Endocrine Flashcards
1
Q
What is DM due to?
A
A lack of or reduced effectiveness of endogenous insulin
2
Q
What does hyperglycaemia cause? (2)
A
- ) Microvascular problems
- ) Macrovascular problems
3
Q
Give 2 microvascular problems
A
- ) Retinopathy
- ) Nephropathy
- ) Neuropathy
4
Q
Give 2 macrovascular problems
A
- ) Stroke
- ) Renovascular disease
- ) Limb ischaemia
- ) Heart disease
5
Q
When does T1DM usually present?
A
Adolescence
6
Q
What causes T1DM?
A
Insulin deficiency from autoimmune destruction of insulin-secreting pancreatic beta cells
7
Q
What is T1DM associated with?
A
Other autoimmune diseases
8
Q
What autoimmune genes are present in 90% of T1DM cases?
A
HLA DR3 +/- DR4
9
Q
Which gene determines islet sensitivity to damage?
A
6q
10
Q
What is latent autoimmune diabetes of adults (LADA) a form of?
A
T1DM
11
Q
What is metabolic syndrome?
A
Central obesity (BMI >30) with 2 of:
- ) BP >130/85
- ) Triglycerides >1.7mmol/L
- ) HDL <1.2mmol/L
- ) Fasting glucose >5.6mmol/L
- ) DM
12
Q
In who is T2DM more prevalent? (3)
A
- ) Asians
- ) Men
- ) Elderly
13
Q
What causes T2DM?
A
Decreased insulin secretion +/- increased insulin resistance
14
Q
Give 2 things T2DM is associated with
A
- ) Obesity
- ) Lack of exercise
- ) Calorie excess
- ) Alcohol excess
15
Q
Which type of DM has a stronger genetic influence?
A
T2DM
16
Q
What does T2DM typically progress from? (2)
A
- ) Impaired glucose tolerance
- ) Impaired fasting glucose
17
Q
What is maturity onset diabetes of the young (MODY)?
A
A rare autosomal dominant form of T2DM affecting young people
18
Q
Give 3 other causes of DM
A
- ) Steroids
- ) Anti HIV drugs
- ) Newer antipsychotics
- ) Pancreas (pancreatitis, surgery, trauma, CF, haemochromatosis, cancer)
- ) Cushing’s disease
- ) Acromegaly
- ) Phaeochromocytoma
- ) Hyperthyroidism
- ) Pregnancy
- ) Congenital lipodystrophy
- ) Glycogen storage diseases
19
Q
How do we diagnose DM?
A
-) Symptoms of hyperglycaemia
-) Raised venous glucose detected once
OR
-) Raised venous glucose on 2 separate occasions OR
-) Oral glucose tolerance test (OGTT)
WITH
-) HbA1c
20
Q
Give 3 symptoms of hyperglycaemia
A
- ) Polyuria
- ) Polydipsia
- ) Unexplained weight loss
- ) Visual blurring
- ) Genital thrush
- ) Lethargy
21
Q
What values do we need for a raised venous glucose?
A
- ) Fasting >7mmol/L
- ) Random >11.1mmol/L
22
Q
What values do we need for an OGTT?
A
2 hour valve of >11.1mmol/L
23
Q
What value do we need for HbA1c?
A
> 48mmol/mol
24
Q
What does HbA1c measure?
A
Average 3 month plasma glucose concentration, glycated Hb
25
Give 3 features of T1DM
- ) Weight loss
- ) Persistent hyperglycaemia despite diet and medications
- ) Autoantibodies (islet cell, anti-glutamic acid decarboxylase)
- ) Ketonuria
26
How do we monitor glucose control? (3)
- ) Fingerprick glucose (before informs about long acting, after - short acting)
- ) HbA1c
- ) Hypoglycaemic attacks
27
What is the general control of DM?
- ) Lifestyle changes
- ) Address vascular risk factors
- ) Diabetic reviews
- ) Foot and eye care
- ) Inform DVLA
28
Give 2 lifestyle changes for DM treatment
- ) Smoking cessation
- ) Low carbohydrate or ketogenic diet
- ) Low glycemic index foods
- ) Weight loss
- ) Exercise
29
How do we treat T1DM?
- ) Insulin (short, medium, long acting)
- ) Self adjust doses with excessive, fingerprick glucose, calorie intake, carb counting
- ) Avoid binge drinking
- ) Give surgary drinks if hypoglycaemic attack
30
Give 3 common insulin regimens
- ) BD biphasic, twice daily premixed insulins by pen
- ) QDS, before meals ultra fast and bedtime long acting
- ) Once daily before bed long acting
31
What are the treatment steps for T2DM?
1) Lifestyle modification
2) Metformin
3) Dual therapy, add DPP4 inhibitor or pioglitazone or sulphonylurea or SGLT-2i
4) Triple therapy
5) Insulin or metformin, sulphonylurea and GLP 1 mimetic
32
What is metformin?
A biguanide that increases insulin sensitivity and helps weight
33
How do DPP4 inhibitors/gliptins work?
Block the action of DPP-4, an enzyme which destroys the incretin hormone
34
How does glitazone work?
Increases insulin sensitivity
35
How does sulfonylurea work?
Increases insulin secretion
36
How does SGLTI work?
Selective sodium-glucose co-transporter-2 inhibitor, blocks reabsorption of glucose in kidneys and promotes excretion of excess glucose in urine
37
Give 3 complications of DM
- ) MI
- ) Stroke
- ) Cataracts
- ) Nephropathy
- ) Retinopathy (blindness)
- ) Foot ulcers
38
What can we use to stop the progression of diabetic retinopathy?
Laser photocoagulation
39
What does laser photocoagulation do? (DM)
Stops production of angiogenic factors from the ischaemic retina
40
What are the 4 types of diabetic retinopathy?
- ) Background
- ) Pre-proliferative
- ) Proliferative
- ) Maculopathy
41
How do we distinguish between ischaemia and peripheral neuropathy in diabetics feet?
Ischaemia - critical toes +/- absent foot pulses
| Peripheral neuropathy - injury/infection over pressure points
42
How do we treat neuropathy complications?
- ) Relieve pressure
- ) Antibiotics for infections
- ) Dressings
43
What is ketoacidosis?
An alternative metabolic pathway used in starvation states, less efficient
44
What does ketoacidosis produce as a by-product?
Acetone
45
How does ketoacidosis occur in diabetics? (4)
- ) Excessive glucose
- ) Cannot be taken up into cells due to lack of insulin
- ) Body into starvation like state
- ) Ketoacidosis only mechanism of energy production
46
Give 4 clinical features of diabetic ketoacidosis
- ) Gradual drowsiness
- ) Vomiting
- ) Dehydration
- ) Abdo pain, polyuria, polydipsia, lethargy, anorexia, ketotic breath, dehydration, coma, deep breathing
47
What type of DM does diabetic ketoacidosis usually affect?
