Endo Flashcards
1
Q
diabetes
what is Maturity onset diabetes of the young (MODY)
A
A group of inherited genetic disorders affecting the production of insulin.
Results in younger patients developing symptoms similar to those with T2DM, i.e. asymptomatic hyperglycaemia with progression to more severe complications such as diabetic ketoacidosis
2
Q
diabetes
which antibodies are present in T1DM
A
- anti-glutamic acid decarboxylase (anti-GAD) (80%)
- Islet cell antibodies (ICA) 70-80%
- Insulin autoantibodies (IAA): correlates strongly with age, found in >90% of young children with T1DM but only 60% of older patients
- Insulinoma-associated-2 autoantibodies (IA-2A)
3
Q
diabetes
what is Latent autoimmune diabetes of adults (LADA)
A
often misdiagnosed as having T2DM because they develop autoimmune diabetes later on in life
4
Q
Thyroid function tests
TSH: low
T3+4: high
A
hyperthyroidism
5
Q
Thyroid function tests
TSH: high
T3+4: low
A
hypothyroidism
6
Q
Thyroid function tests
TSH: low
T3+4: low
A
secondary hypothyroidism (a pituitary or hypothalamic cause)
7
Q
Thyroid function tests
TSH: high
T3+4: high
A
pituitary adenoma (secretes TSH)
8
Q
Thyroid function tests
what antibodies are present in Grave’s disease
A
anti TPO
antithyroglobulin
TSH receptor
9
Q
Thyroid function tests
what antibodies are present in Hashimoto’s Thyroiditis
A
anti TPO
antithyroglobulin
10
Q
Thyroid function tests
what antibodies are present in thyroid cancer
A
antithyroglobulin
11
Q
why should you stop taking metformin before a CT scan
A
the dye/contrast and metformin is filtered out of your blood the kidneys
in an attempt not to overload your kidneys, do not take metformin whilst body is working to eliminate the dye from body (approx 48h).
Taking both could cause metformin to build up in body
could lead to lactic acidosis in pts with decreased kidney function
12
Q
Type 2 Diabetes
pathophysiology
A
repeated exposure to glucose + insulin makes the cells in the body become resistant to the effects of insulin
13
Q
Type 2 Diabetes
non-modifiable RFs
A
- older age
- ethnicity (black, chinese, s.asian)
- FH
14
Q
Type 2 Diabetes
modifiable RFs
A
- obesity
- sedentary lifestyle
- high carb diet (esp refined carbs)
15
Q
Type 2 Diabetes
test to screen for diabetes
A
HbA1C
16
Q
Type 2 Diabetes
symptoms
A
- fatigue
- polydipsia + polyuria
- unintentional weight loss
- opportunistic infections
- slow healing
- glucose in urine (on dipstick)
17
Q
Type 2 Diabetes
what does the OGTT involve
A
fasting plasma glucose result
give 75g glucose drink
measure plasma glucose 2hrs later
tests the ability of the body to cope with a carb meal
18
Q
Type 2 Diabetes
pre-diabetes diagnosis
A
any 1 of:
- HbA1c: 42-47
- impaired fasting glucose: 6.1 - 6.9 mmol/l
- impaired glucose tolerance: OGTT 7.8 - 11.1 mmol/l
19
Q
Type 2 Diabetes
diabetes dx
A
any 1 of:
- HbA1c >48
- Random glucose >11
Fasting glucose >7 - OGTT >11
20
Q
Type 2 Diabetes
mnx (diet)
A
- veg + oily fish
- low glycaemic, high fibre diet
- low carb diet
21
Q
Type 2 Diabetes
mnx (RFs)
A
- exercise + weight loss
- stop smoking
- optimise trx for other illnesses: HTN, hyperlipidaemia, CVD
22
Q
Type 2 Diabetes
what complications to monitor
A
- diabetic retinopathy
- kidney disease
- diabetic foot
23
Q
Type 2 Diabetes
what are the HbA1c targets for someone with new T2DM
A
48mmol/mol
24
Q
Type 2 Diabetes
what are the HbA1c targets for diabetics that have moved beyond metformin alone
A
53 mmol/mol
25
Type 2 Diabetes
1st line medical mnx
metformin
titrated from initially 500mg OD as tolerated
26
Type 2 Diabetes
2nd line medical mnx
add either of:
- sulfonylurea
- pioglitazone
- DPP-4 inhibitor
- SGLT-2 inhibitor
27
Type 2 Diabetes
3rd line medical mnx
triple therapy: metformin + 2 of:
- sulfonylurea
- pioglitazone
- DPP-4 inhibitor
- SGLT-2 inhibitor
or metformin + insulin
28
Type 2 Diabetes
which 2nd line medication is preferred in patients with CVD
SGLT-2 inhibitors
| GLP-1 mimetics (e.g. liraglutide)
29
Type 2 Diabetes
what is metformin
a biguanide
it increases insulin sensitivity
+ decreases liver production of glucose
weight neutral: doesn't increase or decrease body weight
30
Type 2 Diabetes
SEs of metformin
- lactic acidosis
| - diarrhoea + abdo pain
31
Type 2 Diabetes
advantages of metformin
does NOT typically cause hypoglycaemia
weight neutral
32
Type 2 Diabetes
name a sulfonylurea
gliclazide
33
Type 2 Diabetes
how do sulfonylureas work
they stimulate insulin release from the pancreas
34
Type 2 Diabetes
SEs of sulfonylureas
- increased risk of CVD + MI when used as monotherapy
- weight gain
- hypoglycaemia
35
Type 2 Diabetes
how do Pioglitazones work
it's a thiazolidinedione
it increases insulin sensitivity
and decreases liver production of glucose
36
Type 2 Diabetes
SE's of Pioglitazone (5)
- weight gain
- fluid retention
- anaemia
- HF
- extended use may increase risk of bladder cancer
37
Type 2 Diabetes
advantage of Pioglitazone
doe NOT typically cause hypoglycaemia
38
Type 2 Diabetes
what are incretins
hormones produced by the GI tract
they're secreted in response to large meals and act to reduce blood sugar
39
Type 2 Diabetes
what 3 things do incretins do
1. increase insulin secretions
2. inhibit glucagon production
3. slow absorption by the GI tract
40
Type 2 Diabetes
name the main incretin
glucagon-like peptide-1 (GLP-1)
41
Type 2 Diabetes
what enzyme inhibits incretins
dipeptidyl peptidase-4 (DDP-4)
42
Type 2 Diabetes
name the most common DPP-4 inhibitor
sitagliptin
43
Type 2 Diabetes
how do DPP-4 inhibitors work
they inhibit the DPP-4 enzyme
therefore increasing GLP-1 activity
44
Type 2 Diabetes
SE's of DPP-4 inhibitors
- GI tract upset
- sx of URTI
- pancreatitis
45
Type 2 Diabetes
what are GLP-1 mimetics
they mimic the action of GLP-1
46
Type 2 Diabetes
name a common GLP-1 mimetic and how is it given
Exenatide
SC BD by pt or once weekly in a modifiable release form
47
Type 2 Diabetes
