Endocrine Flashcards
(131 cards)
1
Q
what hormones are produced by the pituitary gland?
A
Anterior pituitary: -prolactin -TSH -ACTH -GH -FSH -LH posterior pituitary: -oxytocin -vasopressin (ADH)
connected to the hypothalamus via the pituitary stalk
2
Q
what are the types of hypothyroidism?
A
-primary hypothyroidism- problem with thyroid gland itself
secondary hypothyroidism- usually disorder of the pituitary gland e.g. pituitary apoplexy
congenital hypothyroidism- problem of thyroid dysgenensis or thyroid dyshormogenesis
3
Q
causes of hypothyroidism?
A
- hashimoto’s thyroiditis- autoimmune disease associated with T1DM, Addison’s, pernicious anaemia, anti-TPO
- Subacute thyroiditis (de Quervain’s)- painful goitre and raised ESR
- Post-partum thyroiditis
- Riedel thyroiditis
- Drugs- lithium, amiodarone
- Iron deficiency- most common in developing world
4
Q
causes of thyrotoxicosis?
A
- Grave’s disease- associated thyroid eye disease, pretibial myxoedema
- Toxic multinodular goitre- nodules secrete excess thyroid hormones
- Drugs- amiodarone
5
Q
features of hyperthyroidism?
A
weight loss manic heat intolerance palpitations sweating pretibial myxoedema (lateral malleolus) clubbing diarrhoea oligomenorrhagia anxiety tremor
6
Q
features of hypothyroidism?
A
weight gain lethargy cold intolerance dry non-pitting oedema coarse scalp hair constipation menorrhagia carpal tunnel syndrome decreased deep tendon reflexes
7
Q
what is subclinical hypothyroidism?
A
high TSH, normal T4 (on the way to developing hypothyroidism)
8
Q
what are the TSH and T4 for poor compliance with thyroxine?
A
high TSH, normal T4
TSH is more representative of long-term thyroid control
9
Q
name some thyroid auto-antibodies?
A
anti-TPO (generally seen in hashimotos thyroiditis)
TSH receptor antibody (seen in grave’s disease)
thyroglobulin antibody
10
Q
tx of hypothyroidism?
A
levothyroxine
SEs- hyperthyroidism, reduced BMD, AF, worsening of angina
11
Q
mx of thyrotoxicosis?
A
propranolol- controls symptoms
carbimazole- reduces thyroid hormone production
radioiodine treatment
12
Q
how does PTH work?
A
bone- increases osteoclast activity= more calcium in bloodstream
kidney- increases vit D activation and calcium resorption from the distal convoluted tubule and increase phosphate excretion
13
Q
how does primary hyperparathyroidism work?
A
seen in elderly females with an unquenchable thirst and raised PTH
most commonly due to a solitary adenoma (80%)
symptoms of hypercalcaemia
14
Q
hormone profile for primary hyperparathyroidism?
A
high PTH
high Ca
low phosphate
urine calcium: creatinine ratio >0.01
15
Q
what is seen on XR of primary hyperparathyroidism?
A
pepperpot skull
16
Q
tx of primary hyperparathyroidism?
A
parathyroidectomy if elevated serum calcium >1mg/dL above normal, hypercalciuria, <50 years, neuromuscular symptoms, osteoporosis
17
Q
what is secondary hyperparathyroidism?
A
parathyroid gland hyperplasia occurs as a result of low calcium, almost always due to chronic renal failure
few symptoms or bone disease and soft tissue calcifications
18
Q
Ix of secondary hyperparathyroidism?
A
high PTH, Ca low or normal, high phosphate, low Vit D
19
Q
tx of secondary hyperparathyroidism?
A
medical therapy usually
surgery if bone pain, pruritic, soft tissue calcifications
20
Q
what is tertiary hyperparathyroidism?
A
ongoing hyperplasia after correction of underlying renal disorder
21
Q
features of tertiary hyperparathyroidism?
A
metastatic calcification
bone pain and/or fracture
nephrolithiasis
pancreatitis
22
Q
ix of tertiary hyperparathyroidism?
