Endocrinology Flashcards
(259 cards)
1
Q
What’s the difference between endocrine and exocrine?
A
endocrine- glands pour secretions into bloodstream
exocrine- glands pour secretions though a duct to site of action
2
Q
What happens to TSH if you remove the thyroid/ thyroid is under active?
A
TSH will increase/ be elevated
3
Q
What happens to TSH if you have an overactive thyroid?
A
TSH decreased
4
Q
What happens to FSH and LH after menopause?
A
increases
5
Q
What are the diseases of the pituitary?
A
benign pituitary adenoma
craniopharygioma
trauma
apoplexy/ sheehans (bleeding)
sarcoid/ TB
6
Q
How big is the pituitary?
A
1cm in diameter
7
Q
How do pituitary tumours present?
A
- PRESSIRE OF LOCAL STRUCTURE
bitemporal hemianopia (double vision)
headache
CSF leakage - PRESSURE ON NORMAL PITUITARY
hypopituitarism - FUNCTIONING TUMOUR
prolactinoma
acromegaly and gigantism
Cushing’s disease
8
Q
What is Cushing’s disease?
A
too much cortisol
9
Q
What is acromegaly?
A
too much growth hormone
10
Q
How do you tell the difference between CSF leakage from nose and snot?
A
CSF has glucose in it
11
Q
How does somebody with a hypopituitary present?
A
pale
no body hair
central obesity
12
Q
What happens if you have excess GH as a child? Why only in a child?
A
gigantism
tumour on pituitary presses on it and causes hypothyroidism meaning that the child won’t go through puberty (no testosterone secretion, etc)
13
Q
How does acromegaly present?
A
big hands
big jaw
excess sweating
big heart
14
Q
What is galactorrhea?
A
a milky nipple discharge unrelated to the normal milk production of breast-feeding
15
Q
Can both men and women get prolactinomas?
A
Yes
16
Q
Symptoms of prolactinomas?
A
galactorrhea
infertility
loss of libido
visual field defect
17
Q
How quickly does acromegaly progress?
A
slow onset
18
Q
Symptoms of Cushing’s?
A
main symptoms is weight gain, ulcers, stretch marks, easy bruising
19
Q
What does an orchidometer measure?
A
testicular volume in mL
20
Q
What is normal pre-pubertal testicular volume?
A
1-3 mL
21
Q
What is normal testicular volume for an adult male?
A
15-25mL
22
Q
What is thelarche?
A
breast development signalling first visible change of puberty
23
Q
What induces thelarche?
A
oestrogen
24
Q
How long do thelarche last?
A
3 years approx
25
What are you looking for on a pelvic ultrasound?
check for mullerian structures
morphology of uterus
morphology of ovaries
26
What are mullerian structures?
structures found in the female fetus that eventually develop into a woman's reproductive organs
27
What causes growth of pubic and axillary hair in girls?
adrenal androgens and ovarian androgens
28
What is adrenarche?
maturation of adrenal glands, zona reticularis is formed
29
What happens if adrenarche happens in children?
mild advanced bone age
axillary hair
oily skin
mild acne
body odour
30
Which children most commonly experience adrenarche?
obese children
31
What is the name for early puberty?
precocious puberty
32
What are the types of precocious puberty?
true precocious puberty
precocious pseudopuberty
33
What is the gender distribution of true precocious puberty?
90% female
10% male
34
Why is it alarming if a male child has true precocious puberty?
he is likely to have a brain tumour
35
How do you differentiate between diagnosis of true precocious puberty and precocious pseudopuberty?
GnRH (LHRH) test
inject GnRH
If amount of of FSH and LH rises - true precocious puberty
If amount of TSH and LH stays the same - precocious pseudopuberty
36
What is the treatment for precocious puberty?
GnRH superagonist to suppress pulsatility of GnRH secretion
37
In what percentage of children does delayed puberty occur?
3% of children
38
What are the effects of delayed puberty?
psychological problems
defects in reproduction
reduced peak bone mass
delay in acquisition of sex characteristics
39
What's the average size for an adult penis?
12-14cm
40
What is CDGP?
constitutional delay of growth and puberty
41
What is the most common cause of delayed puberty?