name another GLP-1 mimetic other than Exenatide and how is it given
Liraglutide
OD SC
48
Type 2 Diabetes
in overweight patients, what medications may be given
GLP-1 mimetic + metformin + sulfonylurea
49
Type 2 Diabetes
SE's of GLP-1 mimetics
- GI tract upset
- weight loss
- dizziness
- low risk of hypoglycaemia
50
Type 2 Diabetes
name some SGLT-2 inhibitors
____gliflozin
- empagliflozin
- canagliflozin
- dapagliflozin
51
Type 2 Diabetes
how do SGLT-2 inhibitors work
SGLT-2 protein: reabsorbs glucose from urine into the blood in the proximal tubules of the kidneys
SGLT-2 inhibitors block the action of this protein and cause glucose to be excreted in the urine
52
Type 2 Diabetes
which SGLT-2 inhibitor has been shown to reduce the risk of CVD, HF hospitalisation and mortality
Empagliflozin
53
Type 2 Diabetes
which SGLT-2 inhibitor has been shown to reduce the risk of CV events such as MI, stroke and death and HF hospitalisation
Canagliflozin
54
Type 2 Diabetes
SE's of SGLT-2 inhibitors
- Glucoseuria (glucose in urine)
- diabetic ketoacidosis
- UTIs
- weight loss
55
Type 2 Diabetes
which SE appears to be more common in pts on canagliflozin
lower limb amputation
56
Type 2 Diabetes
how long do rapid-acting insulins work for
10min - 4h
57
Type 2 Diabetes
name 3 rapid acting insulins
- Novorapid
- Humalog
- Apidra
58
Type 2 Diabetes
how long do short-acting insulins work
30min - 8h
59
Type 2 Diabetes
name 3 short-acting insulins
- Actrapid
- Humulin S
- Insuman Rapid
60
Type 2 Diabetes
how long do intermediate-acting insulins work
1h - 16h
61
Type 2 Diabetes
name 3 intermediate-acting insulins
- Insulatard
- Humulin I
- Insuman Basal
62
Type 2 Diabetes
how long do long-acting insulins work for
1h - 24h
63
Type 2 Diabetes
name 3 long-acting insulins
- Lantus
- Levemir
- Degludec ( lasts >40h)
64
Type 2 Diabetes
what do combination insulins contain
a rapid acting and an intermediate acting insulin
65
Type 2 Diabetes
name 3 combinations insulins
In brackets is the proportion of rapid to intermediate acting insulin:
```
Humalog 25 (25:75)
Humalog 50 (50:50)
Novomix 30 (30:70)
```
66
Adrenal Insufficiency
what is it
adrenal glands doesn't produce enough cortisol and aldosterone
67
Adrenal Insufficiency
what is Addison's disease
aka Primary Adrenal Insufficiency
specific condition where the adrenal glands have been damaged, resulting in a reduction in the secretion of cortisol and aldosterone
68
Adrenal Insufficiency
what is the most common cause of Addison's disease
autoimmune
69
Adrenal Insufficiency
what is secondary adrenal insufficiency
loss or damage to the pituitary gland
inadequate ACTH stimulating the adrenal glands
low cortisol release
70
Adrenal Insufficiency
causes of secondary adrenal insufficiency
- surgery to remove pituitary tumour
- infection
- loss of blood flow
- radiotherapy
- Sheehan's syndrome
71
Adrenal Insufficiency
how does Sheehan's syndrome cause secondary adrenal insufficiency
massive blood loss during childbirth leads to pituitary gland necrosis
72
Adrenal Insufficiency
what is tertiary adrenal insufficiency
long term PO steroids causes suppression of the hypothalamus
inadequate CRH release
73
Adrenal Insufficiency
why should long term steroids be tapered down slowly
to allow time for the adrenal axis to regain normal function
to avoid tertiary adrenal insufficiency
74
Adrenal Insufficiency
sx (5)
- fatigue
- nausea
- cramps
- abdo pain
- reduced libido
75
Adrenal Insufficiency
signs (2)
- bronze hyperpigmentation to skin
| - hypotension (esp postural)
76
Adrenal Insufficiency
why is there bronze hyperpigmentation
ACTH stimulates melanocytes to produce melanin
77
Adrenal Insufficiency
what is the key biochemical clue
hyponatraemia
hyperkalaemia is also possible
78
Adrenal Insufficiency
test of choice for dx
short synacthen test
79
Adrenal Insufficiency
ACTH level in primary adrenal failure and why
high
pituitary is trying to stimulate adrenal glands without any negative feedback in the absence of cortisol
80
Adrenal Insufficiency
ACTH level in secondary adrenal failure and why
low
as the reason the adrenal glands are not producing cortisol is that they are not being stimulated by ACTH
81
Adrenal Insufficiency
which adrenal autoantibodies will be present in autoimmune adrenal insufficiency
adrenal cortex antibodies
21-hydroxylase antibodies
82
Adrenal Insufficiency
which inx if suspecting an adrenal tumour, haemorrhage or other structural pathology
CT / MRI adrenals
83
Adrenal Insufficiency
which inx if suspecting pituitary pathology
MRI pituitary
84
Adrenal Insufficiency
what does the short synacthen test involve
measure baseline cortisol
give synacthen (synthetic ACTH)
measure cortisol 30 + 60 min after
85
Adrenal Insufficiency
what should the cortisol level do in a healthy individual in the short synacthen test
at least double
86
Adrenal Insufficiency
what level cortisol in the short synacthen test indicates Addison's
less than double the baseline
87
Adrenal Insufficiency
trx and why
hydrocortisone (glucocorticoid) replaces cortisol
fludrocortisone (mineralcorticoid) replaces aldosterone
for life
88
Adrenal Insufficiency
if pt is acutely ill, how do you manage meds
doses are doubled until they have recovered to match the normal steroid response to illness
89
Adrenal Insufficiency
what are pts given to alert emergency services that they are dependent on steroids for life
steroid card and an emergency ID tag
90
Adrenal Insufficiency
what is Addisonian Crisis
aka adrenal crisis
an acute presentation of severe Addisons, where the absence of steroid hormones leads to a life threatening presentation
91
Adrenal Insufficiency
Addisonian Crisis presentation
- reduced consciousness
- hypotension
- hypoglycaemia
- hyponatraemia
- hyperkalaemia
- pt very unwell
92
Adrenal Insufficiency
what can an Addisonian Crisis be triggered by
- infection
- trauma
- acute illness
- could be their first presentation
