endocrine Flashcards
1
Q
Causes of T1DM
A
HLA-DR/DQ polymorphism, environmental
2
Q
which hypersensitivity is T1DM?
A
type IV
3
Q
What are the effects of a lack of insulin?
A
-lipolysis/muscle breakdown
-Increased hepatic glucose output
-reduced peripheral glucose uptake
-reduces glucagon secretion inhibition
4
Q
What are the key presentations of T1DM
A
days/week of polyuria, polydipisia, weight loss, weakness
5
Q
What are the investigations for T1DM
A
HbA1C (gold standard), serum glucose, U&Es and blood cultures (DKA)
6
Q
what is considered a normal random plasma glucose?
A
<11.1
7
Q
what is considered a normal fasting plasma glucose?
A
<6.1 (>7 in diabetes)
8
Q
what is considered a normal 2hr plasma glucose?
A
<7.8 (>11.1 in diabetes)
9
Q
What is a normal HbA1C?
A
<42 (5.7%)
10
Q
What are the diagnostic criteria for an asymptomatic patient suspected to have T1DM?
A
raised glucose on two separate occasions
11
Q
what is a diabetic HbA1c?
A
> 47 (>6.5%)
12
Q
What is 1st line treatment for T1DM
A
basal-bolus insulin (glargine), amylin analogue (pramlintide or metfromin)
13
Q
What is the 2nd line treatment for T1DM
A
fixed insulin dose
14
Q
What are the complications of T1DM
A
-DKA
-microvascular
-macrovascular
-CVD
-depression
15
Q
What is DKA?
A
hyperglycaemia, ketonaemia, metabolic acidosis
16
Q
Causes of DKA
A
T1DM, infection
17
Q
Risk factors DKA
A
innappropriate insulin therapy, infection etc.
18
Q
pathophysiology of DKA
A
insulin deficiency -> lipolysis/muscle breakdown
lipolysis= FFAs + glycerol
FFAs->ketones
reduced circulating volume
19
Q
presentations of DKA
A
-gradual drowsiness
-vomiting
-dehydration (T1DM)
20
Q
investigations for DKA
A
VBG, acidosis <7.35 or bicarbonate <15mmol/L
blood ketones > 1.6-2.9
blood glucose >11
21
Q
What can insulin treatment for DKA lead to?
A
hypokalaemia due to movement into cells - can cause arrhythmias
22
Q
What is the management of DKA
A
FIG-PICK
Fluids - 0.9% saline
Insulin - actrapid
Glucose - dextrose
Potassium - monitor
Infection - treat underlying cause
Chart - fluids
Ketones - monitor ketones
23
Q
What are the complications of DKA?
A
cerebral oedema
24
Q
What are key presentations of T2DM?
A
Glycosuria, obesity
25
What are the signs of T2DM?
polydipsia
polyuria
polyphagia
glycosuria
26
What is the 2nd line treatment for T2DM?
metformin - if newly diagnosed patients have an HbA1C over 48mmol/L
27
What is the 1st line management of T2DM?
lifestyle modification, weight loss, dietary modifications etc
28
What is the 3rd line management for T2DM?
metformin + 1 of: sulfonylurea, thiazalodinediones, DPP-4 inhibitor or SGLT-2
29
What is the 4th line treatment for T2DM?
insulin
30
how do you monitor T2DM
yearly diabetes reveiw
HbA1c 3-6 months
ACR annually
31
What are the microvascular complications of DM?
neuropathy, retinopathy, nephropathy
32
What are the macrovascular complications of DM?
stroke, hypertension, CAD, peripheral artery disease
33
What are the side effects of insulin treatment?
hypoglycaemia, weight gain, lipodystrophy
34
What are the side effects of metformin?
gastrointestinal upset, lactic acidosis
(nephrotoxic, cannot be used in pts with eGR <30)
35
What is the action of sulfonyureas?
stimulates beta cells to secrete insulin
36
Give an example of a sulfonylurea
gliclazide, glimepiride
37
What are the side effects of sulfonylureas?
