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Phase 2a Lauren > Peer Teaching Endo > Flashcards

Peer Teaching Endo Flashcards

1
Q

What hormone are thyroid disorders to do with?

A

T4

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2
Q

Which hormone is Cushing’s to do with?

A

Too much cortisol

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3
Q

Which hormone is acromegaly to do with?

A

Too much GH

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4
Q

Which hormone is Conn’s to do with?

A

Too much aldosterone

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5
Q

Which hormone is Addison’s to do with?

A

Too little cortisol & too little aldosterone

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6
Q

Which hormone is diabetes insipidus to do with?

A

Not enough ADH

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7
Q

What does CRH released by the hypothalamus do?

A

Act on ant. pituitary —> ACTH —> Adrenal cortex —> glucocorticoids

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8
Q

What does GRH released by the hypothalamus do?

A

Act on ant. pituitary —> LH & FSH —> gonads —> various effects inc. producing testosterone and oestrogen

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9
Q

What does GHRH released by the hypothalamus do?

A

Act on ant. pituitary —> GH —> liver —> IGF-1

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10
Q

What does TRH released by the hypothalamus do?

A

Act on ant. pituitary —> TSH —> thyroid —> T3 & T4

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11
Q

What does dopamine released by the hypothalamus do?

A

Ant. pituitary -x-> DECREASED prolactin

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12
Q

Which two hormones are stored in the posterior pituitary for release?

A

Oxytocin

Vasopressin (ADH)

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13
Q

What is hyperthyroidism?

A

Excess thyroid hormone
Females&raquo_space; males
Mainly 20-40yo

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14
Q

What are the causes of hyperthyroidism?

A

Graves’ - 2/3rds
Toxic multinodular goitre
Toxic thyroid adenoma
Less common: iodine excess congenital

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15
Q

What are the symptoms of hyperthyroidism?

A 
Diarrhoea, 
Weight loss,
Sweats,
Heat tolerance,
Palipitations,
Tremor,
Anxiety,
Menstrual disturbance
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16
Q

Signs of hyperthyroidism?

A 
Tachycardia
Thin hair,
Lid lag,
Onycholysis (nail comes away from the nail bed),
Lid retraction,
Exophthalmos (eyes sticking out)
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17
Q

What would the bloods show in primary hyperthyroidism?

A

Low TSH, High T3/T$

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18
Q

What would the bloods show in secondary hyperthyroidism?

A

High TSH, High T3/T4

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19
Q

Apart from TSH and T3/4, what other investigations could you do to diagnose hyperthyroidism?

A
  • Thyroid autoantibodies (thyroid peroxidase thyroglobulin, TSH receptor antibody)
  • Radioactive iodine isotope uptake scan
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20
Q

What drugs would you use for rapid symptom control in hyperthyroidism?

A

B-Blocker

eg. Propanalol

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21
Q

What drugs would you use to treat hyperthyroidism?

A

Antithyroid drug
Thionamides
eg. CARBIMAZOLE

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22
Q

What non-pharmacological treatments would you use for hyperthyroidism?

A

Radioiodine therapy

Thyroidectomy

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23
Q

What is graves’ diesease?

A
  • AUTOIMMUNE
  • IgG autoantibodies
  • High TSH receptor stimulator antibody (TRAb) = excess TH secretion
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24
Q

What unique signs would you see in graves’ disease?

A

Graves’ opthamlmology - extraocular muscle swelling, eye discomfort, lacrimation, diplopia

Thyroid acropachy (clubbing, finger and toe swelling)

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25
Q

What are the main causes of hypothyroidism?

A

Hashimoto’s thyroisitis,

iodine deficiency, previous radioiodine therapy, overtreatment of hyperthyroidism

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26
Q

What are the symptoms of hypothyroidism?

A 
Fatigue/tiredness/lethargy
Cold intolerance
Weight gain (& anorexia)
Myalgia
Constipation
Oedema
Mennorrhagia
Hoarse voice
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27
Q

What are the signs of hypothyroidism?

