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Year 3 > Endocrine > Flashcards

Endocrine Flashcards

1
Q

define thyrotoxicosis

A

abnormal and excessive quantity of thyroid hormone in the body

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2
Q

Primary hyperthyroidism

A

due to thyroid pathology
thyroid itself is behaving abnormally and producing excessive thyroid hormone

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3
Q

Secondary hyperthyroidisim

A

condition where thyroid is producing excessive thyroid hormone as a result of overstimulation by TSH
Pathology is the hypothalamus or pituitary

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4
Q

Graves disease

A

autoimmune condition where TSH receptor antibodies cause primary hyperthyroidism
TSH receptor antibodies are abnormal antibodies produced by the immune system that mimic TSH and stimulate TSH receptor on the thyroid
(MOST COMMON CAUSE OF HYPERTHYROIDISM)

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5
Q

Toxic multinodular goitre

A

aka = Plummers disease
condition where nodules develop on the thyroid gland that act independently of the normal feedback system and continuously produce excessive thryoid hormone

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6
Q

What is exophthalmos and what causes it

A

bulging eyeball out of socket caused by graves disease
due to inflammation, swelling and hypertrophy of the tissue behind the eyeball that forces the eyeball out

Can be tested from behind patient and getting them to extend their head back to see if you can see the eyeballs bulging
Also if you can see the sclera above their iris

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7
Q

What is pretibial myxoedema and what is it specific to

A

dermatological condition where there are deposits of mucin under the skin on the anterior aspect of the leg
Gives a discoloured, waxy, oedematous appearance to the skin over the area

specific to Graves disease and is a reaction to the TSH receptor antibodies

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8
Q

Causes of hyperthyroidism

A

Graves disease
toxic multinodular goitre
solitary toxic thyroid nodule
thyroiditis (e.g. hashimotos, postpartum and drug induced)

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9
Q

Universal features of hyperthyroidism

A

anxiety and irritability
sweating and heat intolerance
tachycardia
weight loss
fatigue
frequent loose stools
sexual dysfunction

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10
Q

Unique features of Graves disease

A

Diffuse goitre
Graves eye disease
Bilateral exophthalmos
pretibial myoxedema

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11
Q

Unique features of toxic multinodular goitre

A

goitre with firm nodules
most patients are over 50
second most common cause of thyrotoxicosis (after Graves)

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12
Q

What is solitary toxic thyroid nodule

A

single abnormal thryoid nodule is acting alone to release thyroid hormone

nodules are usually benign adenomas
treated with surgical removal of the nodule

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13
Q

De Quervain’s thyroiditis

A

Presentation of a viral infection with fever, neck pain and tenderness, dysphagia and features of hyperthyroidism
hyperthyroid phase followed by a hypothyroid phase as the TSH level falls due to negative feedback

Self-limiting condition and supportive treatment with NSAIDs for pain and inflammation and beta-blockers for symptomatic relief of hyperthyroidism is all that is necessary

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14
Q

Thyroid storm

A

rare presentation of hyperthyroidism
Also known as thyrotoxic crisis
more severe presentation with pyrexia, tachycardia and delirium
requires admission for monitoring and is treated the same way as any other presentation of thyrotoxicosis
may need suppotive care with fluid resus, anti-arrhythmic meds and beta blockers

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15
Q

Hyperthyroidism management

A

Carbimazole (first line) - successful in Graves disease (usually normal thryoid function after 4-8 weeks and full remission within 18months)

Propylthiouracil (second line) - small risk of severe hepatic reactions

Radioactive iodine - destroys some thyroid cells

beta blockers - block adrenalin related symptoms of hyperthyroidism
propanolol is a good option because it non selectively blocks adrenergic activity (particularly useful in thyroid storm)

Surgery - to removed whole thyroid or toxic nodules
will require levothyroxine replacement for life

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16
Q

Hyperthyroidism management

A

Carbimazole (first line) - successful in Graves disease (usually normal thryoid function after 4-8 weeks and full remission within 18months)

Propylthiouracil (second line) - small risk of severe hepatic reactions

Radioactive iodine - destroys some thyroid cells

beta blockers - block adrenalin related symptoms of hyperthyroidism
propanolol is a good option because it non selectively blocks adrenergic activity (particularly useful in thyroid storm)

