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Gen Med and Surg - C.U > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

Cushings disease

A

Raised cortisol level specifically due to raised ACTH from a pituitary tumour

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2
Q

Cushings syndrome is due to? (2)

A

Excess cortisol

Excess ACTH -> raised cortisol

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3
Q 
C
U
S
H
I
N
G 
(mneumonic)
A 
Central obesity / Comedones 
Urinary free cortisol 
Straiae 
Hirutuism 
Immunodeficiency 
Neoplasms 
Glucose (raised)
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4
Q

Cushings caused by raised cortisol (2)

A

Steroids

Adrenal carcinoma / adenoma

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5
Q

Cushings caised by raised ACTH

A

Tumour producing ACTH (not pituitary) e.g. Small cell lung cancer
Cushings disease

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6
Q

Cause of pseudocushings

A

alcohol excess

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7
Q

Dexamethasone suppression test result meanings

Low dose High dose

Cortisol dec Cortisol dec

No change Cortisol dec

No change No change

A

No pathology - dex suppresses cortisol

Cushings disease - high levels able to suppress excess ACTH

Cushings syndrome - levels of cortisol are high INDEPENDENT of ACTH

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8
Q

causes of false +ve dex suppression test

A

obesity
alcoholism
chronic renal failure

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9
Q

Screening test for cushings

A

urine cortisol

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10
Q

3 complications of cushings

A

cardiac problems
diabetes
osteoporosis

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11
Q

Specific clinical presenting feature of cushings disease

A

hyperpigmentation as ACTH activates melanocytes

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12
Q

Action of aldosterone

A

Increased sodium and water reabs

Increase K+ secretion

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13
Q

Commonest cause of primary aldosteronism

A

Conns syndrome - aldosterone producing adenoma

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14
Q

Symptoms of hypokalaemia

A

cramps
abdo pain
muscle weakness
polyuria and polydipsia

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15
Q

Signs of hyperaldosteronism

A

fluid overload
hypertension
metabolic acidosis

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16
Q

Treatment of primary hyperaldosteronism

A

Aldosterone agonist e.g. spironolactone

Calcium channel blockers

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17
Q

Causes of primary aldosteronism

A

Conns syndrome
Adrenal carcinoma
Adrenal hyperplasia

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18
Q

Pathophysiology of secondary aldosteronism

A

Increased renin causing increased aldosterone levels

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19
Q

Causes of secondary aldosteronism

A 
Renal artery stenosis 
Chronic oedema 
Cardiac failure 
Liver failure 
Hypertension
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20
Q

Levels of renin in

1) Primary hyperaldosteronism
2) Secondary hyperaldosteronism

A

LOW

HIGH

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21
Q

Treatments of hyperaldosteronism

A

Aldosterone antagonist

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22
Q

Pathophysiology of primary hypoadrenalism (addisons)

A

Low levels of all adrenal hormones due to acute adrenal destruction

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23
Q

Addisons crisis - patients usually present with one of two conditions

A

Hypoglycaemia

Hypovolaemic shock

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24
Q

Most common cause of addisons disease

A

Autoimmune destruction of the adrenal glands

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25
Q

Signs and symptoms of low cortisol

A

Hyperpigmentation

Hypoglycaemia

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26
Q

Signs and symptoms of low aldosterone

A

Hyponatraemia
Hyperkalaemia
Hypotension - due to fluid and Na+ loss

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27
Q

Signs and symptoms of low androgens

A

Lack of pubic hair in females

Generalised unwell symptoms

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28
Q

Addisons crisis features

A 
Abdo pain 
Vomiting 
Hypotension 
Tachycardia 
Hypovolaemic shock 
Collapse
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29
Q

Important hx to ask if suspect addisions?

A

steroid use?

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30
Q

Key test to help diagnose addisons

A

synacthen test

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31
Q

Short synacthen test result - cortisol not raised

Long synacthen test result - cortisol not raised

A

Primary hypoadrenalism

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32
Q

Short synacthen test result - cortisol not raised

Long synacthen test result - cortisol raised

A

Seconary hypoadrenalism

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33
Q

Short synacthen test result - cortisol raised

Long synacthen test result - cortisol raised

A

NORMAL

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34
Q

SE of steroids

B
E
C
L
O
M
E
T
H
A
S
O
N
E
A 
Buffalo hump 
Easy bruising 
Cateracts 
Large appetite 
Obesity 
Moon face 
Euphoria 
Thin arms / legs / skin 
Hypertension / hyperglycaemia 
Avascular necrosis of femoral head 
Skin thinning 
Osteoporosis 
Negative nitrogen balance 
Emotional liability
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35
Q