- someone on long term steroids suddenly withdrawing those steroids
93
Adrenal Insufficiency
mnx of Addisonian Crisis
- intensive monitoring
- IV hydrocortisone 100mg stat then 100mg every 6hr
- IV fluid resus
- correct hypoglycaemia
- monitor electrolytes and fluids
94
Hyperparathyroidism
which cells produce parathyroid hormone
chief cells in the parathyroid glands
95
Hyperparathyroidism
when is parathyroid hormone released
in response to hypocalcaemia
96
Hyperparathyroidism
how does parathyroid hormone act to raise blood calcium levels
- increases osteoclast activity in bones
- increases calcium absorption from the gut
- increases calcium absorption from the kidneys
- increases Vit D activity
97
Hyperparathyroidism
how does vit D raise blood calcium levels
parathyroid hormone acts on vit D to convert it to its active form
which acts to increase Ca absorption from the intestines
98
Hyperparathyroidism
symptoms of hypercalcaemia
renal stones
painful bones
abdominal groans: constipation, N+V
psychiatric moans: fatigue, depression, psychosis
99
Hyperparathyroidism
cause of primary hyperparathyroidism
uncontrolled parathyroid hormone produced directly by a tumour of the parathyroid gland
100
Hyperparathyroidism
what are the serum calcium levels in primary hyperparathyroidism
hypercalcaemia
101
Hyperparathyroidism
trx of primary hyperparathyroidism
surgically remove tumour
102
Hyperparathyroidism
cause of secondary hyperparathyroidism
- insufficient vit D
or
- Chronic renal failure
leads to low absorption of Ca from the intestines, kidneys and bones
103
Hyperparathyroidism
what are the serum calcium levels and PTH levels in secondary hyperparathyroidism
hypocalcaemia or normal
high PTH
104
Hyperparathyroidism
pathophysiology of secondary hyperparathyroidism
parathyroid glands react to low serum Ca by excreting more PTH
105
Hyperparathyroidism
why is there hyperplasia in the parathyroid gland in secondary hyperparathyroidism
over time the total number of cells in the parathyroid gland increases as they respond to the increased need to produce parathyroid hormone
106
Hyperparathyroidism
trx of secondary hyperparathyroidism
- correct vit D deficiency
| - if in renal failure: renal transplant
107
Hyperparathyroidism
what is tertiary hyperparathyroidism
when secondary hyperparathyroidism continues for a long period of time
when the cause of the secondary hyperparathyroidism is treated the PTH level remains inappropriately high
108
Hyperparathyroidism
what is the cause of tertiary hyperparathyroidism
hyperplasia
109
Hyperparathyroidism
what are the PTH and calcium serum levels in tertiary hyperparathyroidism
high PTH
hypercalcaemia
110
Hyperparathyroidism
why is there hypercalcaemia in tertiary hyperparathyroidism
high PTH in the absence of pathology of secondary hyperparathyroidism leads to high absorption of Ca in the intestines, kidneys and bones
111
Hyperparathyroidism
trx of tertiary hyperparathyroidism
- surgery: remove part of the parathyroid tissue to return the PTH to an appropriate level
112
Hyperaldosteronism
which cells sense BP in the afferent arteriole in the kidney
juxtaglomerular cells
113
Hyperaldosteronism
what do the juxtaglomerular cells secrete in response to low BP
renin (hormone)
114
Hyperaldosteronism and Conn's Syndrome
what does the liver secrete in response to low BP
angiotensinogen
115
Hyperaldosteronism
| what converts angiotensinogen into angiotensin I
renin
116
Hyperaldosteronism
what converts angiotensin I to angiotensin II
ACE (angiotensin converting enzyme)
117
Hyperaldosteronism
where is angiotensin I converted to angiotensin II
in the lungs
118
Hyperaldosteronism
what does angiotensin II do
stimulates the release of aldosterone from the adrenal glands
119
Hyperaldosteronism
what kind of steroid is aldosterone
a mineralocorticoid
120
Hyperaldosteronism
how does aldosterone act on the kidneys
- increase Na reabsorption from the distal tubule
- increase K secretion from the distal tubule
- increase hydrogen secretion from the collecting ducts
121
Hyperaldosteronism
what is Conn's syndrome
primary hyperaldosteronism
the adrenal glands are directly responsible for producing too much aldosterone
122
Hyperaldosteronism
what levels will the serum renin be in Conn's syndrome and why
low as it is suppressed by the high blood pressure from high levels of aldosterone
123
Hyperaldosteronism
what does aldosterone do to BP
it increases it
124
Hyperaldosteronism
causes of Conn's syndrome (primary hyperaldosteronism)
- adrenal adenoma secreting aldosterone (most common)
- bilateral adrenal hyperplasia
- familial hyperaldosteronism type 1 and type 2 (rare)
- adrenal carcinoma (rare)
125
Hyperaldosteronism
what is secondary hyperaldosteronism
excessive renin stimulate the adrenal glands to produce more aldosterone
126
Hyperaldosteronism
what are the serum renin levels in secondary hyperaldosteronism
high
127
Hyperaldosteronism
secondary: when do high renin levels occur
when the BP in the kidneys is disproportionately lower than the BP in the rest of the body:
- renal artery stenosis
- renal artery obstruction
- heart failure
128
Hyperaldosteronism
secondary: which inx is used to confirm renal artery stenosis
doppler US , CT angiogram or magnetic resonance angiography (MRA)
129
Hyperaldosteronism
what is the best screening tool for someone that you suspect has hyperaldosteronism
check the renin and aldosterone levels and calculate the renin/aldosterone ratio
130
Hyperaldosteronism
what does a high aldosterone and low renin indicate
primary hyperaldosteronism
131
Hyperaldosteronism
what does a high aldosterone and high renin indicate
secondary hyperaldosteronism
132
Hyperaldosteronism
what inx relate to the effects of aldosterone
- BP (hypertension)
- serum electrolytes (hypokalaemia)
- blood gas analysis (alkalosis)
133
Hyperaldosteronism
if a high aldosterone is found, what inx nexts?