CDGP
42
What are the hormones of the anterior pituitary?
adrenocorticotrophic hormone (ACTH)
thyroid-stimulating hormone (TSH)
luteinising hormone (LH)
follicle-stimulating hormone (FSH)
prolactin (PRL)
growth hormone (GH)
melanocyte-stimulating hormone (MSH)
43
What are the hormones of the posterior pituitary?
anti-diuretic hormones (ADH)
oxytocin
44
What are the possible co-morbidities associated with acromegaly?
arthritis
headache
arthritis
insulin-resistant diabetes
sleep apnoea
hypertension
heart disease
45
How does acromegaly affect life expectancy?
reduces average life expectancy by approx 10 years
46
What is the difference in the way water-soluble and fat-soluble hormones interact with the cell?
water-soluble hormones bind to a surface receptor, fat-soluble hormones diffuse into the cell
47
Whats the difference in half-life of water-soluble and fat soluble hormones?
water-soluble: short half life
fat-soluble: long half life
48
Whats the difference in transport of water-soluble and fat soluble hormones?
water-soluble: unbound
fat-soluble: protein bound
49
Whats the difference in clearance of water-soluble and fat soluble hormones?
water-soluble: fast
fat-soluble: slow
50
What is the difference in the water peptides/ monoamine hormones are stored vs steroids?
peptides/ monoamines- stored in vesicles
steroids- synthesised on demand
51
What is paracrine?
cellular secretions/ signals that act on adjacent cells
52
What is autocrine?
cellular signals/ secretions that feedback on the same cell that created the hormones
53
How big are peptide hormones?
variable- 3 to 180 amino acids
54
What type of hormone is insulin?
peptide
55
How does insulin exert its effect?
- insulin binds to receptor
- causes phosphorylation of intracellular tyrosine residues associated with the receptor
- this offsets the tyrosine kinase signal transduction pathway inside cell
- leads to decreased plasma glucose
56
By what mechanisms does the action of insulin decrease blood glucose?
- translocation of glut-4 transporter to plasma membrane and influx of glucose
- glycogen synthesis in the liver
-glycolysis
- fatty acid synthesis in liver and adipose tissue
57
What are catecholamines?
type of neurohormone
58
What are the catecholamines and where are they secreted from?
adrenaline and noradrenaline: adrenal medulla
dopamine: hypothalamus
59
What are the catecholamines and where are they secreted from?
adrenaline and noradrenaline: adrenal medulla
dopamine: hypothalamus
60
What receptors do adrenaline and noradrenaline act upon?
adrenoreceptors
61
What are the two lodothyronines?
tyroxine (T4) and triiodothyronine (T3)
61
What are the two lodothyronines?
tyroxine (T4) and triiodothyronine (T3)
62
Where is T4 produced?
thyroid gland
63
Where is T3 produced?
20% of T3 in circulation is secreted directly by thyroid gland, other 80% is T4 that has been converted to T3 after it leaves the thyroid gland
64
What enzyme converts T4 to T3?
iodothyronine deiodinase
65
What are the two classes of steroid hormones?
corticosteroids
sex (gonadal) steroids
66
What are the classes of corticosteroids?
glucocorticoids
mineralocorticoids
67
What are the classes of sex steroid?
androgens
oestrogens
progestogens
68
What are steroid hormones derived from?
cholesterol
69
How is cholesterol converted to each steroid hormone?
- cholesterol converted to pregnenolone
- pregnenolone converted to progesterone
- progesterone converted to cortisol in the adrenal glands
- progesterone converted to androstenedione then to testosterone in the ovaries or testes
- testosterone converted to estradiol in the ovaries
70
How are steroid hormones transported around the body?
vitamine D binding protein
71
Where is glucose stored?
liver
72
What do muscles use for fuel?
free fatty acids
73
What happens if glucose gets too high?
1. inhibition of glucagon secretion
2. stimulation of insulin release
74
Where is insulin and glucagon secreted?
islets of langerhans in the pancreas
insulin- beta cells
glucagon- alpha cells
75
Why is it getting more difficult to differentiate between T1 and T2 diabetes?
Because of increased levels of obesity, T2DM is being diagnosed in younger patients including children
76
What are microvascular complications of T1DM?
In UK, 30% of T1DM patients will develop diabetic nephropathy
Nephropathy tends to lead to retinopathy and severe neuropathy which massively affects quality of life
77
What is nephropathy?
deterioration of kidney function
can end up in kidney failure (end stage renal disease)
78
Define type 1 diabetes mellitus
autoimmune destruction of pancreatic beta cells leading to complete insulin deficiency
79
When do T1DM usually present?
age 5-15
80
What percentage of diabetes is T1DM?
