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Endo Flashcards

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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

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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)
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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

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4
Q

Thyroid function tests

TSH: low
T3+4: high

A

hyperthyroidism

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5
Q

Thyroid function tests

TSH: high
T3+4: low

A

hypothyroidism

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6
Q

Thyroid function tests

TSH: low
T3+4: low

A

secondary hypothyroidism (a pituitary or hypothalamic cause)

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7
Q

Thyroid function tests

TSH: high
T3+4: high

A

pituitary adenoma (secretes TSH)

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8
Q

Thyroid function tests

what antibodies are present in Grave’s disease

A

anti TPO

antithyroglobulin

TSH receptor

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9
Q

Thyroid function tests

what antibodies are present in Hashimoto’s Thyroiditis

A

anti TPO

antithyroglobulin

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10
Q

Thyroid function tests

what antibodies are present in thyroid cancer

A

antithyroglobulin

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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

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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

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13
Q

Type 2 Diabetes

non-modifiable RFs

A
  • older age
  • ethnicity (black, chinese, s.asian)
  • FH
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14
Q

Type 2 Diabetes

modifiable RFs

A
  • obesity
  • sedentary lifestyle
  • high carb diet (esp refined carbs)
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15
Q

Type 2 Diabetes

test to screen for diabetes

A

HbA1C

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16
Q

Type 2 Diabetes

symptoms

A
  • fatigue
  • polydipsia + polyuria
  • unintentional weight loss
  • opportunistic infections
  • slow healing
  • glucose in urine (on dipstick)
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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

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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
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19
Q

Type 2 Diabetes

diabetes dx

A

any 1 of:

  • HbA1c >48
  • Random glucose >11
    Fasting glucose >7
  • OGTT >11
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20
Q

Type 2 Diabetes

mnx (diet)

A
  • veg + oily fish
  • low glycaemic, high fibre diet
  • low carb diet
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21
Q

Type 2 Diabetes

mnx (RFs)

A
  • exercise + weight loss
  • stop smoking
  • optimise trx for other illnesses: HTN, hyperlipidaemia, CVD
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22
Q

Type 2 Diabetes

what complications to monitor

A
  • diabetic retinopathy
  • kidney disease
  • diabetic foot
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23
Q

Type 2 Diabetes

what are the HbA1c targets for someone with new T2DM

A

48mmol/mol

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24
Q

Type 2 Diabetes

what are the HbA1c targets for diabetics that have moved beyond metformin alone

A

53 mmol/mol

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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
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