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Finals (HV) > Endocrine > Flashcards

Endocrine Flashcards

1
Q

What is the clinical chemistry and PTH levels in hypoparathyroidism?

A

Low PTH
Low Calcium
High/Normal PO3

Inappropriate response

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2
Q

List the primary and secondary causes of hypoparathyroidism?

A

Primary- Gland failure
* Autoimmune
* DiGeorge syndrome

Secondary- Gland removal
* Low Magnesium

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3
Q

List the sx of hypocalcaemia?

A

Convulsions
Arrhythmias
Tetany
Spasms
Numbness

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4
Q

List the signs of hypocalcaemia?

A

Chvosteks sign- tapping over parotid causes facial muscles to twitch

Trousseaus sign- ‘Italian hand’

ECG- QT prolongation

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5
Q

What is the clinical chemistry and PTH levels in pseudohypoparathyroidism?

A

High PTH
Low calcium

Appropriate response

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6
Q

What is pseudohypoparathyroidism?

A

Genetic disorder in which the body is resistant to PTH because of mutations

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7
Q

List the features of pseudohypoparathyroidism?

A

Short 4th and 5th metacarpals
Low IQ
Short
Round obesity

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8
Q

What is the clinical chemistry and PTH levels in primary hyperparathyroidism?

A

High PTH
High Calcium
Low PO3

Inappropriate response

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9
Q

List the most common cause of primary hyperparathyroidism?

A

Solitary adenoma (80%)

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10
Q

List the causes of primary hyperparathyroidism?

A

Solitary adenoma
Hyperplasia (15%)
Multiple adenoma/carcinoma

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11
Q

List the sx of hypercalcaemia?

A

BONES, STONES, MOANS, THRONES, GROANS
Bone pain/fractures
Renal stones
depression
polydipsia/polyuria
Abdo pain/constipation/N+V, Pancreatitis, peptic ulceration etc

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12
Q

What is the Gs tx of primary hyperparathyroidism?

A

Parathyroidectomy

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13
Q

What is secondary hyperparathyroidism?

A

Parathyroid hyperplasia due to vit d deficiency or CKD

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14
Q

What is the clinical chemistry and PTH levels in secondary hyperparathyroidism?

A

High PTH
Low Calcium
High/N PO3
Low Vit D

Appropriate response

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15
Q

What is tertiary hyperparathyroidism?

A

Prolonged secondary hyperparathyroidism causes gland to autonomously undergo hyperplasia

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16
Q

What is the clinical chemistry and PTH levels in tertiary hyperparathyroidism?

A

Very High PTH
High calcium

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17
Q

List 5 causes of hypercalcaemia?

A

90% = malignancy + primary hyperparathyroidism
Sarcoidosis
Multiple myeloma
Acromegaly
Thiazides
Thyrotoxicosis

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18
Q

What is the mx of hypercalcaemia?

A

IV fluids (0.9 NaCl) w/ crystalloid
1st line- Bisphosphonates for a week
2nd- calcitonin

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19
Q

What is mx for mild and severe hypocalcaemia?

A

Mild
* Oral supplements

severe
* IV calcium gluconate (10ml of 10% solution over 10 mins) in 100mls sodium chloride 0.9% or glucose 5%
* + ECG monitoring

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20
Q

List 3 causes of pituitary adenomas?

A

Prolactinoma
Acromegaly
Cushing’s syndrome

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21
Q

What is a prolactinoma?

A

A benign adenoma secreting prolactin

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22
Q

What substance inhibits prolactin secretion?

A

Dopamine

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23
Q

List 2 functions of prolactin?

A

Stimulates breast development in puberty
Stimulates milk production

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24
Q

What substances are inhibited by the secretion of prolactin?

A

Sex hormones (oestrogen and testosterone)

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25
Q

List 5 sx of a prolactinoma?

A

Galactorrohoea
Amenorrhoea/Oligo menorrhoea
ED/Loss of libido/Infertility
Bitemporal hemianopia/Headaches

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26
Q

What is the 1st line and Gs Ix in prolactinoma?

A

1st line- serum prolactin
Gs- MRI/CT pituitary

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27
Q

What is the 1st line and Gs mx of prolactinoma?

A

1st line- Cabergoline- Dopamine agonist
Gs- Transphenoidal surgery

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28
Q

What is the difference between acromegaly and gigantism?