10%
81
What is glycosuria?
sugar in the urine
82
What are the risk factors for T1DM?
Northern European
Autoimmune disease
Family History
83
What are the signs and symptoms of T1DM?
- "classic triad": polydipsia, polyruria, weightloss (BMI < 25)
- short history of severe symptoms
- possibly presents with ketosis
84
What is the name for extreme thirstiness?
polydipsia
85
What is the name for frequent urination?
polyuria
86
How is T1DM diagnosed?
Either:
- fasting glucose >= 7.0 mmol/L
- random glucose >= 11.0 mmol/L
- HbA1c >= 6.5% (48 mmol/mol)
87
What is important to remember about diagnosing diabetes using HbA1c?
a value less that 6.5% DOES NOT exclude diabetes as this test is not as sensitive as fasting samples in detecting diabetes
88
What is the treatment for T1DM?
insulin, short or long acting
89
How long does short and long acting insulin work for?
short: 4-6 hrs
long: 12-24 hrs
90
Which antibodies can you check for in T1DM?
Anti GAD
pancreatic islet cell Ab
islet antigen-2 Ab
ZnT8
91
Why does T2DM occur?
patients gradually become insulin resistant AND/OR beta cells fail to secrete enough insulin
non-insulin dependent and progresses from impaired glucose tolerance
92
What causes T2DM?
- reduced insulin secretion/ increased insulin resistance
- gestational diabetes
- steroids
- Cushing's
- chronic pancreatitis
93
What are the risk factors of T2DM?
- lifestyle: obesity, inactivity, calorie and alcohol excess
- higher prevalence in asian men
- >40yrs age
- hypertension
94
What are the signs and symptoms of T2DM?
polydipsia
polyuria
glycosuria
central obesity
slower onset
blurred vision
95
What are the investigations for T2DM?
Exactly the same as type 1:
Either:
- fasting glucose >= 7.0 mmol/L
- random glucose >= 11.0 mmol/L
- HbA1c >= 6.5% (48 mmol/mol)
96
Describe first line management of T2DM
1st line- lifestyle changes
- dietary advice (high complex carbs, low fat)
- smoking cessation
- decrease alcohol intake
- encourage exercise
- regular blood glucose and HbA1c monitoring
97
Describe second line management of T2DM
2nd line- medication
1. METFORMIN (e.g. biguanide)
2. If HbA1c remains high then DUAL THERAPY with metformin:
- DPP4 inhibitor
- Sulphonylurea (e.g. gliclazide)
- pioglitazone
3. If still high = TRIPLE THERAPY with metformin
4. Insulin
98
How does metformin work and what type of patients suit it best?
increases sensitivity to insulin, decreases hepatic gluconeogenesis
first choice in overweight patients as it can cause a slight weight decrease
99
How does sulphonylurea treat T2DM?
increases insulin secretion
100
What are the notable side effects of metformin?
gastrointestinal upset
lactic acidosis
101
Why is sulphonylurea becoming less popular as a 2nd line treatment for T2DM?
causes weight gain
102
What are the notable side effects of sulphonylurea?
hypoglycaemia
weight gain
hyponatraemia
103
Give 2 examples of sulphonylureas
gliclazide
glimepiride
104
What is DKA?
diabetic ketoacidosis- complete lack on insulin resulting in ketone production
105
What causes DKA?
unrelated/ undiagnosed type 1 diabetes
infection/ illness
106
Describe the pathophysiology of DKA
1. absence of insulin causes hyperglycaemia and increased ketones
2. hyperglycaemia causes osmotic diuresis- dehydration
3. glucose and ketones escape in urine
4. circulating ketones are acidic and cause acidosis
107
What is the direct effect of ketones on the body?
anorexia and vomiting
108
What are the signs and symptoms of diabetic ketoacidosis?
extreme diabetes symptoms plus:
nausea and vomiting
weight loss
confusion and reduced mental state
lethargy
abdominal pain
Kussmaul's breathing
'pear drop' breath
hypotension
tachycardia
109
What is kussmaul's breathing?
fast, deep breaths that occur in response to metabolic acidosis
110
What investigations can be done to confirm diabetic ketoacidosis?
- random plasma glucose > 11mmol/L
- plasma ketones >3mmol/L
- blood pH <7.35, or bicarb <15mmol/L
- urine dipstick: glycosuria, ketonuria
- serum U+E:
-raised urea and creatinine
-decreased total K+, increased serum K+
111
What is the treatment for diabetic ketoacidosis?