A
Can (normal or high), high PTH, phosphate low or normal, vit D normal or low, alk phos high
23
Q
tx of tertiary hyperparathyroidism?
A
allow 12 months to elapse following treatment as many cases will resolve
may need surgery
24
Q
cause of primary hypoparathyroidism?
A
decreased PTH secretion
e.g. secondary to thyroid disease
25
Ix of primary hypoparathyroidism?
low calcium, high phosphate
26
features of primary hypoparathyroidism?
hypocalcaemia->
- periorbital paraesthesia
- trousseau's sign- carpal spasm after BP cuff
- chovstek's sign- tapping over parotid gland causes facial muscles to twitch
if chronic- depression, cataracts
ECH- prolonged QT interval
27
tx of primary hypoparathyroidism?
alfacalcidol
28
pseudohypoparathyroidism causes?
target cells are insensitive to PTH
| due to abnormality in a G protein
29
features of pseudohypoparathyroidism?
low IQ, short stature, shortened 4th and 5th metacarpals
30
Ix of pseudohypoparathyroidism?
low calcium, high phosphate, high PTH
diagnosis- urinary cAMP and phosphate levels -following an infusion of PTH = pseudo= no rise in either
hypo= both rise
31
what is pseudopseudohypoparathyroidism?
pseudohypoparathyroidism with normal biochemistry
32
what acid-base balance is caused by hyperkalaemia?
metabolic acidosis
as K+ rises, fewer H+ ions leave bloodstream
They compete with each other for exchange with Na across cell membranes in distal tubule
33
ECG changes of hyperkalaemia?
tall-tended T waves
small p waves
widened QRS leading to a sinusoidal pattern and asystole
34
causes of hyperkalaemia?
```
AKI
metabolic acidosis
addison's disease
rhabdomyolysis
massive blood transfusion
drugs- ACEi, spironolactone, ARBs, ciclosporin, heparin (due to inhibition of aldosterone secretion)
```
35
foods that are high in potassium?
salt substitutes, bananas, oranges, kiwi, avocado
36
mx of hyperkalaemia?
potassium >7 or ECG changes= URGENT
complication= life-threatening arrhythmias
1. stop precipitating drugs
2. stabilisation of the cardiac membrane- IV calcium gluconate
3. short-term shift in potassium from extracellular to intracellular fluid compartment- combined insulin/dextrose infusion, nebulised salbutamol
4. remove potassium from the body- calcium resonium, loop diuretics, dialysis
37
pathophysiology of hypokalaemia?
low K+ in ECF-> water concentration gradient out of cell -> hyperpolarisation of myocyte membrane -> myocyte excitability
38
causes of hypokalaemia?
with hypertension:
-cushings, conns, liddle's syndrome
without hypertension:
-diuretics, GI loss e.g. D&V, renal tubular acidosis, bartter's syndrome, gitelman syndrome
39
features of hypokalaemia?
muscle weakness, hypotonia, predisposition to digoxin toxicity
40
ECG features of hypokalaemia?
U waves
small or absent P waves
long QT
long PR
41
tx of hypokalaemia?
if severe- IV K+ - transfer to high care area with cardiac monitoring, 3x 1L bags of 0.9% saline with 40mmol KCl per bag over 24 hours
42
causes of hypocalcaemia?
```
HAVOC
Hypoparathyrodism
Acute pancreatitis
Vitamin D deficiency
Osteomalacia
CKD
```
43
signs and symptoms of hypocalcaemia?
```
SPASMS
Spasms
Peripheral paraesthesia
Anxious
Seizures
Muscle tone increase
```
44
ix of hypocalcaemia?
ECG- long QT interval
45
tx of hypocalcaemia?
mild- Adcal
| Severe- calcium gluconate
46
causes of primary hyperaldosteronism?
bilateral idiopathic adrenal hyperplasia
adrenal adenoma- Conn's
Adrenal carcinoma- rare
47
features of primary hyperaldosteronism?
hypertension
hypokalaemia e.g. muscle weakness
metabolic alkalosis
48
Ix of primary hyperaldosteronism?