Surgery - to removed whole thyroid or toxic nodules
will require levothyroxine replacement for life

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17
Q

Primary hypothyroidism

A

problem with thyroid gland itself -> autoimmune disorder affecting thyroid tissue

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18
Q

Secondary hypothyroidism

A

due to a disorder with the pituitary gland or a lesion compressing th epituitary gland

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19
Q

Congenital hypothyroidism

A

due to a problem with thyroid dysgenesis or thyroid dyshormonogenesis

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20
Q

Hashimoto’s thyroiditis

A

most common cause in developed world for hyPOthyroidism
autoimmune disease associated with T1DM, addisons or pernicious anaemia
May cause transient thryotoxicosis in acute phase
5-10 times more common in women

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21
Q

Drugs that cause hypothyroidism

A

lithium
amiodarone

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22
Q

TSH and free T4 levels in thyrotoxicosis (graves)

A

low tsh
high free t4

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23
Q

TSH and free T4 levels in primary hypothyroidism (hashimotos)

A

high tsh
low free t4

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24
Q

TSH and free t4 levels in secondary hypothyroidism

A

low tsh
low free t4

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25
Q

tsh and free t4 levels in sick euthyroid syndrome

A

low tsh
low free t4

common in hospital inpatients
changes are reversible upon recovery from systemic illness and no treatment is usually needed

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26
Q

TSH and free T4 levels in subclinical hypothyroidism

A

high tsh and normal free T4

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27
Q

TSH and free t4 levels in someone with poor compliance with thyroxine

A

high tsh and normal free t4
patients who are poorly compliant may tae their thyroxine the day before a routine blood test
the thyroxine levels are hence normal but the TSH lags and reflects longer term low thyroxine levels

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28
Q

Thyroid autoantibodies that can be tested

A

Anti-thyroid peroxidase (anti TPO) antibodies
TSH receptor antibodies
thyroglobulin antibodies

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29
Q

Source of growth hormone

A

anterior pituitary

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30
Q

What is growth hormone responsible for

A

stimulating cell reproduction and growth of organs, muscles, bones and height
stimulates release of insulin like growth factor (IGF-1) by the liver which is also important in promoting growth in children and adolescents

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31
Q

Congenital growth hormone deficiency

A

Results from disruption to growth hormone axis (at hypothalamus or pituitray gland)
can be due to genetic mutation of GH1 or GHRHR(growth hormone releasing hormone receptor)
or due to empty sella syndrome (where pituitary is under developed or damaged

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32
Q

Acquired growth hormone deficiency

A

secondary to trauma, infection or interventions such as surgery

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33
Q

Presentation of growth hormone deficiency in neonates and older infants

A

neonates = micropenis, hypoglycaemia and severe jaundice

older infants = poor growth (usually stopping/severely slowing from 2-3). short stature, slow devlopment of movement and strength and delayed puberty

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34
Q

growth hormone stimulation test

A

involves measuring medications that normally stimulate release of GH (like glucagon, insulin, arginine adn clonidine)
GH levels are monitored for 2-4 hours after administering medication to asses hormonal response
in GH deficiency their will be poor response to the stimulus

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35
Q

Other investigations for GH deficiency

A

other associated hormone deficiencies (thyroid and adrenal deficiency)
MRI brain for structural pituitary or hypothalamus abnormalitites
genetic testing - associated conditions like turner syndrome or prader willi syndrome
Xray of wrist or DEXA scan can determine bone age and help predict final height

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36
Q

Treatment of GH deficiency

A

daily s/c injections of GH (somatropin)
Treatment of other associated hormone deficiencies
close monitoring of height and development

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36
Q

Treatment of GH deficiency

A

daily s/c injections of GH (somatropin)
Treatment of other associated hormone deficiencies
close monitoring of height and development