1. ABC management
2. replace fluid- 0.9% saline IV
3. IV insulin
4. restore electrolytes (e.g. K+)
112
What is HHS?
hyperosmolar hyperglycaemic state
113
What causes HHS?
untreated/ undiagnosed T2DM
infection/ illness
114
What are the signs and symptoms of HHS?
extreme diabetes symptoms plus:
confusions and reduced mental state
lethargy
severe dehydration
115
What investigations confirm a diagnosis of HHS?
- random plasma glucose > 11mmol/L
- urine dipstick: glycosuria
- high plasma osmolality
- U+E
- decreased total body K+
- increased serum K+
116
What is the treatment for HHS?
- replace fluid- 0.9% saline
- insulin- AT LOW RATE OF INFUSION
- restore electrolytes
- low molecular weight heparin (LMWH)
117
Why must patients with HHS be given insulin at a low rate of infusion?
patients with HHS have a high sensitivity to insulin
requires a low infusion rate to prevent cerebral oedema caused by glucose being lowered too quickly
118
What is hypoglycaemia?
low plasma glucose causing impaired brain function
119
What is neutropenia?
abnormally low concentration of neutrophils
120
What glucose value signals hypoglycaemia?
3.9 mmol/L
121
What is hyperthyroidism?
clinical effects of too much thyroid hormone
122
What is the difference between primary and secondary hyperthyroidism?
primary- abnormal increased thyroid function
secondary- abnormal increased TSH production
123
What are the causes of hyperthyroidism?
- 65-75% caused by GRAVES DISEASE
- toxic multi nodular goitre
- toxic adenoma
- metastatic follicular thyroid cancer
- iodine excess
secondary cause: TSH secreting pituitary tumour
124
What is the ratio of F:M diagnosed with Graves disease?
9:1
125
Who is affected by hyperthyroidism?
mostly young women aged 20-40
126
What are the risk factors for hyperthyroidism?
smoking
stress
HLA-DR3
other autoimmune diseases (T1DM, Addisons, vitiligo)
127
What are the signs and symptoms of hyperthyroidism?
hot and sweaty
diarrhoea
hyperphagia
weight loss
palpitations
tremor
irritability
anxiety/ restlessness
oligomenorrhoea
goitre
128
What is goitre?
swelling of thyroid gland causing lump in the front of the neck
129
What is hyperphagia?
abnormally big desire for food/ excessive eating
130
What is oligomenorrhoea?
abnormal menstruation involving infrequent periods
131
Which investigations confirm a diagnosis of hyperthyroidism?
- Thyroid function tests (TFTs) showing increased T4/ T3, plus:
primary: decreased TSH
secondary: increased TSH
- Thyroid autoantibodies (anti-TSHR)
- ultrasound and CT head
132
What is the treatment for hyperthyroidism?
1. DRUG MANAGEMENT
a) beta blockers (rapid symptom relief)
b) 1st line: carbimazole
c) 2nd line: propylthiouracil
2. RADIOIODIDE
3. TYROIDECTOMY
133
How does carbimazole and propylthiouracil treat hyperthyroidism?
carbimazole- blocks synthesis of T4
propylthiouracil- prevents T4 to T3 conversion
134
What are the consequences of untreated hyperthyroidism during pregnancy?
- intrauterine growth resistance (IUGR)
- pre eclampsia
- preterm delivery
- risk of stillbirth/ miscarriage
135
How does Graves disease cause hyperthyroidism?
IgG antibodies bind to TSH receptors to increase T4/ T3 production
136
What are the symptoms of Graves disease?
hyperthyroidism symptoms plus:
- thyroid eye disease
- pretibial myxoedema
- thyroid acropachy
137
What are the features of thyroid eye disease?
eye retraction
periorbital swelling
proptosis/ exophthalmos (bulging eyeballs)
138
What percentage of patients with Graves disease have thyroid eye disease?
25-50%
139
How does thyroid acropachy present?
clubbing
painful finger and toe swelling
periosteal reaction (bone growth)
140
What is hypothyroidism?
clinical effects of lack of thyroid hormone
141
What is the difference between primary and secondary hypothyroidism?
primary: abnormally low thyroid function
secondary: abnormally low TSH production
142
What are the causes of hypothyroidism?
