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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
Q

what autoantibodies might you see in addison’s

A

adrenal cortex antibodies
-21-hydroxylase
-17 alpha hydroxylase

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26
Q

mx of adrenal insufficiency

A

replacement steroids

  • hydrocortisone (glucocorticoid) to replace cortisol
  • fludrocortisone (mineralcorticoid) to replace aldosterone)

Give px a steroid card, ID tag + emergency letter

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27
Q

what to do in acute illness if steroid dependent

A

Double doses (to match normal steroid response to illness)

Px + close contacts to give IM hydrocortisone in emergency

if vomiting take it IM

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28
Q

presentation of adrenal crisis / Addisonian crisis

A

reduced conc
hypotension
hypoglycaemia
hyponatraemia + hyperkalaemia

cld be initial pres or triggered by infection, trauma, acute illness

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29
Q

mx of adrenal crisis

A

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

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30
Q

what is cushing’s disease

A

A pituitary adenoma secreting excessive ACTH -> excessive cortisol release from adrenals

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31
Q

what is cushing’s syndrome

A

the features of prolonged high levels of glucocorticoids in the body.

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32
Q

features of cushing’s syndrome

A

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)

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33
Q

metabolic effects of cushing’s syndrome

A

Hypertension
Cardiac hypertrophy
Type 2 diabetes
Dyslipidaemia (raised cholesterol and triglycerides)
Osteoporosis

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34
Q

causes of cushing’s syndrome

A

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)

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35
Q

ix for cushing’s

A

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

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36
Q

tx of cushing’s syndrome

A

surgical removal of tumour (pituitary/adrenal/ectopic)

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37
Q

what does cortisol do in the body

A

Increases alertness
Inhibits the immune system
Inhibits bone formation
Raises blood glucose
Increases metabolism

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38
Q

what does gastroparesis cause in T1DM

A

erratic blood glucose control
bloating
vomiting

diabetics can get gastroparesis due to neuropathy of the vagus nerve

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39
Q

tx of gastroparesis

A

metoclopramide, domperidone or erythromycin (prokinetic agents)

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40
Q

mx of DKA

A
  • 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

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41
Q

dx of DKA

A

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)

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42
Q

what is SIADH

A

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

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43
Q

sx of SIADH

A

relate to low Na
can be asx

  • headache
  • fatigue
  • muscle aches + cramps
  • confusion

severe hyponatraemia can cause seizures + reduced conc

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44
Q

causes of SIADH

A

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)
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45
Q

diagnosis of SIADH

A

no single test

Euvolaemia
Hyponatraemia
Low serum osmolality
High urine sodium
High urine osmolality

exclude things
establish the cause

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46
Q

SIADH meds

A

Vasopressin receptor antagonists (e.g., tolvaptan)
- needs close monitoring

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47
Q

what is osmotic demyelination syndrome

A

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).

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48
Q

what are the 2 diff ways diabetes insipidus can occur

A

CRANIAL - lack of ADH
NEPHROGENIC - lack of response to ADH

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49
Q

causes of cranial diabetes insipidus

A

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)