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37
Q

Most common case of hypothyroidism in developing world

A

iodine deficiency

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38
Q

Source of cortisol

A

zona fasciculata of adrenal cortex

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39
Q

Functions of cortisol

A

increases BP - permits normal response to angiotensin II and catecholeamine by up regulating alpha 1 receptors on arterioles

inhibits bone formation - decreases osteoblasts, decreases type 1 collagen, decreases absorption of clacium from the gut, increases osteoclastic activity

increases insulin resistance

inhibits inflammatory and immune responses

maintains functions of skeletal and cardiac muscles

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40
Q

Regulation of cortisol

A

Increases secretion:
ACTH from the pituitary gland, itself stimulated by CRH (corticotrophin releasing hormone) released by the hypothalamus

stress

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41
Q

Glucagon source

A

alpha cells of pancreas

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42
Q

Function of glucagon

A

glycogenolysis
gluconeogenesis
lipolysis

(opposite metabolic effects to insulin)

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43
Q

What increases secretion of glucagon

A

hypoglycaemia
stresses (infections, burns, surgery)
Increased catecholeamines + sympathetic nervous system stimulation
increased plasma amino aicds

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44
Q

What decreases secretion of glucagon

A

hyperglycaemia
insulin
somatostatin
increased free fatty acids and keto acid

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45
Q

SGLT-2 inhibitors (-gliflozins)
mechanism of action
route
main side effects
notes

A

inhibits reabsorption of glucose in the kidney
oral
UTI
typically result in weight loss

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46
Q

Insulin
mechanism of action
route
main side effects
notes

A

direct replacement for endogenous insulin
s/c
hypoglycaemia, weight gain, lipodystrophy

used in all patients with T1DM and some patients with poorly controlled T2DM

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47
Q

Metformin
mechanism of action
route
main side effects
notes

A

increases insulin sensitivity and decreases hepatic gluconeogenesis
oral
GI upset, lactic acidosis

first line medication in management of T2DM

cannot be used in patients with an eGFR <30ml/min

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48
Q

Sulfonylureas
mechanism of action
route
main side effects
notes

A

stimulate pancreatic beta cells to secrete insulin
Oral
Hypoglycaemia, weight gain, hyponatraemia
examples include gliclazide and glimepiride

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49
Q

Thiazolidinediones
mechanism of action
route
main side effects
notes

A

activate PPAR-gamma receptor in adipocytes to promote adipogenesis and fatty acid uptake
oral
weight gain, fluid retention

only available one is pioglitazone

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50
Q

DPP-4 inhibitors (-gliptins)
mechanism of action
route
side effects
notes

A

increases incretin levels which inhibit glucagon secretion
oral
generally well tolerated but increased risk of pancreatitis

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51
Q

primary hyperparathyroidism characteristically has hypocalcaemia or hypercalcaeia

A

hypercalcaemia

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52
Q

Pseudohyperkalaemia

A

rise in serum potassium that occurs due to excessive leakage of potassium from cells during or after blood is taken
laboratory artefact and does not represent the true serum potassium
In this case potassium is released as the large number of platelets aggregate and degranulate

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53
Q

Causes of pseudohyperkalaemia

A

haemolysis during venepuncture (excessive vacuum of blood drawing, prolonged tourniquet use or too fine a needle gauge)
delay in processing of blood specimen
abnormally high number of platelets, leukocytes or erythrocytes (such as myeloproliferative disorders)
familial causes

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54
Q

Compartment syndrome

A

particular complication that may occur following fractures

characterised by raised pressure within a closed anatomical space
raised pressure eventually compromises the tissue perfusion resulting in necrosis
two main fractures that cause this are supracondylar fractures and tibial shaft fractures

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55
Q

Features of compartment syndrome

A

pain, especially on movement
paraesthesiae
pallor
arterial pulsation may still be felt as the necrosis occurs as a result of microvascular compromise
paralysis of muscle group

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56
Q

How is a diagnosis of compartment syndrome made

A

measurement of intracompartmental pressure measurements
pressure in excess of 20mmHg are abnormal and >40mmHg is diagnostic

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57
Q

Treatment for compartment syndrome

A

prompt and extensive fasciotomies
in lower limb deep muscles may be inadequately decompressed by inexperienced operator
myoglobinuria may pccur following fasciotomy and result in renal failure (require aggressive IV fluids)
Death of muscle groups occur within 4–6 hours