A

BRADYCARDIAC

Bradycardia
Reflexes relax slowly
Ataxia
Dry thin hair/skin
Yawning 
Cold hands
Ascites
Round puffy face
Defeated demeanor
Immobile
Congestive HF
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28
Q

What is the main cause of acromegaly?

A

Pituitary adenoma

Slow onset over many years

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29
Q

What are the symptoms of acromegaly?

A

Acroparaestesia, arthralgia, sweating, decreased libido, headache

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30
Q

What are the signs of acromegaly?

A 
Massive growth of hands, feet and jaw
Big tongue with widely spaced feet,
Puffy lips, eyelids and skin,
Darkening skin
Obstructive sleep apnoea
deep voice
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31
Q

What investigation is diagnostic for acromegaly?

A

NOT random growth hormone test because GH is a pulsatile protein and levels vary throughout the day

Oral glucose tolerance test:
-Normally a rise in blood glucose will suppress GH levels
-Give glucose and then test GH levels, if still high this is
diagnostic for acromegaly

MRI the pituitary fossa for adenomas

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32
Q

What is the first-line treatment for acromegaly?

A

Trans-sphenoidal surgery

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33
Q

What is the treatment for acromegaly if surgery fails?

A

Somatostatin analogues (SSA) eg. IM Octreotide/IM lanreotide

GH Receptor antagonists
eg. SC Pegvisomant

Dopamine agonist
eg. Oral cabergoline

Radiotherapy

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34
Q

Define Conn’s?

A

Excess production of aldosterone independent of the
renin-angiotensin-aldosterone system

Aldosterone works in the kidney to cause potassium loss,
excess causes hypokalaemia and sodium & water retention

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35
Q

What are the causes of Conn’s?

A 
2/3rds = Conn's syndrome: a solitary aldosterone producing adenoma
1/3 = bilateral adrenocortical hyperplasia
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36
Q

What are the symptoms of hypokalaemia AND HENCE CONN’S?

A 
Constipation
Weakness and cramps
Paraesthesia
polyuria & polydipsia
Heart rhythm changes
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37
Q

What are the signs of hypokalaemia AND HENCE CONN’S?

A

Hypertention

Metabolic alkalosis - due to H secretion in alpha intercalated cells

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38
Q

What are the investigations for Conn’s?

A 
U&Es
Decreased renin
Increased aldosterone
ECG: flat T, long PR, long QT, U waves
Adrenal CT
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39
Q

What are the treatment for Conn’s?

A

Laparoscopic adrenalectomy

Aldosterone antagonist
eg. Spironolactone

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40
Q

When do the parathyroids secrete PTH?

A

In response to low Ca levels

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41
Q

What is the action of PTH?

A

-Increased bone resorption by osteoclasts
-Increased intestinal calcium absorption
-Actives 1,25-dihydroxyVD (calcitriol) in kidney
-Increased calcium reabsorption and
phosphate excretion in the kidney

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42
Q

What is the cause of hyperparathyroidism?

A 
80% = solitary adenoma
20% = parathyroidhyperplasia
Rare = parathyroid cancer
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43
Q

What can hyperparathyroidism be secondary to?

A

CKD, Vitamin D deficiency, GI disease eg. Chron’s

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44
Q

What are the signs and symptoms of hyperparathyroidism?

A

Bones, stones, groans and psychic moans:
-Bones - bone resorption from PTH - pain, fractures, osteopenia etc
Stones - excess Ca - renal colic, biliary stones
-Groans - abdo pain, malaise, nausea, constipation, polydipsia etc
-Psychiatric moans - depression, anxiety etc.

HTN

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45
Q

What are the blood results for primary hyperparathyroidism?

A

High PTH
High Calcium
Low Alk. Phos.

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46
Q

What are the blood results for secondary hyperparathyroidism?

A

High PTH
Low Calcium
High Alk. Phos.

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47
Q

What are the blood results for tertiary hyperparathyroidism?

A

High PTH
High Calcium
High Alk. Phos.

High everything! progression of everything!

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48
Q

What other investigations apart from bloods can you do for hyperparathyroidism?

A

Increased 24hr urinary calcium excretion

DEXA scan for osteoporosis

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49
Q

What is the treatment for hyperparathyroidism?