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50
Q

ix for DI

A

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

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51
Q

MEN 1 tumours

A

3Ps
pArathyroid
p1tuitary
pAncreas

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52
Q

MEN 2

A

2a - 2Ps 1M
PTH
Phaeo
Medullary Ca

2b - 1 P 2Ms
Phaeo
Marfan
Medullary

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53
Q

how is MEN inherited

A

AD

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54
Q

MEN 2a

A

2a - 2Ps 1M
PTH
Phaeo
Medullary Ca

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55
Q

MEN 2b

A

2b - 1 P 2Ms
Phaeochromocytoma - adrenal tumour
Marfan
Medullary thyroid cancer

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56
Q

hypercalcaemia sx

A

bones, stones, groans, moans

polyuria, polydipsia

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57
Q

hypocalcaemia sx

A

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

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58
Q

ECG in hypocalcaemia

A

long QT

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59
Q

hypernatraemia sx

A

thirst + dehydration
weakness, lethargy, irritability, coma

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60
Q

hyponatraemia sx

A

N&V, headache, irritability, confusion, weakness, decreased CGS, seizures

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61
Q

ECG in hyperkalaemia

A

tall tented T waves
prolonged PR
wide QRS
small/absent P

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62
Q

hyperkalaemia sx

A

chest pain
rapid pulse
arrhythmias
headache
decreased power

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63
Q

hypokalaemia sx

A

muscle weakness
hypotonia
palpitations

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64
Q

ECG in hypokalaemia

A

you have no Pot, no Tea, but a long PR and a long QT

flat T waves
ST depression
U waves
prolonged PR

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65
Q

dosing regime for hydrocortisone in adrenal insufficiency

A

majority dosing in the morning, the remainder in the evening

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66
Q

what cancer is hashimotos thyroiditis assoc w

A

MALT lymphoma

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67
Q

what does metformin do

A

increases insulin sensitivity
decreases glucose production

hepatobiliary set of action + cleared renally

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68
Q

SEs metformin

A

GI sx - D&V
lactic acidosis (espesh in hepatic + renal failure but v rare)

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69
Q

when must you stop metformin

A

px not eating/drinking
AKI
raised lactate
prior to IV radiology contrast (risk of renal failure)

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70
Q

what do SGLT-2 inhibitors do (end in -gliflozin)

A

cause more glucose to be excreted in urine

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71
Q

when to add SGLT-2 inhibitors (end in -gliflozin) to metformin

A

when the px has CVD/HF
if their QRISK > 10%

e.g. Dapagliflozin

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72
Q

SEs of SGLT-2 inhibitors (end in -gliflozin)

A

increase urine output and frequency
UTIs
thrush

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73
Q

when to stop SGLT-2 inhibitors (end in -gliflozin)

A

everybody has their SGLT-2 withheld on admission to hx due to risk of EKA during acute illness
need senior review prior to restarting

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74
Q

examples of sulfonureas

A

GLICLAZIDE
tolbutamIDE
glibendamIDE

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75
Q

what does a sulfonylurea do (gliclazide)

A

stimulate insulin release from the pancreas
‘SPANK THE PANC’

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76
Q

SEs of a sulfonylurea (gliclazide)

A

weight gain
hypos

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77
Q

what does pioglitazone do (a thiazolidinedione)

A

increases insulin sensitivity (helps get insulin into the ZONE)
decreases glucose production

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78
Q

SEs of pioglitazone

A

weight gain
HF (don’t start it if px already has this)
fluid retention
increased fracture risk
increased risk of bladder cancer

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79
Q

when to stop pioglitazone

A

acute fluid overload (ie HF)
known or suspected bladder cancer

80
Q

what do DPP-4 inhibitors do (end in -GLIPTIN)

A

enhance the incretin effect
increase insulin secretion + lower glucagon secretion

dont cause weight gain

81
Q

SEs DPP-4 inhibitors (end in -GLIPTIN)

A

nausea
pancreatitis
STOP IN PANCREATITIS

82
Q

what do GLP1 agonists do (exenaTIDE)

A

enhance the incretin effect
increase insulin secretion
inhibit glucagon secretion
delay gastric emptying
suppress appetitie

can result in weight loss

83
Q

SEs GLP1 agonists (exenaTIDE)

A

nausea
pancreatitis
AKI
STOP IN PANCREATITIS/AKI

84
Q

causes of nephrogenic DI

A

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
Q

what is pheochromocytoma

A

tumour of the adrenal glands that secretes unregulated and excessive amounts of catecholamines (adrenaline) from chromaffin cells

releases it in bursts

86
Q

what genetic disorders make pheochromocytoma more common

A

Multiple endocrine neoplasia type 2 (MEN 2)
Neurofibromatosis type 1
Von Hippel-Lindau disease

