endocrine Flashcards

1
Q

triad for pheochromocytoma

A

headache
sweating
tachycardia

a cause of 2ndary HTN in young px

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2
Q

what are the types of thyroid cancer + how do you differentiate them

A

PAPILLARY CANCER
- most common (70%)
- 30-40yrs
- more local invasion via lymphatics
- F
- v good prog

FOLLICULAR CANCER
- second most common
- more common in areas of low iodine + in women
- 30-60
- more likely to spread to lungs + bones haematologically

MEDULLARY CANCER
- Derived from calcitonin producing C-cells -> can present with hypocalcaemia and diarrhoea secondary to raised calcitonin.
- Assoc with Multiple endocrine neoplasia (MEN) syndrome type 2A + B although 75% are sporadic.
- Often metastasis to lymph nodes
- Prognosis worse
- Disease activity can be monitored with calcitonin levels.

ANAPLASTIC CANCER
- least common
- 60-70
- aggressive, presents with rapidly growing masses. pressure sx
- invasion of the trachea, recurrent laryngeal nerve or other local structures by the time of presentation.
- poor prognosis – median survival: 8 months

THYROID LYMPHOMA
- 10% of thyroid cancers
- Non-Hodgkins
- 50-80
- Assoc with Hashimoto’s thyroiditis

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3
Q

sx of prolactinoma (benign tumour of pituitary gland)

A

excess prolactin in women:
- amenorrhoea
- infertility
- galactorrhoea
- osteoporosis

excess prolactin in men:
- impotence
- loss of libido
- galactorrhoea

other symptoms:
- headache
- visual disturbances (classically, a bitemporal hemianopia (lateral visual fields) or upper temporal quadrantanopia)
- symptoms and signs of hypopituitarism

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4
Q

prolactinoma tx

A

dopamine agonists e.g. cabergoline, bromocriptine
(inhibit release of prolactin from pituitary)

surgery

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5
Q

what is a somatroph pituitary adenoma

A

pituitary adenoma that secretes growth hormone causing sx of acromegaly

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6
Q

diagnostic marker for carcinoid syndrome

A

urinary 5-hydroxyindoleacetic acid measurements (5 HIAA)
- measured in 24 hr urine collection

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7
Q

myxoedemic coma

A

rare, life-threatening clinical condition that represents severe hypothyroidism with physiologic decompensation

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8
Q

most common causes of hypercalcaemia

A

Malignancy and primary hyperparathyroidism

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9
Q

what is subacute thyroiditis (De Quervain’s thyroiditis)? + the phases

A

temp inflam of thyroid gland

There are typically 4 phases;
phase 1 (lasts 3-6 weeks): hyperthyroidism, painful goitre, raised ESR, flue-like illness

phase 2 (1-3 weeks): euthyroid

phase 3 (weeks - months): hypothyroidism

phase 4: thyroid structure and function goes back to normal

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10
Q

what is a thyroid storm/thyrotoxic crisis + how does it present?

A

rare and more severe presentation of hyperthyroidism with high fever, tachycardia and delirium, high BP.

It can be life-threatening and requires admission for monitoring.

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11
Q

what is subclinical hyperthyroidism

A

normal T3 + 4 levels

low TSH level

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12
Q

what are the risks of subclinical hyperthyroidism

A

AF

osteoporosis

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13
Q

what is subclinical hypothyroidism

A

high TSH
normal T4

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14
Q

primary hyperthyroidism

A

thyroid behaves abnormally and produces excessive thyroid hormones.
high T3 and T4
low TSH level.

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15
Q

secondary hyperthyroidism

A

pituitary behaves abnormally and produces excessive TSH (e.g., pituitary adenoma), stimulating the thyroid gland to produce excessive thyroid hormones.

TSH, T3 and T4 will all be raised.

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16
Q

Primary hypothyroidism

A

thyroid behaves abnormally and produces inadequate thyroid hormones. Negative feedback is absent, resulting in increased production of TSH.

TSH is raised, and T3 and T4 are low.

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17
Q

Secondary hypothyroidism

A

pituitary behaves abnormally and produces inadequate TSH (e.g., after surgical removal of the pituitary), resulting in under-stimulation of the thyroid gland and insufficient thyroid hormones.

TSH, T3 and T4 will all be low.

