lesion
Carcinomas with necrosis can cause fever

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25
Q

Describe the presentation of adrenocortical adenoma

A

Well circumscribed, encapsulated lesions
Usually small
Yellow / yellow brown cut surface (lipid)
Composed of cells resembling adrenocortical cells
Well differentiated, small nuclei, rare mitoses
Can be functional, but more likely not
Often an incidental finding - usually small

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26
Q

Are adrenocortical carcinomas common

A

No - they are rare

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27
Q

Are adrenal carcinoma non-functional or functional

A

More likely to be functional and malignant

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28
Q

Where do adrenocortical carcinomas usually spread to

A

Local invasion – retroperitoneum, kidney
Metastasis – usually vascular (liver, lung and bone)
Peritoneum and pleura
Regional lymph nodes

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29
Q

What features are suggestive of an adrenocortical carcinoma

A 
Large size 
Haemorrhage and necrosis
Frequent mitoses, atypical mitoses
Lack of clear cells
Capsular or vascular invasion
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30
Q

What can cause primary hyperaldosteronism

A

Conn’s syndrome
Adenoma
Diffuse or nodular hyperplasia of both adrenal glands
It is autonomous production of aldosterone

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31
Q

What can cause hypercortisolism

A

Cushing’s
Steroid therapy - iatrogenic
ACTH secreting tumours - endogenous or exogenous

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32
Q

List causes of acute adrenocortical insufficiency

A

Rapid withdrawal of steroid treatment
Crisis in patient with chronic insufficiency
Massive adrenal haemorrhage

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33
Q

List causes of chronic adrenocortical insufficiency

A
  • Addison’s disease
  • Autoimmune adrenalitis
  • Infections e.g. TB, H|V
    -Metastatic malignancy (lung or breast)
    Unusual causes include amyloid, sarcoidosis and haemochromatosis
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34
Q

Do symptoms of chronic adrenocorticoid insufficiency appear immediately

A

NO

Symptoms only appear once 90% of the gland is damaged

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35
Q

What are the symptoms and signs of Addison’s disease

A 
Weakness, fatigue, anorexia, nausea, vomiting, weight loss, diarrhoea
Hypotension 
Dehydration
Increased pigmentation 
K+ retention and Na+ loss 
Decreased glucocorticoids
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36
Q

What can cause a crisis in Addison’s disease and what are the signs

A

Stress – infection, trauma, surgery

Vomiting, abdominal pain, hypotension, shock and death

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37
Q

What are the 2 types of adrenal medullary tumours

A

Phaeochromocytoma

Neuroblastoma

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38
Q

Which age group is mainly affected by neuroblastoma

A

Children
Usually diagnosed around 18 months
40% diagnosed in infancy

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39
Q

Describe a neuroblastoma

A

40% arise in the adrenal medulla – the remainder mostly along the sympathetic chain
Composed of primitive appearing cells but can show maturation and differentiation towards ganglion cells
Age and stage important for prognosis
Spreads to bones

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40
Q

What is a phaeochromocytoma

A

A neoplasm derived from chromaffin cells of the adrenal medulla
Secrete catecholamines - excess nor-adrenaline and adrenaline
Rare cause of secondary hypertension

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41
Q

What are the signs and symptoms of phaeochromocytoma

A

Hypertension - paroxysmal episodes common during stress, exercise etc
Can lead to cardiac failure, infarction and arrhythmias
Urinary excretion of catecholamines and metabolites can be detected
paroxysmal sweating
Headache
Pallor
Tachycardia
Anxiety/fear

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42
Q

Describe the appearance and behaviour of a phaeochromocytoma

A

Characteristically tumour cells form nests
If malignant they tend to be large and necrotic
Propensity for skeletal metastasis
Other sites include regional lymph nodes, liver and lung

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43
Q

What kind of test would you do if there is too much of a hormone

A

Dynamic suppression test

Introduce a change artificially and see if hormone levels decline in the way you’d expect

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44
Q

What kind of test would you do if there is too little of a hormone

A

Dynamic stimulation test

Try to stimulate hormone release and if it works it suggests the tissue is functional

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45
Q

What is classified as a microadenoma

A

Tumour less than or equal to 1cm

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46
Q

What is classified as a macroadenoma

A

Tumour greater than or equal to 1cm

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47
Q

What symptoms might you get with a pituitary adenoma that is very large

A

Compression of optic chiasm - causes bitemporal hemianopia
Compression of other surrounding cranial nerves (3,4,6) - loss of some eye movements
Headache