1. AUTOIMMUNE: Hashimotos inflammation = goitre), Primary atrophic hypothyroidism (atrophy = no goitre)
2. OTHER PRIMARY: iodine deficiency, drugs (antithyroid drugs, iodine, lithium), post thyroidectomy/ radio iodine)
3. SECONDARY: hypopituitarism
143
How many people are diagnosed with hypothyroidism every year?
4 in every 1000 people
144
Who is most commonly affected by hypothyroidism?
affects F:M in a ratio of 6:1
mainly > 40 yrs old
145
What are the signs and symptoms of hypothyroidism?
fatigue
weight gain
loss of appetite
cold
lethargy
constipation
low mood/ depression
menorrhagia
goitre
146
What is the treatment for hypothyroidism?
levothyroxine (T4)
147
List the hormones of the anterior pituitary
- adrenocorticotropic hormone (ACTH)
- growth hormone (GH)
- luteinising hormone (LH)
- follicle-stimulating hormone (FSH)
- prolactin
- thyroid-stimulating hormone (TSH)
148
List the hormones of the posterior pituitary
- anti-diuretic hormone (ADH)
- oxytocin
149
Where is melanocyte-stimulating hormone produced and what does It do?
pars intima- part of pituitary between anterior and posterior
acts on cells in skin to stimulate production of melanin (pigment which prevents against UV radiation)
150
Where are the hormones released from the posterior pituitary produced?
hypothalamus
151
What is another name for ADH?
vasopressin
152
What does ACTH do?
stimulates adrenal glands to secrete steroids (e.g. cortisol)
153
What does GH do?
regulates growth, metabolism and body composition by acting on liver, bones, adipose tissue and muscles
154
What does LH and FSH do? What are they collectively called?
gonadotrophins
act on ovaries/ testes to stimulate sex hormone production and egg/ sperm maturity
155
What does prolactin do?
stimulates milk production in mammary glands
156
What does TSH do?
stimulates thyroid gland to secrete thyroid hormone
157
What does ADH/ vasopressin do?
controls water balance and blood pressure
158
What does oxytocin do?
stimulates uterine contractions during labour and milk secretion during breast feeding
159
What is Cushing's syndrome?
long term exposure to excessive cortisol hormone released by adrenal glands
160
What is the difference between a syndrome and a disease?
A disease typically has a defining cause, distinguishing symptoms and treatments. A syndrome is a group of symptoms that may not have a definite cause.
161
What are the two types of causes of Cushing's syndrome
ACTH dependent and ACTH independent
162
What is the difference between Cushing's syndrome and Cushing's disease?
Cushing's disease is a specific type of Cushing's syndrome resulting from a pituitary tumour
163
What are the ACTH dependent causes of Cushing's syndrome?
- Cushing's disease- ACTH secreting from pituitary adenoma
- Ectopic ACTH production from small cell lung cancer
164
What are the ACTH independent causes of Cushing's syndrome?
- latrogenic- steroid use (most common)
- adrenal adenoma
165
What are the signs and symptoms of Cushing's?
moon face
central obesity
buffalo hump
acne
hypertension
striae
hirsutism
weight gain
166
What is striae?
stretch marks
167
What is hirsutism?
when women have excessive dark/ coarse hair in a male-like pattern (face/ chest/ back)
168
What investigations are used for Cushing's?
1. random plasma cortisol- raised
2. overnight dexamethasone suppression test- cortisol will not be suppressed in Cushing's
3. urinary free cortisol (24hr)
4. plasma ACTH
169
What is the treatment for Cushing's?
treatment depends on the underlying cause:
- latrogenic: stop medications if possible
- Cushing's disease: removal of pituitary adenoma (transsphenoidal surgery)
- adrenal adenoma: adrenalectomy
cortisol inhibition drugs:
metyrapone
ketoconazole
170
What is acromegaly?
release of excess growth hormone (GH) causing overgrowth of all systems
171
What are the causes of acromegaly?
- 99% of cases caused by pituitary adenoma
- secondary to a malignancy that secretes ectopic GH (e.g. lung cancer)
172
What are some complications of acromegaly?
erectile dysfunction
diabetes mellitus
173
What are the signs and symptoms of acromegaly?
prominent forehead and brow
increased jaw size
large hands, nose, tongue, feet
bitemporal hemianopia
profuse sweating
lower pitch of voice
obstructive sleep apnoea
174
What investigations are used for acromegaly?