A

Gigantism- excess GH in children (before the fusion of growth plates)

Acromegaly- excess GH in adults

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29
Q

List 5sx of acromegaly?

A
  • Frontal bossing
  • Large tongue/nose/jaw/hands/feet
  • Skin tags
  • OSA
  • Headaches/Bitemporal hemianopia
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30
Q

What substance inhibits the release of GH?

A

Somatostatin

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31
Q

What is the 1st line Ix of acromegaly?

A

Serum IGF-1 levels (elevated)

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32
Q

What is the Gs Ix for acromegaly?

A

OGTT- High levels of Glucose should suppress GH

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33
Q

What is the mx of acromegaly (1st - 4th line)

A

1st line- TSS
2nd line- Somatostatin analogue e.g. octreotide
3rd- GH receptor antagonist e.g. pigvisomant
4th line- Dopamine agonist e.g. bromocriptine/cabergoline

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34
Q

What is Cushing’s syndrome?

A

Excess glucocorticoids resulting in distinguished clinical signs and sx

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35
Q

What is Cushing’s disease?

A

Glucocorticoid excess caused by ACTH pituitary tumour

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36
Q

List the causes of Cushing’s?

A

ACTH dependent-Pituitary tumours and Ectopic ACTH tumour

ACTH independent-Adrenal adenoma/carcinoma, exogenous steroids

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37
Q

List 5 sx or signs of Cushing’s?

A

Moon face
obesity
Purple striae
Buffalo hump
Acne
Hirsutism
Mood changes
Irregular menses/ED
WG
High BG/HTN

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38
Q

What is the Ix for Cushing’s?

A
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39
Q

What are the sick day rules regarding patients taking steroids?

A

Patients on long term steroids should have double the dose during intercurrent illness

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40
Q

What drugs can cause gynaecomastia?

A

Spironolactone
Digoxin
Oestrogen
Anabolic steroids
Finasteride
GnRH analogues- gosrelin

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41
Q

What is subclinical hyperthyroidism, and what conditions is it associated with?

A

Normal T4/T3
Low TSH (<0.1mu/L)

Associated with AFib and Osteoporosis

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42
Q

What is cranial diabetes insipidus?

A

Decrease secretion of ADH from pituitary gland

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43
Q

What is nephrogenic diabetes insipidus?

A

Insensitivity to ADH

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44
Q

Where is ADH produced?

A

Supra-optic nucleus in the hypothalamus

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45
Q

Where is ADH released from?

A

Posterior pituitary

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46
Q

How does ADH respond to dehydration/thirst?

A

High ECF osmolality detected by hypothalamus > release of ADH from post. pit > renal water retention >decrease in ECF osmolality

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47
Q

What is the 1st line and gold standard Ix in diabetes insipidus?

A

1st line-Water deprivation test (confirms the presence of DI)

GS- Desmopressin stimulation test (differentiates between NDI and CDI)

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48
Q

What results in the water deprivation test would be indicative of DI?

A

Urine osmolality- Low
Serum Osmolality- High

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49
Q

What would the results of the desmopressin simulation test be in those with CDI and in NDI?

A

CDI-
serum osmolality- low
Urine osmolality- high

NDI
serum osmolality- high
Urine osmolality- low

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50
Q

List the signs of graves disease?

A

Thyroid acropachy (digital clubbing, soft tissue swelling of the hands and feet, and periosteal new bone formation)
Exophthalmos
Pretibial myxoedema
Smooth enlarged non tender goitre

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50
Q

List 5 causes of hyperthyroidism?

A

Toxic multinodular goitre
Iodine excess
Drugs- Amiodarone, Lithium
Gestational
Toxic adenoma
Graves

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51
Q

What is the mx of hyperthyroidism?

A

Carbimazole or Propythiouracil
Thyroidectomy

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52
Q

What is the Ix for Graves disease?

A

TSH/T4 levels (Low TSH, High T4)
Anti TSH antibodies

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53
Q

List the 4 stages in De-quervains thyroiditis?

A

1- hyperthyroidism (painful goitre and high ESR)
2- Euthyroid
3- Hypothyroidism
4- Normalcy

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54
Q

What is the Ix that is used to diagnose De-Quervains/subacute thyroiditis?