hypoglycaemia
weight gain
hyponatraemia
38
What do thiazolidinediones (pioglitazone) do?
they promote adipogenesis and fatty acid uptake
39
What are the side effects of thiazolidinediones?
weight gain and fluid retention
40
What do DPP-4 inhibitors (-gliptins) do?
increase incretin which inhibits glucagon secretion
41
What are the side effects of DPP-4 inhibitors?
tolerated well but can cause pancreatitis
42
Give an example of a DPP4 inhibitor?
sitagliptin
43
What do SGLT-2 inhibs do?
inhibits reabsorption of glucose in the kidney
44
What are the side effects of SGLT-2 inhibs?
UTIs and weight loss
45
Give an example of an SGLT2 inhibitor
dapagliflozin
46
Give an example of a GLP-1 inhibitors
exenatide
47
Explain the pathophysiology of HHS
insulin insufficiency - enough insulin to stop ketogenesis but not enough to stop hepatic glucose production
48
How does hyperglycaemia effect osmolality?
it results in osmotic diuresis with a loss of sodium and potassium
49
What are the causes of Hyperosmolar Hyperglycaemic state
diabetes + infection
50
What are the key presentations of HHS?
acute cognitive impairment - psychosis, coma, seizures
51
What are the physiological characteristics of HHS?
severe hyperglycaemia >30
hypotension
hyperosmolality >320
52
1st line investigation for HHS
blood glucose >30
blood ketones -ve
VBG - mild acidosis
serum osmolality >320
U&Es, abnormal K
53
management of HHS
rehydrate - 0.9% saline over 48 hrs
replace K+ when urine flows
use insulin if blood sugar not falling
LMWH for VTE prophylaxis
54
What are the complications of HHS
stroke, MI, PE
treatment related hypokalcaemia/glycaemia
55
What are the symptoms of hypoglycaemia?
hypotension, tachycardia, sweating, anxiety, hunger, dizziness
56
How does decreased blood glucose effect adrenaline, GH and cortisol?
all of these hormones are produced in order to increase blood glucose rapidly
57
Below what glucose level do autonomic symptoms show?
<3.3mmol/L
58
Below what glucose level do neuroglycopenic symptoms show?
<2.8mmol/L
59
What are the symptoms of neurocytopenic hypoglycaemia?
weakness, vision changes, confusion, dizziness
60
management for hypoglycaemia
food- carbs
OR
IV 10% glucose 200ml/h (conscious)
IV 10% glucose 200ml/15mins (inconscious)
61
complications of hypoglycaemia
siezure
coma
brain damage
62
what is cushings syndrome
hypercorticolism
63
What are the causes of ACTH independent cushings?
iatrogenic - steroids e.g. prednisolone (glucocorticoid)
adrenal adenoma
64
What are the causes of ACTH dependent cushings?
anterior pituitary adenoma
ectopic ACTH
ACTH dependent are more rare
65
What are the risk factors for cushings?
female
20-50 yrs
pituitary/adrenal adenoma, carcinoma, neuroendocrine tumours
66
What are the effects of hypercorticolism?
increases gluconeogenesis/glycogenesis, reduced insulin secretion, increased proteolysis/lipolysis/bone resporption, Na+ reabsorption, K+ excretion, anti-inflammatory/immunosuppressive
67
What are the key presentation of cushings?
round "moon" face
central obesity
abdominal striae
buffalo hump
proximal limb muscle wasting
supraclavicular fat distribution
68
What is the first line investigation for cushings?
plasma cortisol - elevated
69
gold standard investigations for cushings
dexamethasone supression test
(48hr_
low dose 1mg: low cortisol->normal, high/normal cortisol->cushings
high dose 8mg: low cortisol->cushings, High/normal cortisol->ACTH low->adrenal cushings
->ACTH high->ectopic ACTH
70
What is the management of cushings?
depends on cause
iatrogenic -> stop medication
surgical removal of adenoma/tumour
removal of adrenal glands + replacement hormones
71
What are the complications of cushings?