1st line: insulin like growth factor 1 test - raised
gold standard: oral glucose tolerance test
other tests: random serum GH raised, MRI of pituitary fossa
175
What is the treatment for acromegaly?
1st line- transsphenoidal resection surgery (if cause is adenoma)
2nd line- somatostatin analogue e.g. ocreotide
3rd line- GH receptor antagonist e.g. pegvisomant
4th line- dopamine agonist e.g. cabergoline
176
What is transsphenoidal resection?
most common way to remove pituitary tumours
tumour removed via the sphenoid sinus, accessed through the nose
177
What is a prolactinoma?
benign adenoma of pituitary gland producing excess prolactin
178
What causes prolactinoma?
cause is unknown but there is a genetic association
179
What is hyperprolactinaemia?
too much prolactin in the blood of men and women who aren't pregnant
180
What are some causes of hyperprolactinaemia other than prolactinoma?
non-functional pituitary tumour (compresses pituitary stalk hence no inhibition of prolactin release)
antidopaminergic drugs
181
What are the 2 classifications of prolactinoma?
micro- tumour < 10mm diameter on MRI (most common, accounts for 90% of cases)
macro- tumour > 10mm diameter on MRI
182
Why does prolactinoma cause galactorrhoea?
increased release of prolactin can cause galactorrhea by stimulating milk production from mammary gland as well as inhibiting FSH and LH
183
What are the signs and symptoms of prolactinoma?
visual field defect
headache
menstrual irregularity
infertility
galactorrhea
184
What investigations are used to diagnose prolactinoma?
prolactin levels
head CT
185
What is the treatment for prolactinoma?
- gold standard: transphenoidal resection surgery
- 1st line: dopamine agonists: bromocriptine/ cabergoline
186
Why are dopamine agonists used to treat prolactinoma?
dopamine has an inhibitory effect on prolactin
187
What is Conn's syndrome?
primary hyperaldosteronism due to an aldosterone producing adenoma
188
Describe the pathophysiology of Conn's syndrome
excess production of aldosterone independent of renin-angiotensin system:
- high sodium and water retention
- increased potassium excretion in kidneys
- low renin release
189
What are the signs and symptoms of Conn's syndrome?
hypertension
hypokalaemia
nocturia
polyuria
mood disturbance
190
What investigations can confirm a diagnosis of Conn's syndrome?
- aldosterone-renin ratio blood test: increased
- plasma potassium: reduced
- U+E
191
What is the treatment for Conn's syndrome?
- 1st line: spironolactone (pre-op controls BP and K+ levels)- if hyperplasia
- gold standard: laparoscopic adrenalectomy- if adenoma
Aim is to lower BP, decrease aldosterone levels and resolve electrolyte imbalance
192
What is Addison's disease?
primary adrenal insufficiency
193
Describe the pathophysiology of Addison's disease
destruction of adrenal cortex leads to decreased production of glucocorticoid (cortisol) and mineralocorticoid (aldosterone)
194
What are the causes of Addison's disease?
- autoimmune destruction (80% of cases in UK + developed countries)
- TB (most common cause worldwide)
- adrenal metastases
195
What are the signs and symptoms of Addison's disease?
tanned
lean
fatigue
pigmented palmar creases
postural hypotension
often diagnosed late
196
What investigations can confirm a diagnosis of Addison's disease?
- 1st line:
U+E confirms hyponatraemia, hypokalaemia
Blood glucose confirms hypoglycaemia
- Gold standard:
Short SynACTHen test (ACTH stimulation test) presents with low cortisol, high ACTH
- Plasma renin and aldosterone:
high renin, low aldosterone
197
What are some less commonly used test that can also confirm a diagnosis of Addison's disease?
- adrenal CT or MRI
- 2l-hydroxylase adrenal autoantibodies- is positive in autoimmune diseases in more than 80% of cases
198
What is the treatment for Addison's disease?
replace steroids depending on signs and symptoms:
hydrocortisone- replaces cortisol
fludrocortisone- replaces aldosterone
treat underlying cause and warn against abruptly stopping steroids
199
What does SIADH stand for?
syndrome of inappropriate ADH
200
What is SIADH?
inappropriately large amounts of ADH secretion causing water to be reabsorbed in collecting duct
201
What are the causes of SIADH?