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18
Q

causes of secondary adrenal insufficiency

A

inadequate ACTH due to loss or damage to pituitary -> lack of stim to adrenals -> low cortisol

  • tumours (pituitary adenoma)
  • surgery to pituitary
  • radiotherapy
  • sheehan’s syndrome (where major PPH -> AVN to pituitary)
  • trauma
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19
Q

causes of tertiary adrenal insufficiency

A

inadequate CRH by the hypothalamus

usually result of px taking long-term oral steroids (>3wks) causing -ve feedback
when they are withdrawn the hypothalamus cannot release the amounts needed fast enough

therefore need to be tapered down

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20
Q

cause of primary adrenal insufficency

A

addison’s

damage to adrenals - AI

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21
Q

sx of adrenal insufficiency

A

Fatigue
Muscle weakness
Muscle cramps
Dizziness and fainting
Thirst and craving salt
Weight loss
Abdominal pain
Depression
Reduced libido

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22
Q

signs of adrenal insufficiency

A

Bronze hyperpigmentation of the skin (ACTH stimulates melanocytes to produce melanin)

Hypotension (particularly postural hypotension – with a drop of more than 20 mmHg on standing)

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23
Q

biochemical findings in adrenal insufficiency

A

hyponatraemia (low Na)

maybe:
hyperkalaemia
hypoglycaemia
raised creatinine + urea due to dehydration
hypercalcaemia

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24
Q

ix for adrenal insufficiency

A

short Synacthen test (ACTH stim test)
- failure of cortisol to double after dose of synthetic ACTH = addison’s / v signif atrophy of adrenals after long time w 2ndary