Pathophysiology of secondary hypoadrenalism

A

Dysfuction of hypothalamus, pituitary axis

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36
Q

Main causes of secondary hypoadrenalism (2)

A

Iatrogenic - long term steroid use

Pituitary / hypothalamus tumour / infection / infarction

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37
Q

Difference between sign and symptoms of primary and secondary hypodrenalism

A

Secondary
ACTH low - so no hyperpigmentation

Aldosterone not low so no electrolyte imbalance

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38
Q

ACTH levels in

1) Primary hypoadrenalism
2) Secondary hypoadrenalism

A

HIGH

LOW

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39
Q

When should a new drug be added in T2D treatment (HbA1c)

A

> 58

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40
Q

T2D diagnosis criteria

A

If the patient is symptomatic:
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)

If the patient is asymptomatic the above criteria apply but must be demonstrated on two separate occasions.

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41
Q

Hyperparathyroidism leads to

Ca2+ levels to…?

PO4 levels to…?

A

High

Low

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42
Q

6 key features of hypercalcaemia

A 
Renal stones 
Abdominal groans - pain
Polydypsia 
Bones (bone pain) 
Psychiatric overtones - depression
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43
Q

Impact of hypercalcaemia on the ECG

A

shortened QT

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44
Q

Most cases of primary hyperparathyroidism are due to?

A

parathyroid adenoma

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45
Q

Primary hyperparathyroidism

Ca2+ results

PTH result

A

high

high

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46
Q

Main therapy in hypercalcaemia

A

fluid rehydration

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47
Q

Secondary hyperparathyroidism

Ca2+ results

PTH results

A

low

high

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48
Q

Two causes of secondary hyperparathyrodism

A

renal failure

low vit d

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49
Q

tertiary hyperparathyrodism

A

prolonged secondary so PTH becomes so high, calcium is produced at a v high level. Vit D must be corrected

Increased Ca2+
Vit D normal
PTH high

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50
Q

Clinical signs of hypocalcaemia

A

pins and needles
muscle aches
tetany

chvostek’s sign - twitching of facial muscles when the facial nerve is tapped

Arrhythmias

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51
Q

Blood tests in hypocalcaemia

A 
Ca2+ 
PTH
Vit D 
Phosphate
Magnesium 
U&Es
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52
Q

Most common cause of hypoparathyroidism

A

iatrogenic - removal during thyroidecomy / post radiation

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53
Q

pseudohypoparathyrodism is due to?

A

resistance to PTH

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54
Q

Impaired glucose tolerance

Fasting glucose -

2h post glucose load

A
  1. 0 - 7.0

7. 8 - 11.0

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55
Q

Presentation of T1D

A

Age 12
Polydypsia
Polyuria
+/- ketoacidosis

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56
Q

Tests in suspected T1D

A

FBC
Glucose - HbA1C
U&Es

Urine dip - ketone / glucose

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57
Q

What other organs should be monitored in diabetes

A

Eyes
Renal
Vascular

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58
Q

Precipitants of diabetic ketoacidosis

A

Sepsis
Not taking insulin
MI

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59
Q

Presentation of ketoacidosis

A 
N&V 
Confusion
Abdo pain 
Lethargy 
Tachypnoea
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60
Q

infusion rate of insulin in ketoacidosis

A

infuse at a fixed rate of 0.1 units/kg/hour w/ 0.9% NaCl

61
Q

Metformin action

A

Improves insulin sensitivity

62
Q

Glicalzide action (sulphonylurea)

A

Stimulates pancreas to secrete insulin

63
Q

Pioglitazone (thiazolidinedones) action

A

Improves insulin sensitivity

64
Q

Alpha glucose inhibitors

A

Prevents sugar absorption in the intestine

65
Q

HbA1c target for those managed by diet and lifestyle (+/- drug not causing hypoglycaemia)

A

48 mmol/mol (6.5%).

66
Q

HbA1c target for people who are taking a drug associated with hypoglycaemia (such as a sulphonylurea)

A

53 mmol/mol (7.0%)

67
Q

two causes of diabetes insipidus

A

Cranial e.g. brain tumour / trauma

Nephrogenic e.g. hypercalcaemia, hypokalaemia, CKD

68
Q

diabetes insipidus =

A

inability of the kidneys to conserve water

69
Q

Symptoms of diabetes insipidus

A

Polyuria and polydypsia

70
Q

Invesigations in diabetes insipidus

A

urine / plasma osmolalitty

Water deprivation test - give desmopressin and see response.