A

Thyroid Scintigraphy- globally reduced uptake of I2-131

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55
Q

What is the most common type of thyroid cancer?

A

Papillary (70%)

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56
Q

List 5 sx and signs of hypothyroidism?

A

Cold intolerance
Constipation
Lethargy
Menorrhagia
Dry/coarse hair
Loss of lateral 1/3 eyebrow
Carpal tunnel syndrome
Dry skin
WG

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57
Q

What is the mx of hypothyroidism?

A

Levothyroxine

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58
Q

What Ix relevant to Hashimoto’s?

A

Anti TPO
TSH/T4 (High TSH, low t4)

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59
Q

What is SIADH?

A

Syndrome where too much ADH is released

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60
Q

List 5 causes of SIADH?

A

Malignancy (ectopic/pituitary)
Neurological (stroke/SAH/meningitis)
Infections
Post-operative
Drugs

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61
Q

What drugs can cause SIADH?

A

CARDISH
Chemotherapy
Antidepressants
Recreational
Diuretics
Inhibitors (SSRIs, ACEIs)
Sulfonyureas
Hormones (Desmopressin)

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62
Q

What is the triad of features that is present in SIADH?

A

Hyponatraemia
High urine Na+
Euvolaemia

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63
Q

What ix are conducted to make a diagnosis of SIADH?

A

SIADH is a diagnosis of exclusion.
Addison’s disease must be excluded via short synACTHen test

Urine osmolality-high
Serum Osmolality-low

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64
Q

List the sx of SIADH?

A
  • Absence of hypo/hypervolaemia
  • Nausea and Vomiting
  • Headaches
  • Fatigue
  • Muscle cramps and aches
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65
Q

What is Addison’s disease?

A

Autoimmune destruction of adrenal glands thus decrease secretion of cortisol and aldosterone

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66
Q

What is the most common cause of Addison’s in the world?

A

TB

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67
Q

What is the most common cause of Addison’s in the UK/Developed world?

A

Autoimmune

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68
Q

List the layers of the adrenal glands and what hormones are subsequently released?

A

Medulla - Adrenaline and noradrenaline
Cortex:
1. Zona Glomerulosa- Mineralocorticoids (Aldosterone)
2. Zona Fasiculata- Glucocorticoids (Cortisol)
3. Zona Reticularis- Sex hormones (DHEA)

69
Q

List the sx of Addison’s disease?

A

Tanned
Lean
Palmar hyperpigmentation
WL
Hypotension
N+V

70
Q

What is the Ix’s for Addison’s disease?

A

Short Synacthen Test-
give synthetic ACTH, in healthy pts cortisol should be produced (x2 of baseline), however in Addison’s since the glands are damaged no/little cortisol is produced.

Electrolytes- Hyponatraemia, Hyperkalaemia, Hypoglycaemia

High renin, High ACTH, Low cortisol, Low aldosterone

71
Q

What is the mx of Addison’s disease?

A

Lifelong Fludrocotisone and Hydrocortisone

72
Q

What are signs of Addison’s crisis?

A

Hypotension
Altered consciousness
Hyponatraemia, Hyperkalaemia

73
Q

What is the mx of Addison’s crisis?

A

IV hydrocortisone
IV fluids resus
Correct hypoglycaemia

74
Q

What is Conn’s syndrome?

A

Primary hyperaldosteronism

75
Q

List the 2 most common causes of Conn’s syndrome?

A

Adrenal adenoma
Bilateral adrenal hyperplasia (*)

76
Q

What is the job of aldosterone?

A
  1. Acts on distal tubule which increases Na+ reabsorption
  2. Acts on distal tubule which increases K+ secretion
77
Q

What are the sx of Conn’s syndrome?

A

HTN**
Lethargy
mood disturbances
Nocturia
Polyuria
Metabolic alkalosis

78
Q

What is the first line Ix of Conn’s syndrome?

A

Aldosterone:Renin ratio
Primary-High Aldosterone to Renin ratio
Secondary-Low aldosterone to renin ratio

79
Q

What is the mx for Conn’s Syndrome?

A

Adrenal adenoma- Surgery
BL adrenal hyperplasia- Spironolactone (aldosterone antagonist)

80
Q

What is secondary adrenal insufficiency?

A

Affects pituitary therefore low ACTH production thus less cortisol but normal aldosterone and renin

81
Q

What Ix and results would indicate secondary adrenal insufficiency?