- post-operative from major surgery
- infection (atypical pneumonia and lung abscess)
- head injury
- medications (thiazide diuretics)- most common cause
202
What are the signs and symptoms of SIADH?
very non-specific
headache
nausea
fatigue
muscle cramps
confusion
severe hyponatraemia
203
What investigations can confirm a diagnosis of SIADH?
DIAGNOSIS BY EXLCUSION
- U+E shows hyponatraemia
- high urine sodium
- high urine osmolality
Causes of hyponatraemia that need to be excluded:
- -ve short SynACTHen test- exclude adrenal insufficiency
- no diarrhoea, no vomiting
- no history of diuretic use
- no AKI/CKD
204
How is SIADH managed?
treat underlying cause:
stop causative medicine
fluid restriction
tolvaptan (ADH receptor blocker)
205
What is hyperkalaemia?
blood potassium level > 5.5mmol/L
206
What are the causes of hyperkalaemia?
3 categories:
IMPAIRED EXCRETION:
- AKI/CKD
- drug affect (ACEi, NSAIDS, beta blockers)
- renal tubular acidosis
- addison's disease (low aldosterone)
INCREASED INTAKE:
- IV K+ therapy
- increased dietary intake
SHIFT TO EXTRACELLULAR:
- metabolic acidosis
- rhabdomyolysis
- decreased insulin
- tumour lysis syndrome
207
How does metabolic acidosis cause hyperkalaemia?
cells switch H+ for K+ to reduced acidosis
208
Why does tumour lysis syndrome cause hyperkalaemia?
the intracellular contents (including potassium) are released
209
What are the symptoms of hyperkalaemia?
fatigue
light-headedness
chest pain
palpitations
210
What are the signs of hyperkalaemia?
arrhythmia (potential cardiac arrest)
reduced power and reflexes
flaccid paralysis
signs of underlying cause
211
How will hyperkalaemia present on an ECG?
- small/ absent p waves
- prolonged PR interval (> 200ms)
- wide QRS interval (> 120ms)
- TALL TENTED T WAVES
212
What investigations are used to confirm a diagnosis of hyperkalaemia?
ECG
bloods- FBC, U+E
213
What is the treatment for hyperkalaemia?
- ABC
- cardiac monitoring
- calcium gluconate- to protect myocardium
- insulin and dextrose or nebuliser salbutamol - drives K+ intracellularly
- treat underlying cause
214
What is hypokalaemia?
blood potassium < 3.5mmol/L
215
What are the causes of hypokalaemia?
3 categories:
INCREASED EXCRETION
- renal disease
- drug effect (thiazide, loop diuretics, laxatives)
- GI loss (D+V)
- Conn's Syndrome
DECREASED INTAKE:
- dietary deficiency/ fasting
- liquorice abuse
SHIFT TO INTRACELLULAR:
- metabolic alkalosis
- drug effect (insulin, B2 agonists (SABAs and LABAs)
216
What are the symptoms of hypokalaemia?
can be asymptomatic
fatigue + light headedness
weakness
cramps
palpitations
constipation
217
What are the signs of hypokalaemia?
arrhythmia
hypotonia
hypereflexia
muscle paralysis
rhabdomyolysis
218
How does hypokalaemia present on an ECG?
- prolonged PR interval
- ST depression
- flat T waves
- prominent U waves
219
What investigations are used to confirm a diagnosis of hypokalaemia?
ECG
Bloods- FBC, U+E
220
What are the two types of diabetes insipidus?
cranial
nephrogenic
221
What are the symptoms of diabetes insipidus?
polyuria
polydipsia
dehydration
222
Describe the pathophysiology of diabetes insipidus
caused by impaired water reabsorption from the kidneys
large volumes of dilute urine due to reduced ADH due to:
impaired secretion from posterior pituitary (cranial) OR impaired response of the kidney to ADH (nephrogenic)
223
What are the causes of cranial diabetes insipidus?
can be idiopathic
congenital
tumour
trauma
infection
224
What are the causes of nephrogenic diabetes insipidus?
inherited
metabolic (low potassium, high calcium)
drugs (lithium)
chronic renal disease
224
What are the causes of nephrogenic diabetes insipidus?
inherited
metabolic (low potassium, high calcium)
drugs (lithium)
chronic renal disease
225
How is diabetes insipidus diagnosed?
gold standard: 8hr water deprivation test to diagnose, then desmopressin test to establish if cranial or nephrogenic
other possible investigation: cranial MRI
226
What is the treatment for diabetes insipidus?
treat underlying cause, mild cases can just undergo rehydration
cranial- desmopressin (synthetic ADH) to replace ADH
nephrogenic- if cause persists, give bendroflumethiazide
227
What is desmopressin?
synthetic ADH
228
What is hyperparathyroidism?
excessive secretion of parathyroid hormone (PTH)
229
What are the categories of hyperparathyroidism?