1st line- plasma aldosterone:renin ratio (high aldosterone and low renin. Negative feedback due to sodium from aldosterone)
high resolution CT abdomen and adrenal vein sampling
49
mx of primary hyperaldosteronism?
bilateral adrenocortical hyperplasia: spironolactone (aldosterone antagonist)
adrenal adenoma: surgery
50
what is the hypothalamic-pituitary-adrenal axis?
stress-> hypothalamus -> CRH -> pituitary -> ACTH -> adrenal cortex -> cortisol -> mineralocorticoid effects, anti-inflammatory, protein synthesis, lipolysis
51
what is cushing's syndrome?
excess cortisol and loss of HPA axis feedback and loss of circadian rhythm
52
what is cushing's disease?
above caused by a pituitary adenoma
53
causes of cushing's syndrome?
ACTH dependent causes-
- cushing's disease- tumour secreted ACTH
- ectopic ACTH production e.g. SCLC
ACTH independent causes-
- iatrogenic- steroids
- adrenal adenoma
- adrenal carcinoma
- carney complex: syndrome including cardiac myoxma
- micronodular adrenal dysplasia
54
what is pseudo-cushings?
mimics cushings but due to alcohol excess or severe depression
causes first positive dexamethasone suppression test or 24 hour urinary free cortisol
insulin stress test may be used to differentiate
55
symptoms of cushing's disease?
```
personality changes, CNS irritability, hyperglycaemia, moon face
oedema, purple striae
gynaecomastia
increased susceptibility to infections
thin extremities, thin skin
fat deposits on face and back of shoulders
OP
amenorrhora, hirsutism
```
56
Ix of cushing's syndrome?
1. overnight dexamethasone suppression test
2. 24 hr urinary free cortisol
FBC, U&E
MRI brain if adenoma suspected
CT
57
how does a dexamethasone suppression test work?
the patient has a dose of dexamethasone (a synthetic glucocorticoid steroid) at night (i.e. 10pm) and their cortisol and ACTH is measured in the morning (i.e. 9am). The intention is the find out whether the dexamethasone suppresses their normal morning spike of cortisol.
if cortisol remains high after low-dose= cushing's syndrome not due to primary cause e.g. secondary to steroids
if cortisol remains high after low dose but not high dose= cushing's disease
if cortisol not suppressed by either= ectopic ACTH e.g. lung cancer or adrenal adenoma producing cortisol
58
tx of cushing's syndrome?
if iatrogenic- stop steroids
cushing's disease- remove pituitary adenoma
remove adrenal adenoma
ectopic ACTH- remove tumour
59
hormone production of adrenal gland?
1. medulla- produces catecholamines and adrenaline
2. cortex-
- glucocorticoids- cortisol
- mineralocorticoids- aldosterone
- gonadocorticoids- androgens
60
what is addison's disease?
autoimmune destruction of adrenal glands
61
other causes of destruction of adrenal glands?
TB, mets, HIV, antiphospholipid syndrome, pituitary disorders, exogenous glucocorticoid therapy
62
features of addison's disease?
```
lethargy
weakness
anorexia
N&V
weight loss
salt-craving
hyperpigmentation- esp palmar creases, vitiligo, hypotension, hypoglycaemia
```
63
electrolyte abnormalities of addisons?
low Na and high K
64
features of addisons crisis?
collapse, shock, pyrexia
65
Ix of addison's disease?