A

Short synacthen test- Give synthetic ACTH and cortisol would increase

Low cortisol, Low ACTH, Normal renin and Normal Aldosterone

82
Q

What is carcinoid syndrome?

A

The release of serotonin into systemic circulation from a carcinoid tumour

83
Q

Where do carcinoid tumours commonly arise from?

A
  1. GI tract
  2. Lungs
  3. Liver
  4. Ovaries
  5. Thymus
84
Q

What is the most common GI site for carcinoid tumours?

A

Appendix

85
Q

What is the most common site for carcinoid mets?

A

Liver

86
Q

List sx and signs of carcinoid syndrome?

A

Flushing
Diarrhoea
Bronchospasm- Wheezing
Pulmonary stenosis
Abdo pain
Pellagra (Niacin/B3 deficiency)

87
Q

What is the triad of sx in pellagra?

A

Diarrhoea
Dementia
Dermatitis

88
Q

What is the first line Ix of Carcinoid syndrome?

A

1st- High urinary 5-hydroxyindoloacetic acid

89
Q

What is the GS ix for Carcinoid syndrome?

A

Chromogranin A and Octreoscan

90
Q

What is the mx of carcinoid syndrome?

A

Somatostatin analogue- Octreotide
Surgery

91
Q

What amino acid is converted into serotonin?

A

Tryptophan

92
Q

What is a carcinoid crisis?

A

When a tumour outgrows its blood supply. It is a life-threatening crisis which causes Vasodilation, Hypotension, Tachycardia, Bronchoconstriction and hyperglycaemia

93
Q
A
94
Q

What is serotonin syndrome?

A

Excess synaptic serotonin in CNS that clinically manifests as a triad of sx (Neuromuscular excitation, Autonomic effects and altered mental status)

94
Q

What is phaechromocytoma?

A

A tumour arising from catecholamine producing chromaffin cells of adrenal glands (Adrenaline and Noradrenaline)

94
Q

List the sx of phaechromocytoma?

A

5Ps
Perspiration
Palpitations
Pallor
High BP
Pain (headache)

95
Q

What is the 1st line and other important Ix?

A

1st line- 24 hour collection of catecholamines- High

Other- CT/MRI abdo

96
Q

What is the mx of phaechromocytoma?

A

Alpha and Beta Blockers
GS- Surgery

97
Q

What is the primary anion in the ECF

A

Cl-

98
Q

What is the primary cation in ECF?

A

Na+

99
Q

What is the primary cation in ICF?

A

K+

100
Q

What is T1DM?

A

Autoimmune destruction of beta cells of the pancreas resulting in absolute deficiency of insulin, thus increasing glucose levels.

101
Q

Where is glucagon released from and what does it do?

A

Glucagon released from alpha cells (Turns Glycogen into Glucose)

102
Q

Where is insulin released from and what does it do?

A

Beta cells (Glucose to glycogen)

103
Q

What are the Ix necessary to diagnose T1DM?

A

Fasting glucose >7.0mmol/L
Random glucose >11.1mmol/L
HbA1c >48mmol/L

104
Q

What is the Tx for T1DM?

A

Insulin and Education

105
Q

What are the complications of T1DM?

A

Lipodystrophy, Hypoglycaemia, WG, micro/macro vascular complications, DKA

106
Q

How does insulin work?

A

Insulin activates insulin-receptors on the membranes of insulin-responsive tissues (e.g. peripheral muscle and adipose tissue), stimulating the migration of glucose transporters to the cell membrane to facilitate uptake of circulating glucose into these tissues.

In the absence of insulin (as in T1DM), glucose cannot be taken up by insulin-responsive tissues, causing hyperglycaemia.

107
Q

list the micro and macrovascular complications of diabetes?

A

Micro- nephropathy, retinopathy and neuropathy

Macro- Cardiovascular, cerebrovascualr, aor peripheral vascualr disease

108
Q

List the sx of T1DM?

A

Polydipsia
Polyuria
Nocturia
WL
Fatigue
Blurred vision

109
Q

What is DKA?

A

Complication of T1DM

110
Q

What is the pathophysiology of DKA?

A

DKA is caused by uncontrolled lipolysis, which results in an excess of free fatty acids that are ultimately converted to ketone bodies

111
Q

List the clinical features of DKA?