CVD, hypertension, DM
72
What is Addisons disease?
failure of adrenal cortex to secrete cortisol and aldosterone (primary adrenal insufficiency)
73
What are the causes of primary adrenal insufficiency (Addisons)?
autoimmune adrenalitis - most common in developed countries
TB - most common worldwide
74
What are causes of secondary adrenal insufficiency?
inadequate ACTH production due to damage/loss of pituitary
75
What are the causes of tertiary adrenal insufficiency?
inadequate CRH from the hypothalamus, often due to long term (>3 weeks) oral steroids
76
What are the key presentations of addisons?
weight loss
hyperpigmentation (bronzing of hands)
fatigue
anorexia
salt cravings
77
What is the gold standard investigation for addisons?
short synacthen test (ACTH stimulation test)
78
How does the short synacthen test work?
synacthen (synthetic ACTH) given in the morning, cortisol measured at baseline, 30 and 60 mins, in healthy pt, cortisol should double
79
What is the management of Addisons?
hydrocortisone (glucocorticoid) to replace cortisol
fludrocortisone (mineralcorticoid) to replace aldosterone
80
What is the management of an addisonian crisis?
parenteral steroids - hydrocortisone 100mg
fluid resus
correct hypoglycaemia
monitor electrolytes
81
what is Conns syndrome?
hyperaldosteronism
82
What is primary hyperaldosteronism and what is it caused by?
the adrenal glands are responsible for producing too much aldosterone (renin will be low) - adrenal adenoma e.g. bilateral adrenal hyperplasia
83
What is secondary hyperaldosteronism?
high levels of aldosterone due to and increase in renin secretion
84
What are the key presentations of conns?
hypertension
85
What are the symptoms of conns?
muscle cramps
86
What are the investigations for conns?
aldosterone renin ratio - high in primary (gold standard)
plasma K+ will be low
87
What confirmatory investigation can be done for Conns?
MRI/CT to locate adrenal lesions
elective adrenal venous sampling
88
What medications can help manage Conns?
aldosterone antagonists
eplerenone
spironolactone
89
What surgical/interventional remedies are there for Conns?
adrenalectomy
percutaneous renal artery angioplasty
90
What are the Causes of hypokalaemia?
INCREASED EXCRETION:
drugs(thiazide/loops)
renal disease
GI loss
REDUCED INTAKE:
dietary deficiency
SHIFT TO INTRACELLULAR:
insulin/salbutamol
91
What does K+ do in the body
heart function, muscle contraction, water balance, nervous impulses
92
What are the signs of hypokalaemia?
arrhythmias, muscle paralysis, hypotonia. hyporeflexia, tetany
93
Gold standard investigations for hypokalaemia
ECG-> inverted T waves, ST depression, prominent U wave
U&Es <3.5 (<2.5 is severe)
94
What is the management of mild hypokalaemia?
oral potassium replacement
95
What is the management of severe hypokalaemia?
IV potassium chloride 40mmol in 1L 0.9% NaCl
96
Causes of hyperkalaemia
IMPAIRED EXCRETION:
AKI/CKD
drugs
renal tubular acidosis
INCREASED INTAKE:
IV therapy
increased dietary intake
SHIFT FROM INTRACELLULAR:
metabolic acidosis
97
key presentations of hyperkalaemia
arrhythmias, reduced power/reflexes, palpitations, chest pain
98
What are the gold standard Investigations for hyperkalaemia?
ECG-> peaked T waves, P wave flattening, PR prolongation, wide QRS complex
U&Es
99
How should you manage hyperkalaemia with ECG changes?