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48
Q

What symptoms might you get with a pituitary adenoma that is supressing hormone release

A

Hypoadrenalism – not enough cortisol
Hypothyroid – due to lack of TSH
Hypogonadism – due to lack of FSH/LH (may result in amenorrhea, loss of libido and erectile dysfunction)
Diabetes insipidus – no ADH
GH deficiency - children stop growing, low mood, poor muscle function in adults
Loss of prolactin - only noticed in lactating mums

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49
Q

List the physiological causes of raised prolactin

A

Breast feeding
Pregnancy
Stress
Sleep

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50
Q

List the pharmacological causes of raised prolactin

A

Dopamine antagonists- metoclopramide
Anti-psychotics
Anti-depressants - TCA, SSRIs
Cocaine

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51
Q

List the pathological causes of raised prolactin

A

Hypothyroidism
Stalk lesions - caused by surgery or severe trauma (e.g. RTA)
Prolactin secreting tumour of the pituitary – prolactinoma (most common pituitary tumour)

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52
Q

Which other hormone has a mild stimulatory effect on prolactin production

A

TRH

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53
Q

What are the symptoms of prolactinoma in women

A 
Galactorrhoea - milk production 
Menstrual irregularity 
Amenorrhoea 
Infertility 
Tend to present early as they notice the symptoms - obvious
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54
Q

What are the symptoms of prolactinoma in men

A 
Impotence 
Visual field abnormality 
Headache 
Anterior pituitary malfunction 
Tend to present later with mass effects
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55
Q

What investigations can be done if you suspect a prolactinoma

A

Serum Prolactin concentration - would be high
This is only normal in breastfeeding mums
MRI of pituitary - look for adenoma
Visual field test - bitemporal hemianopia
Pituitary Function tests - may be other hormones affected

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56
Q

How do you treat prolactinoma

A

Only pituitary adenoma which is amenable to medical therapy - Dopamine agonists
Cabergoline is usually 1st line as has the least side effects
Other drugs in this class are - bromocriptine (only one safe in preganacy) and quinagolide

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57
Q

List potential side effects of dopamine agonists

A

nausea/vomiting
low mood
may cause fibrosis of heart valves etc

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58
Q

What causes acromegaly

A

GH excess - most commonly from tumour

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59
Q

What are the symptoms of acromegaly

A

Giant due to bone growth (before epiphyseal fusion)
Thickened soft tissues - skin, large jaw, sweaty, large hands, prominent brow (frontal bossing)
Increased shoe size and large hands
Snoring/Sleep apnoea due to thickened nasopharynx
Tiredness
Hypertension and cardiac failure
All soft tissue and organs enlarge (hepato, spleno and cardiomegaly)
Overgrowth of bone leads to premature arthritis
Headaches
Diabetes mellitus
Local pituitary effects - visual fields, hypopituitarism
Early CV Death
Colonic polyps and colon cancer

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60
Q

What causes the headaches in acromegaly

A

Increased dynamic blood flow - vascular effect of condition

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61
Q

How would you diagnose acromegaly

A

IGF1 levels tested - usually raised as GH stimulates its release
Then do a glucose tolerance test - suppression test for GH (will not be suppressed if affected)
Visual field examination
MRI of pituitary

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62
Q

How do you treat acromegaly

A

Drugs to help symptoms include: somatostatin analogues such as sandostatin
GH antagonist - pegvisomant
May use dopamine agonists

Pituitary surgery - trans-sphenoidal
If GH still high after then can use radiotherapy and drugs

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63
Q

What are the side effects of somatostatin analogues

A 
Local Stinging
Short term: 	
Flatulence
Diarrhoea
Abdominal pains

Long term:
Gallstones - stop gallbladder contracting

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64
Q

When are dopamine agonists more effective in acromegaly

A

If the pituitary tumour causing the excess GH is co-secreting prolactin

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65
Q

How does pegvisomant work

A

GH antagonist - Binds to the growth hormone receptor and blocks its activity
Does not decrease tumour size
IGF1 levels decrease but GH stays the same or increases

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66
Q

Obesity has similar presentations to Cushing’s - how you differentiate

A 
Cushing's is characterised by:
Thin Skin
Proximal myopathy
Frontal balding in women
Conjunctival oedema (chemosis)
Osteoporosis

You wont see these symptoms in classic obesity

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67
Q

Describe the screening test for Cushing’s

A

Overnight 1mg dexamethasone suppression test
Measure cortisol levels the next morning - if still high it is considered abnormal and Cushing’s should be suspected
The dexa should supress the ACTH and therefore cortisol

