Endocrine Flashcards

1
Q

What hormones to anterior pituitary release

A
  • FSH and LH
  • ACTH
  • TSH
  • Prolactin and endorphins
  • Growth hormone
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2
Q

Posterior pituitary hormones

A
  • Oxytocin
  • ADH
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3
Q

Actions of cortisol

A
  • Increase alertness
  • Inhibit immune system
  • Inhibit bone formation
  • Raise blood glucose
  • Increases metabolism
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4
Q

Adrenal axis

A
  • Hypothalamus produces CRH
  • AP produces ACTH
  • Adrenal produces cortisol
  • neg fb loop
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5
Q

what is cushings

A
  • prolonged levels of corticosteroid in body
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6
Q

Causes cushing

A
  • Disease = pituitary adenoma
  • Corticosteroids
  • Paraneoplastic
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7
Q

Cushing S+S

A
  • Round face
  • Central obesity and stretch marks
  • Proximal wasting
  • hirsutism
  • Bruising
  • buffalo hump
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8
Q

metabolic affects cushings

A
  • HTN
  • DM2
  • cardiac hypertrophy
  • Dyslipidaemia
  • Osteoporosis
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9
Q

cushings Ix

A
  • 24hr urinary free cortisol
  • bloods
  • MRI for PA
  • CT if cancerour cause
  • dex suppression test = gold standard
  • hypokalaemic metabolic alkalosis
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10
Q

Mx cushings

A
  • adenoma = trans sphenoidal
  • surgery on tumours
  • adrenalectomy
  • metyrapone
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11
Q

dex suppression test results

A
  • Normal = respond to dex and suppress cortisol
  • Adrenal adenoma = high even after high dose, acth low
  • Pituitary adenoma = low dose not suppressed, high dose is suppressed and ACTH high
  • Ectopic = all high
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12
Q

Whats primary adrenal insufficiency

A
  • Addisson’s
  • Damaged glands = reduced cortisol and aldosterone
  • ACTH high as no neg FB
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13
Q

Secondary adrenal insufficiency

A
  • Inadequate ACTH
  • Lack of stimulation to glands
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14
Q

Tertiary adrenal insufficiency

A
  • Inadequate CRH
  • steroids cause hypothalamus suppression
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15
Q

Addisons specific S+S

A
  • Bronze hyperpigmentation
  • Hypotension
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16
Q

General adrenal insufficiency S+S

A
  • fatigue
  • muscle weakness and cramps
  • dizzy
  • thirsty
  • weight loss
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17
Q

Ix adrenal insufficiency

A
  • hyponatraemia
  • short synacthen test = synthetic ACTH
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18
Q

S+S adrenal crisis

A
  • reduced consciousness
  • hypotension
  • hypoglycaemia
  • hyponatraemia
  • hyperkalaemia
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19
Q

Mx adrenal crisis

A
  • A-E
  • 100mg hydrocortisone
  • IV fluids
  • correct hypo
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20
Q

GH axis

A
  • GHRH released from hypothalamus
  • causes AP to release GH
  • GH stimulates IGF-1 from liver
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21
Q

Actions GH

A
  • Bone growth
  • Bone density and strength
  • Cell regeneration and reproduction
  • Internal organ growth
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22
Q

causes acromegaly

A
  • pituitary adenoma
  • lung/panc cancer
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23
Q

S+S acromegaly

A
  • Bitemporal hemianopia if space occ
  • frontal bossing
  • sweating
  • macroglossia, large nose
  • large hands and feet
  • prognathism
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24
Q

metabolic affects acromegaly

A
  • hypertrophic heart
  • HTN
  • T2DM
  • arthritis
  • Carpal tunnel
  • colorectal cancer
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25
Q

Ix acromegaly

A
  • IGF1
  • GH suppression test
  • MRI
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26
Q

Mx acromegaly

A
  • Trans-sphenoidal surgery
  • Pegvisomant
  • Ocreotide = somatostatin anologue
  • Dopamine agonist
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27
Q

Parathyroid axis

A
  • PTH released in response to low Ca
  • Kidney increases reabsorption of Ca
  • Increased osteoclast activity
  • Intestinal absorption of Ca through vit D
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28
Q

S+S hypercalcaemia

A
  • Kidney stones
  • Painful bones
  • Abdo groans = cnstipation, N+V, polyuroa and dipsia
  • psych moans
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29
Q

Primary hyperparathyroidism

A
  • Uncontrolled PTH production by tumout of glands
  • Hypercalcaemia
  • Remove surgically
  • PTH and Ca high
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30
Q

Secondary hyperparathyroidism

A
  • Insufficient Vit D reduces Ca reabsorption from intestines, kidneys and bones
  • Serum Ca normal/low, PTH high
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31
Q

Tertiary hyperparathyroidism

A
  • When secondary HPT goes on too long = hyperplasia
  • High PTH and Ca
  • Remove PT tissue
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32
Q