87
Q

ix pheochromocytoma

A

Plasma free metanephrines
24-hour urine catecholamines
CT/MRI to look for tumour

88
Q

mx pheochromocytoma

A

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
Q

what to do if there is difficulty distinguishing T1DM from other types

A

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
Q

what is Maturity onset diabetes of the young (MODY)

A

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
Q

what is a hyperosmolar hypergycaemic state (HHS)

A

occurs in people with type 2 diabetes who experience very high blood glucose levels (often over 40mmol/l)
med emergency

92
Q

pathophysiology of hyperosmolar hypergycaemic state (HHS)

A

hyperglycaemia → ↑ serum osmolality (high conc stuff) → osmotic diuresis (wee) → severe volume depletion

93
Q

precipitating factors for hyperosmolar hypergycaemic state (HHS)

A

intercurrent illness
dementia
sedative drugs

94
Q

presentation hyperosmolar hypergycaemic state (HHS)

A

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
Q

dx hyperosmolar hypergycaemic state (HHS)

A

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
Q

mx hyperosmolar hypergycaemic state (HHS)

A

fluid replacement
insulin should not be given unless blood glucose stops falling while giving IV fluids (cld lead to CPM)
venous thromboembolism prophylaxis

97
Q

normal range for BM

A

4-7

98
Q

what is primary hyperparathyroidism

A

excess secretion of PTH resulting in hypercalcaemia
usually tumour in parathyroid glands

high PTH (or inappropriately normal)
high Ca

99
Q

what is secondary hyperparathyroidism

A

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
Q

what is tertiary hyperparathyroidism

A

secondary hyperparathyroidism continues for an extended period, after which the underlying cause is treated
parathyroid gland hyperplasia has occured

101
Q

when can you dx T2DM

A

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
Q

when to add a second drug in T2DM

A

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
Q

when is metformin CI

A

severe CKD

104
Q

what is the most common cause of impaired hypoglycaemia awareness in T1DM

A

if longstanding - neuropathy of parts of the autonomous nervous system

105
Q

Drug causes of gynaecomastia

A

spironolactone (most common drug cause)
cimetidine
digoxin
cannabis
finasteride
GnRH agonists e.g. goserelin, buserelin
oestrogens, anabolic steroids

106
Q

grave’s disease tx

A

initially: propranolol
refer to 2nday care
carbimazole if this does not control sx

107
Q

side effects of glucocorticoids

A

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
Q

any change in vision w graves

A

urgent referral as risk of thyroid eye disease

109
Q

acid-base imbalance in cushings

A

hypokalaemic metabolic alkalosis

110
Q

what is sick euthyroid syndrome

A

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
Q

causes of primary hyperaldosteronism

A

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
Q

features of primary hyperaldosteronism

A

hypertension
hypokalaemia
e.g. muscle weakness
metabolic alkalosis

113
Q

ix for primary hyperaldosteronism

A

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
Q

mx primary hyperaldosteronism

A

adrenal adenoma: surgery (laparoscopic adrenalectomy)
bilateral adrenocortical hyperplasia: aldosterone antagonist e.g. spironolactone

115
Q

The Hba1c target for patients on a drug which may cause hypoglycaemia

A

53 mmol/mol

116
Q

what can lead to lower than expected HbA1c levels

A

reduced red blood cell lifespan

Sickle-cell anaemia
GP6D deficiency
Hereditary spherocytosis
Haemodialysis

117
Q

what can lead to higher than expected HbA1c levels

A

increased red blood cell lifespan

Vitamin B12/folic acid deficiency
Iron-deficiency anaemia
Splenectomy

118
Q

mx thyroid storm

A

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
Q

calcitonin

A

Released from the parafollicular cells
Usually found in patients with medullary carcinoma of the thyroid

120
Q

antibodies found in autoimmune disease affecting the thyroid (Hashimotos 100%) and Graves (70%)

A

Thyroid peroxidase (microsomal) antibodies

121
Q

antibodies found in individuals with Graves disease (95%)