A

Abdominal pain
Polyuria, polydipsia, dehydration
Kussmaul respiration (deep hyperventilation)
pear drop smelling breath

112
Q

What is the diagnostic criteria for DKA?

A

Random glucose >11mmol/L
pH <7.3
Bicarbonate <15mmol/L
Ketone >3mmol/l or ++ urinary ketones

113
Q

What is the mx of DKA?

A
  1. Fluid replacement- Isotonic saline
  2. Insulin infusion (start on 0.1unit/kg/hour)
    - Once blood glucose is < 14 mmol/l an infusion of 10% dextrose should be started at 125 mls/hr in addition to the 0.9% sodium chloride regime
  3. Correction of electrolyte disturbances
  4. Long acting insulin should be continued, short-acting insulin should be stopped
114
Q

What is T2DM?

A

A polygenic disorder in which there is progressive relative insulin deficiency and cells become insulin resistance

115
Q

List the RF for T2DM diabetes?

A

Obesity, Male, South Asians, Lack of exercise, FHx

116
Q

What is pre-diabetes?

A

HbA1c level of 42-47 mmol/mol

117
Q

What are the 2 types of impaired glucose regulation?

A

Impaired fasting glucose (IFG) - due to hepatic insulin resistance

Impaired glucose tolerance (IGT) - due to muscle insulin resistance

118
Q

What is IFG?

A

IFG is defined by elevated blood glucose levels after an overnight fast but not high enough to be classified as diabetes.

fasting glucose greater than or equal to 6.1 but less than 7.0 mmol/l implies impaired fasting glucose (IFG)

119
Q

What is IGT?

A

IGT is characterized by elevated blood glucose levels after consuming a glucose-rich drink (oral glucose tolerance test) but not high enough to be classified as diabetes.

fasting plasma glucose less than 7.0 mmol/l and OGTT 2-hour value greater than or equal to 7.8 mmol/l but less than 11.1 mmol/l

120
Q

What is HHS?

A

a metabolic emergency of uncontrolled T2DM

121
Q

List the sx of HHS?

A

Hypovolaemia
Marked hyperglycaemia
Raised serum osmolarity
Fatigue
N+V
Altered level conciousness
Dehydration
Hypotension/Tachy

122
Q

What is the mx of HHS?

A

Normalise Osmolality

  1. Replace fluid and electrolytes (IV 0.9 Saline)
  2. Insulin
  3. VTE Prophylaxis
123
Q

What are the causes of hyperglycaemia?

A

Reduced Insulin Secretion
Reduced insulin utilisation
Increase glucose production
Pancreatitis

124
Q

What are the hypoglycaemia?

A

Diabetes
Non diabetic causes (EXPLAIN)
Exogenous drugs
Pituitary Insufficiency
Liver failure
Addisons
Insulinoma
Non pancreatic neoplasm

125
Q

List the ECG changes seen in Hypokalaemia?

A

Small/Inverted T waves
Prominent U waves
Long PR interval
Depressed ST segment

126
Q

List the ECG changes seen in Hyperkalaemia?

A

Tall tented T waves
Small/Absent P waves
Wide QRS complex
Prolonged PR interval

127
Q

What is the mx of hyperkalaemia?

A

if cardiotoxicity- IV calcium gluconate

if no cardiotoxic and no ECG-Insulin dextrose infusion w/ nebulised salbutamol

128
Q

What’s the 1st line thx for DMT2

A

Lifestyle modifications

129
Q

What drug class does metformin belong to?

A

Biguanide

130
Q

What is the MOA of metformin?

A

Increases insulin sensitivity and decreases hepatic gluconeogenesis

131
Q

What are the side effects of metformin

A

Lactic acidosis*

GI upset

132
Q

What is the MOA of sulfonylureas

A

Stimulate beta pancreatic cells to produce insulin by binding to ATPk channels on beta cells