- CT/MRI to look for an adrenal tumour
| - renal doppler US, CT angiogram or magnetic resonance angiography (MRA) for renal artery stenosis or obstruction
134
Hyperaldosteronism
medical mnx
aldosterone antagonists:
- Eplerenone
- Spironolactone
135
Hyperaldosteronism
mnx to treat underlying cause
- adenoma: surgical removal
| - renal artery stenosis: percutaneous renal artery angioplasty via the femoral artery
136
what is the most common cause of secondary hypertension
hyperaldosteronism
137
pt with high BP that is not responding to trx and perhaps a low K level
what do you do
consider screening for hyperaldosteronism with a renin:aldosterone ratio
138
Syndrome of Inappropriate Anti-Diuretic Hormone
where is ADH produced
hypothalamus
139
Syndrome of Inappropriate Anti-Diuretic Hormone
where is ADH secreted
posterior pituitary gland
140
Syndrome of Inappropriate Anti-Diuretic Hormone
what is ADH aka
vasopressin
141
Syndrome of Inappropriate Anti-Diuretic Hormone
what does ADH do
stimulates water reabsorption from the collecting ducts in the kidneys
142
Syndrome of Inappropriate Anti-Diuretic Hormone
what is it
where there is inappropriately large amounts of ADH
143
Syndrome of Inappropriate Anti-Diuretic Hormone
2 general causes
- posterior pituitary producing too much ADH
| - ADH secreted from elsewhere: small cell lung cancer
144
Syndrome of Inappropriate Anti-Diuretic Hormone
what does excessive ADH result in
excessive water reabsorption in the collecting ducts
this water dilutes the Na in the blood
hyponatraemia
145
Syndrome of Inappropriate Anti-Diuretic Hormone
what kind of hyponatraemia do you get and why
euvolaemic hyponatraemia
because the excessive water reabsorption is not significant enough to cause fluid overload
146
Syndrome of Inappropriate Anti-Diuretic Hormone
what will the urine osmolality and sodium be and why
high urine osmolality
high urine sodium
the urine becomes more concentrated as less water is excreted by the kidneys
147
Syndrome of Inappropriate Anti-Diuretic Hormone
symptoms
- severe hyponatraemia: seizures, reduced consciousness
- headache
- fatigue
- muscle aches and cramps
- confusion
148
Syndrome of Inappropriate Anti-Diuretic Hormone
causes (6)
- post-op
- infection: atypical pneumonia + lung abscesses
- head injury
- medications
- malignancy: small cell lung cancer
- meningitis
149
Syndrome of Inappropriate Anti-Diuretic Hormone
what medications can cause SIADH
- thiazide diuretics
- carbamazepine
- vincristine
- cyclophosphamide
- antipsychotics
- SSRIs
- NSAIDs
150
Syndrome of Inappropriate Anti-Diuretic Hormone
how to establish diagnosis
```
diagnosis of exclusion
+
clinical exam: euvolaemia
U+E: hyponatraemia
high urine Na + osmolality
```
151
Syndrome of Inappropriate Anti-Diuretic Hormone
when establishing diagnosis, what needs to be excluded
- adrenal insufficiency: -ve short synacthen test
- no diuretic use
- no diarrhoea, vomiting, burns, fistula, XS sweat
- no XS water intake
- no CKD or AKI
152
Syndrome of Inappropriate Anti-Diuretic Hormone
mnx
- stop causative medication
- fluid restriction: 500ml-1L
- Tolvaptan (ADH receptor blocker)
- Demeclocycline (tetracycline abx)
153
Syndrome of Inappropriate Anti-Diuretic Hormone
what is Tolvaptan
an ADH receptor blocker
v. powerful, can cause a rapid increase in Na
close monitoring: 6 hourly sodium levels
154
Syndrome of Inappropriate Anti-Diuretic Hormone
what is demeclocycline
a tetracycline abx
inhibits ADH
it was used prior to vaptans and is now rarely used
155
Syndrome of Inappropriate Anti-Diuretic Hormone
what is a complication of severe hyponatraemia (<120 mmols/l) being treated too quickly (>10 mmol/l increase over 24hrs)
central pontine myelinolysis (CPM)
aka osmotic demyelination syndrome
156
Syndrome of Inappropriate Anti-Diuretic Hormone
how does the brain adapt to low blood Na
as blood Na falls, water will move across the BBB by osmosis
brain swells
brain adapts by reducing solutes in brain cells so water is balanced across the BBB. Takes a few days
157
Syndrome of Inappropriate Anti-Diuretic Hormone
why does the brain cells have a low osmolality in severe or long time hyponatraemia
as blood Na falls, water will move across the BBB by osmosis
brain swells
brain adapts by reducing solutes in brain cells so water is balanced across the BBB. Takes a few days
158
Syndrome of Inappropriate Anti-Diuretic Hormone
CPM: what happens when
the blood Na suddenly rises
water will rapidly shift out of the brain cells and into the blood causing 2 phases of sx
159
Syndrome of Inappropriate Anti-Diuretic Hormone
CPM: what are the 1st phase symptoms
encephalopathic and confused
headache, N+V
due to electrolyte imbalance
160
Syndrome of Inappropriate Anti-Diuretic Hormone
CPM: what are the 2nd phase symptoms
- spastic quadriparesis
- pseudobulbar palsy
- cognitive and behavioural changes
due to demyelination of neurones
161
Syndrome of Inappropriate Anti-Diuretic Hormone
CPM: mnx
prevention is essential as trx is only supportive
162
T2DM
whom is metformin CI'd in
those with an eGFR<30 due to lactic acidosis
use gliclazide instead
163
what recreational drug is known to deplete B12 reserves
laughing gas (NO)
164
Diabetes Insipidus
what is it
a lack of ADH or a lack of response to ADH
this prevents the kidney from being able to concentrate the urine leading the polyuria + polydipsia
165
Diabetes Insipidus
what can it be classified into
nephrogenic or cranial
166
Diabetes Insipidus
what is primary polydipsia
when the pt has a normally functioning ADH system but they are drinking excessive quantities of water leading to excessive urine production
they don't have diabetes insipidus
167
Diabetes Insipidus
what is nephrogenic diabetes insipidus
when the collecting ducts of the kidneys do not respond to ADH
168
Diabetes Insipidus
what are the causes of nephrogenic diabetes insipidus (4)
- lithium
- mutations in the AVPR2 gene on the X chromosome that codes for the ADH receptor
- intrinsic kidney disease
- electrolyte disturbance (hypokalaemia and hypercalcaemia)
169
Diabetes Insipidus
mutation in which gene can cause nephrogenic diabetes insipidus
AVPR2 gene on the X chromosome that codes for the ADH receptor
170
Diabetes Insipidus
what is cranial diabetes insipidus
when the hypothalamus does not produce ADH for the pituitary gland to secrete
171
Diabetes Insipidus
cranial causes (6)
- idiopathic
- brain tumours
- head injury
- brain malformations
- brain infections: meningitis, encephalitis, TB)
- brain surgery or radiotherapy
172
Diabetes Insipidus
presentation (5)
- polyuria
- polydipsia
- dehydration
- postural hypotension
- hypernatraemia
173
Diabetes Insipidus
what will the urine osmolality be
low
174
Diabetes Insipidus
what will the serum osmolality be
high
175
Diabetes Insipidus
what is the diagnostic inx
water deprivation test
176
Diabetes Insipidus
what is the water deprivation test aka
the desmopressin stimulation test
177
Diabetes Insipidus
describe the method for the water deprivation test
- fluid deprivation for 8h
- measure urine osmolality
- administer desmopressin (synth ADH)
- measure urine osmolality 8h later
178
Diabetes Insipidus
what are the results of urine osmolality in cranial DI after fluid deprivation
low
179
Diabetes Insipidus
what are the results of urine osmolality in cranial DI after desmopressin (ADH)?