T1DM
48
Give 3 triggers of diabetic ketoacidosis
- ) Infection
- ) Surgery
- ) MI
- ) Pancreatitis
- ) Chemotherapy
- ) Antipsychotics
- ) Wrong insulin dose
- ) Non compliance
49
What 3 things do we diagnose diabetic ketoacidosis with?
- ) Acidaemia
- ) Hypergylcaemia
- ) Ketonaemia
50
What tests do we do in diabetic ketoacidosis?
- ) ECG
- ) CXR
- ) Dipstick
- ) MSU
- ) Glucose
- ) Ketones
- ) pH
- ) U&E
- ) HCO3-
- ) Osmolality
- ) FBC
- ) Blood cultures
51
Give 3 things that would make diabetic ketoacidosis severe
- ) Very high ketones
- ) Low venous bicarbonate
- ) Low pH
- ) Low K
- ) Low GCS
- ) Low O2
- ) Low systolic BP
- ) Pulse high/low
- ) High anion gap
52
What is the management of diabetic ketoacidosis? (8)
- ) Saline bolus
- ) Tests
- ) IV insulin and aim for fall in blood ketones or rise in venous bicarbonate
- ) Potassium if needed
- ) Consider catheter, NG
- ) LMWH
- ) Avoid hypoglycaemia by giving glucose when <14mmol/L
- ) Treat cause
53
What type of DM does hyperglycaemic hyperosmolar state usually affect?
T2DM
54
What is hyperglycaemic hyperosmolar state?
Longer history with marked dehydration and glucose, no switch to ketone metabolism
55
What do we give in hyperglycaemic hyperosmolar state?
LMWH as occlusive events are a danger
56
How do we treat hyperglycaemic hyperosmolar state?
- ) Fluid
- ) K+ when urine flows
- ) Maybe insulin
- ) Treat cause
57
What does hypoglycaemia present with?
- ) Odd behaviour
- ) Sweating
- ) Increased pulse
- ) Seizures
58
How do we treat hypoglycaemia?
- ) Conscious - quick acting carb snack
- ) Conscious but uncooperative - glucose gel in mouth
- ) Unconscious - glucose IVI or glucagon
59
What is a phaeochromocytoma?
Rate catecholamine producing tumours
60
What do phaeochromocytoma arise from?
Sympathetic paraganglia cells (phaeochrome bodies), which are collections of chromatin cells
61
Where are phaeochromocytomas usually found?
Within the adrenal medulla
62
Where are rarer extra-adrenal phaeochromocytomas found?
By the aortic bifurcation
63
What is the 10% rule of phaeochromocytomas? (4)
10% malignant
10% extra-adrenal
10% bilateral
10% familial
64
Give a gene that is mutated in phaeochromocytoma
SDH, succinyl dehydrogenase
65
What can phaeochromocytoma cause?
HTN
66
Give 2 things phaeochromocytoma is associated with
Hereditary cancer syndromes:
- ) Thyroid
- ) MEN-2A and 2B
- ) Neurofibromatosis
- ) von Hippel-Lindaue syndrome
67
What is the classic triad of presentation of a phaeochromocytoma?
- ) Episodic headache
- ) Sweating
- ) Tachycardia
68
What other presenting features of phaeochromocytoma may there be?
- ) Difficult to control BP
- ) Palpitation
- ) High pulse
- ) Dyspnoea
- ) Angina
- ) Headache
- ) Anxiety
69
What do tests show in phaeochromocytoma?
- ) Metanephrines/metadrenaline in 25h urine
- ) Increased WCC
- ) Abdominal CT/MRI to localise
70
How do we treat a phaeochromocytoma?
- ) Surgery
- ) Alpha blockade pre-op
- ) With beta-blocker if heart disease or tachycardia
- ) Chemo if malignancy
71
What are tumours from each one of the adrenal glands associated with?
GFR=MINER-GA
Zona glomerulosa - mineralocorticoids
Zona fasciculata - glucocorticoids
Zona reticularis - androgens
72
What is acromegaly due to?
An increased secretion of growth hormone from a pituitary tumour or hyperplasia
73
What are 5% of acromegaly cases associated with?
MEN-1
74
What does growth hormone stimulate?
Bone and soft tissue growth through increased secretion of insulin like growth factor 1
75
Give 3 symptoms of acromegaly
- ) Acroparaesthesia
- ) Amenorrhoea
- ) Loss of libido
- ) Headache
- ) Sweating
- ) Snoring
- ) Arthralgia
- ) Backache
- ) Skin darkening
- ) Goitre
- ) Malocclusion of jaw
- ) Increased size of hands and feet and face
- ) Curly hair
- ) Weight gain
- ) Oily large pored skin
- ) Scalp folds
- ) Gigantism if before bony epiphyses fuse
76
What do tests show/what tests do we do in acromegaly?
- ) High glucose, calcium, phosphate
- ) GH secretion fails to be suppressed by high glucose (OGTT)
- ) MRI of pituitary fossa
- ) Hypopituitarism
- ) Visual fields and acuity
- ) ECG
- ) Old photos
77
How do we treat acromegaly?
- ) Transphenoidal surgery to prevent compression
- ) Somatostatin analogues or radiotherapy if surgery doesn't work
- ) Growth hormone antagonist pegvisomant if resistant/intolerant to somatostatin analogue
78
What gender is Grave's disease more common in?
Females
79
When does Grave's disease typically present?
40-60
80
What does Grave's disease cause?
Hyperthyroidism
81
What is Grave's disease caused by? (4)
- ) Circulating IgG autoantibodies bind to and activate G protein coupled thyrotropin receptors
- ) Smooth thyroid enlargement
- ) Increases hormone production (especially T3)
- ) React with orbital autoantigens
82
Give 2 diseases Grave's disease is associated with
- ) Vitiligo
- ) T1DM
- ) Addison's
83
Give 2 triggers for Grave's disease
- ) Stress
- ) Infection
- ) Childbrith
84
Give 3 symptoms of Grave's disease
- ) Diarrhoea
- ) Weight loss
- ) Increased appetite
- ) Sweats
- ) Heat intolerance
- ) Tremor
- ) Oligomenorrhoea
- ) Subfertility
- ) Eye disease
- ) Oedema above ankles
- ) Clubbing
85
Give 4 things tests show in Grave's disease
- ) TSH suppressed
- ) T4 and T3 high
- ) Maybe mild normocytic anaemia or mild neutropenia
- ) High ESR
- ) High caclium
- ) High LFT
86
How do we treat Grave's disease?
- ) Beta blockers
- ) Carbimazole to titrate against TH levels
- ) Can block replace - carbimazole and thyroxine
- ) Radioiodine or thyroidectomy if relapse
87
What gender is hypothyroidism more common in?