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68
Q

What is the definitive test for Cushing’s

A 
If screening (overnight dexa) test is positive then carry out a low dose dexamethasone suppression test 
Give 2mg of dexa per day for 2 days 
measure cortisol 6 hrs after last dose 
If still >130 nmol/l then definitely Cushing's
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69
Q

What is the high dose dexamethasone test used for

A

Determines what the type of Cushing’s it is

If cortisol level is supressed by the high dose then it’s pituitary in origin

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70
Q

How do you treat pituitary Cushing’s

A

Hypophysectomy and external radiotherapy if recurs

Trans-sphenoidal removal of the causative tumour

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71
Q

How do you treat adrenal Cushing’s

A

bilateral adrenalectomy - remove glands

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72
Q

How do you treat ectopic Cushing’s

A

Remove source

OR bilateral adrenalectomy

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73
Q

What drugs can be used in the treatment of Cushing’s

A

Metyrapone - only if other treatments fail or not suitable in elderly, side effects common
Ketoconazole - hepatotoxic
Both stop synthesis of cortisol
Pasireotide LAR - somatostatin analogue

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74
Q

What can cause hypopituitarism (low pituitary action)

A 
Pituitary tumours 
Secondary metastatic tumours 
Local brain tumours - mass effect if nearby 
Granulomatous disease - TB, sarcoidosis 
Vascular disease - polyarteritis 
Trauma - RTA 
Hypothalamic disease - e.g. syphilis 
iatrogenic - surgical mistake 
Autoimmune - sheenan disease post-partum 
Infection - meningitis
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75
Q

What are the symptoms of anterior hypopituitarism

A 
Menstrual irregularities (F)
Infertility, impotence
Gynaecomastia (M)
Abdominal obesity
Loss of facial hair (M)
Loss of axillary and pubic hair (M and F)
Dry skin and hair
Hypothyroid faces
Growth retardation - in kids
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76
Q

How can you treat hypothyroidism

A

Thyroxine - 100-150mcg/day

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77
Q

How can you treat low cortisol levels

A

Hydrocortisone
10-25 mg/day
Day and night

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78
Q

How can you treat low GH levels

A

GH nightly as SC injection

It increases muscle mass, bone density and improves cardiac function

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79
Q

How do you treat low testorone levels

A

Testosterone replacement
IM injection every 3-4 weeks or 10-14 weeks depending on type
Can get skin gels

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80
Q

What are the risks of testosterone replacement

A

Prostate enlargement - doesn’t cause cancer
Polycythaemia - too many blood cells
Hepatitis

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81
Q

List the causes of diabetes insipidus

A

Familial - isolated or part of DIDMOAD
Idiopathic - 50%
Due to trauma such as RTA
Rarely: tumours, sarcoidosis, meningitis

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82
Q

What conditions are included in DIDMOAD

A

Diabetes insipidus
Diabetes mellitus
Optic atrophy
deafness

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83
Q

How do you test for diabetes insipidus

A

Water deprivation test
Stimulation test – trying to cause ADH release (patient should try and retain water to counteract test)

Measure plasma and urine osmolality and then stop patient drinking from 8am-4pm. If they have DI then urine will continue to be inappropriately diluted and plasma osmolality increases

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84
Q

How do you treat cranial diabetes insipidus

A

Give desmopressin - synthetic ADH
Can be in nasal spray, tablet or injection forms

Titrate dose according to plasma sodium and symptoms

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85
Q

List common causes of midline neck swellings

A

Thyroid pathology
Thyroglossal cyst
Dermoid cyst

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86
Q

List common causes of anterior triangle swellings

A

Lymph nodes
Branchial cyst
Salivary gland pathology
Carotid body tumour

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87
Q

List common causes of posterior triangle swellings

A

lymphadenopathy

cystic hygroma

88
Q

What is Conn’s syndrome

A

An excess of aldosterone
Caused by a tumour presents in the cells of the zona glomerulosa which secretes excess aldosterone
Results in high NaCl and water levels in the body
Low potassium due to Na/K ATPase action

89
Q

What are the symptoms of Conn’s syndrome

A

Hypertension - increase in Na resorption causes water to follow which increases circulating volume
Hypokalaemia
Will have a high aldosterone and unrecordable renin

90
Q

Describe adrenal hyperplasia

A

Cause of secondary hypertension
Usually occurs bilaterally
Similar symptoms to Conn’s