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58
Q

first hormone secreted in hypoglycaemia

A

glucagon

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59
Q

Community management of hypoglycaemia

A

oral glucose 10-20g in liquid, gel or tablet form
alternatively quick acting carbohydrate like GlucoGel or DextroGel
HypoKit may be prescribed which contains a syringe and vial of glucagon IM or SC injection

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60
Q

Hospital management of hypoglycaemia

A

quick acting carbohydrate (GlucoGel or DextroGel) if alert
if unalert Sc/IM injection of glucagon
alternatively IV 20% glucose solution through a large vein

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61
Q

Carcinoid syndrome

A

occurs when metastases are present in liver and release serotonin into systemic circulation
may also occur with lung carcinoid as mediators are not cleared by liver

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62
Q

Features of carcinoid tumours

A

flushing
diarrhoea
bronchospasm
hypotension
right heart valvular stenosis
ACTH and GHRH may be secreted resulting in cushings

63
Q

Investigations for carcinoid tumours

A

urinary 5-HIAA
plasma chromogranin A y

64
Q

management of carcinoid tumours

A

somatostatin analogues (octreotide)
for diarrhoea cyproheptadine may help

65
Q

How does loperamide slow down bowel movements

A

acts on mu opioid receptors in the myenteric plexus of the large intestine

66
Q

features of hypocalcaemia

A

tetany - muscle twitching, cramping and spasm
perioral paraesthesia
if chronic - depression, cataracts
ECG: prolonged QT interval

67
Q

Trousseau’s sign

A

sign of hypocalcaemia
carpal spasm if brachial artery occluded by inflating BP cuff and maintaining pressure above systolic
seen in around 95% patients

68
Q

Chvostek’s sign

A

sign of hypocalcaemia
tapping over parotid causes facial muscles to twitch

69
Q

Second line therapy for patients who are unable to tolerate side effects of statins

A

ezetimibe

70
Q

what is ezetimibe

A

lipid-lowering drug which inhibits cholesterol receptors on enterocytes, decreasing cholesterol absorption in small intestine

71
Q

What medication acutely prescribed may cause issues with diabetic control?

A

Corticosteroids like prednisolone

72
Q

How does Antidiuretic hormone promote water reabsorption

A

by the insertion of aquaporin-2 channels in the collecting ducts of the kidneys

73
Q

Causes of hypercalcaemia

A

CHIMPANZEES
Calcium supplementation
Hyperparathyroidism
Iatrogenic (drugs: thiazides)
Milk Alkali syndrome
Paget disease of the bone
Acromegaly and Addisons disease
Neoplasia
Zollinger Ellison syndrome
Excessive vitamin D
Excessive vitamin A
Sarcoidosis

74
Q

First sign of male puberty

A

testicular enlargement

75
Q

What might happen if you abruptly stop someone’s long term steroids

A

Longer-term systemic corticosteroids suppress the natural production of endogenous steroids. They should therefore not be withdrawn abruptly, as this may precipitate an Addisonian crisisAddisonian crisis is characterised by vomiting, hypotension, hyperkalaemia, and hyponatremia.

76
Q

Where is prolactin secreted

A

Anterior pituitary gland

77
Q

Function of prolactin

A

stimulates breast development
stimulates milk production
decreases GnRH pulsatility at the hypothalamic level and to a lesser extent, blocks the action of LH on the ovary or testis.

78
Q

What increases the secretion of prolactin

A

thyrotropin releasing hormone
pregnancy
oestrogen
breastfeeding
sleep
stress
drugs, metoclopramide and antipyschotics

79
Q

What decreases secretion of prolactin

A

dopamine
dopaminergic agonists

80
Q

What is Leptin

A

Leptin is a hormone secreted by adipose tissue, playing an important role in satiety and fullness. Mutations that disrupt leptin signalling have been implicated in monogenic obesity, manifesting clinically as severe childhood-onset obesity.

81
Q

What is Ghrelin

A

Ghrelin is known as the ‘hunger hormone’, mediating feelings of hunger. Decreased ghrelin synthesis would result in diminished hunger and does not manifest clinically as obesity.