Women
88
Give clinical features of hypothyroidism
- ) Lethargy
- ) Low mood
- ) Dislike of cold
- ) Increased weight
- ) Constipation
- ) Menorrhagia
- ) Dementia
- ) Myalgia
- ) Cramps
- ) Bradycardic symptoms
89
Give 3 bradycardic symptoms
- ) Slow relaxation of reflexes
- ) Ataxia
- ) Dry thin hair/skin
- ) Cold hands
- ) Ascites
- ) Round puffy face
- ) Defeated demeanour
- ) Immobile
- ) Congestive HF
90
What do tests show in hypothyroidism?
- ) TSH high
- ) T4 low
- ) Autoantibodies if Hashimoto's
91
What is a main cause of primary autoimmune hypothyroidism?
Hashimoto's thyroiditis
92
What is goitre due to?
Swelling of the neck due to lymphocytic and plasma cell infiltration
93
In who is Hashimoto's thyroiditis commoner in?
Women, 60-70
94
What can Hashimoto's thyroiditis be? (2)
Hypothyroid or euthyroid
95
What is the treatment for hypothyroidism? (2)
Young and healthy - levothyroxine (T4)
| Elderly/comorbid - lower dose of levothyroixine
96
What may levothyroxine precipitate in the elderly/comorbid?
Angina or MI
97
What do we find in tests for thyroid cancer?
- ) T3, T4, TSH, thyroid autoantibodies
- ) CXR may show tracheal goitres and mets
- ) US, fine needle aspiration, cytology
- ) Radionuclide scans may show malignant lesions as hypofunctioning/cold (hyperfunctioning/hot suggests adenoma)
98
What are the 5 types of thyroid cancer?
- ) Papillary (60%)
- ) Follicular (<25%)
- ) Medullary (5%)
- ) Lymphoma (5%)
- ) Anaplastic (rare)
99
Who does papillary thyroid cancer occur in, and how does it spread?
Younger patients, to lymph nodes and lungs
100
How do we treat papillary thyroid cancer?
- ) Total thyroidectomy
- ) +/- node excision
- ) +/- radioiodiine
- ) Levothyroxine
101
Who does follicular thyroid cancer occur in, and how does it spread?
Middle aged, via blood to bone and lungs
102
How do we treat follicular thyroid cancer?
- ) Total thyroidectomy
- ) T4 suppression
- ) Radioiodine ablation
103
Who does medullary thyroid cancer occur in?
Sporadic or part of MEN syndrome
104
What may medullary thyroid cancer produce?
Calcitonin (can be used as tumour marker)
105
How do we treat medullary thyroid cancer?
- ) Phaeochromocytoma scan pre-op
- ) Thyroidectomy
- ) Node clearance
- ) Maybe beam radiotherapy to prevent recurrance
106
Who does lymphoma thyroid cancer occur more in, and how does it present?
Females, stridor or dysphagia
107
What do we assess for in lymphoma thyroid cancer?
Histology for MALT
108
What does MALT stand for?
Mucosa-associated lymphoid tissue
109
How do we treat lymphoma thyroid cancer?
Chemoradiotherapy
110
Who does anaplastic thyroid cancer occur in?
Rare, females more, elderly
111
What is Cushing's syndrome? (3)
Clinical state produced by:
- ) Chronic glucocorticoid excess
- ) Loss of normal feedback mechanisms of hypothalamo-pituitary-adrenal axis
- ) Loss of circadian rhythm of cortisol secretion
112
What is the main cause of Cushing's syndrome?
Oral steroids
113
What is the most common endogenous cause of Cushing's syndrome?
Increased adrenocorticotropic releasing hormone (ACTH) due to pituitary adenoma (Cushing's disease)
114
What is the peak age of Cushing's disease?
30-50
115
What is Cushing's disease?
Bilateral adrenal hyperplasia from an ACTH-secreting pituitary adenoma
116
Give 3 symptoms of Cushing's syndrome
- ) Weight gain
- ) Mood change
- ) Proximal weakness
- ) Gonadal dysfunction
- ) Acne
- ) Recurrent Achilles tendon rupture
117
Give 3 signs of Cushing's syndrome
- ) Central obesity
- ) Plethoric moon face
- ) Buffalo hump
- ) Supraclavicular fat distribution
- ) Skin and muscle atrophy
- ) Bruises
- ) Purple abdominal striate
- ) Osteoporosis
- ) Increased BP
- ) Increased glucose
- ) Infection prone
- ) Poor healing
118
How do we diagnose Cushing's syndrome? (4)
- ) Raised plasma cortisol
- ) Overnight dexamethasone suppression test (no suppression by cortisol)
- ) 24hr free cortisol
- ) 48hr dexamethasone suppression test
119
Give 3 localisation tests for Cushing's syndrome
- ) Plasma ACTH (undetectable, adrenal tumour likely)
- ) CT/MRI adrenal glands
- ) Adrenal vein sampling
- ) High dose suppression test if ACTH detectable
- ) Cortisol rises with pituitary disease but not with ectopic ACTH production
- ) MRI pituitary
120
How do we treat Cushing's syndrome? (4)
- ) Iatriogenic - stop medications
- ) Cushing's disease - selective removal of pituitary adenoma, bilateral adrenalectomy if unlocatable or recurrence
- ) Adrenal tumour - adrenalectomy, radiotherapy if carcinoma
- ) Ectopic ACTH - surgery
121
What is Conn's syndrome?
A solitary aldosterone producing adenoma that causes primary hyperaldosteronism
122
What is primary hyperaldosternoism?
Excess production of aldosterone independent of the renin-angiotensin system
123
What does primary hyperaldosteronism cause?
Increased sodium and water retention, and decreased renin release
124
Give 3 symptoms of primary hyperaldosteronism
- ) Asymptomatic
- ) Signs of hypokalaemia
- ) Weakness
- ) Cramps
- ) Paraesthesiae
- ) Polyuria
- ) Polydipsia
- ) Increased BP sometimes
125
What tests do we do for primary hyperaldosteronism?
- ) U&E
- ) Renin
- ) Aldosterone
- ) Adrenal vein sampling
126
What is the treatment for Conn's syndrome? (2)
- ) Laparoscopic adrenalectomy
| - ) Spironolactone for 4wks pre-op to control BP and K+
127
What is primary adrenocortical insufficiency?
Addison's disease
128
What is the pathophysiology of primary adrenocortical insufficiency?
Destruction of the adrenal cortex leads to glucocorticoid (cortisol) and mineralocorticoid (aldosterone) deficiency
129
Give 3 causes of primary adrenocortical insufficiency
- ) Autoimmunity
- ) TB
- ) Adrenal mets
- ) Lymphoma
- ) Opportunistic infections in HIV
- ) Adrenal haemorrhage
- ) Congenital
130
What is the most common cause of secondary adrenal insufficiency?