high
180
Diabetes Insipidus
what are the results of urine osmolality in nephrogenic DI after fluid deprivation
low
181
Diabetes Insipidus
what are the results of urine osmolality in nephrogenic DI after desmopressin (ADH)?
low
182
Diabetes Insipidus
what are the results of urine osmolality in primary polydipsia after fluid deprivation
high
183
Diabetes Insipidus
what are the results of urine osmolality in primary polydipsia after desmopressin (ADH)?
high
184
Diabetes Insipidus
mnx in mild cases
- treat underlying cause
| - manage conservatively
185
Diabetes Insipidus
mnx in cranial DI
desmopressin (synthetic ADH)
186
Diabetes Insipidus
mnx in nephrogenic DI
desmopressin in higher doses (under close monitoring)
187
Phaeochromocytoma
where is adrenaline produced
by the chromaffin cells in the adrenal medulla of the adrenal glands
188
Phaeochromocytoma
what is it
a tumour of the chromaffin cells that secretes unregulated and excessive amounts of adrenaline
189
Phaeochromocytoma
what is adrenaline
a catecholamine hormone and neurotransmitter that stimulates the sympathetic nervous system and responsible for the fight or flight response
190
Phaeochromocytoma
why are there periods of worse symptoms followed by more settled periods
adrenaline tends to be secreted in bursts
191
Phaeochromocytoma
25% are familial and associated with what?
multiple endocrine neoplasia type 2 (MEN2)
192
Phaeochromocytoma
what is the 10% rule to describe the patterns of tumour
10% bilateral
10% cancerous
10% outside the adrenal gland
193
Phaeochromocytoma
inx
- 24h urine catecholamines
| - plasma free metanephrines
194
Phaeochromocytoma
why is measuring catecholamines unreliable
they naturally fluctuate and so will be difficult to interpret the result
195
Phaeochromocytoma
what is metanephrines
a breakdown product of adrenaline
196
Phaeochromocytoma
what is the half life of adrenaline
a few minutes
197
Phaeochromocytoma
why are metanephrine levels a more diagnostic tool
metanephrines have a longer half life than adrenaline so less prone to dramatic fluctuations
198
Phaeochromocytoma
presentation
- peaks and troughs
- anxiety
- sweating
- headache
- HTN
- palpitations, tachyardia + paroxysmal AF
199
Phaeochromocytoma
mnx initially
Phentolamine IV (short acting alpha blocker) - to initially control BP
Phenoxybenzamine (longer acting alpha blocker) - to control BP before surgery can be arranged
200
Phaeochromocytoma
mnx once established on alpha blockers
beta blockers
201
Phaeochromocytoma
what is the definitive mnx
adrenalectomy
202
trx of symptomatic prolactinomas
dopamine agonists (e.g. cabergoline, bromocriptine) which inhibit the release of prolactin from the pituitary gland
trans-sphenoidal surgery if medicine failed
203
Cushing Syndrome definition
the signs and sx that develop after prolonged abnormal elevation of cortisol
204
Cushing's Disease definition
the specific condition where a pituitary adenoma secretes excessive ACTH
205
Cushing syndrome presentation
- round in the middle with thin limbs
- high levels of stress hormones
- extra effects
206
Cushing syndrome presentation (round in the middle with thin limbs)
- round moon face
- central obesity
- abdominal striae
- buffalo hump
- proximal limb muscle wasting
207
Cushing syndrome presentation (high levels of stress hormone)
- HTN
- cardiac hypertrophy
- hyperglycaemia (T2DM)
- depression
- insomnia
208
Cushing syndrome presentation (extra effects)
- osteoporosis
| - easy bruising and poor skin healing
209
Cushing syndrome
causes
- exogenous steroids
- cushing's disease
- adrenal adenoma
- paraneoplastic cushing's
210
Cushing syndrome
what is paraneoplastic cushing's
excess ACTH is released from a cancer (not the pituitary) and stimulates excessive cortisol release (ectopic ACTH)
211
Cushing syndrome
what is the most common cause of paraneoplastic Cushing's
Small Cell Lung Cancer
212
Cushing syndrome
test of choice for dx
dexamethasone suppression test
213
Cushing syndrome
what can be used as an alternative to the dexamethasone suppression test to dx but not indicate underlying cause
24 hr urinary free cortisol
214
Cushing syndrome
trx
surgically remove tumour- trans-sphenoidal (pituitary adenoma)
215
Cushing syndrome
mnx if surgical removal is not possible
remove both adrenal glands and give replacement steroid hormones for life
216
Cushing syndrome
describe what happens in the dexamethasone test
give low dose dexamethasone at 10pm
measure cortisol and ACTH at 9am
then repeat but with high dose
217
Cushing syndrome
normal response to low dose dexamethasone
- suppresses CRH
- supresses ACTH
- LOW CORTISOL
218
Cushing syndrome
Result of low dose dexamethosone if pt has Cushing's syndrome
- CORTISOL REMAINS HIGH as a little bit of dexamethasone makes no difference to axis
219
Cushing syndrome
result of high dose dexamethasone if someone has cushing's disease (pituitary adenoma)
- high enough to suppress ACTH
| - LOW CORTISOL
220
Cushing syndrome
Result of high dose dexamethasone if pt has an adrenal tumour
- suppresses CRH
- suppresses ACTH
- but no effect on adrenal gland and is still pumping out cortisol
- HIGH CORTISOL
221
Cushing syndrome
Result of high dose dexamethasone on an ectopic ACTH tumour
- suppresses CRH
- but ectopic still releasing high ACTH
- so HIGH CORTISOL
222
pt had thyroidectomy, then tingling of face and hands and spasms. what is it
Iatrogenic hypocalcaemia
The parathyroids may be damaged during thyroidectomy causing post-operative hypocalcaemia
223
Hyperthyroidism
define hyperthyroidism
over-production of thyroid hormone by the thyroid gland.
224
Hyperthyroidism
define thyrotoxicosis
an abnormal and excessive quantity of thyroid hormone in the body
225
Hyperthyroidism
define primary hyperthyroidism
the thyroid itself that is behaving abnormally and producing excessive thyroid hormone
226
Hyperthyroidism
define Secondary hyperthyroidism
thyroid is producing excessive thyroid hormone as a result of overstimulation by TSH. The pathology is in the hypothalamus or pituitary.