-ACTH stimulation test (short synacthen test)
plasma cortisol measured-> given IM synacthen 250ug -> cortisol measured 30 mins after
-in primary care, do 9am cortisol
100-500= prompts ACTH stimulation test
66
tx of addison's diaease?
replace glucocorticoids- hydrocortisone
| replace mineralocorticoids- fludrocortisone (isn't required in an Addisonian crisis)
67
what is acromegaly?
excess growth hormone secretion
68
causes of acromegaly?
pituitary adenoma
ectopic GHRH
GH production by tumours e.g. pancreatic
69
features of acromegaly?
coarse facial appearance, spade-like hands, increased feet size
large tongue, prognathism, interdental spaces
sweat gland hypertrophy- excessive sweating and oily skin
features of pituitary tumour- hypopituitarism, headaches, bitemporal hemianopia
raised prolactin in 1/3 of cases-> galactorrhoea
6% have MEN 1
70
complications of acromegaly?
hypertension
diabetes
cardiomyopathy
colorectal cancer
71
Ix of acromegaly?
GH levels not reliable on their own
IGF-1 levels
oral glucose load-> lack of suppression of GH to <1ug/L
pituitary MRI-> pituitary adenoma
72
tx of acromegaly?
trans-sphenoidal surgery- remove adenoma
DA agonists- bromocriptine
Somatostatin analogue- directly inhibit the release of GH e.g. octreotide
GH receptor antagonist e.g. pegvisomant
73
what is diabetes insipidus?
a condition characterised by either a deficiency of anti-diuretic hormone, ADH (cranial DI) OR an insensitivity to ADH (nephrogenic DI)
74
causes of cranial DI?
```
Idiopathic
post-head injury
pituitary surgery
craniopharyngiomas
DIDMOAD
haemochromatosis
```
75
causes of nephrogenic DI?
Genetics- affects vasopressin receptor
hypercalcaemia, hypokalaemia
demeclocycline, lithium
tubulo-interstitial disease: obstruction, sickle-cell, pyelonephritis
76
features of DI?
polyuria, polydipsia
77
Ix of DI?
High plasma osmolality
low urine osmolality- >700 excludes DI
water deprivation test
78
mx of DI?
Nephrogenic- thiazides, low salt/protein diet
| Central- desmopressin
79
how does vasopressin (ADH) work?
V1- blood vessels (constriction)- increases arterial pressure
V2- kidneys (fluid reabsorption)- increases arterial pressue
80
what causes T2DM?
A relative deficiency of insulin due to an excess in adipose tissue
81
symptoms of T1DM and T2DM?
T1DM- weight loss, polydispia, polyuria, DKA- vomiting, abdo pain, reduced consciousness level
T2DM- often picked up incidentally on routine bloods cells, polyuria, polydipsia
82
diagnosis of diabetes?
if the patient is symptomatic only one of the following, if asymptomatic must be demonstrated twice-
- fasting glucose >7mmol/L
- random glucose >11.1mmol/L
HbA1C- glycosylated Hb
>6.5% (48mmol/mol)= diagnostic
false positives for increased red cell turnover e.g. haemolytic anaemia, HIV
83
what is pre-diabetes?
HbA1C 42-47
or fasting glucose 6.1-6.9
also called impaired fasting glucose
84
what is impaired glucose tolerance?
fasting glucose <7 and OGTT 2-hour value >7.8mmol/L but less than 11.1mmol/L
85
mx of T1DM?
HbA1c monitored every 3-6 months target of <48
blood glucose
insulin- long-acting e.g. insulin detemir
self-testing at least 4 times a day, more frequent monitoring during periods of illness, before,during and after sport
metformin- add if BMI >25
86
mx of T2DM?
```
1st line= metformin
if HbA1c >58mmol/mol, add 1 of:
-gliptin
-sulphonylurea
-pioglitazone
-SGLT-2 inhibitor
```
if HbA1c continues to remain >58-
- insulin or
- metformin and sulphonylurea and 1 of:
- gliptin
- pioglitazone
- SGLT-2 inhibitor
if triple therapy not tolerated, CI'd or not effective AND BMI >35-> metformin, sulphonylurea and GLP-1 mimetic
87
lifestyle advice for T2DM?
diet and exercise
BP target <140/80
statin if QRISK2 >10%
88
what to give if metformin CI'd for T2DM?
gliptin OR
sulphonylurea OR
pioglitazone
89
meds for diabetic neuropathy and N&V?