RAAS

A
  • Renin prodiced in afferent arterioles in response to hypoTN
  • Renin converts angiotensin to AG1
  • In lungs ACE converts AG1 to AG2
  • AG2 = vasocinstricts = increases BP
  • AG2 = aldosterone from adrenals = hypertrophy of myocytes
  • Aldosterone acts on kidneys = Na reabsorption in DT = water into kidneys = increases BP
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33
Q

Conns syndrome

A
  • Adrenal adenoma
  • Causes high levels of aldosterone
  • ARR = high aldosterone and low renin
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34
Q

Secondary hyperaldosteronism

A
  • excessive renin = excess aldosterone
  • Renal artery stenosis and HF
  • ARR = high both
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35
Q

Mx hyperaldosteronism

A
  • Aldosterone antagonists = spironolactone, eplerenone
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36
Q

ADH axis

A
  • Low water content in blood
  • PP releases more ADH
  • High volume water reabsorbed by kidney
  • Concentrated urine and more water in blood
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37
Q

SAIDH is

A
  • Increased ADH from PP = increased water reabsorbed = hyponatraemia
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38
Q

causes SIADH

A
  • Increased secretion
  • SCLC
  • Post operation
  • SSRI
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39
Q

S+S SIADH

A
  • Hyponatramia
  • headache
  • fatigue
  • cramps and confusion
  • seizures if severe
40
Q

Clinical features SIADH

A
  • Euvolaemia
  • Hypona
  • Low serum osmolality
  • high urine Na
  • high urine osmolality
41
Q

Mx siadh

A
  • admit if Na <125
  • find and treat underlying cause
  • fluid restrict
  • Vasopressor receptor antagonists = tolvaptan
  • Correct slowly to prevent demyelination = no more than 10mmol/l change in 24hrs
42
Q

nephrogenic diabetes insipidus

A

collecting ducts dont respond to ADH

43
Q

Cranial DI

A

hypothalamus doesnt produce ADH for PP to secrete

44
Q

S+S DI

A
  • polyuria >3l
  • polydypsia
  • dehydration
  • postural hypotension
45
Q

Ix DI

A
  • low urine osmolality
  • High serum osmolality
  • Water deprivation test
46
Q

water deprivation test results

A
  • Primary polysipis = urine osmolality after deprivation high
  • CDI = UO low after deprivation, high after desmopressin
  • NDI = UO low after deprivation and desmopressin
47
Q

Phaeochromocytoma

A
  • Adrenal tumour = excessive adrenaline release
  • Ix = plasma free metaneprines and 24hr urine catecholamines
  • Mx = removal, BB, AB
48
Q

thyroid axis

A
  • hypothalamus releases TRH
  • Stimulates AP to release TSH
  • = thyroid gland produces T3 and T4
  • Neg FB
49
Q

Primary hyperthyroidism

A
  • thyroid produces excess thyroid hormone
50
Q

Secondary hyperthyroidism

A
  • Hypothalamus or pituitary patholody
  • pituitary produces too much TSH
51
Q

Graves

A
  • Autoimmune
  • TSH receptor antibodies cause primary hyperthyroidism
  • TSHRA = stimulate TSHR on thyroid
  • Causes exophthalmos and pretibial myxoedema
52
Q

thyroiditis causes

A

= hyperthyroidism followed by hypothyroidism
- De Quervains
- Hashimotos
- Postpartum
- Drug induced

53
Q

S+S hyperthyroid

A
  • Anxiety
  • Sweating
  • Tachy
  • Weight loss, fatigue and insomnia
  • Loose stools
  • Sexual dysfunction
54
Q

S+S graves

A
  • Diffuse goitre
  • Exopthalmos
  • Pretibial myxoedema
  • hand swelling and finger clubbing
55
Q

WHat is the intitial thyrotoxic phase

A
  • Excessive thyroid hormones
  • Thyroid swelling and tenderness
  • Flu like illness
  • Raised inflamatory markers
  • Self limiting but some remain hypo
56
Q

thyrotoxic crisis

A
  • Fever, tachy and delirium
  • May need fluid resus, anti-arrythmic meds and BB
57
Q

Mx hyperthyroid

A
  • carbimazole (Can cause pancreatitis and agranulocytosis)
  • BB
58
Q

primary hypothyroidism

A
  • Thyroid behaves abnomrally = produces inadequate thyroid hormones
  • _ve FB absent
59
Q

secondary hypothyroidism

A
  • pituitary produces inadequate tsh
  • = tumours and surgery
60
Q

causes primary hypothyroid

A
  • Hashimotos = autoimmune anti TPO and andi tG
  • Iodine deficiency
  • Lithium
61
Q

S+S hypothyroid

A
  • Weight gain
  • Dry skin
  • Coarse hair and loss
  • fluid retention
  • heavy periods
  • constipation
62
Q