IV calcium gluconate/chloride - stabilised cardiac membrane
insulin + dextrose
100
How should you manage hyperkalaemia with NO ECG changes?
shift potassium into cells with IV insulin/dextrose or with nebulised salbutamol
101
What medications/procedures can remove potassium from the body?
calcium resonium, loop diuretics, dialysis
102
what are phaechromocytomas?
tumours arising from catecholamine-producing chromaffin cells of the adrenal medulla
103
causes of phaechromocytomas
MEN 2
neurofibromatosis
bilateral/malignant/extra-adrenal in 10%
104
pathophysiology of phaechromocytomas
tumour secreted catecholamines: adrenaline, noradrenaline and sometimes dopamine (metanephrines/normetanephrines)
105
key presentations of phaechromocytomas
episodic, hypertension, headaches, palpitations, sweating, pallor
106
gold standard investigation for phaechromocytomas
24hr urine collection for catecholamines, metaneprhines, normetanephrines plus same metabolites in blood
107
Management of phaechromocytomas
non emergency: alpha(phenoxybenzamine)/beta blockers, surgical excision (curative in 85%)
HTN crisis: antihypertensive agents (phentolamine)
108
what is Carcinoid syndrome?
symptoms due to release of vasoactive peptides (serotonin) into the blood stream, namely serotonin
109
What causes carcinoid syndrome?
most commonly arise from the gut followed by lungs, liver, ovaries and thymus
110
What is the pathophysiology of carcinoid syndrome?
neuroendocrine tumours secrete serotonin in to bloodstream
Gi tumours secrete hormones which are inactivated by the liver (enterohepatic system) unless there are liver metastases which cause liver dysfunction
111
What are the key presentations of carcinoid syndrome?
diarrhoea, flushing, wheeze, abdominal cramps/masses
112
gold standard investigations for carcinoid syndrome
high 5-hydroxyindoleacetic acid (breakdown product of serotonin, will be high)
liver ultrasound ( will show metastasis)
113
Management of localised carcinoid syndrome
1st line - surgical recision
AND perioperative octreotide infusion
114
Management of metastatic carcinoid syndrome
1st line - surgical recision AND perioperative octreotide infusion
adjunct - radiofrequency ablation
(somatostatin analogue or interferon alfa if not suitable for resection)
115
complications of carcinoid syndrome
carcinoid heart disease
bowel obstruction/intestinal bleeding
pellagra
carcinoid crisis
116
What is serotonin syndrome?
An excess of synaptic serotonin in the CNS
117
What are the causes of serotonin syndrome?
SSRI, SNRIS, antidepressants, opioids, lithium
118
What are the key presentations of serotonin syndrome?
Clonus
hyper-reflexia
119
Symptoms of serotonin syndrome
anxiety, agitation, confusion, tremor, sweating, seizure
120
investigations for serotonin syndrome
signs of serotonin toxicity
121
Management of severe serotonin toxicity
Cessation of medications
adjuncts
- activated charcoal
- chlorpromazine
122
Management of serotonin syndrome with rhabdomyolysis
cessation of medications
adjuncts
- activated charcoal
- chlorpromazine
AND
muscle paralysis and cooling
123
What serum Na+ level constitutes hyponatraemia?
<135mmol/L
124
What is a severely low Na+ serum level?
<125mmol/L
125
What are the causes of hypovolaemic hyponatraemia?
volume depletion - third spacing of fluids (interstitial)
126
What are the causes of euvolemic hyponatraemia?
- hypothyroidism
- adrenal insufficiency
- polydipsia or potomania
- medications
127
What are the causes of hypervolemic hyponatraemia?
decreased arterial volume
- congestive heart failure
- cirrhosis
- nephrotic syndrome
128
key presentations of hyponatraemia?
anorexia, nausea, lethargy
129
symptoms of hyponatraemia?
headache, irritability, confusion, seizures, decreased GCS
130
Management of asymptomatic chronic hyponatraemia
fluid restriction or demeclocycline (ADH antagonist)
131
Management of acute or symptomatic hyponatraemia
cautious rehydration w/ 0.9% saline (do not correct rapidly -> central pontine myelinolysis)
consider using furosemide when not hypovolaemic to avoid fluid overload
132
What medication is used to treat hyponatraemia to promote water excretion?