PRIMARY- 1 parathyroid gland produced excessive PTH
SECONDARY- increased secretion of PTH to compensate hypocalcaemia
TERTIARY- autonomous secretion of PTH even after correction of calcium deficiency due to chronic kidney disease (CKD)
230
What are the causes of primary hyperparathyroidism?
80% caused by adenoma
20% caused by hyperplasia of all glands
231
What are the causes of secondary hyperparathyroidism?
chronic kidney disease (CKD)
low vitamin D
232
What causes tertiary hyperparathyroidism?
develops from prolonged secondary hyperparathyroidism
233
What are the signs and symptoms of hyperparathyroidism?
Bones, Stones, Moans, Groans, Hypercalcaemia
Bones- bone pain
Stones- renal calculi (kidney stones)
Moans- psychic moans (depression)
Groans- abdominal moans
Hypercalcaemia
234
What investigations can be used to confirm a diagnosis of hyperparathyroidism?
PTH/ BONE PROFILE: high PTH, high calcium, low phosphates
PRIMARY- raised calcium
SECONDARY- low serum calcium, high PTH
TERTIARY- raised calcium + raised PTH
Can also do a DEXA scan X-ray which will show "salt and pepper" degradation of bone, and an ultrasound to look for kidney stones
235
How is hyperparathyroidism managed?
"watchful waiting"
PRIMARY- surgical removal of adenoma, give bisphosphates
SECONDARY- calcium correction, treat underlying cause
TERTIARY- cinacalet (calcium mimetic), total/ part thyroidectomy
236
What is hypoparathyroidism?
reduced PTH production
primary- due to gland failure
secondary- other causes
237
What are the causes of hypoparathyroidism?
PRIMARY- failure of gland caused by:
autoimmune destruction
congenital (DiGeorge Syndrome)
SECONDARY-
surgical removal of thyroid gland
decreased magnesium (required for PTH secretion)
238
What is DiGeorge Syndrome?
22q11 deletion
239
What are the risk factors for hypoparathyroidism?
other autoimmune disorders
240
Describe the pathophysiology of hypoparathyroidism
low PTH results in hypocalcaemia and hyperphosphateaemia which makes neurons more excitable
241
What are the symptoms of hypoparathyroidism?
acronym: CATS go numb
Convulsions
Arrhythmias
Tetany
Spasm
Numbness
242
What is tetany?
involuntary contraction of muscles
243
What are the signs of hypoparathyroidism?
- Chvostek's sign- facial nerve tap induces spasm
- Trousseau's sign- BP cuff causes wrist flexion and fingers to pull together
244
What investigations confirm a diagnosis of hypoparathyroidism?
Bloods- bone profiling
- decreased calcium
- increased or normal phosphate
- decreased PTH
ECG:
prolonged QT and ST segments
245
What is the role of basal insulin in T1DM?
controls glucose levels between meals and at night
concentration can be adjusted as needed between 5-7mmol/L
246
What is the role of bolus insulin?
manage glucose according to carbohydrate intake and pre-meal glucose
247
Where is PTH secreted from?
chief cells in parathyroid gland
248
How does PTH act on bone to increase serum calcium?
stimulates osteoclasts to release ionic calcium for reabsorption
249
What hormone regulates the decrease in serum calcium?
calcitonin
250
Where does calcitonin secretion occur?
c-cells in the thyroid, stimulated by increased serum calcium
251
What is a normal level for serum calcium?
2.2 to 2.6 mmol/L
252
What calcium levels would indicate hypocalcaemia?
mild-moderate: 1.9-2.2 mmol/L
severe: < 1.9 mmol/L
253
What calcium levels would indicate hypocalcaemia?
mild-moderate: 1.9-2.2 mmol/L
severe: < 1.9 mmol/L
254
Prolactinoma is a tumour of what cell type?
lactotroph
255
Prolactinoma is a tumour of what cell type?
lactotroph
256
What makes up the HPA axis?
hypothalamus
pituitary
adrenals
257
What makes up the HPA axis?
hypothalamus
pituitary
adrenals