A

Antibodies to TSH receptor

122
Q

antibodies to check as thyroid cancer follow up

A

Thyroglobulin antibodies for most

Calcitonin for medullary

123
Q

ix thyroid nodules

A

TFTs
Ultrasonography

124
Q

causes of benign thyroid nodules

A

Multinodular goitre
Thyroid adenoma
Hashimoto’s thyroiditis
Cysts (colloid, simple, or hemorrhagic)

125
Q

causes of malignant thyroid nodules

A

Papillary carcinoma (most common malignant cause)
Follicular carcinoma
Medullary carcinoma
Anaplastic carcinoma
Lymphoma

126
Q

what is an insulinoma

A

a neuroendocrine tumour deriving mainly from pancreatic Islets of Langerhans cells
assoc w MEN-1
most common pancreatic endocrine tumour

127
Q

features of insulinoma

A

1) hypoglycaemia with fasting or exercise
2) reversal of symptoms with glucose
3) recorded low BMs at the time of symptoms

128
Q

skin lesions in grave’s disease

A

pretibial myxoedema - deposits of glycosaminoglycans under the skin on the anterior aspect of the leg
shiny, orange peel like

129
Q

what can cause falsely low HbA1c readings

A

sickle cell anaemia
GP6D deficiency
hereditary spherocytosis
haemodialysis

as they reduce RBC lifespan

130
Q

what can cause higher than expected HbA1c readings

A

VB12/folic acid deficiency
iron-deficiency anaemia
splenectomy

131
Q

phaeochromocytoma presentation

A

triad of sweating, headaches, and palpitations in association with severe hypertension

132
Q

Pheochromocytoma dx

A

urinary metanephrines

133
Q

what is the incretin affect

A

the insulin response to oral glucose is much greater than the response to IV

this effect is diminished in T2DM

134
Q

what is grave’s disease

A

AI condition where TSH receptor antibodies cause primary hyperthyroidism - they stim TSH receptors on the thyroid
most common cause hyperthyroidism

135
Q

causes of hyperthyroidism

A

G – Graves’ disease
I – Inflammation (thyroiditis)
S – Solitary toxic thyroid nodule
T – Toxic multinodular goitre

136
Q

causes of thyroiditis

A

De Quervain’s thyroiditis
Hashimoto’s thyroiditis
Postpartum thyroiditis
Drug-induced thyroiditis

137
Q

general course of thyroiditis

A

often causes an initial period of hyperthyroidism, followed by under-activity of the thyroid gland (hypothyroidism)

138
Q

presentation hyperthyroidism

A

Anxiety and irritability
Sweating and heat intolerance
Tachycardia
Weight loss
Fatigue
Insomnia
Frequent loose stools
Sexual dysfunction
Brisk reflexes on examination

139
Q

features of Grave’s disease

A

Diffuse goitre (without nodules)
Graves’ eye disease, including exophthalmos
Pretibial myxoedema
Thyroid acropachy (hand swelling and finger clubbing)

140
Q

tx De Quervain’s Thyroiditis

A

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
Q

mx hyperthryroidism

A

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
Q

risk whilst taking carbimazole

A

agranulocytosis
acute pancreatitis

143
Q

second line anti-thyroid drug (+ its risk)

A

Propylthiouracil

(small risk of severe liver reactions)

144
Q

what can both anti-thyroid drugs cause

A

Agranulocytosis

  • vulnerable to severe infections
  • look out for px on these drigs w sore throat + get urgent FBC
145
Q

how does radioactive iodine tx work

A

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
Q

radioactive iodine tx rules

A

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
Q

most common cause of hypothyroidism in developed world

A

Hashimoto’s thyroiditis

148
Q

antibodies assoc w Hashimoto’s thyroiditis

A

anti-thyroid peroxidase (anti-TPO) antibodies and anti-thyroglobulin (anti-Tg) antibodies