ACTH is high in primary and low in secondary

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25
what autoantibodies might you see in addison's
adrenal cortex antibodies -21-hydroxylase -17 alpha hydroxylase
26
mx of adrenal insufficiency
replacement steroids - hydrocortisone (glucocorticoid) to replace cortisol - fludrocortisone (mineralcorticoid) to replace aldosterone) Give px a steroid card, ID tag + emergency letter
27
what to do in acute illness if steroid dependent
Double doses (to match normal steroid response to illness) Px + close contacts to give IM hydrocortisone in emergency if vomiting take it IM
28
presentation of adrenal crisis / Addisonian crisis
reduced conc hypotension hypoglycaemia hyponatraemia + hyperkalaemia cld be initial pres or triggered by infection, trauma, acute illness
29
mx of adrenal crisis
ABCDE IM/IV hydrocortisone (initial dose = 100mg, followed by an infusion or 6 hrly doses) IV fluids Correct hypoglycaemia (IV dextrose) monitor electrolytes + fluid balance
30
what is cushing's disease
A pituitary adenoma secreting excessive ACTH -> excessive cortisol release from adrenals
31
what is cushing's syndrome
the features of prolonged high levels of glucocorticoids in the body.
32
features of cushing's syndrome
Round face (known as a “moon face”) Central obesity Abdominal striae (stretch marks) Enlarged fat pad on the upper back (known as a “buffalo hump”) Proximal limb muscle wasting (with difficulty standing from a sitting position without using their arms) Male pattern facial hair in women (hirsutism) Easy bruising and poor skin healing Hyperpigmentation of the skin in patients with Cushing’s disease (due to high ACTH levels)
33
metabolic effects of cushing's syndrome
Hypertension Cardiac hypertrophy Type 2 diabetes Dyslipidaemia (raised cholesterol and triglycerides) Osteoporosis
34
causes of cushing's syndrome
C – Cushing’s disease (a pituitary adenoma releasing excessive ACTH) A – Adrenal adenoma (an adrenal tumour secreting excess cortisol) P – Paraneoplastic syndrome (when ACTH is released from a tumour somewhere other than the pituitary e.g. small cell lung cancer) E – Exogenous steroids (patients taking long-term corticosteroids)
35
ix for cushing's
dexamethasone suppression tests low dose test - cortisol decreased rules out cushing's - cortisol remains high -> cushing's measure serum ACTH - if low due to an adrenal tumour (primary) - if still high there is a secondary cause high dose test - cortisol now low = pituitary adenoma - cortisol still high = ectopic ACTH secretion
36
tx of cushing's syndrome
surgical removal of tumour (pituitary/adrenal/ectopic)
37
what does cortisol do in the body
Increases alertness Inhibits the immune system Inhibits bone formation Raises blood glucose Increases metabolism
38
what does gastroparesis cause in T1DM
erratic blood glucose control bloating vomiting diabetics can get gastroparesis due to neuropathy of the vagus nerve
39
tx of gastroparesis
metoclopramide, domperidone or erythromycin (prokinetic agents)
40
mx of DKA
- fluid replacement w isotonic saline FIRST (i.e 0.9% NaCl) (1L over 1 hr, 500ml over 5 mins if BP <90) - IV insulin at 0.1 unit/kg/hr once blood glucose is <14 mmol/l start an infusion of 10% dextrose as well as fluids - correction of electrolyte dist (K+) - monitor closely treat underlying triggers such as infection if the ketonaemia and acidosis have not been resolved within 24 hours then the patient should be reviewed by a senior endocrinologist
41
dx of DKA
Hyperglycaemia (e.g., blood glucose above 11 mmol/L) Ketosis (e.g., blood ketones above 3 mmol/L) Acidosis (e.g., pH below 7.3)
42
what is SIADH
increased release of ADH (vaspressin) from the posterior pituitary increasing water reabsorption from the urine, diluting the blood + leading to hyponatraemia urine becomes more conc
43
sx of SIADH
relate to low Na can be asx - headache - fatigue - muscle aches + cramps - confusion severe hyponatraemia can cause seizures + reduced conc
44
causes of SIADH
SIADH pneumonic Small cell lung tumours Infection Abscess Drugs (carbemazepine + antipsychotics) Head injury - post-operative after major surgery - Lung infection, particularly atypical pneumonia and lung abscesses - Brain pathologies, such as a head injury, stroke, intracranial haemorrhage or meningitis - Medications (e.g., SSRIs and carbamazepine) - Malignancy, particularly small cell lung cancer - Human immunodeficiency virus (HIV)
45
diagnosis of SIADH
no single test Euvolaemia Hyponatraemia Low serum osmolality High urine sodium High urine osmolality exclude things establish the cause
46
SIADH meds
Vasopressin receptor antagonists (e.g., tolvaptan) - needs close monitoring
47
what is osmotic demyelination syndrome
or CPM a comp of long-term severe hyponatraemia being treated too quickly (e.g., more than a 10 mmol/L increase per 24 hours).
48
what are the 2 diff ways diabetes insipidus can occur
CRANIAL - lack of ADH NEPHROGENIC - lack of response to ADH
49
causes of cranial diabetes insipidus
Brain tumours Brain injury Brain surgery Brain infections (e.g., meningitis or encephalitis) Genetic mutations in the ADH gene (autosomal dominant inheritance) Wolfram syndrome (a genetic condition also causing optic atrophy, deafness and diabetes mellitus)
50
ix for DI