Iatrogenic - due to long term steroid therapy leading to suppression of the pituitary-adrenal axis
131
When does secondary adrenal insufficiency become apparent?
On withdrawal of steroids
132
Give 4 symptoms of adrenal insufficiency
- ) Toned/lean
- ) Tanned
- ) Tired
- ) Tearful
- ) Possible weakness, anorexia, dizzy, faints, flu-like myalgia/arthralgias
- ) Depression, psychosis
- ) N&V, abdominal pain, diarrhoea/constipation
- ) Pigmented palmar creases
- ) Buccal mucosa
- ) Postural hypotension
- ) Vitilago
133
What do tests show in adrenal insufficiency?
- ) Decreased sodium
- ) Increased potassium
- ) Low glucose
- ) Ureaemia
- ) High calcium
- ) Eosinophilia
- ) Anaemia
134
What should we suspect in all with unexplained abdominal pain or vomiting?
Addison's
135
What is the diagnostic test for adrenal insufficiency?
Short ACTH stimulation test
- ) Plasma cortisol before and 30mins after tetracosactide
- ) Exclude Addison's if cortisol high
- ) Also test renin and aldosterone if high
136
What other tests should we do in adrenal insufficiency?
- ) 21-hydroxylase adrenal autoantibodies
| - ) CT, CXR for TB, mets
137
What is the treatment of adrenal insufficiency?
- ) Replace steroids with daily hydrocortisone
- ) Mineralocorticoids correct postural hypotension, low Na+, high K+ (fludrocortisone)
- ) Steroid use bracelet
- ) Double steroids in febrile injury, stress, illness
138
What is diabetes insipidus? (DI)
The passage of large volumes of dilute urine due to impaired water resorption by the kidney
139
What are the 2 types of DI?
Cranial DI - reduced ADH secretion from the posterior pituitary
Nephrogenic DI - impaired response of kidney to ADH
140
Give 4 causes of cranial DI
- ) Idiopathic
- ) Congenital
- ) Tumour
- ) Trauma
- ) Hypophysectomy
- ) Autoimmune hypophysitis
- ) Infiltration
- ) Vascular
- ) Infection
141
Give 4 causes of nephrogenic DI
- ) Inherited
- ) Metabolic (low K, high Ca)
- ) Lithium
- ) Chronic renal disease
- ) Post obstructive uropathy
142
Give 3 symptoms of DI
- ) Polyuria
- ) Polydipsia
- ) Dehydration
- ) Symptoms of hypernatraemia
143
What tests do we do in DI?
- ) U&E
- ) Ca
- ) Glucose
- ) Serum and urine osmolalities
- ) Water deprivation test
144
What is the urine like in DI?
Dilute, despite raised plasma osmolality (U:P>2)
145
How do we differential cranial and nephrogenic DI?
Urine osmolality increases after desmopressin in cranial DI
146
What is the treatment for cranial DI?
- ) MRI
- ) Test anterior pituitary function
- ) Desmopressin
147
What is the treatment for nephrogenic DI?
- ) Treat cause
- ) Bendroflumethiazide if persists
- ) NSAIDs low urine volume and plasma Na+
148
What is syndrome of inappropriate ADH secretion (SIADH) a cause of?
Hyponatraemia
149
How do we diagnose SIADH?
- ) Concentrated urine
- ) Hyponatraemia
- ) Low plasma osmolality
- ) In absence of hypovolaemia, oedema, diuretics
150
Give 4 causes of SIADH
- ) Malignancy (SCLC, pancreas)
- ) CNS disorders (meningoencephalitis, absess, stoke)
- ) Chest disease (TB, pneumonia)
- ) Endocrine disease (hypothyroidism)
- ) Drugs (opiates, SSRIs)
- ) Other (trauma, surgery, HIV)
151
How do we treat SIADH?
- ) Treat cause
- ) Restrict fluid
- ) Consider salt +/- loop diuretic if severe
- ) Possible vasopressin receptor antagonists
152
What level of plasma potassium is a potential emergency?
>6.5mmol/L
153
Give 3 concerning clinical features of hyperkalaemia
- ) Fast irregular pulse
- ) Chest pain
- ) Weakness
- ) Palpitations
- ) Light headedness
154
What does an ECG show in hyperkalaemia? (4)
- ) Tall tented T waves
- ) Small P waves
- ) Wide QRS complex
- ) Ventricular fibrillation
155
What may an artefactual hyperkalaemia be due to?
- ) Haemolysis
- ) Contamination with potassium EDTA anticoagulant
- ) Delayed analysis
156
Give 3 causes of hyperkalaemia
- ) Oliguric renal failure
- ) K+ sparing diuretics
- ) Rhabdomyolysis
- ) Metabolic acidosis
- ) Excess K+ therapy
- ) Addison's
- ) Massive blood transfusion
- ) Burns
- ) Drugs
- ) Artefactual result
157
How do we treat non-urgent hyperkalaemia?
- ) Treat cause
- ) Review medications
- ) Polystyrene sultanate resin (binds to K+ in gut)
158
What does hypokalaemia exacerbate?
Digoxin toxicity
159
Give 3 clinical features of hypokalaemia
- ) Muscle weakness
- ) Hypotonia
- ) Hyporeflexia
- ) Cramps
- ) Tetany
- ) Palpitations
- ) Light-headedness
- ) Constipation
160
What does an ECG show in hypokalaemia? (4)
- ) Small or inverted T waves
- ) Prominent U waves
- ) Long PR interval
- ) Depressed ST segments
161
Give 4 causes of hypokalaemia
- ) Diuretics
- ) Vomiting and diarrhoea
- ) Pyloric stenosis
- ) Rectal villous adenoma
- ) Intestinal fistula
- ) Cushing's syndrome/steroids/ACTH
- ) Conn's syndrome
- ) Alkalosis
- ) Purgative and liquorice abuse
- ) Renal tubular failure
162
What is the best indication that hypokalaemia is long standing on diuretics?
Increased bicarbonate
163
What makes hypokalaemia harder to correct?
Low Mg2+ levels
164
What is the treatment of mild hypokalaemia?
- ) Oral K+ supplement
| - ) Consider K+ sparing diuretic
165
What is the treatment of severe hypokalaemia?
Give IV potassium slowly
166
Give 4 symptoms of hypercalcaemia
Bones, stones, groans, psychic moans
- ) Abdominal pain
- ) Vomiting
- ) Constipation
- ) Polyuria
- ) Polydipsia
- ) Depression
- ) Anorexia
- ) Weight loss
- ) Tiredness
- ) Weakness
- ) HTN
- ) Confusion
- ) Pyrexia
- ) Renal stones
- ) Renal failure
- ) MI
167
What does an ECG show in hypercalcaemia?