227
Hyperthyroidism
what is Grave's disease
an autoimmune condition where TSH receptor antibodies cause a primary hyperthyroidism
228
Hyperthyroidism
Grave's: what are TSH receptor antibodies
abnormal antibodies produced by the immune system that mimic TSH and stimulate the TSH receptors on the thyroid
229
Hyperthyroidism
what is the most common cause
Grave's disease
230
Hyperthyroidism
what is Toxic multinodular goitre aka
Plummer’s disease
231
Hyperthyroidism
what is Toxic multinodular goitre
nodules develop on the thyroid gland that act independently of the normal feedback system and continuously produce excessive thyroid hormone
232
Hyperthyroidism
what is exophthalmos caused by
Grave's disease
inflammation, swelling and hypertrophy of the tissue behind the eyeball that forces the eyeball forward
233
Hyperthyroidism
what is Pretibial myxoedema
deposits of mucin under the skin on the anterior aspect of the leg (the pre-tibial area).
discoloured, waxy, oedematous appearance to the skin over this area
234
Hyperthyroidism
cause of Pretibial myxoedema
specific to Grave’s disease and is a reaction to the TSH receptor antibodies.
235
Hyperthyroidism
causes (4)
- Grave’s disease
- Toxic multinodular goitre
- Solitary toxic thyroid nodule
- Thyroiditis (e.g. De Quervain’s, Hashimoto’s, postpartum and drug-induced thyroiditis)
236
Hyperthyroidism
unique features of Grave's (all relate to presence of TSH receptor antibodies)
- Diffuse goitre (without nodules)
- Graves eye disease
- Bilateral exophthalmos
- Pretibial myxoedema
237
Hyperthyroidism
unique features of Toxic Multinodular Goitre
- Goitre with firm nodules
- Most patients are >50
- 2nd most common cause of thyrotoxicosis (after Grave’s)
238
Hyperthyroidism
mnx of
Solitary Toxic Thyroid Nodule
surgical removal of the nodule.
nodules are usually benign adenomas
239
Hyperthyroidism
presentation of De Quervain’s Thyroiditis
- viral infection with fever, neck pain and tenderness
- dysphagia
- features of hyperthyroidism
240
Hyperthyroidism
why is there a hyperthyroid phase followed by a hypothyroid phase in De Quervain’s Thyroiditis
the TSH level falls due to negative feedback
241
Hyperthyroidism
mnx of De Quervain’s Thyroiditis
supportive treatment with NSAIDs for pain and inflammation
BB for symptomatic relief of hyperthyroidism
242
Hyperthyroidism
presentation of a thyroid storm/thyrotoxic crisis
- hyperthyroidism
- pyrexia
- tachycardia
- delirium
243
Hyperthyroidism
mnx of thyroid storm
- same for thyrotoxicosis
| + fluid resus, anti-arrhythmic med + BB
244
Hyperthyroidism
1st line mnx
carbimazole
245
Hyperthyroidism
carbimazole: what is titration-block
The dose is carefully titrated to maintain normal levels
246
Hyperthyroidism
carbimazole: what is block and replace
The dose is sufficient to block all production and the patient takes levothyroxine titrated to effect
247
Hyperthyroidism
2nd line mnx
Propylthiouracil
248
Hyperthyroidism
what is the risk with Propylthiouracil
small risk of severe hepatic reactions
249
Hyperthyroidism
how does radioactive iodine work as mnx
drinking a single dose of radioactive iodine
taken up by the thyroid gland and the emitted radiation destroys a proportion of the thyroid cells.
250
Hyperthyroidism
what are the strict rules with radioactive iodine
- Must not be pregnant and are not allowed to get pregnant within 6m
- Avoid close contact with children and pregnant women for 3w
- Limit contact with anyone for several days after receiving the dose
251
Hyperthyroidism
what are BB used for
to block the adrenalin related symptoms of hyperthyroidism
esp in a thyroid storm
252
Hyperthyroidism
what is the BB of choice for mnx of sx and why
Propranolol
| it non-selectively blocks adrenergic activity as opposed to more “selective” beta blockers the work only on the heart
253
important safety info for carbimazole
- Neutropenia and agranulocytosis: signs of infection
- increased risk of congenital malformations
- risk of acute pancreatitis
254
when first starting carbimazole trx, how often should bloods be taken
every 6w
255
Once your hormone levels are stable on carbimazole, how often should bloods be taken
every 3m
256
Hypothyroidism
what is the most common cause of hypothyroidism in the developed world
Hashimoto’s Thyroiditis
257
Hypothyroidism
what autoantibodies is Hashimoto’s Thyroiditis associated with
antithyroid peroxidase (anti-TPO) antibodies
and antithyroglobulin antibodies
258
Hypothyroidism
does Hashimoto’s Thyroiditis cause a goitre
yes
259
Hypothyroidism
what is the most common cause of hypothyroidism in the developing world
iodine deficiency
260
Hypothyroidism
which foods is iodine added to to prevent iodine deficiency
table salt
261
Hypothyroidism
which treatments can cause it
All of the treatments for hyperthyroidism:
- carbimazole
- propylthiouracil
- radioactive iodine
- thyroid surgery
262
Hypothyroidism
which medications can cause it (not the hyperthyroid treatments)
lithium: inhibits the production of thyroid hormones and can cause a goitre and hypothyroidism.
amiodarone: interferes with thyroid hormone production and metabolism. Usually can cause hypothyroidism but also thyrotoxicosis
263
Hypothyroidism
what does it mean by central causes
secondary hypothyroidism
the pituitary gland is failing to produce enough TSH
hypopituitism
264
Hypothyroidism
central causes
- tumours
- infection
- vascular (Sheehan Syndrome)
- radiation
265
Hypothyroidism
presentation and features
- weight gain
- fatigue
- dry skin
- coarse hair + hair loss
- Fluid retention (oedema, pleural effusions, ascites)
- Heavy or irregular periods
- Constipation
266
Hypothyroidism
what is primary hypothyroidism caused by
thyroid gland insufficiency
267
Hypothyroidism
primary hypothyroidism TSH, T3 + T4 results
high TSH
low T3 + T4
268
Hypothyroidism
what is secondary hypothyroidism caused by
pituitary pathology
269
Hypothyroidism
secondary hypothyroidism TSH, T3 + T4 results
low TSH
low T3 +T4
270
Hypothyroidism
mnx
PO levothyroxine
271
Hypothyroidism
how does levothyroxine work
synthetic T4, and metabolises to T3 in the body.