Low urine osmolality (lots of water diluting the urine) High/normal serum osmolality (water loss may be balanced by increased intake) More than 3 litres on a 24-hour urine collection WATER DEPRIVATION TEST I.E. desmopressin stimulation test cranial low urine osmolarity after water deprivation high urine osmolarity after synthetic ADH given nephrogenic urine osmolarity always low
51
MEN 1 tumours
3Ps pArathyroid p1tuitary pAncreas
52
MEN 2
2a - 2Ps 1M PTH Phaeo Medullary Ca 2b - 1 P 2Ms Phaeo Marfan Medullary
53
how is MEN inherited
AD
54
MEN 2a
2a - 2Ps 1M PTH Phaeo Medullary Ca
55
MEN 2b
2b - 1 P 2Ms Phaeochromocytoma - adrenal tumour Marfan Medullary thyroid cancer
56
hypercalcaemia sx
bones, stones, groans, moans polyuria, polydipsia
57
hypocalcaemia sx
CATs go numb Convulsions Arrythmias Tetany Chvostek's (facial nerve spasm) and Trousseau's (BF cuff causing wrist to flex + fingers to draw together) signs
58
ECG in hypocalcaemia
long QT
59
hypernatraemia sx
thirst + dehydration weakness, lethargy, irritability, coma
60
hyponatraemia sx
N&V, headache, irritability, confusion, weakness, decreased CGS, seizures
61
ECG in hyperkalaemia
tall tented T waves prolonged PR wide QRS small/absent P
62
hyperkalaemia sx
chest pain rapid pulse arrhythmias headache decreased power
63
hypokalaemia sx
muscle weakness hypotonia palpitations
64
ECG in hypokalaemia
you have no Pot, no Tea, but a long PR and a long QT flat T waves ST depression U waves prolonged PR
65
dosing regime for hydrocortisone in adrenal insufficiency
majority dosing in the morning, the remainder in the evening
66
what cancer is hashimotos thyroiditis assoc w
MALT lymphoma
67
what does metformin do
increases insulin sensitivity decreases glucose production hepatobiliary set of action + cleared renally
68
SEs metformin
GI sx - D&V lactic acidosis (espesh in hepatic + renal failure but v rare)
69
when must you stop metformin
px not eating/drinking AKI raised lactate prior to IV radiology contrast (risk of renal failure)
70
what do SGLT-2 inhibitors do (end in -gliflozin)
cause more glucose to be excreted in urine
71
when to add SGLT-2 inhibitors (end in -gliflozin) to metformin
when the px has CVD/HF if their QRISK > 10% e.g. Dapagliflozin
72
SEs of SGLT-2 inhibitors (end in -gliflozin)
increase urine output and frequency UTIs thrush
73
when to stop SGLT-2 inhibitors (end in -gliflozin)
everybody has their SGLT-2 withheld on admission to hx due to risk of EKA during acute illness need senior review prior to restarting
74
examples of sulfonureas
GLICLAZIDE tolbutamIDE glibendamIDE
75
what does a sulfonylurea do (gliclazide)
stimulate insulin release from the pancreas 'SPANK THE PANC'
76
SEs of a sulfonylurea (gliclazide)
weight gain hypos
77
what does pioglitazone do (a thiazolidinedione)
increases insulin sensitivity (helps get insulin into the ZONE) decreases glucose production
78
SEs of pioglitazone
weight gain HF (don't start it if px already has this) fluid retention increased fracture risk increased risk of bladder cancer
79
when to stop pioglitazone
acute fluid overload (ie HF) known or suspected bladder cancer
80
what do DPP-4 inhibitors do (end in -GLIPTIN)
enhance the incretin effect increase insulin secretion + lower glucagon secretion dont cause weight gain
81
SEs DPP-4 inhibitors (end in -GLIPTIN)
nausea pancreatitis STOP IN PANCREATITIS
82
what do GLP1 agonists do (exenaTIDE)
enhance the incretin effect increase insulin secretion inhibit glucagon secretion delay gastric emptying suppress appetitie can result in weight loss
83
SEs GLP1 agonists (exenaTIDE)
nausea pancreatitis AKI STOP IN PANCREATITIS/AKI
84
causes of nephrogenic DI
idiopathic genetic: - more common form affects the vasopression (ADH) receptor x-linked recessive - less common form results from a mutation in the gene that encodes the aquaporin 2 channel electrolytes - hypercalcaemia (HIGH Ca) - hypokalaemia (LOW K+) lithium - lithium desensitizes the kidney's ability to respond to ADH in the collecting ducts tubulo-interstitial disease: obstruction, sickle-cell, pyelonephritis Kidney diseases (e.g., polycystic kidney disease)
85
what is pheochromocytoma
tumour of the adrenal glands that secretes unregulated and excessive amounts of catecholamines (adrenaline) from chromaffin cells releases it in bursts
86
what genetic disorders make pheochromocytoma more common
Multiple endocrine neoplasia type 2 (MEN 2) Neurofibromatosis type 1 Von Hippel-Lindau disease
87
ix pheochromocytoma
Plasma free metanephrines 24-hour urine catecholamines CT/MRI to look for tumour
88
mx pheochromocytoma
Alpha blockers (e.g., PHENOXYBENZAMINE or doxazosin) Beta blockers, only when established on alpha blockers or labetalol as it blocks alpha + beta receptors Surgical removal of the tumour
89
what to do if there is difficulty distinguishing T1DM from other types
measure C-peptide low in T1DM (as the pancreas is not making enough insulin precursor, which breaks down to form C-peptide and insulin) normal or high in T2DM or measure Anti-GAD (present in most px w T1DM)
90
what is Maturity onset diabetes of the young (MODY)
A group of inherited genetic disorders affecting the production of insulin -> younger px developing sx similar to those with T2DM, i.e. asymptomatic hyperglycaemia with progression to more severe complications such as diabetic ketoacidosis