149
Q

most common cause of hypothyroidism in developing world

A

iodine deficiency

150
Q

what drugs can interfere w thyroid hormone production

A

lithium inhibits production
amiodarone interferes w production + metabolism

151
Q

Causes of Secondary Hypothyroidism

A

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

152
Q

hypothyroidism presentation

A

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

153
Q

mx hypothyroidism

A

Oral levothyroxine (synthetic T4 that metabolises to T3 in the body)

dose titrated based on TSH level, initially every 4 wks

154
Q

what is acromegaly

A

the result of excessive growth hormone (GH)

155
Q

causes of acromegaly

A

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

156
Q

acromegaly presentation

A

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

157
Q

acromegaly ix

A

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

158
Q

acromegaly tx

A

Trans-sphenoidal surgery, through the nose and sphenoid bone, to remove the pituitary tumour

Surgical removal of ectopic tumours

159
Q

medical options for reducing GH

A

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

160
Q

diabetic neuropathy

A

diabetes leads to sensory loss, typically glove + stocking distribution, lower legs affected first
can be painful

161
Q

mx diabetic neuropathy

A

same way as all neuropathic pain
1 = amitriptyline, duloxetine, gabapentin or pregabalin
2 = swap to another ^
tramadol for rescue therapay

162
Q

diabetic retinopathy
what does it cause + why

A

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)

163
Q

grading of diabetic retinopathy

A

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

164
Q

Diabetic maculopathy

A

Exudates within the macula
Macular oedema

165
Q

comps of diabetic retinopathy

A

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

166
Q

mx diabetic retinopathy

A

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

167
Q

why do you get diabetic foot disease

A
  • neuropathy - so loss of protective sensation
  • PAD
168
Q

what is charcot’s arthropathy

A

syndrome in patients who have peripheral neuropathy, or loss of sensation, in the foot and ankle

169
Q

presentation diabetic foot disease

A

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

170
Q

when to screen px w DM for diabetic foot dis + how

A

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

171
Q

when to screen to diabetic nephropathy + how

A

Annually

urinary albumin:creatinine ratio (ACR)
should be an early morning specimen
ACR > 2.5 = microalbuminuria

172
Q

mx diabetic nephropathy

A

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

173
Q

what is secondary hyperaldosteronism caused by

A

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

174
Q

insulin sick day rules

A

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

175
Q

when to add 10% dextrose infusion in DKA mx

A

once blood glucose is < 14 mmol/l

176
Q

blood results if poor compliance w meds in px w primary hypothyroidism

A

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.

177
Q

what to give everyone when prescribing insulin

A

glucagon kit for emergencies

178
Q

what is a sliding scale + what must you accompany it w

A

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
179
Q

when to use a sliding scale

A

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

180
Q

what monitoring is needed whilst a px is on a sliding scale

A

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

181
Q

what to stop / ctu whilst a sliding scale is running

A

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)

182
Q

when to come off a sliding scale

A

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

183
Q

hypoglycaemia definition

A

glucose < 4
less than 4 on the floor

start tx if sx - seating, pallor, trmor, irritable

184
Q

tx hypoglycaemia conscious + orientated

A

oral glucose load
- lucozade, orange juice, glucose gel

185
Q

tx hypoglycaemia lower GCS w access

A

IV 10% glucose
-200 mls over 10 mins

-or 100mls 20% glucose stat

186
Q

tx hypoglycaemia lower GCS no access

A

1mg IM glucagon

187
Q

how often to monitor blood glucose in diabetic px

A

4x/day

188
Q

when to omit insulin

A

NEVER in T1DM
(even if hypo!!!!)

189
Q

criteria for GLP1 agonists (exenaTIDE) therapy

A

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
190
Q

when to consider insulin in T2DM

A

Hba1C > 58 after 3 mths of dual oral therapy
sld be intermediate-acting (due to hypo risk)

191
Q

what is usual total daily dose of insulin

A

0.5units per kg

192
Q

best insulin regime for T1DM

A

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

193
Q

mx nephrogenic DI

A

thiazide diuretics
low salt/protein diet

194
Q

mx cranial DI

A

desmopressin

195
Q

Endocrine parameters reduced in stress response:

A

Insulin
Testosterone
Oestrogen

finals (27 decks)

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