Decreased QT interval
168
Give 3 causes of hypercalcaemia
- ) Malignancy
- ) Primary hyperparathyroidism
- ) Sacoidosis
- ) Vitamin D intoxication
- ) Thyrotoxicosis
- ) Lithium
- ) Tertiary hyperparathyroidism
- ) HIV
169
What are the pointers to malignancy in hypercalcaemia? (6)
- ) Decreased albumin
- ) Decreased chloride
- ) Alkalosis
- ) Decreased potassium
- ) Increased phosphate
- ) Increased ALP
170
What is the pointer to hyperparathyroidism in hypercalcaemia?
Increased PTH
171
What tests do we do in hypercalcaemia?
- ) FBC
- ) Protein electrophoresis
- ) CXR
- ) Isotope bone scan
- ) 24hr urinary Ca2+ excretion
172
How do we treat hypercalacemia?
- ) Treat cause
- ) Correct dehydration
- ) Bisphosphonates (prevent bone resorption)
- ) Chemo for malignancy
- ) Steroids for sarcoidosis
173
What are the features of hypocalcaemia?
SPASMODIC
- ) Spasms
- ) Perioral paraesthesia
- ) Anxious, irritable, irrational
- ) Seizures
- ) Muscle tone increased in smooth muscle (wheeze, dysphagia, colic)
- ) Orientation impaired and confusion
- ) Dermatitis
- ) Impetigo herpetiformis
- ) Chvostek's sign, choreoathetosis, cataract, cardiomyopathy
174
What does an ECG show in hypocalcaemia?
Long QT interval
175
What is Chvostek's sign?
Tapping over the parotid/facial nerve makes the facial muscles twtich
176
Give 3 causes of hypocalcaemia with increased phosphate
- ) CKD
- ) Hypoparathroidism (& pseudo)
- ) Acute rhabdomyolysis
- ) Hypomagnesaemia
177
Give 3 causes of hypocalcaemia with normal or decreased phosphate
- ) Vitamin D deficiency
- ) Osteomalacia
- ) Acute pancreatitis
- ) Over-hydration
- ) Respiratory alkalosis
178
How do we treat hypocalcemia?
- ) Mild - daily calcium
- ) CKD - alfacalcidol
- ) Severe - calcium glutamate IV
179
What is primary hypoparathyroidism due to?
Gland failure
180
What do tests show in primary hypoparathyroidism?
- ) Decreased Ca
- ) Increased/normal phosphate
- ) Normal ALP
181
Give a sign of primary hypoparathyroidism
- ) Those of hypocalcaemia (SPASMODIC)
| - ) Autoimmune signs
182
Give a cause of primary hypoparathyroidism
- ) Autoimmune
| - ) Congenital
183
What is the treatment for primary hypoparathyroidism?
Calcium supplements and calcitriol
184
What is secondary hypoparathyroidism due to? (3)
- ) Radiation
- ) Surgery
- ) Hypomagnesaemia
185
What is pseudohypoparathyroidism?
Failure of the target ell to respond to PTH
186
What is PTH secreted in response to?
Low ionised calcium levels
187
What are the parathyroid glands controlled by?
Negative feedback via calcium levels
188
How does PTH act by? (3)
- ) Increases osteoclast activity releasing calcium and phosphate from bones
- ) Increases calcium and decreases phosphate reabsorption in the kidney
- ) Increases active 1,25-dihydroxyvitamin D3 production
189
What is the overall effect of PTH?
Increased calcium and decreased phosphate
190
Give 2 causes of primary hyperparathyroidism
- ) Solitary adenoma (80%)
- ) Hyperplasia of all glands
- ) Parathyroid cancer
191
What is primary hyperparathyroidism associated with?
MEN, multiple endocrine neoplasia
192
How does primary hyperparathyroidism present?
- ) Increased calcium - weak, tired, depressed, thirsty, polyuric, renal stones, abdominal pain, pancreatitis, ulcers
- ) Bone reabsorption - pain, fractures, osteopenia/porosis
- ) Increased BP
193
What should we check for in everyone with HTN?
Calcium levels
194
What do tests show in primary hyperparathyroidism?
- ) Increased calcium
- ) Increased PTH
- ) Decreased phosphate
- ) Increased ALP (from bone activity)
- ) 24hr urinary calcium increased
- ) Imaging shows bone lesions
- ) DEXA
195
What is the treatment for primary hyperparathyroidism?
- ) Mild - increase fluid, avoid thiazides and high calcium/vitamin D intake
- ) Excision of adenoma/all 4 hyperplastic glands
- ) Cinacalcet
196
What does cinacalcet do?
Increases sensitivity of parathyroid cells to calcium
197
Give 2 complications of primary hyperparathyroidism
- ) Hypoparathyroidism
- ) Recurrant laryngeal nerve damage
- ) Symptomatic calcium decrease
198
What is secondary hyperparathyroidism?
Calcium is decreased and PTH is increased
199
What is secondary hyperparathyroidism caused by?
Decreased vitamin D intake, chronic renal failure
200
How do we treat secondary hyperparathyroidism?
- ) Treat causes
- ) Phosphate binder
- ) Vitamin D
- ) Cinacalcet if PTH very high
201
What is tertiary hyperparathyroidism?
Calcium is increased and PTH is very high
202
What does tertiary hyperparathyroidism occur after?
Prolonged secondary hyperparathyroidism, causing the glands to act autonomously having undergone hyper plastic or adenomatous change
203
Why is calcium increased in tertiary hyperparathyroidism?
Increased secretion of PTH unlimited by feedback control
204
What condition is tertiary hyperparathyroidism seen in?
Chronic renal failure
205
What is carcinoid syndrome?
Occurs in 5% of carcinoid tumours, implying hepatic involvement
206
What is a carcinoid tumour?
A diverse group of tumours of enterochromaffin cell (neural crest) origin capable of producing 5HT (serotonin)
207
Give 3 common sites of carcinoid tumours
- ) Appendix (45%)
- ) Ileum (30%)
- ) Rectum (20%)
- ) GI tract, ovary, testis, bronchi
208
Give 3 clinical features of a carcinoid tumour
- ) Initially few
- ) GI tumours - appendicitis, intussusception, obstruction
- ) Hepatic tumours - RUQ pain
209
What may carcinoid tumours secrete?
- ) Bradykinin
- ) Tachykinin
- ) Substance P (pain)
- ) VIP
- ) Gastrin
- ) Insulin
- ) Glucagon
- ) ACTH (Cushing's syndrome)
- ) PTH
- ) THs
210
What are 10% of carcinoid tumours part of?
MEN
211
Give 3 symptoms of carcinoid syndrome
- ) Bronchoconstriction
- ) Paroxysmal flushing in upper body
- ) Diarrhoea
- ) CCF
212
Why does congestive HF occur in carcinoid syndrome?