71
Q

pathophysiology of DI caused by cranial causes

A

failure of posterior pituitary to produce vasopressin

72
Q

pathophysiology of DI caused by nephrogenic causes

A

failure of the kidney to respond to vasopressin

73
Q

Water deprivation test

Cranial cause result ->

Nephrogenic cause result ->

A

Urine osmolality increases (water retained)

Urine osmolality doesn’t change

74
Q

CNS disorders causing SIADH

A

Tumour
Meningitis
Encephalitis
SAH

75
Q

Pulmonary causes of SIADH

A

TB
Cancer
COPD

76
Q

Drugs causing SIADH

A

Diuretics

Antidepressants

77
Q

Malignancy causing SIADH

A

Lung
Lymph
Pancrease

78
Q

SIADH creates what type of hyponatramiea

A

Euvolaemic

79
Q

Symptoms of hyponatraemia

A

confusion
irrritability
headache
weakness

can get delirum / psychosis / ataxia

80
Q

Hypovolaemia hyponatraemia due to

A

due to salt loss and water follows

81
Q

Hypervolaemia hyponatraemia due to

A

excess water

82
Q

Normovolaemic hyponatraemia due to

A

Na+ loss > water

83
Q

Causes of normovolaemic hyponatraemia

A

SIADH

Post op

84
Q

causes of hypervolaemic hyponatraemia

A

Cardiac failure
Liver failure
Renal failure

Excess intake

85
Q

causes of hypovolaemic hyponatraemia

A

Extra renal - burns , N&V, dehydration

Renal - diuretic, hypoaldosteronism

86
Q

Bedside investigations in hyponatraemia

A

UandE
Serum osmolality
Urine osmolality

87
Q

two functions of the testes

A

produce testosterone

spermatogenesis

88
Q

Presentation of hypogonadism in men

A 
decreased libido 
erectyle dysfuncton 
gynaecomastia 
fatigue 
delayed puberty
89
Q

Main blood test in hypogonadism in med

A

serum testosterone

90
Q

Main cause of secondary hypogonadism in men

A

Prolactinoma

91
Q

SE of Sulfonylureas e.g gliclazide

A

Hypoglycaemic episodes
• Increased appetite and weight gain
• Syndrome of inappropriate ADH secretion
• Liver dysfunction (cholestatic)

92
Q

Glitazones SE

A

• Weight gain
• Fluid retention
• Liver dysfunction
• Fractures

93
Q

Metformin SE

A

• Gastrointestinal side-effects

• Lactic acidosis

94
Q

Causes of primary hyperparathyroidism

A

single adenoma
diffuse hyperplasia of parathyroid gland
carcinoma

95
Q

Imagining in primary hyperparathyrodism

A

US
FNA
SESTANIBI - radionuclear scan

96
Q

Treatment of primary hyperparathyrodism

A

resection

97
Q

Primary hyperparathyrodism blood test results

A

PTH high
Ca2+ high
Normal vit D

98
Q

Secondary hyperparathyrodism

A

Something is causing low Ca2+

Kidney - CKD (Vit D not activated)
Low vit D
Osteomalacia

99
Q

Secondary hyperparathyrodism blood test results

A

PTH high
Ca2+ low
Vit D low

100
Q

Treatment of secondary hyperparathyroidism

A

alpha calcidol - replace Vit D

101
Q

Treatment of tertiary hyperparathyroidism

A

Should improve in a year

or remove

102
Q

Causes for hypercalcaemia

A

Mets
HyperPara
Myeloid
Sarcoidosis

103
Q

What does the anterior pituitary produce?

A 
ACTH 
TSH 
LH
FSH
GH
Prolactin
104
Q

What does the posterior pituitary produce?

A

ADH and oxytocin

105
Q

Causes of hyperprolactinaemia

A

Physiological - pregnancy
Drugs - metoclopramide, haloperidol, methyldopa
Neoplasia - prolactinoma
PCOS

106
Q

Presentation of hyperprolactinaemia

A

amenorrhoea
infertility
galatorrhoea

107
Q

What is myxoedema

A

infiltraiton of the skin with mucopolysaccharies -> leads to dry waxy skin swelling in those with hypoT

108
Q

Causes of hypothyroidism

A 
hashimotos - most common 
idiopathic 
drug induced e.g. amiodarone, lithium 
Iatrogenic 
Iodine deficiency 
Congenital
109
Q

General features of hypothyrodism

A 
cold intolerance 
letheragy 
weight gain 
dry skin and hair 
low hoarse voice
110
Q