A

Fluids,
Surgically manage underlying cause
Bisphosphonates

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50
Q

What are the causes of hypoparathyroidism?

A 
Autoimmune destruction of PT glands
Congenital
Surgical removal (secondary) 
Mg deficiency
VD deficiency
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51
Q

What are the signs and symptoms of hypoparathyroidism?

A

Same as hypocalcaemia..

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52
Q

What is the treatment of hypoparathyroidism?

A

Calcium supplements

Vitamin D analogue
eg. CALCITRIOL

Synthetic PTH

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53
Q

What is pseudohypothyroidism?

A

Decreased RESPONSE to PTH

54
Q

What is the bloodwork for pseudohypothyroidism?

A

Low Ca, high PTH

Treat as hypoparathyroidism

55
Q

What is the range for hypokalemia?

A

<3.5mmol/L

56
Q

What does hypokalemia cause?

A

Low K+ in serum = water concentration gradient out of cell

Increased leakage from ICF = hyperpolarisation of monocyte membrane = myocyte excitability

57
Q

What are the ECG changes for hypokalemia?

A

U have NO POT (K+), NO Tea but a LONG PR and a LONG QT.

1) U waves
2) No T waves/inversion
3) Long PR
4) Long QT

58
Q

What is the treatment for hypokalemia?

A

Give potassium

Oral/IV

59
Q

What are the ECG changes for hyperkalemia?

A

Tall tented T waves, small P, wide QRS

60
Q

What is the treatment for hyperkalemia?

A

Non urgent-
Polystyrene sulphonate resin = binds K+ in gut decreasing uptake

Urgent-
Calcium gluconate = decreases VF risk in the heart
Insulin = drives K+ into cells

61
Q

Why could ACEi cause hyperkalemia?

A

Blocks the binding of aldosterone to receptor

62
Q

Why could AKI cause hyperkalemia?

A

Decreased filtration rate so more K+ is maintained in blood

63
Q

Why could cause hypokalemia?

A

High aldosterone

64
Q

Would hypokalemia cause acidosis or alkalosis?

A

Alkalosis as H+ is transported out of cells and K+ in

65
Q

Would hyperkalemia cause acidosis or alkalosis?

A

Alkalosis as H+ is transported in of cells and K+ out

66
Q

What drugs could cause hypokalemia?

A

B2 agonists (SABA/LABA) - increase B2 pumping of K+ into cell

Insulin - K+ follows insulin into cells

67
Q

What drugs could cause hypokalemia?

A

B blocker - inhibits pumping of K+ into cell

68
Q

Potassium is important in maintaining resting potential.. what does this lead to?

A

Hypo - slows everything down
Constipation, weakness/cramps, arrythmias & palpitations

Hyper - speeds everything up
Cramping, weakness/flaccid paralysis, arrythmias & arrest

69
Q

Causes of hypocalemia?

A 
H - hypoparathyroidism (low phos)
A - acute pancreatitis (high phos)
V - vitamin D deficiency (high phos)
O - osteomalacia (high phos)
C - chronic kidney disease (low phos)
70
Q

Presentation of hypocalcemia?

A

SPASMODIC

Spasms
Perioral paraesthesia
Anxious, irritable, irrational
Seizures
Muscle tone increases in smooth muscle = wheeze
Orientation impaired & confusion
Dermatitis
Impetigo herpetiformis - reduced Ca2+& pustules in pregnancy
Chvostek’s sign, cataract, cardiomyopathy

71
Q

What ECG changes can you see in hypocalcaemia?

A

Long QT interval

72
Q

What is the treatment of hypocalcaemia?

A

Mild - Adcal

Severe - calcium gluconate

73
Q

What are the symptoms of hypercalcemia?

A

Bones, stones, moans and psychic moans

Painful bones
Kidney stones
Nausea, vomiting, constipation, indigestion
Lethargy, fatigue, memory loss, psychosis, depression

74
Q

What investigations would you do for hypercalcemia?

A

Find the cause:

  • Corrected calcium levels - big in cancer
  • PTH - high in hyperparathyroidism, low in cancer

Damage?