133
Q

What is the side effects of sulfonylureas

A

Weight gain
Hypoglycaemia*
Hyponatremia
GI upset

134
Q

What do sulfonylureas drugs end in

A

Glimepride

Glicazide

135
Q

What is the MOA of thiazolidinediones

A

Promote adipogenesis and ffa uptake

136
Q

What are the side effects of thiazolidinediones

A

Weight gain

Fluid retention

137
Q

Name a thiazolidinediones drug

A

Pioglitazone

138
Q

What is the MOA do DPP-4 inhibitors

A

Increase incretin levels which inhibit glucagon secretion

139
Q

What are the side effects of DPP-4 Inhibitors

A

Generally well tolerated but increase risk of pancreatitis

140
Q

What to DPP-4 inhibitors drugs name end in

A

Gliptins

141
Q

What is the MOA of SGLT2- inhibitors

A

Inhibit reabsorption of glucose in the kidneys

142
Q

What are the side effects of SGLT2-Inhibitors

A

Weight loss, UTI

143
Q

What do SGLT2-Inhibitors drug name end in

A

Gliflozins

144
Q

What is the MOA of GLP-1 agonists

A

Incretin mimetic thus inhibit glucagon secretion (s/c)

145
Q

Side effects of GLP-1 agonists

A

Weight loss, N+V, Pancreatitis

146
Q

What do glp-1 agonist drugs end in

A

-tides

147
Q

What test can differentiate between Cushing’s and pseudo-cushing’s?

A

Insulin stress test

148
Q

High-dose dexamethasone suppression test shows:

Cortisol- not suppressed

ACTH- suppressed

What is the most likely diagnosis?

A

Adrenal adenoma

149
Q

High-dose dexamethasone suppression test shows:

Cortisol- suppressed

ACTH- suppressed

What is the most likely diagnosis?

A

Cushing’s Disease- Pituitary adenoma

150
Q

High-dose dexamethasone suppression test shows:

Cortisol- not suppressed

ACTH- not suppressed

What is the most likely diagnosis?

A

Ectopic ACTH syndrome

151
Q

What is congenital adrenal hyperplasia?

A

An autosomal recessive disorder that impairs adrenal steroid biosynthesis

152
Q

What is the most common cause of CAH?

A

21 hydroxylase deficiency

also, 11 beta hydroxylase deficiency, and 17 hydroxylase deficiency

153
Q

List the sx present in CAH?

A

Ambiguous genitalia
Salt wasting crisis
Precocious puberty
Infertility
Height and growth abnormalities

154
Q

What is the Ix of choice for diagnosing CAH?

A

ACTH stimulation test

155
Q

What is the thyroid function test results in sick euthyroid syndrome?

A

Acute illness
Normal TSH
Low T3/T4

156
Q

What is the preferred tx for MODY?

A

Gliclazide

157
Q

What is kallman’s syndrome?

A

X linked recessive disorder causing delayed puberty secondary to hypogonadotropic hypogonadism

158
Q

List the sx associated with kallmans?

A

Anosmia
delayed puberty
Low sex hormones
Low FSH, LH

159
Q

What is the HbA1c Target in order to start a second drug in T2DM mx?

A

> 58mmol/L

160
Q

What is the maximum dose of metformin in T2DM?

A

2g/day

161
Q

What are features associated with MEN type 1?

A

3Ps
Parathyroid- hyperparathyroidism
Pituitary
Pancreas- insulinoma, gastrinoma. Recurrent peptic ulceration

162
Q

What are the features of MEN type IIa?

A

Medullary thyroid cancer
2Ps
Parathyroid
Phaechromocytoma

163
Q

What are the features MEN type IIb?

A

Medullary thyroid cancer
Phaechromocytoma
Marfanoid body habitus, Neuroma

164
Q

What is the MOA of carbimazole?

A

Inhibits thyroid peroxidase

165
Q

What malignancy is closely linked with acromegaly?

A

Colorectal cancer

166
Q

In unexplained hypoglycaemia, what further test can you perform to differentiate between exogenous and endogenous insulin?

A

C-Peptide and Proinsulin
High serum insulin and High C peptide and proinsulin = Endogenous e.g. insulinoma

High serum insulin and low C peptide and proinsulin = Exogenous

167
Q

What is the sick day rules for T1DM?

A

Continue taking insulin as normal, but check BMs more regularly

168
Q

What are the T1DM blood glucose targets?

A

5-7mmol/l on waking
4-7mmol/l before meals and other times

169
Q

How does hyperthyroidism and hypothyroidism affect menses?

A

Hyperthyroidism- Oligo menorrhoea/Amenorrhoea

Hypothyroidism- Menorrhagia

Finals (HV) (19 decks)

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