272
Hypothyroidism
monitoring with levothyroxine
TSH levels monthly until stable, then once stable it can be checked less frequently
273
which abx can cause diabetes insipidus
Demeclocycline
274
what is Waterhouse-Friderichsen syndrome
adrenal gland failure due to bleeding into the adrenal gland
usually caused by severe meningococcal infection or other severe, bacterial infection
275
symptoms of Waterhouse-Friderichsen syndrome
acute adrenal gland insufficiency, and profound shock
276
1st line mnx for steroid induced hyperglycaemia
Gliclazide
277
Type 1 Diabetes
what is a normal blood glucose conc
4.4 - 6.1 mmol/l
278
Type 1 Diabetes
where is insulin produced
beta cells in the Islets of Langerhans in the pancreas
279
Type 1 Diabetes
how does insulin reduce blood sugar
- causes cells in the body to absorb glucose from the blood and use it as fuel
- causes muscle and liver cells to absorb glucose from the blood and store it as glycogen
280
Type 1 Diabetes
where is glucagon produced
by the alpha cells in the Islets of Langerhans in the pancreas.
281
Type 1 Diabetes
what does glucagon do
- glycogenolysis: tells the liver to break down stored glycogen into glucose.
- gluconeogenesis: tells the liver to convert proteins and fats into glucose
282
Type 1 Diabetes
when does ketogenesis occur
when there is insufficient glucose supply and glycogens stores are exhausted
283
Type 1 Diabetes
what happens in ketogenesis
The liver takes fatty acids and converts them to ketones
they can be used as fuel
284
Type 1 Diabetes
how can ketones levels be measured
in the urine by “dip-stick” and in the blood using a ketone meter
285
Type 1 Diabetes
what is it
a disease where the pancreas stops being able to produce insulin
286
Type 1 Diabetes
who does DKA occur in and why
occurs in Type 1 Diabetes
body does not have enough insulin to use and process glucose
287
Type 1 Diabetes
what are the main problems
- ketoacidosis
- dehydration
- potassium imbalance
288
Type 1 Diabetes
why is there dehydration in DKA
glucose starts being filtered into the urine.
which draws water out with it (osmotic diuresis).
patient urinates more and drinks more
289
Type 1 Diabetes
why is there hypokalaemia in DKA
- Insulin normally drives potassium into cells
- Without insulin potassium is not added to and stored in cells
- Serum potassium can be high or normal
- total body potassium is low because no potassium is stored in the cells
- when trx with insulin starts, patients can develop severe hypokalaemia
290
Type 1 Diabetes
signs of DKA
- Hyperglycaemia
- Dehydration
- Ketosis
- Metabolic acidosis (with a low bicarbonate)
- Potassium imbalance
291
Type 1 Diabetes
sx of DKA
- Polyuria, Polydipsia
- N + V
- Acetonic breath
- Dehydration --> hypotension
- Altered consciousness
- sx of underlying trigger (i.e. sepsis)
292
Type 1 Diabetes
diagnosis of DKA
1. Hyperglycaemia (BG > 11 mmol/l)
2. Ketosis (blood ketones > 3 mmol/l)
3. Acidosis (pH < 7.3)
293
Type 1 Diabetes
mnx of DKA
- IV fluid resus (1 litre stat)
- Insulin infusion (Actrapid at 0.1 Unit/kg/hour)
- potassium replacement (no more than 10mmol/hr
294
Type 1 Diabetes
how is the insulin prescribed
combination of
- background, long acting insulin OD
- short acting insulin injected 30 min before meals
295
Type 1 Diabetes
what can injecting in the same spot cause
lipodystrophy: SC fat hardens and do not absorb insulin properly
296
Type 1 Diabetes
short term complications
- hypoglycaemia
| - hyperglycaemia (and DKA)
297
Type 1 Diabetes
typical sx of hypoglycaemia
- tremor
- sweating
- irritability
- dizziness
- pallor
severe:
- reduced consciousness
- coma
- death unless treated
298
Type 1 Diabetes
why are there vascular long term complications
Chronic exposure to hyperglycaemia causes damage to the endothelial cells of blood vessels.
This leads to leaky, malfunctioning vessels that are unable to regenerate
299
Type 1 Diabetes
why are there infection related complications
High levels of sugar in the blood also causes suppression of the immune system
and provides an optimal environment for infectious organisms to thrive
300
Type 1 Diabetes
macrovascular complications
- Coronary artery disease: a major cause of death
- Peripheral ischaemia: poor healing, ulcers and “diabetic foot”
- Stroke
- Hypertension
301
Type 1 Diabetes
microvascular complications
- Peripheral neuropathy
- Retinopathy
- Kidney disease, particularly glomerulosclerosis
302
Type 1 Diabetes
infection related complications
- UTIs
- pneumonia
- skin + soft tissue infections esp in feet
- candidiasis
303
Type 1 Diabetes
what is HbA1c
glycated haemoglobin: how much glucose is attached to Hb molecule
the average glucose level over the last 3 months because red blood cells have a lifespan of around 3-4 months
304
Type 1 Diabetes
what is capillary blood glucose
used for self monitoring glucose
gives immediate result
305
Type 1 Diabetes
what is Flash Glucose Monitoring (e.g. FreeStyle Libre)
sensor on the skin that measures the glucose level of interstitial fluid
a lag of 5 minutes behind blood glucose
306
Acromegaly
what is it
the clinical manifestation of excessive growth hormone (GH)
307
Acromegaly
where is GH produced
by the anterior pituitary gland
308
Acromegaly
what is the most common cause
unregulated growth hormone secretion by a pituitary adenoma.
309
Acromegaly
what is a rare cause
cancer (lung or pancreatic) secreting ectopic growth hormone releasing hormone (GHRH) or growth hormone
310
Acromegaly
how can the presentation be separated into
- space occupying lesion
- overgrowth of tissues
- organ dysfunction
- sx suggesting active raised GH
311
Acromegaly
presentation (space occupying lesion)
- headaches
| - bitemporal hemianopia
312
Acromegaly
presentation (overgrowth of tissues)
- frontal bossing: prominent forehead and brow
- large nose, tongue, hands, feet
- large protruding jaw (prognathism)
- arthritis from imbalanced growth of joints
313
Acromegaly
presentation (organ dysfunction)
- hypertrophic heart
- HTN
- T2DM
- colorectal cancer
314
Acromegaly
presentation (sx suggesting active raised GH)
- new skin tags
| - profuse sweating
315
Acromegaly
why is a random GH level not a helpful inx
it will fluctuate, giving false positives and false negatives
316
Acromegaly
what is the initial screening test
Insulin-like Growth Factor 1 (IGF-1)
raised
317
Acromegaly
other inx (apart from IGF-1)
- OGTT whilst measuring GH (high glucose normally suppresses GH)
- MRI brain for pituitary tumour
- formal visual field testing: refer to opth
318
Acromegaly
definitive mnx of acromegaly secondary to pituitary adenoma
trans-sphenoidal surgical removal of the pituitary tumour
319
Acromegaly
what medications can block GH
- Pegvisomant (GH antagonist OD, SC)
- Somatostatin analogues to block GH release (e.g. ocreotide)
- Dopamine agonists to block GH release (e.g. bromocriptine)
320
Acromegaly
what is one of the functions of somatostatin
block GH release from the pituitary gland.