  • U&E - renal
  • X Ray

Treatment:
Saline (NaCl)
Bisphosphonates

75
Q

What is hypercalcemia of malignancy?

A

Causes osteoclast stimulation = increased bone breakdown
Inhibits osteoblast prrecursors

Most commonly in myeloma & non-hodgkin lymphoma

76
Q

What bloods would you expect in hypercalcemia?

A

CXR

Bloods = high Ca, high phosphate

77
Q

What ECG results would you expect in hypercalcemia?

A

Tented T waves, short QT interval

78
Q

What is the pathophysiology of cushing’s SYNDROME?

A

Excess cortisol
Loss of hypothalamic pituitary axis feedback
Loss of circadian rhythm

79
Q

What is the pathophysiology of cushing’s DISEASE?

A

All the factors of cushing’s syndrome + caused by pituitary adenoma

80
Q

What is the first line of treatment for iatrogenic causes of Cushing’s?

A

STOP STEROIDS

81
Q

What is the treatment for Cushing’s disease?

A

Trans-sphenoidal removal of pituitary adenoma

Bilateral adrenalectomy

82
Q

What is the treatment for ectopic Cushing’s syndrome?

A

Surgery if tumour is located and hadn’t spread

Adrenal Steroid Synthesis Inhibitors (inhibit cortisone synthesis) eg. MetyraponeTr

83
Q

Symptoms of Cushing’s?

A 
Cushing
Cataracts
Ulcers
Skin - striae
HTN, hyperglycaemia
Infections increase
Necrosis
Glucosuria
Aesthetic:
Truncal obesity
Moon face
Buffalo hump
Acne
Hirsutism
Weight gain
84
Q

What investigations would you undertake for Cushing’s?

A

NOT random plasma cortisol - pulsatile, stress, illness etc

Dexamethasone supression test: failure to suppress in 24hrs = cushing’s

24hr urinary free cortisol, normal = unlikely

85
Q

Treatment for adrenal adenoma cushing’s?

A

Adrenalectomy, radiotherapy

86
Q

Risk factors for DMT2?

A 
Male
Asian
Older
Obese
Lack of exercise
High calorie intake
87
Q

Symptoms for DMT2?

A

Asymptomatic

Late: hyperglycaemia, polyuria, polydipsia

88
Q

Investigations and diagnostic for DMT2?

A

Random plasma glucose - >11.1
Fasting plasma glucose >7
2 hr post-prandial >11.1
HbA1c >48mmol/mol

89
Q

Investigation and diagnostic levels for impaired glucose tolerance?

A

Abnormal 2hr post-prandial result but glucose level not high enough to be diabetic

90
Q

Investigation and diagnostic levels for impaired fasting glucose?

A

Abnormal fasting result but glucose level not high enough to be diabetic

91
Q

DMT2 treatment?

A 
Lifestyle changes and advice
Sort out HTN - ACEi eg. ramipril
1. Metformin (biguanides)
2. 43-58mmol/mol
Metformin + DPP4 inhbitor eg. sitagliptin
OR
metformin + pioglitazone (glitazone)
OR
metformin + sulphonylurea eg. oral gliclazide
OR
Metformin + SGLT-2i (glifazon) 
3. >58
Triple therapy (met + SU + GLP1)
OR 
Insulin
92
Q

Weight change when taking biguanides (metformin)?

A

Weight loss

93
Q

Weight change when taking sulfonylurea (gliclazide)?

A

Weight gain

94
Q

Weight change when taking DPP4 inhibitors (sitagliptin)?

A

No change

95
Q

Weight change when taking glitazones (plioglitazone)?

A

Weight gain

96
Q

What genes increase the risk of DMT1?

A

HLA-DR3-DQ2

HLA-DR4-DQ8

97
Q

What is the cause of DMT2?

A

Autoimmune B-cell destruction

98
Q

What is the cause of DKA?

A

Insufficient insulin

=More ketogenesis due to less glucose available = more ketones produced

99
Q

What are the signs & symptoms of DKA?

A

Pear breath
Vomiting & abdo pain
Dehydration
Kussmaul’s breathing (deep and rapid)

100
Q

What is used to diagnose DKA?