91
what is a hyperosmolar hypergycaemic state (HHS)
occurs in people with type 2 diabetes who experience very high blood glucose levels (often over 40mmol/l) med emergency
92
pathophysiology of hyperosmolar hypergycaemic state (HHS)
hyperglycaemia → ↑ serum osmolality (high conc stuff) → osmotic diuresis (wee) → severe volume depletion
93
precipitating factors for hyperosmolar hypergycaemic state (HHS)
intercurrent illness dementia sedative drugs
94
presentation hyperosmolar hypergycaemic state (HHS)
can come on over days (unlike DKA which is hrs) consequences of vol less - dehydration - polyuria + polydipsia systemic - lethargy - N&V neuro - altered conc - focal neuro def haem - hyperviscosity
95
dx hyperosmolar hypergycaemic state (HHS)
hypovolaemia marked hyperglycaemia (>30 mmol/L) significantly raised serum osmolarity (> 320 mosmol/kg) can be calculated by: 2 * Na+ + glucose + urea no significant hyperketonaemia (<3 mmol/L) no significant acidosis (bicarbonate > 15 mmol/l or pH > 7.3 – acidosis can occur due to lactic acidosis or renal impairment)
96
mx hyperosmolar hypergycaemic state (HHS)
fluid replacement insulin should not be given unless blood glucose stops falling while giving IV fluids (cld lead to CPM) venous thromboembolism prophylaxis
97
normal range for BM
4-7
98
what is primary hyperparathyroidism
excess secretion of PTH resulting in hypercalcaemia usually tumour in parathyroid glands high PTH (or inappropriately normal) high Ca
99
what is secondary hyperparathyroidism
insufficient VD or CKD reduces Ca absorption from the intestines, kidneys and bones. This results in hypocalcaemia. The parathyroid glands react to the low serum calcium by excreting more parathyroid hormone Ca low or normal PTH high
100
what is tertiary hyperparathyroidism
secondary hyperparathyroidism continues for an extended period, after which the underlying cause is treated parathyroid gland hyperplasia has occured
101
when can you dx T2DM
fasting glucose greater than or equal to 7.0 mmol/l random glucose greater than or equal to 11.1 mmol/l (or after 75g oral glucose tolerance test) or HbA1c >48 mmol/mol (6.5%) in adults (less than this does not exclude as less sensitive that above tests) If the patient is asymptomatic the above criteria apply but must be demonstrated on two separate occasions.
102
when to add a second drug in T2DM
titrate up metformin and encourage lifestyle changes to aim for a HbA1c of 48 mmol/mol (6.5%), but should only add a second drug if the HbA1c rises to 58 mmol/mol (7.5%)
103
when is metformin CI
severe CKD
104
what is the most common cause of impaired hypoglycaemia awareness in T1DM
if longstanding - neuropathy of parts of the autonomous nervous system
105
Drug causes of gynaecomastia
spironolactone (most common drug cause) cimetidine digoxin cannabis finasteride GnRH agonists e.g. goserelin, buserelin oestrogens, anabolic steroids
106
grave's disease tx
initially: propranolol refer to 2nday care carbimazole if this does not control sx
107
side effects of glucocorticoids
Endocrine - impaired glucose regulation - increased appetite/weight gain - hirsutism - hyperlipidaemia Cushing's syndrome sx Musculoskeletal - osteoporosis - proximal myopathy - avascular necrosis of the femoral head Immunosuppression Psychiatric - insomnia - mania - depression - psychosis Gastrointestinal - peptic ulceration - acute pancreatitis Ophthalmic - glaucoma - cataracts Suppression of growth in children Intracranial hypertension Neutrophilia
108
any change in vision w graves
urgent referral as risk of thyroid eye disease
109
acid-base imbalance in cushings
hypokalaemic metabolic alkalosis
110
what is sick euthyroid syndrome
a condition in which serum levels of thyroid hormones are low in patients who have nonthyroidal systemic illness but who are actually euthyroid it is often said that everything (TSH, T4, T3) is low. In the majority of cases however the TSH level is within the >normal range (inappropriately normal given the low thyroxine and T3) Changes are reversible upon recovery from the systemic illness and hence no treatment is usually needed.
111
causes of primary hyperaldosteronism
bilateral idiopathic adrenal hyperplasia: the cause of around 60-70% of cases adrenal adenoma (Conn's syndrome): 20-30% of cases unilateral hyperplasia familial hyperaldosteronism adrenal carcinoma
112
features of primary hyperaldosteronism
hypertension hypokalaemia e.g. muscle weakness metabolic alkalosis
113
ix for primary hyperaldosteronism
1st line = plasma aldosterone/renin ratio - shows high aldosterone levels alongside low renin levels (negative feedback due to sodium retention from aldosterone) high-resolution CT abdomen and adrenal vein sampling
114
mx primary hyperaldosteronism
adrenal adenoma: surgery (laparoscopic adrenalectomy) bilateral adrenocortical hyperplasia: aldosterone antagonist e.g. spironolactone
115
The Hba1c target for patients on a drug which may cause hypoglycaemia
53 mmol/mol
116
what can lead to lower than expected HbA1c levels
reduced red blood cell lifespan Sickle-cell anaemia GP6D deficiency Hereditary spherocytosis Haemodialysis
117
what can lead to higher than expected HbA1c levels
increased red blood cell lifespan Vitamin B12/folic acid deficiency Iron-deficiency anaemia Splenectomy
118