91
Q

How do you diagnose primary aldosteronism

A

Plasma aldosterone and renin are measured in the blood and expressed as a ratio
If ratio is >750 then do a saline suppression test (give 2L saline and would expect aldosterone to decrease due to RAAS feedback)
If it is not fully supressed then confirmation of primary aldosteronism (e.g, Conns)

Would then do a CT adrenal to determine if Conn’s or hyperplasia

92
Q

What conditions are included in primary aldosteronism

A

Conn’s syndrome

adrenal hyperplasia

93
Q

How do you treat Conn’s syndrome

A

Surgery

Remove the adenoma laparoscopically

94
Q

How do you treat adrenal hyperplasia

A

Aldosterone receptor antagonist - e.g. spironolactone or eplerenone
Spironolactone comes with lots of side effects (gynaecomastia and hyperkalaemia)

95
Q

How does Cushing’s affect DHEA levels

A

Increased secretion due to higher ACTH levels
As it’s the prohormone to the sex hormones you get excess testosterone
Can get acne, amenorrhea, frontal balding, facial hair growth, lack of libido and impotence

96
Q

What are the symptoms of adrenaline hypersecretion

A 
Hypertension 
Increased heart rate and strength 
Pallor or excessive flushing 
Arrhythmias 
Palpatation
Sweating 
Headaches 
Anxiety 
Polyuria and polydipsia 
Slows digestion - ileus
97
Q

Why is phaechromocytomas called 10% tumours

A 
10% extra-adrenal 
10% are malignant (mets)
10% bilateral 
10% occur in children 
10% are part of an associated hereditary syndrome
98
Q

How would you diagnose phaeochromocytomas

A

Urinary catecholamines and metabolites collected and measured over 24hrs
Typically do this over 2-3 days

If abnormal you do a CT or MRI to look for tumours
Then do more specific MIBG scan - type of nuclear medicine scan that looks for tumour/mets by attaching radioactive marker to MIBG (adrenaline precursor)

99
Q

How do you treat phaeochromocytomas

A

Surgery to remove the tumour - usually lap
Alpha and beta blockade to counteract symptoms before surgery
If malignant tumour then chemo can be used

100
Q

List primary causes of primary adrenal insufficiency

A 
Addison's disease - autoimmune condition
Congenital Adrenal Hyperplasia
Adrenal TB 
Malignancy 
Adrenal haemorrhage 
Haemochromatosis
101
Q

List secondary causes of adrenal insufficiency

A

Due to lack of ACTH stimulation
Iatrogenic (excess exogenous steroid) - most common
Pituitary/hypothalamic disorders - e.g. tumour

102
Q

Addison’s disease only becomes symptomatic once most of the damage is done - true or false

A

True

Usually only once 90% of the adrenal gland is destroyed

103
Q

How would you diagnose Addison’s

A 
Blood tests: 
Low Na and high K+ 
Hypoglycaemia 
ACTH levels - will be high 
High renin and low aldosterone 
Adrenal antibodies

Short synacthen test - give ACTH injection then measure cortisol

104
Q

How do you treat adrenal insufficiency

A

DONT DELAY - START TREATMENT
Give steroids (hydrocortisone IV) and fluid (saline to replace Na)
Give fludrocortisone as aldosterone replacement
Basically syntehtically replace the missing hormones
Give sick day rules and identification

105
Q

Adrenal insufficiency can be fatal if not treated - true or false

A

TRUE

106
Q

How are steroids used in treatment

A

Suppression of inflammation, the immune system and replacement treatment
Treats allergic disease, inflammatory disease, malignant

107
Q

Do you get hyperpigmentation with secondary adrenal insufficiency

A

NO

Pigmentation caused by excess ACTH which is low in secondary causes

108
Q

What are the implications of long term steroid treatment

A

Supresses ACTH production - negative feedback acts on anterior pituitary
Unable to properly respond to stress
Need extra dose when ill
Cannot stop suddenly - need gradual withdrawal over 4-6 weeks

109
Q

How do you diagnose primary aldosteronism

A

Measure plasma aldosterone and renin
If ratio is raised then carry out saline suppression test -should supress aldosterone and renin – if that doesn’t happen (e.g. aldosterone high) then you can get biochemical diagnosis of alsosteronism

Then confirm subtype through CT or adrenal vein sampling

110
Q

What are the symptoms of classical congenital adrenal hyperplasia

A

Males:
Adrenal insufficiency
Poor weight gain

Females
Genital ambiguity

111
Q

What are the symptoms of non-classical congenital adrenal hyperplasia

A 
Hirsute 
Acne
Oligomenorrhoea
Precocious puberty
Infertility or sub-fertility
112
Q