Vasopressor receptor antagonists (vaptans) e.g. tolvaptan, effective in treating hyper and euvolemic
133
In emergency, what should be given to a hyponatraemic patient
hypertonic saline (1.8%) at 70mmol Na+/hr
134
What are the complications of hyponatraemia?
cerebral oedema, osteoporosis, osmotic demyelination syndrome, increased risk of falls
135
What serum Na+ concentration is considered hypernatraemic?
>145 mmol/L
136
What serum Na+ concentration is considered severe hypernatraemia
>160mmol/L
137
What are the 3 causes of hypernatraemia?
free water loss, pure free water intake deficit, sodium overload
138
Give an example of free water loss hypernatraemia
renal concentrating defect, osmotic diuresis, diabetes insipidus
139
give an example of sodium overload hypernatraemia
mineralcorticoid excess, ingestion of too much salt, administration of hypertonic fluids
140
key presentations of hypernatraemia
lethargy, thirst, weakness
141
symptoms of hypernatraemia
mood changes, coma/fits, decreased JVP
142
Management of hypernatraemia
oral rehydration, IV glucose 5% 1L/hr
if hypovolaemic - use 0.9% saline
143
complications of hypernatraemia
treatment related brain oedema
low chance of:
- myelinolysis
- rhabdomyolysis
- cardiac toxicity
- metabolic effects
144
What is the difference between primary and secondary hypothyroidism?
secondary results from pituitary failure, primary is a due to thyroid dysfunction
145
What is the most common form of hypothyroidism in the developed world?
hashimotos thyroiditis
146
What antibodies is hashimoto's thyroiditis associated with?
antithyroid peroxidase (anti-TPO)
and antithyroglobulin antibodies
147
other than autoimmune, what are the other causes of hyothyroidism?
iodine deficeincy
hyperthyroid meds/treatment (carbimazole etc)
148
What medications can cause hypothyroidism?
lithium, amiodarone
149
What are some secondary causes of hypothyroidism?
tumours
150
What is the gold standard investigation for hashimoto's hypothyroidism?
antithryoid peroxidase antibodies positive
151
How does hypothyroidism present?
weight gain, lethargy, dry skin, coarse hair/hair loss (lateral aspect of eyebrow), menorrhagia, constipation
152
How does Graves cause hyperthyroidism?
circulating IgG antibodies target G coupled TSH receptors causing hypertrophy and hyperplasia of the thryoid gland
153
What do thyroid hormones effect?
metabolic rate, thermogenesis, HR, cardiac contractility, CO, vasodilation
154
What are the key presentations of hyperthyroidism
unintentional weight loss, heat intolerance, tremor, palpitations, diffuse goitre
Graves - exophthalmos and pretibial myxedema
155
What are the symptoms of hyperthyroidism?
diarrhoea, menstrual irregularity, alopecia, fatigue, sexual dysfunction, hyperphagia (excessive appetite)
156
What are the first line Investigations for hyperthyroidism?
TFTs
elevated T3/4, low TSH in primary, high in secondary
157
What is the 1st line management of hyperthyroidism?
anti-thyroid drugs carbimazole (propylthiouracil, 2nd line) PLUS beta blockers
158
What medication is used to treat thyrotoxic symptoms in hyperthyroidism?
propranolol
159
What is used to treat de quervains hyperthryoidism?
NSAIDS
160
Other managements for hyperthyroidism
radioactive iodine therapy
surgery to remove nodules/thyroid
anticoag if in AF
161
complications of hyperthyroidism
hypothyroidsim (iatrogenic)
thyroid storm
HF
angina
osteoporosis
162
What type of antibodies attack the thyroid in Graves disease?
IgG autoantibodies attack thyrotropin (TSH) receptor
163
What are the key presentations of Graves disease?
exophthalmos, pretibial myxoedema, thyroid acropachy
164
What is thyroid acropachy?
a triad of clubbing, soft tissue swelling of hands and feet and periosteal new bone formation
165
What is de quervains thyroiditis?
inflammation of the thyroid gland resulting in pain and discomfort
166
What are the key presentations of de quervains thyroiditis?
neck pain, thyroid enlargement, fever, palpitations
167
What with TFTs and CRP show in de quervains thryoiditis?