mx thyroid storm
beta-blockers: typically IV propranolol anti-thyroid drugs: e.g. methimazole or propylthiouracil (PTU) Lugol's iodine dexamethasone - e.g. 4mg IV qds - blocks the conversion of T4 to T3 symptomatic treatment e.g. paracetamol treatment of underlying precipitating event
119
calcitonin
Released from the parafollicular cells Usually found in patients with medullary carcinoma of the thyroid
120
antibodies found in autoimmune disease affecting the thyroid (Hashimotos 100%) and Graves (70%)
Thyroid peroxidase (microsomal) antibodies
121
antibodies found in individuals with Graves disease (95%)
Antibodies to TSH receptor
122
antibodies to check as thyroid cancer follow up
Thyroglobulin antibodies for most Calcitonin for medullary
123
ix thyroid nodules
TFTs Ultrasonography
124
causes of benign thyroid nodules
Multinodular goitre Thyroid adenoma Hashimoto's thyroiditis Cysts (colloid, simple, or hemorrhagic)
125
causes of malignant thyroid nodules
Papillary carcinoma (most common malignant cause) Follicular carcinoma Medullary carcinoma Anaplastic carcinoma Lymphoma
126
what is an insulinoma
a neuroendocrine tumour deriving mainly from pancreatic Islets of Langerhans cells assoc w MEN-1 most common pancreatic endocrine tumour
127
features of insulinoma
1) hypoglycaemia with fasting or exercise 2) reversal of symptoms with glucose 3) recorded low BMs at the time of symptoms
128
skin lesions in grave's disease
pretibial myxoedema - deposits of glycosaminoglycans under the skin on the anterior aspect of the leg shiny, orange peel like
129
what can cause falsely low HbA1c readings
sickle cell anaemia GP6D deficiency hereditary spherocytosis haemodialysis as they reduce RBC lifespan
130
what can cause higher than expected HbA1c readings
VB12/folic acid deficiency iron-deficiency anaemia splenectomy
131
phaeochromocytoma presentation
triad of sweating, headaches, and palpitations in association with severe hypertension
132
Pheochromocytoma dx
urinary metanephrines
133
what is the incretin affect
the insulin response to oral glucose is much greater than the response to IV this effect is diminished in T2DM
134
what is grave's disease
AI condition where TSH receptor antibodies cause primary hyperthyroidism - they stim TSH receptors on the thyroid most common cause hyperthyroidism
135
causes of hyperthyroidism
G – Graves’ disease I – Inflammation (thyroiditis) S – Solitary toxic thyroid nodule T – Toxic multinodular goitre
136
causes of thyroiditis
De Quervain’s thyroiditis Hashimoto’s thyroiditis Postpartum thyroiditis Drug-induced thyroiditis
137
general course of thyroiditis
often causes an initial period of hyperthyroidism, followed by under-activity of the thyroid gland (hypothyroidism)
138
presentation hyperthyroidism
Anxiety and irritability Sweating and heat intolerance Tachycardia Weight loss Fatigue Insomnia Frequent loose stools Sexual dysfunction Brisk reflexes on examination
139
features of Grave's disease
Diffuse goitre (without nodules) Graves’ eye disease, including exophthalmos Pretibial myxoedema Thyroid acropachy (hand swelling and finger clubbing)
140
tx De Quervain’s Thyroiditis
self-limiting, sx tx NSAIDs for symptoms of pain and inflammation Beta blockers for the symptoms of hyperthyroidism Levothyroxine for the symptoms of hypothyroidism
141
mx hyperthryroidism
Carbimazole Once the patient has normal levels (within 4-8 weeks), they continue on maintenance carbimazole and either: - The dose is titrated to maintain normal levels (known as titration-block) - A higher dose blocks all production, and levothyroxine is added and titrated to effect (known as block and replace)
142
risk whilst taking carbimazole
agranulocytosis acute pancreatitis
143
second line anti-thyroid drug (+ its risk)
Propylthiouracil (small risk of severe liver reactions)
144
what can both anti-thyroid drugs cause
Agranulocytosis - vulnerable to severe infections - look out for px on these drigs w sore throat + get urgent FBC
145
how does radioactive iodine tx work
drink a single dose of radioactive iodine, the thyroid gland takes this up + the emitted radiation destroys a proportion of the thyroid cells -> decrease in thyroid hormone production. Remission can take 6 months, after which the thyroid is often underactive, requiring long-term levothyroxine
146
radioactive iodine tx rules
no preg / breastfeeding, must not get preg within 6 mths of tx men must not father children within 4 mths tx limit contact w ppl after the dose
147
most common cause of hypothyroidism in developed world
Hashimoto’s thyroiditis
148
antibodies assoc w Hashimoto’s thyroiditis
anti-thyroid peroxidase (anti-TPO) antibodies and anti-thyroglobulin (anti-Tg) antibodies
149
most common cause of hypothyroidism in developing world
iodine deficiency
150
what drugs can interfere w thyroid hormone production
lithium inhibits production amiodarone interferes w production + metabolism
151
Causes of Secondary Hypothyroidism
Tumours (e.g., pituitary adenomas) Surgery to the pituitary Radiotherapy Sheehan’s syndrome (where major post-partum haemorrhage causes avascular necrosis of the pituitary gland) Trauma
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hypothyroidism presentation