neuropathy- amitriptyline, duloxetine
| N&V- metoclopramide
90
SEs of insulin?
hypoglycaemia
weight gain
lipodystrophy
91
how does metformin work?
| SEs, CIs and positives?
increases insulin sensitivity and decreases hepatic gluconeogenesis
SE- GI upset, lactic acidosis, CI- eGFR <30ml/min
positives- can cause weight loss
92
examples, mechanism, SEs and CI of sulphonylureas?
e.g. gliclazide
stimulates pancreatic beta cells to secrete insulin
SE- hypoglycaemia, weight gain, hyponatraemia
CI- pregnancy and breastfeeding- causes neonatal hypoglycaemia
93
examples, mechanism, SE and CI of glitazones?
pioglitazone
activates PPAR-gamma receptor in adipocytes to promote adipogenesis andfatty acid uptake
SE- weight gain, fluid retention, fractures
CI- heart failure
94
examples, SE and positives of DPP4 inhibitors?
```
e.g. gliptins
increases incretin levels which inhibits
glucagon secretion
SE- pancreatitis
positive- no weight changes
```
95
example, SE and positive of SGLT-2 inhibitors?
e.g. glifozins
inhibits resorption of glucose in the kidney
SE- UTI, DKA
positives- typically results in weight loss
96
pathophysiology of DKA?
caused by uncontrolled liplysis which results in an excess of free fatty acids that are ultimately converted to ketone bodies
97
precipitating features of DKA?
Infection
MI
missed insulin doses
98
features of DKA?
abdo pain
polyuria, polydipsia, dehydration
Kussmaul respiration (deep hyperventilation)
Acetone-smelling breath ('pear drop' breath)
99
diagnostic criteria for DKA?
Glucose >11mmol/L or known DM
pH <7.3
BICARB <15
ketones >3 or urine ketones ++ on dipstick
100
mx of DKA?
1. Fluid replacement- 0.9% saline 1L in first hour then 0.9% saline and KCl over 2 hours and continued with increased time intervals
(slower in 15-25y/o due to risk of cerebral oedema)
2. Insulin- IV .1 unit/kg/hour
3. Once BG is <15mmol/l start 5% dextrose infusion
4. Correction of hypokalaemia if 3.5-5.5 (senior review if lower)
5. Continue with long-acting insulin
101
complication of DKA?
```
gastric stasis
VTE
arrhythmias
cerebral oedema
ARDs
AKI
```
102
what is hyperosmolar hyperglycaemic state?
hyperglycaemia in T2DM-> resulting in osmotic diuresis, severe dehydration and electrolyte deficiencies
-typically presents in the elderly
103
clinical features of hyperosmolar hyperglycaemic state?
onset in slower than T2DM (over days) and therefore dehydration and metabolic disturbances are worse
fatigue- lethargy, N&V
neuro- decreased consciousness, headaches, papilloedema, weakness
haem- hyperviscosity- increased risk of VTE, stroke
CV- dehydration, hypotension, tachycardia
104
diagnosis of hyperosmolar hyperglycaemic state?
1. hypovolaemia
2. marked hyperglycaemia (>30mmol/L) without sigf ketonuria or acidosis
3. Significantly raised serum osmolarity (>320mosmol/kg)
- 2Na + glucose + urea
105
mx of hyperosmolar hyperglycaemic state?
1. normalise the osmolality
2. replace fluid and electrolyte imbalance
3. normalise blood glucose
106
most common type of pituitary adenoma?
prolactinomas
107
symptoms of pituitary adenoma?
excess hormone e.g. cushings
depletion of hormone
stretching of dura around pituitary fossa -> headache
compression of optic chiasm -> bitemporal hemianopia
108
Ix of pituitary adenoma?
pituitary bloods- GH, prolactin, ACTH, TFT, FSH/LH
visual field testing
MRI
109
mx of pituitary adenoma?
hormonal therapy (e.g. bromocriptine for prolactinomas), surgery
110
what is MEN type 1?