Tricuspid incompetence and pulmonary stenosis from 5HT induced fibrosis
213
What tests and results do we get in carcinoid tumours?
- ) Increased 24hr 5HIAA
- ) CXR and chest/pelvis MRI/CT to localise
- ) Plasma chromogranin A (tumour mass)
214
What is 5HIAA?
5-hydroxyindoleacetic acid, 5HT metabolite
215
How do we treat carcinoid syndrome?
- ) Octerotide
- ) Treat symptoms
- ) Resection to cure
216
What does octerotide do?
Somatostatin analogue that blocks
217
What is acne?
A disorder of the pilosebaceious follicles
218
What is the pathogenesis of acne?
Occurs as a result of androgenic simulation on the sebaceous gland causing excessive sebum, outflow obstruction, leakage into dermis and infection with propionibacterium acnes (skin commensal), leads to inflammation
219
What does acne present with? (6)
```
Greasy skin and lesions
-) Open comedones (blackheads)
-) Closed comedones (whiteheads)
-) Papules (deep)
-) Pustules (more superficial)
-) Nodules
-) Cysts
On face, chest, neck, back
```
220
What is the treatment for acne?
- ) Wash twice daily with soap/acne soap and water
- ) Topical treatments
- ) Systemic treatments
221
How do topical treatments help in acne?
Encourage skin peeling, reduce inflammation, have antibiotic effect
222
Give 2 topical treatments used in acne
- ) Benzoyl peroxide
- ) Clindamycin/erythromycin
- ) Retinoids
223
Give 2 systemic treatments used in acne
- ) Antiobiotics oxytetracycline, clindamycin, erythromycin
- ) Isotrenoin
- ) Antiandrogens (e.g. pill)
224
Why do we only use isotrenoin as a last resort in acne treatment?
SEs include severe drying of skin and possible depressive effects
225
What does atopic eczema result from?
IgE mediated T cell autoimmune response to allergens
226
What increases the likelihood of atopy?
Increased cleanliness so decreased germ exposure in early life results in over production of pro allergy T cells
227
Give 2 clinical features of eczema
- ) Rash (inside of elbows, knees, around eyes and neck)
| - ) Pruritus
228
What is the pruritus of eczema worse with?
- ) Dry air
- ) Sweating
- ) Local irritation
- ) Stress
229
When does eczema usually onset?
First 3 months of life
230
What course does eczema follow?
Chronic relapsing/remitting course (but usually improves throughout childhood)
231
Give 2 complications of eczema
- ) Lichenification
| - ) Infection
232
What is lichenification?
The skin becomes thick and leathery as a result of epidermal hypertrophy from excessive scratching
233
What is the usual infectious organism in eczema?
Staphylococcus
234
What is the treatment for eczema?
- ) Remove precipitating factors
- ) Emollients
- ) Steroid creams
- ) Antibiotics for infections
- ) Immune modulating agents
- ) Phototherapy
- ) Systemic steroids
235
Whats psoriasis?
An autoimmune disease characterised by patches of abnormal skin (genetic disease triggered by environmental factors)
236
What are the susceptibility genes for psoriasis?
PSORS1-9
237
What is psoriasis due to?
Keratinocyte hyperproliferation
238
What is the differentiation in psoriasis?
Basal layer to horny layer
239
When does psoriasis onset peak?
30s
240
Give the 5 types of psoriasis
- ) Classical
- ) Guttate
- ) Palmoplanar pustular
- ) Flexoral
- ) Erythrodermic
241
What are the patches like in classical psoriasis?
Well circumscribed erythematous plaques with silver scaling (itchy)
242
Where are the plaques in classical psoriasis?
Elbow, knees, scalp
243
Where are the plaques in guttate psoriasis?
Trunk
244
In who does guttate psoriasis occur?
Children following strep throat
245
What are the patches like in palmoplanar pustular psoriasis?
Yellow brown pustules on palms and soles
246
What are the patches like in flexoral psoriasis?
Erythematous but not scaly
247
Where are the plaques in flexural psoriasis?
Submammary, axially, anogenital
248
What is erythrodermic psoriasis?
An acute onset of erythroderma, medical emergency
249
Give 3 clinical features of psoriasis
- ) Classical itchy painful patches
- ) Nails - pitting, lifting off bed, subungal hyperkeratosis
- ) Psoriatic arthritis possible
250
What can make psoriasis worse? (4)
- ) Trauma
- ) Stress
- ) Sunlight
- ) Some drugs (NSAIDs, ACEIs)
251
What is the treatment for eczema?
- ) Emollients
- ) Topical corticosteroids
- ) Vitamin D analogues
- ) Coal tar preparations
- ) Dithranol cream
- ) Keratolytics
- ) Retinoids (topical/systemic)
- ) Immunosuppression
- ) Phototherapy if resistant
252
What do vitamin D analogues do?
Decrease cell proliferation
253
What do coal tar preparations do?
Inhibit DNA synthesis
254
What does dithranol cream do?
Decreases cell proliferation
255
What is cellulitis?
Bacterial infection involving the inner layers of the skin
256
What is cellulitis usually caused by?
Group A strep or staph entering via a break in the kin
257
Give 3 predisposing conditions to cellulitis
- ) Blistering
- ) Bite
- ) Pruritic rash
- ) Eczema
- ) Dry skin
- ) Injections
- ) DM
- ) Obesity
258
Give a risk factor of cellulitis
- ) Age
| - ) Immunodeficiency
259
Give 2 clinical features of cellulitis
- ) Area of skin is red, hot, painful
- ) Lethargy possible
- ) Fever possible
260
Where does cellulitis most commonly involve?
Legs and face
261
What is the treatment for cellulitis?
- ) Antibiotics - flucloxacillin
| - ) Surgical draining if abscess
262
What is necrotising fasciitis?
Rapidly progressive infection of the deep fascia causing necrosis of subcutaneous tissue
263
What is necrotising fasciitis caused by?
- ) Group A beta haemolytic streptococci
| - ) Often polymicrobial
264
Give a symptom of necrotising fasciitis
Intense pain over skin surface of affected area and underlying muscle
265
What is the treatment of necrotising fasciitis?
- ) Radical debridement of dead tissue
- ) Amputation if gangrene
- ) IV antibiotics (benzylpenicillin and clindamycin)
266
What are ulcers?
Abnormal breaks in an epithelial surface
267
What causes skin ulceration? (7)
- ) Venous disease (70%)
- ) Arterial and venous disease (15%)
- ) Arterial disease (2%)
- ) Neuropathic
- ) Infective
- ) Traumatic
- ) Vasculitis
268
How do we differentiate between venous and arterial causes of skin ulceration?
Ankle brachial pressure index ABPI
269
How do we treat skin ulceration?