321
Acromegaly
where is somatostatin secreted
by the brain, GI tract and pancreas in response to complex triggers
322
Acromegaly
which has a more of an inhibitory effect on GH release: somatostatin or dopamine
somastostatin
323
In which part of the adrenal gland is the mineralocorticoid produced?
The zona glomerulosa produces mineralocorticoids (e.g aldosterone)
324
In which part of the adrenal gland is glucocorticoid produced?
The zona fasciculata produces glucocorticoids (e.g. cortisol)
325
what is a complication of DKA
cerebral oedema
326
when should 5% glucose be added in mnx in DKA
until blood glucose is <14 mmol/L
327
what is the first line treatment of primary hypogonadism in men.
testosterone therapy
328
is TB adrenalitis is a well recognised cause of Addison's disease
yes
329
what is a carcinoid tumour
rare, slow growing malignant tumours that develop in the neuroendocrine system
330
what hormone do 5-10% of carcinoid tumours secrete
serotonin
331
clinical features of carcinoid tumours
- Abdominal pain
- Diarrhoea
- Flushing
- Wheeze
- Pulmonary stenosis
332
mnx of carcinoid tumours
- octreotide: an analogue of Somatostatin in order to inhibit tumour products
- surgical resection
333
when to inform the DVLA and stop immediately driving if patient has hypoglycaemia
>1 severe episode of hypoglycaemia whilst awake
or 1 episode of severe hypoglycaemia whilst driving
334
what is classed as severe hypoglycaemia
an episode the patient required help from another person to manage
335
what is impaired fasting glucose
a pre-diabetic state defined as:
- Fasting glucose 6.1-7mmol/L
- 2h glucose <7.8mmol/L
336
when is metformin CI'd
if eGFR <30 ml/min
337
definition of Impaired glucose tolerance is a pre-diabetic state
Fasting glucose <7mmol/L
| 2h glucose 7.8-11mmol/L
338
why does Hypoglycaemia unawareness occur
due to a blunting of the body's autonomic and stress responses because of recurrently low blood glucose levels
339
1st line approach to hypoglycaemia unawareness
Reduce the patients insulin doses and set higher than normal blood glucose targets.
340
According to NICE guidelines, gestational diabetes mellitus is diagnosed if the woman has either:
- fasting plasma glucose level of ≥5.6 mmol/L;
or
- 2 hour post-oral glucose tolerance test plasma glucose level of ≥7.8 mmol/L.
341
what are 1st line medications for diabetic neuropathic pain
duloxetine, gabapentin, pregabalin or amitriptyline.
342
TSH normal
T4 elevated
what could this be
Subacute (De Quervain's) Thyroiditis.
starts with hyperthyroidism followed by a hypothyroid phase following depletion of TSH
343
what do medullary thyroid cancers secrete
cancer of the parafollicular cells and so secrete calcitonin
344
why is there abdo pain in DKA
theories:
- acidosis
- hyperglycaemia increasing gastric motility
- rapid expansion of the hepatic capsule
- mesenteric ischaemia due to volume depletion (secondary to dehydration)
345
what is pseudohypoparathyrodism
a rare genetic condition resulting in failure of target organs to respond to normal levels of parathyroid hormone
346
how is pseudohypoparathyroidism different to hypoparathyroidism
hypoparathyroidism: PTH deficiency
pseudo: failure to respond to PTH
347
```
15 year old
low Ca
high phosphate
high PTH
no kidney disease
blunting of the 4th and 5th knuckles
```
what could this be
Pseudohypoparathyroidism - Type 1a
348
low Ca
low phosphate
normal PTH
what could this be
Vitamin D deficiency
349
what is Psuedopseudohypoparathryoidism
the patient has the phenotypic appearance of a patient with Pseudohypoparathyroidism but has no biochemical abnormality
350
clinical presentation of hypocalcaemia
- Numbness/tingling of fingers and toes
- Muscle cramps
- Carpopedal spasm
- Seizures
- Chvostek's sign
- Trousseau's sign
351
hypocalcaemia: what is Chvostek's sign
tapping the facial nerve results in twitching of the face
352
hypocalcaemia: what is Trousseau's sign
inflation of a blood pressure cuff results in carpopedal spasm
353
what modifications would you make to someone's diabetic medication if on end of life care
- stop PO hypoglycaemic agents in T2DM
- Insulin: convert to OD long-acting, at a 25% dose reduction.
- Metformin is safe unless eGFR < 30 ml/L/1.73m2.
354
why stop PO hypoglycaemic agents in end of life care
carry a significant risk of precipitating hypoglycaemia in patients at the end of their lives, due to their reduced oral intake
355
Which type of thyroid cancer carries the worst prognosis?
Anaplastic
356
how does a thyroid lymphoma present as
- rapidly expanding mass in the neck
- hoarseness
- difficulty swallowing
- difficulty breathing
357
is Hashimoto's Thyroiditis a RF for developing thyroid lymphoma
yes
358
What is the most common type of thyroid cancer?
Papillary thyroid cancer
359
what is the gold standard test for establishing the diagnosis of insulinoma
A 72 hour fast
360
what is a by product of insulin production
serum c-peptide
361
what does a high insulin and high c-peptide indicate
excessive endogenous production of insulin
362
what does a high insulin and low c-peptide indicate
exogenous administration of insulin
363
features of MEN-1
- pituitary tumours
- parathyroid hyperplasia
- pancreatic tumours
364
features of MEN-2
- medullary thyroid cancer
- Adrenal: pheochromocytoma
- Parathyroid: hyperplasia/adenomas
365
Which of the 6 anterior pituitary hormones tends to stop first?
Go Look For The Adenoma
growth hormone -> LH -> FSH -> thyroid -> ACTH
366
The most important initial treatment for symptomatic hypercalcaemia
aggressive intravenous fluid therapy.
367
what would you expect to see in the WBC of someone with an Addisonian crisis
raised WBC esp eosinophilia
368
consequences if you start her on too high a dose of levothyroxine
1. Hyperthyroidism -->thyroid storm
2. MI, arrythmias (AF)
3. sweating, palpitations, N+V, diarrhoea, coma, psychosis
369
2 commonest causes of hypercalcaemia
Primary hyperparathyroidism
Malignancy: bony mets, myeloma
370
mnx of hypercalcaemia
- aggressive IV fluids typically 3-4 litres/day.
- Bisphosphonates
- calcitonin
- furosemide
371
ECG findings of hypokalaemia
- small/inverted T waves
- U waves
- prolonged PR interval
- ST-segment depression
372
If the patient is unwell due to their hyponatraemia (e.g. having seizures, or is comatose), how do you manage
hypertonic (3%) saline