How do you treat CAH

A 
Glucocorticoid replacement 
Some need mineralocorticoid 
Achieve max growth potential in kids 
Control androgen excess 
Restore fertility
113
Q

List the biochemical changes seen in phaeochromocytoma

A 
Hyperglycaemia 
May have low potassium 
High haematocrit - raised Hb conc 
Mild hypercalcaemia 
Lactic acidosis 
High catecholamines
114
Q

How do you diagnose phaechromocytoma

A

Confirm catecholamine excess: 24hr urine test or plasma levels
Identify source by MRI, MIBG or PET scan

115
Q

How do you treat phaechromocytoma

A 
Full α and β- blockade (A before B) - phenoxybenzamine and propranolol 
Fluid and/or blood replacement 
Surgery to remove tumour 
Chemo if malignant 
Genetic and family testing
116
Q

What are the symptoms of hypercalcaemia

A 
Increased stimulation of smooth muscle, nerves and heart 
Tiredness 
Confusion 
Depression and lethargy 
May have abnormal ECG 
Arrhythmia 
Kidney stones 
Muscle weakness - decreased excitability 
Constipation 
Polyuria and polydipsia
Osteoporosis
117
Q

What are the symptoms of hypocalcaemia

A

Muscle tetany - increased excitability
Pins and needles in extremities
Extreme cases can cause contraction of respiratory muscle - breathing issues and even death by asphyxiation

118
Q

What are the symptoms of hyperparathyroidism

A 
Hypercalcaemia - associated symptoms 
Renal stones 
Osteoporosis 
Low serum phosphate
High PTH and calcium
119
Q

What are the 3 types of hyperparathyroidism

A

Primary - caused by overactive parathyroid gland
Secondary - physiological response to low calcium
Tertiary - parathyroid becomes autonomous after years of secondary

120
Q

How do you diagnose hyperparathyroidism

A

Raised serum calcium
Raised serum PTH
Increased urine calcium excretion
Do a sestimibi scan - overactive gland will take up labelled solution if primary hyperparathyroidism

121
Q

How do you treat hyperparathyroidism

A

Surgical removal of causative adenoma - only if suffering with renal issues or severe osteoporosis
High fluid intake
Avoid high calcium and Vit D diet
Bisphosphonates are mainly a holding measure

122
Q

What causes hypoparathyroidism

A

Lack of cells in the parathyroid gland which secrete PTH
Can be genetic: Di George Syndrome (absence of glands)
Acquired - destruction via malignancy in gland or autoimmune disease

123
Q

What are the symptoms of hypoparathyroidism

A

Symptoms of hypocalcaemia
Chvostek’s sign
Trousseau’s sign
Fractures due to high remodelling

124
Q

What is Chvostek’s sign

A

Twitching of facial muscle when you gently tap the facial nerve

125
Q

What is Trousseau’s sign

A

Inflating a BP cuff at systolic pressure will cause tetany of hand muscles

126
Q

How do you diagnose hypoparathyroidism

A

Blood tests: hormone and serum electrolyte

Look for low PTH, low Ca, high phosphate

127
Q

How do you treat hypoparathyroidism

A

Calcium and Vitamin D supplements

128
Q

what causes pseudohypoparathyroidism

A

Genetic receptor abnormality leading to resistance of PTH hormone

129
Q

Describe the blood electrolyte levels in pseudohypoparathyroidism

A

Increased PTH
Low Ca
High phosphate

130
Q

What are some complications of pseudohypoparathyroidism

A 
Subcutaneous calcification 
Mental retardation 
Blunting of 4th metacarpal
Obesity 
Bone abnormalities
131
Q

List causes of vitamin D deficiency

A

Lack of sunlight absorption - winter, skin pigmentation, not outdoors enough
Lack of absorption of prohormone - poor diet or malabsorption
Problem with hormone activation - liver failure

132
Q

what does vitamin D deficiency result in

A

Decreased absorption of Ca and phosphate
PTH secretion increases to compensate but this causes more bone reabsorption - weaker and less dense bones
Lack of mineralisation which causes low bone quality
Leads to rickets and Osteomalacia

133
Q

Describe rickets

A

Occurs in kids with low vit D
Bones become soft - legs bow under their weight, skull bones are soft and tender, widened epiphyses at wrists, abnormalities of costochondral joints

134
Q

describe Osteomalacia

A

Similar to rickets but in adults
Low mineralisation leads to increased fracture risk
Bone and muscle tenderness
Gait deformity