Weight gain Fatigue Dry skin Coarse hair and hair loss Fluid retention (including oedema, pleural effusions and ascites) Heavy or irregular periods Constipation iodine def causes goitre
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mx hypothyroidism
Oral levothyroxine (synthetic T4 that metabolises to T3 in the body) dose titrated based on TSH level, initially every 4 wks
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what is acromegaly
the result of excessive growth hormone (GH)
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causes of acromegaly
pituitary adenoma (GH produced by anterior pituitary gland) can be 2ndary to cancer e.g. lung/pancreatic cancer w a tumour that secretes ectopic GH
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acromegaly presentation
if space-occupying pituitary tumour: - headaches - visual field defect (bitemporal hemianopia) excess GH: Prominent forehead and brow (frontal bossing) Coarse, sweaty skin Large nose Large tongue (macroglossia) Large hands and feet Large protruding jaw (prognathism) other: Hypertrophic heart Hypertension Type 2 diabetes Carpal tunnel syndrome Arthritis Colorectal cancer
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acromegaly ix
Insulin-like growth factor-1 (IGF-1) tested on blood sample - indicates GH level (can't test GH directly as fluctuated throughout the day) OGTT ie GH suppression test (where glucose drink sld suppress GH level if normal) - do after IGF-1 test to confirm dx pituitary MRI
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acromegaly tx
Trans-sphenoidal surgery, through the nose and sphenoid bone, to remove the pituitary tumour Surgical removal of ectopic tumours
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medical options for reducing GH
Pegvisomant is a GH receptor antagonist given daily by a SC injection Somatostatin analogues (e.g., octreotide) block GH release Dopamine agonists (e.g., bromocriptine) block GH release
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diabetic neuropathy
diabetes leads to sensory loss, typically glove + stocking distribution, lower legs affected first can be painful
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mx diabetic neuropathy
same way as all neuropathic pain 1 = amitriptyline, duloxetine, gabapentin or pregabalin 2 = swap to another ^ tramadol for rescue therapay
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diabetic retinopathy what does it cause + why
most common cause of blindness in adults aged 35-65 years-old Hyperglycaemia damages the retinal small vessels and endothelial cells. Increased vascular permeability -> leaking BVs, blot haemorrhages + hard exudates (yellow-white deposits of lipids and proteins in the retina) Damage to BV walls -> microaneurysms and venous beading Damage to nerve fibres -> cotton wool spots on retina Intraretinal microvascular abnormalities (IRMA) = dilated + tortuous capillaries in the retina that act as a shunt between the arterial and venous vessels Neovascularisation (dev of new BVs)
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grading of diabetic retinopathy
Background – microaneurysms, retinal haemorrhages, hard exudates and cotton wool spots Pre-proliferative – venous beading, multiple blot haemorrhages and intraretinal microvascular abnormality (IMRA) Proliferative – NEOVASCULARISATION and vitreous haemorrhage
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Diabetic maculopathy
Exudates within the macula Macular oedema
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comps of diabetic retinopathy
Vision loss Retinal detachment Vitreous haemorrhage (bleeding into the vitreous humour) Rubeosis iridis (new blood vessel formation in the iris) – this can lead to neovascular glaucoma Optic neuropathy Cataracts
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mx diabetic retinopathy
Non-proliferative = close monitoring and careful diabetic control. Proliferative - Pan-retinal photocoagulation (PRP) – extensive laser treatment across the retina to suppress new vessels - Anti-VEGF medications by intravitreal injection - Surgery (e.g., vitrectomy) may be required in severe disease
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why do you get diabetic foot disease
- neuropathy - so loss of protective sensation - PAD
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what is charcot's arthropathy
syndrome in patients who have peripheral neuropathy, or loss of sensation, in the foot and ankle
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presentation diabetic foot disease
neuropathy: loss of sensation ischaemia: absent foot pulses, reduced ankle-brachial pressure index (ABPI), intermittent claudication complications: calluses, ulceration, Charcot's arthropathy, cellulitis, osteomyelitis, gangrene
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when to screen px w DM for diabetic foot dis + how
annually screen for ischaemia - palpate for both the dorsalis pedis pulse and posterial tibial artery pulse screen for neuropathy - a 10 g monofilament is used on various parts of the sole of the foot
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when to screen to diabetic nephropathy + how
Annually urinary albumin:creatinine ratio (ACR) should be an early morning specimen ACR > 2.5 = microalbuminuria
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mx diabetic nephropathy