A

Acidaemia (blood pH)
Hyperglycaemia
Ketonaemia/ketoniuria

101
Q

What is the management of DKA?

A

Fluid

Insulin

102
Q

What is the cause of hypoglycaemia?

A

Too much insulin/oral hypoglycaemic agents

Insufficient glucose to the brain

103
Q

What are the signs & symptoms of hypoglycaemia?

A

Odd behaviour (aggression)
Sweating (fight or flight)
Raised pulse
Seizures

104
Q

What is used to diagnose hypogylcaemia?

A

Blood glucose levels

105
Q

What is the management of hypoglycaemia?

A

Glucose

Glucagon

106
Q

What is the cause of HHS?

A

Insufficient oral hypoglycaemic agents

Not ketones, just hyperglycaemia

107
Q

What are the signs & symptoms of HHS?

A

Dehydration

watered down DKA

108
Q

What is used to diagnose HHS?

A

Blood glucose level

109
Q

What is the management of HHS?

A

Low molecular weight heparin
Fluids
Insulin (if severe)

110
Q

What is the most common cause of primary adrenal insufficiency?

A 
TB = worldwide
Addison's = UK
111
Q

Signs and symptoms of Addison’s?

A

Lean, tanned (pigmented)
Depressed, tearful
N&V, abdo pain

Tanned, tired, tones, tearful

112
Q

Diagnosis of Addison’s?

A

Short ACTH stimulation test (Give ACTH (synacthen), then measure cortisol
level; in Addison, cortisol remains low after giving ACTH)

Test for 21-hydroxylase adrenal autoabs (+ve in 80% of Addison’s)

Bloods will show low sodium and high potassium due to low aldosterone

113
Q

Treatment of Addison’s?

A

Hydrocortisone (glucocorticoids) to replace cortisol, fludrocortisone (glucocorticoids) to replace aldosterone

114
Q

What emergency is associated with Addison’s?

A

Addisonian crisis@

Patients present with shock, treat with fluids and hydrocortisone

115
Q

Causes of cranial DI?

A

Head injury, pituitary tumours

116
Q

Causes of nephrogenic DI?

A

Drugs eg. lithium

117
Q

Signs and symptoms of DI?

A

Polyuria, polydipsia, dehydration

118
Q

Diagnosis of DI?

A

Water Deprivation Test

  1. Restrict fluid
  2. Measure urine osmolarity (+ve for DI if urine osmolarity is low)
  3. Desmopressin (ADH analogues) to differentiate cranial or nephrogenic.
    Urine will NOT be concentrated in nephrogenic DI, will in cranial
  4. MRI hypothalamus for masses in cranial DI
119
Q

Treatment of DI?

A

Cranial DI - desmopressin

Nephrogenic DI - bendroflumethizide, NSAIDs

120
Q

Causes of SIADH?

A

Malignancy, dugs, CNS disorder

121
Q

Signs and symptoms of SIADH?

A

Confusion
Anorexia
Nausea
Concentrated urine

122
Q

Diagnosis of SIADH?

A

Measure urine and plasma osmolarity

123
Q

Treatment of SIADH?

A

Treat the underlying cause
Restrict fluid

Vasopressin receptor antagonists (vaptans)

124
Q

Upon waiting for an adrenalectomy, what medication would you use to stabilise BP & K+?

A

Spironolactone

125
Q

Both renin and aldosterone are raised. Diagnosis?

A

Renin screting tumour or

Secondary hyperaldosteronism

126
Q

Low aldosterone. Dx?

A

Addison’s

127
Q

Low renin, high aldosterone. Dx?

A

Adrenal adenoma/carcinoma. Adrenal hyperplasia syndromes

128
Q

Classic Cushing’s presentation?

A

abdominal striae, moon face, buffalo hump

and weight loss in extremities

129
Q

Classic Addison’s presentation?

A

hyperpigmentation, central

weight loss as well as hypotension

130
Q

Classic carcinoid syndrome?

A

triad of cardiac

involvement, diarrhoea and flushing. Its due to the tumour cells producing 5-HT

Phase 2a Lauren (15 decks)

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