T3/4 and CRP will be raised
168
What is the management for de quervains thyroiditis in the hyperthyroid stage?
NSAIDs or corticosteroids
169
What is a thyroid storm?
the severe end of thryotoxicosis, a
170
What are the key presentations of a thyroid storm?
agitation, confusion, coma
171
What are the symptoms of thyroid storm?
diarrhoea, goitre, acute abdomen (abdominal pain)
172
Investigation for thyroid storm?
TFTs, high T3/4, low TSH primary, high in secondary
173
What is the first line management for thyroid storm?
carbimazole - antithyroid treatment
174
Why is hydrocortisone given in a thryoid storm?
it treats relative adrenal insufficiency and prevents conversion of T4 to T3
175
what other treatments may be given in a thyroid storm?
supportive care, fluid resus, anti-arrhythmetics, beta blockers
176
What are the complications of thyroid storm
thromboembolism, coma, heart failure, arryhthmia, death
177
What is the prognosis of thyroid storm?
75% mortality without treatment
178
What is the relationship between thyroid hormone levels and cholesterol and triglyceride levels?
They are inversely proportional
179
What are the symptoms of hypothyroidism?
weight gain
coarse hair/hair loss
goitre
eyelid oedema
180
What are the investigations for hypothyroidism?
TFTs low T3/4, high TSH in primary, low in secondary
181
How do you manage hypothyroidism?
1st line levothyroxine (T4)
if over 65 with CAD -> low dose levothyroxine
182
What are the 4 types of thyroid cancer?
papillary, follicular, anaplastic and medullary
183
What do medullary thyroid cancers secrete? this can be tested in the blood to screen for recurrence
calcitonin
184
What are the investigations for thyroid cancer?
TFTs, fine needle biopsy
185
How do you treat a papillary or follicular thyroid cancer?
surgery + radioactive iodine ablation + TSH suppression
if recurrent/metastatic - chemo - sorafenib/lenvatinib
186
How do you treat medullary thyroid cancer?
1st line - surgery + thyroid replacement
2nd line - vandentanib + thyroid replacement
187
how do you treat anaplastic thyroid cancer?
palliative surgery + chemoradiation + thyroid replacement
188
How do you treat lymphoma (thyroid cancer)?
chemo, external radiation - TSH suppression
(TSH suppression bc thyroid needs TSH to grow)
189
Which of the thyroid cancers has the best prognosis
papillary>follicular>medullary>lymphoma>anaplastic
190
What is the most common cause of acromegaly?
pituitary somatotroph adenoma ( benign anterior pituitary adenoma)
191
What are the effects of growth hormone?
lipolysis
gluconeogenesis
glycogenolysis
decreased peripheral glucose uptake
protein synthesis
osteoblast stimulation
cell resistance to insulin increases
192
What are the Symptoms of acromegaly?
excessive sweating
headache
tiredness
weight gains
deep voice
amenorrhea
change in appearance
193
How can acromegaly effect vision?
pituitary adenoma -> bitemporal hemianopia
194
What inhibits the release of GH?
somatostatin, high glucose levels and dopamine
195
What are the investigations for acromegaly?
insulin like growth factor-1 (IGF-1) blood test
OGTT- GH nadir >1microgram/L
196
Why is the OGTT used to diagnose acromegaly?
glucose should inhibits GH production but does not in acromegaly
197
what is the 1st line treatment for acromegaly
transsphenoidal surgery
198
what is the 2nd line treatment for acromegaly?
2nd line - octreotide (somatostatin analogue)
199
What is the third line treatment for acromegaly?