- ) Treat cause
- ) Prevention (smoking, nutrition, DM control)
- ) 4 layer compression bandaging if arterial pulse ok
- ) Debridement and gels for necrosis
- ) Antibiotics for infection
270
Give 3 risk factors for developing skin cancer
- ) Age
- ) Sun bed use
- ) Fair skin
- ) History of sunburn or living overseas
- ) FHx
- ) Phototherapy
271
Who is commonly affected by malignant melanomas?
Younger patients
272
What is the main cause of malignant melanoma?
Short period of intense UV exposure
273
What is the main symptoms of a melanoma?
Skin mole changes
274
Give 2 major and minor signs for melanomas
Major - change in size, shape, colour
| Minor - inflammation, sensory change, large, irregular colour, irregular border
275
What does ABCDE stand for in melanoma?
Skin mole changes:
- ) Asymmetry
- ) Border irregular
- ) Colour non-uniform
- ) Diameter large
- ) Elevation
276
Give the 3 types of melanoma
- ) Superficial spreading (70%)
- ) Nodular (10-15%)
- ) Lentigo (15%)
277
What are superficial spreading melanomas like?
Grow slowly and met later
278
What are nodular melanomas like?
Invade deeply and met early
279
What are lentigo melanomas like?
Usually on the face of elderly patients, large, flat and dark
280
How do we treat melanomas?
- ) Early excision can be curative with wide margins
| - ) Chemo for mets
281
What does a squamous cell skin cancer usually present with?
Ulcerated lesion with hard, raised edges in sun exposed sites
282
What may squamous cell skin cancer begin as?
Solar keratoses (crumbly, yellow white crusts)
283
Where may squamous cell skin cancers be found?
- ) Lips of smokers
| - ) In long standing ulcers
284
What is the spread of squamous cell skin cancer like?
Local destruction may be extensive but metastasis is rare
285
How do we treat squamous cell skin cancer?
Excision with radiotherapy for recurrence/nodes
286
What are the 2 types of basal cell skin cancer?
Nodular or superficial
287
Give 3 features of nodular basal cell skin cancer
- ) Pearly nodule with rolled telangiectatic edge
- ) Face/sun exposed site
- ) May have central ulcer
- ) Mets rare
288
Give 3 features of superficial basal cell skin cancer
- ) Red scaly plaques with raised smooth edge
- ) Trunk or shoulders
- ) Usually due to UV exposure
- ) Excision, cyrotherapy
- ) Topical flurouracil or imiquimod cream
289
How does topical flurouracil or imiquimod cream work?
Causes necrosis and healing of cancerous skin and leaves normal skin unharmed
290
What is amyloidosis?
A group of disorders characterised by extracellular deposits of a protein in abnormal fibrillar form that is resistant to degradation
291
What are the 2 systemic forms of amyloidosis?
AL and AA
292
Give 2 other conditions amyloid deposition is a feature of
- ) AD
- ) T2DM
- ) Haemodialysis related amyloidosis
293
How do we diagnose amyloidosis?
Biopsy of affected tissue with positive staining under a polarised light microscopy
294
What is the median survival of amyloidosis?
1-2 years
295
What is AL amyloid?
The proliferation of a plasma cell clone leading to amyloidogenic monoclonal immunoglobulins and fibrillary light chain protein deposition
296
What can AL amyloid lead to?
Organ failure and death
297
Give 2 associations of AL amyloid
Myeloma and lymphoma
298
How do we treat AL amyloid?
- ) Optimise nutrition
- ) Oral melphalan and prednisolone extends survival by months
- ) High dose IV melphalan and autologous peripheral blood stem cell transplant
299
What does kidney involvement in AL amyloid lead to?
Glomerular lesions - proteinuria and nephrotic syndrome
300
What does heart involvement in AL amyloid lead to?
Restrictive cardiomyopathy, arrhythmias, angina
301
What does nerve involvement in AL amyloid lead to?
Peripheral and autonomic neuropathy, carpal tunnel syndrome
302
What does gut involvement in AL amyloid lead to?
Macroglossia (big tongue), malabsorption, weight loss, perforation, haemorrhage, obstruction, hepatomegaly
303
What does vascular involvement in AL amyloid lead to?
Purpura, especially periorbital
304
What type of amyloidosis is AL amyloid?
Primary
305
What is AA amyloid?
Amyloid is derived from serum amyloid A, an acute phase protein, reflecting chronic inflammation in RA, UC, Crohn's, chronic infections (TB, OM, bronchiectasis)
306
Where does AA amyloid affect?
Kidneys, liver, spleen
307
How does AA amyloid present?
- ) Proteinuria
- ) Nephrotic syndrome
- ) Hepatosplenomegaly
308
How do we treat AA amyloid?
Manage underlying condition
309
What type of amyloidosis is AA amyloid?
Secondary
310
What is familial amyloidosis?
Autosomal dominant condition that usually causes a sensory or autonomic neuropathy
311
Give 3 diseases of the breast
- ) Fibroadenoma
- ) Breast cysts
- ) Intraductal papilloma
312
What is fibroadenoma?
Benign overgrowth of collagenous mesenchyme of one breast lobule
313
Who does fibroadenoma present in?
Usually <30 but can be up to menopause
314
What does fibroadenoma present as?
Firm, smooth, mobile lump, painless, may be multiple
315
How do we treat fibroadenoma?
- ) Observe and reassure
- ) US and fine needle aspiration if doubt
- ) Surgical excision if large
316
What is a breast cyst?
A benign fluid filled rounded lump not fixed to surrounding tissue, occasionally painful
317
Who do breast cysts present in?
Common >35, especially perimenopausal
318
How do we diagnose breast cysts?
Aspiration
319
How do we treat breast cysts?
Aspirate if large
320
What is an intraductal papilloma?
Benign breast lesion
321
Where do intraductal papillomas develop?
- ) Near nipple (solitary, more near menopause)
| - ) Peripheral breast (multiple, more in younger, associated with higher chance of malignancy)
322
What symptom is an intraductal papilloma the most common cause of?
Bloody nipple discharge
323
How do we diagnose a biopsy in intraductal papilloma?
Galactogram
324
How do we treat an intraductal papilloma?
Microdochectomy excision
325
Give 4 risk factors for breast cancer
- ) Family history
- ) Age
- ) Long uninterruped oestrogen exposure
- ) Nulliparity/first pregnancy >30, not breastfed
- ) Early menarche and late menopause
- ) HRT, pill
- ) BRCA genes, act breast cancer
- ) Obesity
326
Give 5 types of breast cancer
- ) Non-invasive ductal carcinoma in situ
- ) Non-invasive lobular carcinoma in situ
- ) Invasive ductal carcinoma
- ) Invasive lobular carcinoma
- ) Medullary cancers
- ) Colloid/mucoid
- ) Papillary
- ) Tubular
- ) Paget's of the nipple
327
What is the most common type of breast cancer?