Mx hypothyroid

A
  • levothyroxine
63
Q

Thyroid blood results

A

1 hyper = low TSH, high T3/4
2 hyper = both high
1 hypo = high TSH low T3/4
2 = both low

64
Q

What is type 1 diabetes

A
  • Pancreas stops being able to produce adequate insulin
  • Less insulin = less glucose absorption
65
Q

what cells produce insulin

A

beta cells in islet of langerhans

66
Q

how dies insulin reduce glucose

A
  • causes cells to absorb glucose as fuel
  • Causes muscle and liver to absorb glucose as glycogen
67
Q

what is glucagon

A
  • hormone produced by alpha cells in islets of langerhans
68
Q

when is glucagon released

A
  • in response to low blood sugar
  • glycogenolysis and gluconeogenesis
69
Q

when are ketones produces

A

when there is insufficient glucose supply = ketones are water soluble fatty acids used as fuel = can cross BBB

70
Q

3 key features of DKA

A
  • Ketoacidosis
  • Dehydration
  • K imbalance
71
Q

how does polyruia occur in DM

A
  • Hyperglycaemia = overwhelms kidneys
  • GLucose leaks to urine
  • Glucose draws water by osmotic diuresis
72
Q

How os K affected in DM

A
  • Insulin drives K into cells
  • No insulin = K not stored in cells
73
Q

presentation DKA

A
  • Hyperglycaemia
  • Dehydration
  • Ketosis
  • Met acidosis
  • K imbalance
  • Polyuria and dipsia, N+V, acetone, hypotn
74
Q

diagnosisn DKA requires all 3 of…

A
  • Hyperglycaemia >11
  • Ketosis blood >3mmol
  • Acidosis <7.3
75
Q

Mx DKA

A

FIG PICK
- Fluids = IV resus normal saline
- Insulin = fixed rate e.g. actrapid 0.1/kg/hr
- Glucose = monitor and infuse if <14
- Potassium = add K to fluids
- Infection = treat cause
- Chart fluid balance
- Ketones monitor

76
Q

Complications DKA

A
  • Hypo
  • HypoK
  • Cerebral oedema
  • Pulmonary oedema
77
Q

T1DM Mx

A
  • Basal bolus
78
Q

Mx hypoglycaemia

A
  • <4 on the floor
  • Conscious and alert = juice, gel 15g etc.
  • Conscious and confused = 200mls 10% glucose over 10 mins or 1mg IM glucagon
79
Q

DM macrovascular complications

A
  • CAD
  • Peripheral ischaemia
  • Stroke
  • HTN
80
Q

Microvascular complications

A
  • Peripheral neuropathy
  • Retinopathy
  • Kidney disease
81
Q

T2DM patho

A
  • Exposure to glucose and insulin = resistant to insulin
  • More and more insulin needed to stimulate cells = fatigues the pancreas and output reduced
82
Q

Pre diabetes

A

HbA1c 42-47 mmol/mol

83
Q

diabetes HbA1c

A

48mmol/mol or higher

84
Q

Mx T2DM

A
  1. Metformin then…
  2. SGLT2 inhibitors (dapaglifozin)
85
Q

Metformin SE

A
  • diarrhoea, vomiting, lactic acidosis
86
Q

When to stop metformin

A
  • Not E+D
  • AKI
  • Raised lactate
  • Contrast
87
Q

Sulfonureas SE

A
  • ides = gliclazide = spank the panc
  • weight gain, hypo
  • stop in hypo
88
Q

thiazolidediones SE

A
  • glitazones
  • weight gain, retention, HF
  • stop in fluid overload of bladder cancer
89
Q

Gliptin SE

A
  • pancreatitis, nausea
  • eanatide also cause pancreatitis
90
Q

SGLT2 inhibitors SE

A
  • = flozins
  • candidiasis
  • UTI
91
Q

Hyperosmolar hyperglycaemic state

A
  • T2DM complication
  • Hyperosmolality, hyperglycaemia and absence of ketones
  • Polyuria, dipsia, WL, confision, tach and htpotn
  • IV fluids
92
Q

metformin MoA

A
  • Improves insulin sensitivity in liver/muscle
  • suppresses hepatic gluconeogenesis
  • se = nausea, diarrhoea
93
Q

DDP4i example, MoA, SE

A
  • Linagliptin
  • Incretin effect
  • Pancreatitis
94
Q

Sulfonylurea MoA example SE

A
  • Gliclazide
  • enhances insulin secretion
  • hypoglycaemia
95
Q

SGLT2 example moa se

A
  • emagliflozin
  • reduced renal glucose reabosrption
  • euglycaemic ketoacidosis, thrush
96
Q

thyroid swell movement on exam

A
  • moves upwards on swallowing
97
Q

thyroglossal cyst

A
  • midline, between thyroid and hyoid
  • upwards on tongue protrusion