GH receptor antagonist - pegvisomant OR
dopamine agonists - bromocriptine
200
What are the complications of acromegaly?
carpal tunnel syndrome
T2DM
sleep apnea
hypertension
cardiac complications
201
what are prolactinomas?
benign lactotroph adenomas (pituitary) expressing and secreting prolactin
202
What does prolactin do?
it causes breasts to grow and make milk during pregnancy
203
Risk factors for prolactinoma?
female
20-50yrs old
FH
oestrogen therapy
204
What is the pathophysiology of prolactinomas?
hypersecretion of prolactin -> secondary hypogonadism (breast milk production)
dopamine has -ve feedback on prolactin, disruption of transport/ secretion = hyerprolactinaemia
205
key presentations of prolactinomas?
women present with amenorrhea and galactorrhea
men present with sexual dysfunction, hypogonadism and gynaecomastia
206
What are the investigations for preolactinomas?
serum prolactin - 1st line
MRI of pituitary - 2nd line
207
What is the 1st line of management for prolactinomas?
dopamine agonists - bromocriptine/cabergoline
208
What are the other treatments for prolactinomas?
2nd line - hormone therapy
3rd line surgery (medical treatments more effeicient)
209
What are the complications of prolactinomas?
infertility, sight loss, anterior pituitary failure
210
What is SIADH?
euvolemic, hypotonic, hyponatraemia - impaired water excretion due to ADH release
211
What can cause SIADH?
many causes:
drugs- SSRIs amiodarone, NSAIDs
malignancy - lung
head injury
infection
212
what is the pathophysiology of SIADH?
more ADH means more water retention, diluting electrolytes
213
What are the key presentations of SIADH?
Mainly due to hyponatraemia:
headache
lethargy
muscle cramps
weakness
confusion
214
What are the investigations for SIADH?
U&Es (low Na+), serum osmolality (low)
high urine osmolality and Na+
215
How do you manage SIADH?
fluid restriction, 500mls-1L
vasopressor receptor antagonist - tolvaptan
216
How do you manage severe SIADH?
IV hypertonic saline + fluid restriction + vasopressin receptor antagonist
+
furosemide
217
What can happen as a result of rapid treatment of hyponatraemia?
central pontine myelinolysis
218
What are the complications of SIADH?
cerebral oedema, seizure, coma, death, central pontine myelinolysis
219
What is diabetes insipidus?
a disease characterised by decreased secretion of ADH (cranial) from posterior pituitary or an insensitivity to ADH (nephrogenic)
220
What are the two causes of diabetes inspidus?
cranial, nephrogenic
221
give examples of cranial causes of diabetes insipidus
idiopathic -50%
tumour
trauma
haemorrhage
222
give an example of a nephrogenic cause of diabetes insipidus
hereditary
drugs- lithium, demeclocycline
chronic renal disease
223
What is the pathophysiology of cranial diabetes insipidus
lack of ADH secretion post pituitary
reduced water reabsorption
high serum osmolality
224
What is the pathophysiology of nephrogenic diabetes insipidus?
resistance to action of ADH
225
What are the key presentations of diabetes inspidus?
polyuria
polydipsia
226
What are the symptoms of diabetes insipidus?
nocturia, dry mucosa, sunken eyes, changes to skin turgor
227
What are the gold standard investigations for diabetes insipidus?
water deprivation test, urine osmolality tested before and after synthetic ADH (desmopressin) given
228
What is the difference in urine osmolality between cranial and nephrogenic DI in the water deprivation test?
urine osmolality remain lows in nephrogenic
urine osmolality will rise after desmopressin given in cranial (kidneys still respond to ADH)
229
What is the treatment for cranial DI?
desmopressin
230
What is the treatment for nephrogenic DI?
thiazide diuretics e.g bendroflumethiazide
231
What can cause hypocalcaemia?
hypoparathyroidism
vit D deficiency
drugs
malignancy
232
What is calcium used for in the body?
neurotransmission and muscle contraction, bone mineralisation, regulator of ion transport and membrane integrity
233
What are the key presentations of hypocalcaemia?
CATs go numb
convulsions
arrhythmias
tetany
numbness in hands and feet
234
What are the investigations of hypocalcaemia?
- bone profile
- corrected calcium
- ECG - prolonged QT
- parathyroid function
235
What is the management of hypocalcaemia?