Invasive ductal carcinoma
328
What is non-invasive ductal carcinoma in situ seen as on a mammography?
Microcalcification
329
Which breast cancer tends to affect younger people?
Medullary
330
Which breast cancer tends to affect older people?
Colloid/mucoid
331
What genetic feature gives a better prognosis in breast cancer?
Oestrogen receptor positive
332
What genetic feature gives a worse prognosis in breast cancer?
Overexpression of HER2 (growth factor receptor gene)
333
How do we assess breast cancer? (3)
- ) Clinical examination
- ) Radiology by US and mammography
- ) History and cytology by fine needle aspiration or core biopsy
334
What are the 4 stages of breast cancer?
1) Confined to breast, mobile
2) With lymph nodes in ipsilateral axilla
3) Tumour fixed to muscle but not chest wall, ipsilateral nodes make be fixed, skin involved
4) Complete fixation to chest wall, distant mets
335
What are the surgical options for breast cancer treatment?
- ) Wide local excision
- ) Mastectomy
- ) With axillary node sampling/clearance or sentinel node biopsy
336
What treatments do we give along with surgery?
- ) Radiotherapy
| - ) Adjuvant chemotherapy
337
What is the endocrine therapy for post-menopausal oestrogen receptor positive breast cancers?
- ) Tamoxifen (blocks oestrogen)
| - ) Aromatase inhibitors (blocks peripheral oestrogen synthesis)
338
What is the endocrine therapy for pre-menopausal oestrogen receptor positive breast cancers?
- ) Ovarian ablation
| - ) Gonadotropin releasing hormone analogues
339
What is the endocrine therapy for HER2 positive breast cancers?
Perception (trastuzumab) with chemo
340
How do we treat metastases?
CNS surgery or radiotherapy with bisphosphonates for bone protection
341
Give 2 reconstruction options for breast cancer treatment
- ) Tissue expanders
- ) Implants
- ) Latissimus dorsi flap
- ) Transverse abdominis myocutaneous flap
342
What can occur in those undergoing axially node sampling/dissection?
Arm lymphoedema
343
Give the difference between endocrine and exocrine glands
Endocrine - secretions into the blood stream
| Exocrine - glands through a duct to site of action
344
Give an endocrine gland
Thyroid, adrenal
345
Give an exocrine gland
Pancreas
346
Define endocrine function
Blood bourne, acting at distant sites
347
Define paracrine function
Acting on adjacent cells
348
Define autocrine function
Feedback on the same cell that secreted the hormone
349
How are peptides/monoamines stored?
In vesicles
350
How are steroids stored?
Nope, synthesised on demand
351
Give the 4 steps of from synthesis to secretion of peptides
Synthesis - preprohormone to pro hormone
Packaging - prohormone to hormone
Storage - hormone
Secretion - hormone
352
How are peptides released?
In pulses/bursts
353
How do we measure amine molecules?
Normetanephrines and metanephrines in the blood/urine - breakdown products
354
Where are amines produced?
Adrenal medulla
355
What does cortisol do?
Increases the conversion of norepinephrine to epinephrine
356
What is most of T3 from?
T4
357
Is T3 or T4 active?
T3
358
What do we need to synthesis thyroid hormones?
Iodine
359
Where do cholesterol derivates and steroids go in the cell?
To the nucleus
360
What sort of rhythm does cortisol have?
Diurnal
361
What sort of rhythm does GH have?
Pulses
362
How are the anterior and posterior pituitaries different anatomically?
Anterior - endocrine outpouching
| Posterior - continuous projection from hypothalamus (hypothalamus synthesises, posterior pituitary releases)
363
Give 3 hormones the anterior pituitary secretes and what these have an effect on
- ) TSH - thyroid
- ) ACTH - adrenal cortex
- ) FSH and LH - testes/ovaries
- ) Growth hormone - entire body
- ) Prolactin - mammary glands
364
Give the 4 steps of the hypothalamo-pituitary-thyroid axis
1) Hypothalamus secretes TRH
2) Anterior pituitary secretes hormones
3) Affects thyroid gland
4) Thyroid hormones produced
Negative feedback loops at each step
365
Give 3 functions of thyroid hormones
- ) Accelerates food metabolism
- ) Increased protein synthesis
- ) Stimulation of carbohydrate metabolism
- ) Enhances fat metabolism
- ) Increase in ventilation rate
- ) Increase in CO and HR
- ) Brain development during foetal life and postnatal development
- )Growth rate accelerated
366
What switches off prolactin secretion?
Dopamine
367
What are the 3 layers of the adrenal cortex?
GFR
Zona glomerulosa
Zona fasciculata
Zona reticularis
368
What does each layer of the adrenal gland secrete, and give an example of each (4)
Zona glomerulosa - mineralcorticoids, aldosterone
Zona fasciculata - glucocorticoids, cortisol
Zona reticularis - androgens, dehydroepiandosterone
Adrenal medulla - stress hormones, epinephrine
369
What is the anterior pituitary gland also known as?
Adenohypophysis
370
What is the posterior pituitary gland also known as?
Neurohypophysis
371
What does the anterior pituitary review its blood supply from?
Portal venous circulation from the hypothalamus
372
Give 3 things a pituitary tumour can cause
- ) Pressure on local structures (optic nerves)
- ) Pressure on normal pituitary (hypopituitarism)
- ) Functioning tumour (Cushing's, acromegaly)
373
Is hyper or hypothyroidism more prevalent?
Hypothyroidism
374
Give 2 antibodies that are found in almost all patients with autoimmune hypothyroidism
Thyroglobulin and thyroid peroxidase
375
What is the cause of Grave's disease?
Autoimmune, thyroid stimulating antibodies
376
Give 2 environmental risk factors for thyroid autoimmunity
- ) Stress
- ) High iodine intake
- ) Smoking
377
What is thyroid associated opthalmopathy?
Swelling in extraocular muscles due to autoantigen in muscle crossreacting with thyroid autoantigen
378
What barrier may thyroid stimulating antibodies cross?
Placenta
379
What is thyrotoxicosis?
An excess of thyroid hormones in the blood
380
Give 3 mechanisms for increase levels of thyroid hormones
- ) Overproduction
- ) Leakage of preformed hormone from thyroid
- ) Ingestion of excess thyroid hormone
381
Give 2 causes of hyperthyroidism
- ) Grave's disease
- ) Toxic multinodular goitre
- ) Toxic adenoma
382
What is a common side effect of thionamides?
Rash
383
What is adrenal crisis?
Common presentation of adrenal insufficiency
384
Give 3 symptoms/signs of an adrenal crisis
- ) Hypotension
- ) Cardiovascular collapse
- ) Fatigue
- ) Fever
- ) Hypoglycaemia
- ) Hyponatraemia
- ) Hyperkalaemia