Skin changes in HypoT

A

Dry skin and hair

loss of outer 1/3 of eyebrow

111
Q

Psychological and neurological aspects of hypoT

A

Depression
Slow reflexes
Carpal tunnel syndrome

112
Q

CV features of hypoT

A

Bradycardia
Angina
Non pitting oedema

113
Q

Reproductive features of HypoT

A

Menorrhagia

Infertility

114
Q

Thyrotoxic storm

A

Thyrotoxicosis causes acutely increased metabolism

Life threatening tachycardia
Hypertension
Fever

115
Q

Blood results in

Primary HyperT

Secondary HyperT

A

High T4 but low TSH

High TSH and T4

116
Q

Causes of primary hyperT

A

Graves disease
Toxic Multinodular goitre
Toxic adenoma
Over treating of hypothyrodism

117
Q

Cause of secondary HyperT

A

Pituitary adenoma

118
Q

General features of HyperT

A 
Heat intolerance 
Weight loss 
Diarrhoea 
Sweating 
Muscle wasting 
TREMOR m
119
Q

Skin features of HyperT

A

Dry skin

120
Q

Psychological features of HyperT

A

Pychosis
Emotional liability
Restlessness

121
Q

Muscular features of HyperT

A

Myopathy

122
Q

Cardiac features of HyperT

A

AF
Tachycardia
Palpiations

123
Q

menstrual features of HyperT

A

Oligomenorrhoea

124
Q

HyperT treatment

Medical

Interventional

Surgical

A

Carbimazole and Beta blocker

Radioactive iodine

Thyroidectomy

125
Q

Features ONLY found in Graves disease

A 
Proptosis 
Lid retraction 
Preorbital oedema 
Diplopia 
Limited eye movements 
Pretibial myxoedema 
Thyroid acropachy
126
Q

Specific antibodies to test for in HyperT

A

Against thyroid peroxidase and thyroglobulin

127
Q

Main cause of benign thyroid cancer

A

follicular adenoma

128
Q

Types of thyroid carcinoma

A

medullarly
papillary
follicular

129
Q

Questions to ask about in suspected thyroid cancer

A 
Thyroid mass 
Usually painless 
Dysphagia 
Dyspnoea 
Hoarseness 
Weight loss 
B symptoms
130
Q

Investigations in suspected thyroid cancer

A

CXR
US
FNA
Radioisotope

131
Q

Specific test for phaeochromocytoma

A

24 hr urinary collection of metanephrines (sensitivity 97%*)

this has replaced a 24 hr urinary collection of catecholamines (sensitivity 86%)

132
Q

treatment of thyrotoxic storm

A

carbimazole
beta blocker
hydrocortisone

133
Q

Which type of lung cancer causes cushing’s syndrome

A

small cell carcinoma

134
Q

paraneoplastic manifestations of squamous cell lung cancer

A

Parathyroid related protein - hypercalcaemia

135
Q

test to differentiate between T1D and T2D

A

C- peptide

136
Q

blood pressure targets for diabetics

A

Diabetes mellitus: hypertension management

NICE recommend the following blood pressure targets for diabetics:
if end-organ damage (e.g. renal disease, retinopathy) < 130/80 mmHg
otherwise < 140/80 mmHg

137
Q

T1D blood glucose targets

A

In type 1 diabetics, blood glucose targets:
5-7 mmol/l on waking and
4-7 mmol/l before meals at other times of the day

138
Q

2nd line treatment in TD2 who are obese

A

DPP-4 inhibitors are useful in T2DM patients who are obese

139
Q

only add a second drug in T2D when HbA1c is?

A

> 58 mmol/mol

140
Q

Which patients who take insulin DON’T need to inform the DVLA

A

Not all patients on insulin have to inform the DVLA. The exceptions are those on temporary treatment for 3 months or less, or gestational diabetes that are taking insulin for less than 3 months post delivery

141
Q

In diabetic foot what has been lost?

A

loss of protective sensation

142
Q

what ratio can be checked when looking for diabetic nephropathy

A

albumin: creatine ratio

143
Q

how does hyperglycaemia cause diabetic nephropathy

A

leads to nephron loss, so RAAS activated and glomerular hypertension -> hyperfiltration of proteins and eventual tubular damage

144
Q

HONK =

hyperosmoler non-ketotic acidosis

A

emergency where hyperglycaemia leads to dehydration and hyperosmolality without significant ketoacidosis

145
Q

Bed side tests in HONK

A

Glucose test
Urine dip and culture
Observations
ECG

146
Q

Further tests in HONK

A

CXR - likely precipitant is infection

147
Q

Bloods in HONK

A 
FBC 
U&amp;E 
ABG 
Glucose 
Lactate 
Blood cultures
148
Q

Treatment

A

ABCDE

  • fluids
  • insulin infusion - slower than in DKA
  • regular monitoring
  • consider LMWH because at risk of clotting

Gen Med and Surg - C.U (16 decks)

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