135
Q

What is the most common cause of female infertility

A

PCOS

136
Q

List some potential causes of amenorrhea

A 
PCOS 
Anorexia nervosa 
Bulimia nervosa 
Depression 
Endocrine disorders 
Pregnancy 
Premature menopause or ovarian failure
137
Q

What is oestradiol

A

Potent oestrogen produced by the ovary

138
Q

Which cancer is most likely to spread to the adrenals

A

Lung

139
Q

What is a periosteal reaction

A

Reacts when the bone has been attacked or damaged
Thick rind appearing around bone
Periosteum becomes hypertrophic in cancers (often lung)

140
Q

Describe a diffuse bone abnormality

A

all bones are too brittle
all bones are too soft
tends to be a systemic problem
Includes osteoporosis, rickets, Osteomalacia and Paget’s

141
Q

Describe a focal bone abnormality

A

Occurs in a single location

Can be traumatic, neoplastic, inflammatory or degenerative

142
Q

Which bones are most commonly fractured in osteoporosis

A

proximal femur
sacrum and pubic rami
thoracolumbar vertebral bodies
distal radius

143
Q

Describe the appearance of lytic bone destruction

A

Medullary lucency and loss of trabeculae
Loss of inner cortex
Complete loss of cortex
Potential for pathological fracture

144
Q

Describe the appearance of sclerotic bone lesions

A

Subtle medullary density and loss of trabeculae
Spreading zone of density which includes cortex
Featureless white bone
Expansion of bone
Most commonly caused by prostate and breast cancer

145
Q

What is the definition of osteoporosis

A

Progressive systemic skeletal disease characterised by low bone mass and deterioration of bone tissue, with a increase in bone fragility and susceptibility to fracture

146
Q

Bone is constantly undergoing remodelling - true or false

A

TRUE

continuous cycle

147
Q

Describe how bone mass changes with age

A

Increases as we grow up
Peaks at around 30 and is maintained until mid-late 40’s
Starts to decrease as we age
Accelerated in women due to menopause

148
Q

Which factors contribute to bone loss

A 
Sex hormone deficiency
Body weight
Genetics
Diet
Immobility
Diseases
Drugs especially glucocorticoids, aromatase inhibitors
149
Q

In which sex is osteoporosis more common

A

Women

150
Q

List common fracture sites in osteoporosis patients

A

Neck of femur
Vertebral body
Distal radius
Humeral neck

151
Q

What can multiple vertebral fractures lead to

A

Thoracic kyphosis

152
Q

Fracture incidence increases with age - true or false

A

True

153
Q

How do you measure bone density

A

DEXA scan

Compares bone density to peak young adult level and an age matched group

154
Q

What are the risk factors for fragility fracture

A

Non-modifiable: age, gender, ethnicity, previous fracture, family history, early menopause, co-existing disease

Modifiable - bone density, alcohol, weight, smoking, inactivity, certain medications

155
Q

Who do you assess for fracture risk

A

Anyone >age 50 years with risk factors
Anyone under 50 years with very strong clinical risk factors:
Early menopause
Glucocorticoids

156
Q

As bone density decreases, fracture risk increases - true or false

A

True

157
Q

List some secondary causes of low bone density/osteoporosis

A

Endocrine: Cushing’s, hyperthyroidism, hyperparathyroidism
GI: Coeliac, IBD, chronic liver disease
Chronic kidney disease
CF or COPD

158
Q

Which lifestyle factors can be modified to manage osteoporosis

A 
Exercise: high intensity strength training and low impact weights 
Avoid excess alcohol 
Avoid smoking 
Fall prevention
Increased dietary calcium
159
Q

Which drugs can be used in the treatment of osteoporosis

A 
Calcium & vitamin D supplementation
Bisphosphonates
Denosumab
Teriparatide
HRT
SERMS (Selective Estrogen Receptor Modulators)
Testosterone
160
Q

How do bisphosphonates work

A

Anti-resorptive agents
Prevent bone loss at all sites vulnerable to osteoporosis - ingested by osteoclasts and cause cell death
Reduce risk of hip and spine fracture

161
Q

Give examples of bisphosphonates

A

Aledronate

Risedronate

162
Q

When is zoledronic acid given in treatment of osteoporosis

A

Given if they cannot tolerate the bisphosphonate oral therapy
Annual IV infusion for 3 years

163
Q

How does denosumab work

A

fully human monoclonal antibody which binds to target and inhibits development and activity of osteoclasts
Decreases bone resorption and increases bone density
Given as SC injection every 6 months