82
Q

What is mydriasis

A

dilation of pupils

83
Q

What increases secretion of ADH

A

ECF osmolality increase
Volume decrease
pressure decrease
angiotensin II

84
Q

What decreases secretion of ADH

A

ECF osmolality decrease
volume increase
temperature decrease

85
Q

How does carbimazole work

A

blocks thyroid peroxidase from coupling and iodinating the tyrosine residues on thyroglobulin → reducing thyroid hormone production

86
Q

Parathyroid hormone effects on the bone

A

Binds to osteoblasts which signal to osteoclasts to cause resorption of the bone and release calcium

87
Q

Parathyroid hormone effects on the kidneys

A

Active reabsorption of calcium and magnesium from the distal convoluted tubule
decreases reabsorption of phosphate

88
Q

Parathyroid hormone effects on the intestine via the kidneys

A

Increases intestinal calcium absorption by increasing activated vitamin D
Active vitamin D increases calcium reabsorption

89
Q

What do SGLT-2 inhibitors do

A

reversibly inhibit sodium-glucose co-transporter 2 (SGLT-2) in the renal proximal convoluted tubule to reduce glucose reabsorption and increase urinary glucose excretion.
Examples include canagliflozin, dapagliflozin and empagliflozin.

90
Q

Important adverse effects of SGLT-2

A

urinary and genital infection (secondary to glycosuria). Fournier’s gangrene has also been reported
normoglycaemic ketoacidosis
increased risk of lower-limb amputation: feet should be closely monitored

91
Q

What does an excess of growth hormone increase the risk of

A

developing diabetes mellitus type 2

This is because the hormone mobilises glucose from fat stores (to build muscle), thus increasing its concentration in the blood. Subsequently, the pancreas has to secrete greater amounts of insulin to combat the increased levels of glucose.

92
Q

Symptoms of excess growth hormones

A

Other symptoms of excess growth hormone may include thickened skin, enlarged hands and feet, a prominent jaw, carpal tunnel syndrome, tiredness, muscle weakness and hypertension.

93
Q

Difference between a pancreatic psuedocyst and a pancreatic cyst

A

A pseudocyst is surrounded in granulation tissue, as opposed to a true cyst which is surrounded with epithelial tissue

94
Q

what do Dipeptidyl peptidase-4 (DPP-4) inhibitors (e.g. Vildagliptin, sitagliptin) do

A

dipeptidyl peptidase-4, DPP-4 inhibitors increase levels of incretins (GLP-1 and GIP) by decreasing their peripheral breakdown

95
Q

Pretibial myxoedema

A

localised skin lesion
classically on the skin in front of the tibia
development is due to an increase of glycosaminoglycans in the pretibial dermis
associated with grave’s disease

96
Q

Sulfonyureas mechanism of action

A

Increase stimulation of insulin by pancreatic B cells and decrease hepatic clearance of insulin

97
Q

Where is ACE produced

A

pulmonary endothelium

98
Q

Features of addisons

A

lethargy, weakness, anorexia, nausea and vomiting, weight loss, salt craving
hyperpigmentation (especially palmar creases), vitiligo, loss of pubic hair in women, hypotension, hypoglycaemia
hyponatraemia and hyperkalaemia may be seen
crisis: collapse, shock, pyrexia

99
Q

Primary causes of hypoadrenalism

A

TB
metastases (bronchial carcinoma)
Meningococcal septicaemia (Waterhouse-Fredrichsen syndrome)
HIV
Antiphospholipid syndrome

100
Q

Empagliflozin mechanism of action

A

SGLT-2 inhibitor - reversibly inhibit sodium-glucose co-transporter 2 in the renal proximal convoluted tubule

101
Q

Insulin and potassium

A

decreases serum potassium through stimulation of the sodium potassium ATPase pump

102
Q

Pathophysiology of DKA

A

Caused by uncontrolled lipolysis (not proteolysis) which results in an excess of free fatty acids that are ultimately converted to ketone bodies

103
Q

Most common precipitating factors of DKA

A

Infection
missed insulin
MI

104
Q

Features of DKA

A

abdominal pain
polyuria, polydipsia, dehydration
Kussmaul respiration (deep hyperventilation)
acetone smelling breath

105
Q

Management of DKA

A

Fluid replacement: isotonic saline is used initially (even if severly acidotic)

Insulin: IV infusion at 0.1unit/kg/hour
Once glucose < 15mmol/l 5% dextrose infusion should be started