dietary protein restriction tight glycaemic control BP control: aim for < 130/80 mmHg ACEi or ARB should be start if urinary ACR of 3 mg/mmol or more control dyslipidaemia e.g. Statins
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what is secondary hyperaldosteronism caused by
excessive renin stimulating release of excessive aldosterone excessive renin may be released due to disproportionately lower BP in the kidneys - renal artery stenosis - HF - liver cirrhosis + ascites
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insulin sick day rules
if a patient is on insulin, they MUST NOT STOP IT due to the risk of DKA check blood glucose more frequently (e.g. every 1–2 hours including through the night) consider checking blood or urine ketone levels regularly maintain normal meal pattern if possible if appetite is reduced meals could be replaced with carbohydrate-containing drinks (such as milk, milkshakes, fruit juices, and sugary drinks) aim to drink at least 3 L of fluid (5 pints) a day to prevent dehydration
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when to add 10% dextrose infusion in DKA mx
once blood glucose is < 14 mmol/l
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blood results if poor compliance w meds in px w primary hypothyroidism
TSH level will be high implying that over recent days/weeks the body is thyroxine deficient. If px starts taking meds properly just b4 appt free T4 will be within normal range. As thyroxine level wld be corrected but the TSH takes longer to normalise.
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what to give everyone when prescribing insulin
glucagon kit for emergencies
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what is a sliding scale + what must you accompany it w
variable rate IV insulin infusions (act rapid) - according to capillary blood glucose measurements always accompanied by an infusion of fluid containing GLUCOSE + potassium to prevent insulin induced hypoglycaemia + hypokalaemia - so 2 cannulas
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when to use a sliding scale
px w know DM unable to take oral food + for whom their own insulin regime is not poss vomiting (first exclude DKA/HHS) NBM + who will miss more than one meal (ie pre-surgery, want them to be 1st on list) severe illness + need to achieve good glycaemic control reduced GCS
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what monitoring is needed whilst a px is on a sliding scale
actual need for it - daily CBG - hourly if hypo -> tx + swap to insulin sensitive regime U&Es - daily monitor K fluid status - daily no overload concern -> 5% glucose (w K) 125ml/hr overload concern -> 83ml/hr v elderly/frail -> 42ml/hr if hepatic/renal impairment -> insulin sensitive regime
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what to stop / ctu whilst a sliding scale is running
stop all oral hypoglycaemic agents i.e. no diabetets tablets stop all short acting insulins stop all pre-mixed insulins (all the ones w a number in) ctu all long-acting + basal insulins (levemir)
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when to come off a sliding scale
asap when px has normal biochem px is E+D give the next meal related long-acting insulin dose, wait for 1 hr, then remove sliding scale (imp as it only has a half-life of 5 mins) restart all other DM meds + review them
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hypoglycaemia definition
glucose < 4 less than 4 on the floor start tx if sx - seating, pallor, trmor, irritable
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tx hypoglycaemia conscious + orientated
oral glucose load - lucozade, orange juice, glucose gel
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tx hypoglycaemia lower GCS w access
IV 10% glucose -200 mls over 10 mins -or 100mls 20% glucose stat
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tx hypoglycaemia lower GCS no access
1mg IM glucagon
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how often to monitor blood glucose in diabetic px
4x/day
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when to omit insulin
NEVER in T1DM (even if hypo!!!!)
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criteria for GLP1 agonists (exenaTIDE) therapy
if triple therapy not effective/CI then give metformin + sulfonurea + GLP1 agonist if: - BMI > 35 w obesity related probs - BMI < 35 + insulin wld have serious occupational implications / not tolerated
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when to consider insulin in T2DM
Hba1C > 58 after 3 mths of dual oral therapy sld be intermediate-acting (due to hypo risk)
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what is usual total daily dose of insulin
0.5units per kg
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best insulin regime for T1DM
basal-bolus split long and short acting 50/50 1-2 long acting 3 short acting w meals round down not up can knock some off as hypo risk
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mx nephrogenic DI
thiazide diuretics low salt/protein diet
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mx cranial DI
desmopressin
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Endocrine parameters reduced in stress response:
Insulin Testosterone Oestrogen