164
Q

What are the side effects of desonumab

A

Hypocalcaemia, eczema, cellulitis

165
Q

How does teriparatide work

A

It is recombinant parathyroid hormone - mimics its action
Stimulates bone growth rather than reducing bone loss
Only used in a small number

166
Q

Describe the effects of corticosteroids on bone health

A

Reduction of osteoblast activity and lifespan
Suppression of replication of osteoblast precursors
Reduction in calcium absorption
Inhibition of gonadal and adrenal steroid production

Increases fracture risk - dose dependent

167
Q

Describe Paget’s disease of bone

A

Abnormal osteoclastic activity followed by increased osteoblastic activity
Results is abnormal bone structure with reduced strength and increased fracture risk
May be single or multiple sites

168
Q

Which bones are commonly affected by Paget’s

A

long bones, pelvis, lumbar spine and skull predominantly

169
Q

Incidence of Paget’s decreases with age - true or false

A

False
It increases
Rare in the under 40’s

170
Q

How does Paget’s present

A

Bone pain
Deformity
Deafness
Compression neuropathies

Can be asymptomatic and an incidental finding

171
Q

How do you treat Paget’s

A

Analgesia

Bisphosphonates

172
Q

What is osteogenesis imperfecta

A

Rare group of genetic disorders mainly affecting bone
Mostly caused by defects in collagen genes
Most are autosomal dominant
Different forms to mild to severe

173
Q

What are the signs and symptoms of osteogenesis imperfecta

A

Increased fracture risk - may present with fracture
Hypermobility
Blue sclera
dentinogenesis imperfecta - teeth issues
More severe present with childhood fractures
Mild may not present until adulthood

174
Q

How do you manage osteogenesis imperfecta

A

No cure
Fracture fixation
Surgery to correct deformities
Bisphosphonates

175
Q

What are the most common endocrinopathies

A

Thyroid issues and diabetes

176
Q

In general how do you approach the diagnosis of an endocrine issue

A

First look for a phenotype
Then can do biochemical tests
Then look to imaging to try and find an anatomical issue (CT best for adrenal and MRI for pituitary)

177
Q

Loss of pituitary hormones usually occurs all at once - true or false

A

False
Loss of pituitary hormone is often sequential as some areas more susceptible to being squeezed by mass
Gonadotrophins lost first then ACTH then TSH

178
Q

Non-functional or non-secreting adenomas present with structural symptoms first - true or false

A

True
They don’t secrete any hormones so don’t get these affects

Secreting ones produce hormones so these effects usually make you sick first

179
Q

Which pituitary hormones are released at a steady state

A

FSH,LH and TSH

Therefore any low readings would be a true low

180
Q

Which pituitary hormones are not released at a steady state

A

GH and ACTH
Growth hormone is released in spikes so may get a false low if you catch it at the wrong time
ACTH is diurnal - big spike in the morning
These ones require a stimulation or suppression test

181
Q

What is Sheehan syndrome

A

Pituitary dysfunction following post-partum hemorrhage

The drop in BP caused ischaemia and necrosis of pituitary and results in loss of function

182
Q

List tumours can affect the pituitary

A

Pituitary adenoma
Craniopharyngioma
Cerebral and secondary tumours

183
Q

Which infections can lead to pituitary hypofunction

A

Meningitis
Syphilis
HIV/AIDs

184
Q

List some iatrogenic causes of pituitary hypofunction

A

Cranial radiation

Removal of the pituitary

185
Q

What is the most common cause of pituitary hormone excess

A

Most common cause is a secreting adenoma - present earlier than non-secreting
Benign - don’t met but do cause symptoms

186
Q

How does excess FSH and LH present

A

No real clinical symptoms
Gonads don’t make a high level of hormone in response
Usually present later with structural effect from pituitary

187
Q

Which types of tumours can produce ACTH

A

Small cell lung cancer and other neuroendocrine tumours can produce huge amounts of ACTH

188
Q

How does excess ACTH lead to hyper pigmentation

A

ACTH cleaved from pro-hormone POMC
Other products include melanocyte stimulating hormone
Therefore if you have increased ACTH production you get excess MSH which leads to pigmentation

189
Q

How can you determine the source of excess ACTH

A

Measure ACTH and cortisol levels
If an adrenal issue then cortisol would be high and ACTH low
If caused by exogenous steroids then ACTH and cortisol will both be low If a pituitary issue then ACTH high and cortisol low