Correction of electrolyte disturbance: serum potassium is often high on admission despite total body potassium being low
potassium supplements may be needed

Long acting insulin should be continued and short acting insulin should be stopped

106
Q

DKA resolution

A

Defined as
pH >7.3
blood ketones <0.6mmol/L
Bicarbonate >15mmol/L

107
Q

Complications

A

gastric stasis
thromboembolism
arrythmias secondary to hyperkalaemia/iatrogenic hypokalaemia
iatrogenic due to incorrect fluid therapy: cerebral oedema, hypokalaemia, hypoglycaemia
ARDS
AKI

108
Q

Magnesium and parathyroid hormone

A

enables secretion and function of parathyroid hormones
levels must be sufficient to allow parathyroid hormone to exert its effects

109
Q

Which metabolic disorder is hyperkalaemia associated with

A

Addisons

110
Q

Klinefelter’s syndrome

A

associated with karyotype 47, XXY
often taller than average
lack of secondary sexual characteristics
small, firm testes
infertile
gynaecomastia
elevated gonadotrophin levels but low testosterone

Diagnosis by karyotype

111
Q

What decreases the secretion of prolactin

A

dopamine
dopaminergic agonists

112
Q

Where are phaeochromocytomas found

A

adrenal medulla

113
Q

What are phaeochromoctomas associated with

A

MEN type II
neurofibromatosis
von hippel-lindau syndrome

114
Q

Features of phaeocromocytomas

A

hypertension
headache
palpitations
sweating
anxiety

115
Q

Tests for phaeochromocytomas

A

24hr urinary collection of metanephrines
(has replaced 24hr urinary collection of catecholamines)

116
Q

Management of phaeochromocytomas

A

surgery is definitive management
must first be stabilized with medical management
alpha blocker (phenocybenzamine) given before a beta blocker (propranolol)

117
Q

Kallmann’s syndrome

A

Recognised cause of delayed puberty secondary to hypogonadotropic hypogonadism
usually inherited as an X-linked recessive trait
thought to be caused by failure of Cn-RH secreting neurons to migrate to the hypothalamus

118
Q

Typical clue of kallmann’s syndrome in questions

A

associated with a lack of smell (anosmia) in a boy with delayed puberty

119
Q

Features of Kallmann’s syndrome

A

delayed puberty
hypogonadism
anosmia
sex hormone levels are low
LH, FSH levels are inappropriately low/normal
patients are typically of normal or above average height

120
Q

Source of prolactin

A

anterior pituitary

121
Q

Source of somatostatin

A

Delta cells of the pancreas, pylorus and duodeum

122
Q

Graves pathophysiology

A

Formation of IgG antibodies on the TSH receptors on the thyroid gland

123
Q

How can corticosteroids worsen diabetic control

A

due to their anti-insulin effects

124
Q

Example of minimal glucocorticoid activity but very high mineralocorticoid activity

A

fludrocortisone

125
Q

Example of glucocorticoid activity and high mineralocorticoid activity

A

hydrocortisone

126
Q

Example of predominant glucocorticoid activity and low mineralocorticoid activity

A

prednisolone

127
Q

Example of very high glucocorticoid activity and minimal mineralocorticoid activity

A

dexamethasone
betmethasone

128
Q

Glucocorticoid endocrine side effects

A

impaired glucose regulation
increased appetite/weight gain
hirsutism ( where women have thick, dark hair on their face, neck, chest, tummy, lower back, buttocks or thighs. )
hyperlipidaemia

129
Q

Glucocorticoid cushings side effect

A

moon face
buffalo hip
striae

130
Q

Glucocorticoid MSK side effects

A

Osteoporosis
proximal myopathy
avascular necrosis of the femoral head

131
Q

Glucocorticoid immunosuppresion side effects

A

increased susceptibility to severe infection
reactivation of TB

132
Q

Glucocorticoid psychiatric side effects

A

Insomnia
mania
depression
psychosis

133
Q

Glucocorticoid Gi side effects

A

Peptic ulceration
acute pancreatitis

134
Q

glucocorticoid ophthalmic side effects

A

glaucoma
cataracts

135
Q

T2DM medication that doesnt typically cause weight gain or hypoglycaemia

A

Metformin
Gliptins (DPP-4 inhibitors)