- parathyroid (95%)- hyperparathyroidism due to parathyroid hyperplasia
- pituitary (70%)
- pancreas (50%) e.g. insulinoma, gastrinoma (leading to recurrent peptic ulceration)
111
what is MEN type 2?
medullary thyroid cancer e.g. phaeochromocytoma
112
what is the most common drug cause of gynaecomastia?
spirinolactone
113
symptoms of addisonian crisis?
hypovolaemia
hyponatraemia
hyperkalaemia
114
causes of addisonian crisis?
sepsis or surgery causing an acute exacerbation of chronic insufficiency (Addison's, Hypopituitarism)
adrenal haemorrhage eg Waterhouse-Friderichsen syndrome (fulminant meningococcemia)
steroid withdrawal
115
mx of addisonian crisis?
hydrocortisone 100 mg im or iv
1 litre normal saline infused over 30-60 mins or with dextrose if hypoglycaemic
continue hydrocortisone 6 hourly until the patient is stable. No fludrocortisone is required because high cortisol exerts weak mineralocorticoid action
oral replacement may begin after 24 hours and be reduced to maintenance over 3-4 days
116
what is the most common presentation for MEN 1?
Hypercalcaemia
117
2 tests to confirm cushing's syndrome?
overnight dexamethasone suppression test (most sensitive)
| 24 hr urinary free cortisol
118
what to do in a hypoglycaemic attack with impaired GCS?
give IV glucose if there is IV access
| if GCS not impaired, give quick-acting carbohydrate such as GlucoGel®
119
causes of raised prolactin?
```
prolactinoma
pregnancy
oestrogens
physiological: stress, exercise, sleep
acromegaly: 1/3 of patients
polycystic ovarian syndrome
primary hypothyroidism
```
120
rules of radioactive iodine?
Involves drinking a single dose of radioactive iodine
This is taken up by the thyroid, and the emitted radiation destroys a portion of the thyroid cells
Patients can be left hypothyroid afterwards and require levothyroxine replacement
There are rules regarding:
Not pregnant or allowed to get pregnant within 6 months
Avoiding contact with children and pregnant women
Limiting contact with others for several days after receiving the dose
121
What cells secrete PTH?
chief cells
122
how to investigate pheochromocytoma?
| adrenal tumour
plasma metanephrines or 24 hour urine catecholamines (both breakdown products of adrenalin).
123
mx of acromegaly?
Both somatostatin analogues (e.g. ocreotide) and dopamine agonists (e.g. bromocriptine)
124
causes of SIADH?
Post-operative from major surgery
Infection, particularly atypical pneumonia and lung abscesses
Head injury
Medications (thiazide diuretics, carbamazepine, vincristine, cyclophosphamide, antipsychotics, SSRIs, NSAIDSs,)
Malignancy, particularly small cell lung cancer
Meningitis
125
electrolyte abnormality of SIADH?
hyponatraemia (dilutional)
| Clinical examination will show euvolaemia
126
mx of SIADH?
Fluid restriction
| vaptans (ADH receptor blockers such as tolvaptan).
127
risk of rapid correction of hyponatraemia?
A rise in sodium that is too fast gives a risk of central pontine myelinolysis (a neurological condition).
128
antibodies in thyroid disease?
anti-TPO- Grave’s Disease and Hashimoto’s Thyroiditis
Antithyroglobulin Antibodies- Grave’s Disease, Hashimoto’s Thyroiditis and thyroid cancer.
TSH Receptor Antibodies- graves
129
what is levothyroxine?
synthetic T4 and metabolises to T3 in the body.
130
what causes pretibial myxoedema?
a reaction to the TSH receptor antibodies- there are deposits of mucin under the skin on the anterior aspect of the leg
131
what is De Quervain’s Thyroiditis?
De Quervain’s Thyroiditis describes the presentation of a viral infection with fever, neck pain and tenderness, dysphagia and features of hyperthyroidism. There is a hyperthyroid phase followed by hypothyroid phase as the TSH level falls due to negative feedback.