190
Q

Which is the only pituitary tumour that does not require neurosurgery

A

Prolactinoma - responds to medical therapy

All others require surgery

191
Q

How do you access the pituitary surgically

A

Trans-sphenoidal

Put scope up the nose

192
Q

What is the function of oxytocin

A

Triggers let-down reflex in breastfeeding mums

193
Q

What is the function of ADH

A

Conserves water
Binds to receptors in the kidney which causes recruitment of AQP2 to the cell membrane
This AQP2 allows water to move back into the blood

Also causes vasoconstriction

Overall increase in BP

194
Q

How does diabetes insipidus present

A

Presents with increased urination, very dilute urine, constant thirst

195
Q

What can cause diabetes insipidus

A

Can be caused by production issue in pituiatry or lack of recognition by kidney receptors

196
Q

What happens to plasma osmolality in diabetes insipidus

A

It is very high - sodium and urea are high

In contrast urine osmolality is very low (peeing out a lot of water

197
Q

What is the main determinant of plasma osmolality

A

Sodium

Other solutes include: potassium, urea and glucose

198
Q

What is osmolality

A

The concentration of a solution expressed as the total number of solute particles per kilogram

199
Q

How do you differentiate between cranial and nephrogenic diabetes insipidus

A

After the water deprivation test you give artificial ADH
If a cranial issue their urine will immediately concentrate, if nephrogenic there will be no effect (get them to drink to recover instead!)

200
Q

What is the main differential for suspected diabetes insipidus

A

Psychogenic polydipsia
Excessive water drinking which means they flush their kidneys so much they lose the concentration gradient and cannot concentrate anymore

201
Q

At what point must you stop a water deprivation test for diabetes insipidus

A

Must stop if they lose >3% of body weight as they dehydrate very quickly
Therefore they are weighed throughout

202
Q

How do you treat nephrogenic diabetes insipidus

A

It is very hard. Look for and reverse underlying causes if there.
Sometimes massive ADH dose can cause some retention.
May use thiazide diuretics.
Must carry a warning card that if unconscious they need fluids stat

203
Q

How do you treat SIADH

A

Treat underlying cause
Fluid restriction - 1-1.5L per day (unpleasant as brain will be telling them to drink)
Demeclocycline - old antibiotic which uncouples AQP2 from the receptor (expensive now)
Tolvaptan - holy grail V2 receptor antagonist but very expensive

204
Q

How does SIADH present

A

Presents with confusion, lethargy, normovolaemic (no dehydration or overload), symptoms of underlying cause

Low plasma osmolality and urine is very high
Low sodium

205
Q

What causes the confusion in SIADH

A

Caused by swelling in the brain as excess water moves into the cells

206
Q

What must you exclude before diagnosing SIADH

A

Always need to exclude hypothyroid and low cortisol as they present similarly on biochemistry

207
Q

All cortical hormones from the adrenals are derived from what

A

Cholesterol

208
Q

What is the risk of excessive sodium shift

A

Central pontine myelinosis - loss of myelin in the midbrain (pons)
Nerves will then dysfunction - pain, dysphagia, dysarthria, diplopia. LOC

209
Q

What is the maximum acceptable sodium shift

A

No more than 8mmol/L shift in 24 hours

210
Q

ACTH acts on which zones of the adrenal glands

A

All 3 zones stimulated by ACTH but only glucocorticoids negatively feedback on ACTH

211
Q

Where is aldosterone produced

A

Adrenal glomerulosa

212
Q

What is the purpose of aldosterone

A

Activates NaK ATP channel and resorbs Na in the kidney

Na absorption which water follows - increased circulating volume and BP

213
Q

You tend to lose all 3 hormones in adrenocortical disease - true or false

A

True

214
Q

How does adrenocortical deficiency present

A 
Weight loss
Lethargy 
Diarrhoea
Hypotension, 
Hypoglycaemia
Hyperpigmentation due to excess ACTH
Hyponatraemia and hyperkalaemia (due to aldosterone loss) 
 Lack of cortisol leads to hypoglycaemia
215
Q

Why MUST you give alpha blockers before beta in the treatment of phaeochromocytoma

A

If you give beta first it can kill them

If beta blocked all adrenaline goes to alpha receptors causing massive vasoconstriction, hypertension and stroke

216
Q

Why does phaeochromocytoma cause labile BP

A
  • BP labile as the adrenaline acts on alpha receptors which cause vasoconstriction and in response
217
Q

You see a patient newly diagnosed with Addison’s disease. What advice should you give them about their steroid medication in the event of becoming unwell or going for surgery?

A

They will need to increase their corticosteroid medication dose

Endocrinology (13 decks)

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