136
Q

What is leptin secreted by

A

adipose tissue

137
Q

DPP-4 inhibitors mechanism

A

work by inhibiting enzyme dipeptidyl peptidase 4
this enzyme acts to break down endogenos incretins such as GLP1 and GIP
in the body these molecules are released in response to food (they decrease appetite, increase insulin secretion and inhibit glucagon secretion to lower blood glucose levels)
as DPP 4 inhibitors inhibit the breakdown of these molecules their effect is increased leading ot the anti-diabetic role of this medication

138
Q

What step is essential for the formation of all steroid hormones?

A

conversion of cholesterol to pregnenolone
pregnenolone is precursor for all steroid hormones
takes place within mitochondria

139
Q

Primary hypogonadism (Klinefelter’s syndrome)
Lh and testosterone levels

A

LH - high
testosterone Low

140
Q

Hypogonadotrophic hypogonadism (Kallman’s syndrome)
LH and testosterone levels

A

LH-low
testosterone - low

141
Q

Androgen insensitivity syndrome
LH and testosterone levels

A

LH high and testosterone normal/high

142
Q

Testosterone-secreting tumour
LH and testosterone levels

A

LH low
Testosterone high

143
Q

How does orlistat work and what is it used for

A

reduces fat digestion by inhibiting lipase
anti-obesity agent

144
Q

What are these examples of?
gliflozin (dapagluflozin)
tolbutamide
exenatide
linagliptin
pioglitazone

A

gliflozin - SGLT-2 inhibitor
tolbutamide - sulfonylurea
exenatide - glp-1 receptor agonist
linagliptin is a DPP 4 inhibitor
piolitazone is a thiazonlidinedione

145
Q

What can you use to assess endogenous insulin production

A

C-peptide is secreted in proportion to insulin

146
Q

What is fragment E

A

fibrinogen degradation product produced alongside D dimer upon break down of a clot

147
Q

What is Addison’s disease

A

Specific condition where the adrenal glands have been damaged, resulting in reduced secretion of cortisol and aldosterone. Most common cause is autoimmune

148
Q

Symptoms of Addison’s disease

A
  • Fatigue
  • Nausea
  • Cramps
  • Abdominal pain
  • Reduced libido
149
Q

Signs of Addison’s disease

A
  • Bronze hyperpigmentation to skin (ACTH stimulates melanocytes to produce melanin)
  • Hypotension (particularly postural hypotension)
150
Q

Investigations for Addison’s disease

A

FBC & U&Es - hyponatraemia and hyperkalaemia
Short synacthen test - first line to diagnose adrenal insufficiency
ACTH - ACTH is high
Adrenal autoantibodies - adrenal cortex antibodies and 21-hydroxylase antibodies

151
Q

Short synacthen test

A

Synacthen is synthetic ACTH
Test used to diagnose adrenal insufficiency (like for Addison’s)
Ideally performed in the morning
Blood cortisol is measure at baseline, 30 & 60 mins after synacthen administration
Synthetic ACTH will stimulate healthy adrenal glands to produce cortisol and the cortisol level should at least double
Failure of this process is indicative of primary adrenal insufficiency (Addison’s)

152
Q

Treatment for Addison’s

A

Replacement steroids titrated to signs, symptoms and electrolytes
Hydrocortisone to replace cortisol
Fludrocortisone to replace aldosterone (if needed)
Patients also given steroid card and emergency ID for emergency services to know they are on long term steroids

153
Q

How does an Addisonian crisis typically present

A

Reduced consciousness
Hypotension
Hypoglycaemia, hyponatraemia, hyperkalaemia
Patients can be very unwell

154
Q

Do you do investigations for someone presenting in an addisonian crisis

A

you don’t wait for a definitive diagnosis before treating because it is life threatening

155
Q

Management for addisonian crisis

A

intensive monitoring
parenteral steroids (IV hydrocortisone 100mg stat then 100mg every 6 hours)
Iv fluid resus
Correct hypoglycaemia
Careful monitoring of electrolytes and fluid balance

Year 3 (14 decks)

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