10ml calcium gluconate/chloride 10% slow IV
oral calcium
vit D
236
What are the complications of hypocalcaemia?
seizure, cardiac arrest, convulsions, osteoporosis
237
How can you treat acute hypocalcaemia?
IV calcium gluconate, 10%, 10ml, 10 mins
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How can you treat persistent hypocalcaemia?
vit D 50000 IU orally once a week for 8 weeks
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What can cause hypercalcaemia?
hyperparathyroidism, malignancy, sarcoidosis
240
What are the key presentations for hypercalcaemia?
kidney stones, psychic groans (confusion), abdominal moans (constipation, acute pancreatitis)
241
What is the gold standard investigation for hypercalcaemia?
PTH, bone profile
elevated PTH, high calcium, low/normal phosphates
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What are the main managements of hypercalcaemia?
rehydration with 0.9% saline, bisphosphonates, sometimes use loop diuretics e.g. furosemide
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What are the complications of hypercalcaemia?
pancreatitis, confusion, coma, death
244
What is the most common cause of primary hyperparathyroidism?
parathyroid adenomas
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What else can cause primary hyperparathyroidism?
hyperplasia
congenital
lithium therapy
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What causes secondary hyperparathyroidism?
insufficient vit D or chronic renal failure resulting in low serum calcium
247
What causes tertiary hyperparathyroidism?
occurs after prolonged secondary hyperparathyroidism, parathyroid becomes autonomous and secreted PTH without stimulation
248
What is the pathophysiology of hyperparathyroidism?
PTH increase->increased renal Ca absorption, phosphate excretion, renal vit D synthesis, calcium intestinal absorption and bone remodelling
249
What are the key presentations of hyperparathyroidism?
bones (osteoporosis)
kidney stones
psychic groans - fatigue/depression
abdominal moans - nausea/constipation
250
What are the best investigations for hyperparathyroidism?
PTH/bone profile - high PTH, high calcium - low phosphates (depending on type of hyperparathyroidism)
251
What is the treatment for primary hyperparathryoidism?
parathyroidectomy
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What is the treatment for secondary hyperparathyroidism?
vit D supplements or renal transplant in CKD
253
What is the treatment for tertiary hyperparathyroidism?
surgical removal of part of the parathyroid to bring PTH to the right level
254
What is cinacalet and what does it do?
its a calcimimetic, it increases the sensitivity of parathyroid to calcium causing less PTH secretion
255
What are the key presentations of secondary/tertiary hyperparathyroidism?
CATs go numb
convulsions, arrhythmias, tetany and numbness in the hands and feet and around mouth
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What are the key presentations of hypoparathyroidism?
CATs go numb
convulsions, arrhythmias, tetany and numbness of extremities
257
What is the gold standard investigation for hypoparathyroidism?
bone profile- low calcium, high phosphate, low PTH
258
How do you manage hypoparathyroidism?
IV calcium and Vit D
magnesium supplement (if hypomagnesemic)
Ca supplements and calcitriol
259
What are the side effects of SGLT-2 inhibs?
UTIs and weight loss
260
What with TFTs and CRP show in de quervains thryoiditis?
T3/4 and CRP will be raised
261
What with TFTs and CRP show in de quervains thryoiditis?
T3/4 and CRP will be raised
262
What with TFTs and CRP show in de quervains thryoiditis?
T3/4 and CRP will be raised
263
What with TFTs and CRP show in de quervains thryoiditis?
T3/4 and CRP will be raised
264
What with TFTs and CRP show in de quervains thryoiditis?
T3/4 and CRP will be raised
265
What with TFTs and CRP show in de quervains thryoiditis?
T3/4 and CRP will be raised
266
What with TFTs and CRP show in de quervains thryoiditis?
T3/4 and CRP will be raised
267
What with TFTs and CRP show in de quervains thryoiditis?
T3/4 and CRP will be raised
268
Why is hydrocortisone given in a thryoid storm?
it treats relative adrenal insufficiency and prevents conversion of T4 to T3
269
How can you treat persistent hypocalcaemia?
vit D 50000 IU orally once a week for 8 weeks
