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Phase 2 > Endocrine > Flashcards

Endocrine Flashcards

1
Q

Define endocrine

A

These glands ‘pour’ secretions directly into blood stream, without ducts
e.g. thyroid, adrenal, beta cells of pancreas

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2
Q

Define exocrine

A

These glands ‘pour’ secretions through a duct to site of action
e.g. submandibular, parotid, pancreas (amylase & lipase)

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3
Q

Describe the action of endocrine hormones

A

Blood-borne, acting on distant sites

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4
Q

Describe the action of paracrine hormones

A

Acting on nearby adjacent cells

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5
Q

Describe the action of autocrine hormones

A

Feedback on same cell that secreted hormone - acts on itself

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6
Q

Define Diabetes Mellitus T1

A

Autoimmune disease, causes the destruction of beta cells leading to insulin deficiency
∴ hyperglycaemia

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7
Q

Epidemiology DMT1

A

Usually younger < 30 years
↑ Northern Europe, esp Finland!
Incidence is increasing

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8
Q

22yr old woman with DMT1 is pregnant - what is the chance of her child also having DMT1?

A

1 in 25

(It is accepted that the child of any women below 25 years has a 1 in 25 chance of getting T2DM)

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9
Q

Monitoring of T2DM

A

HbA1c checked after 6 months
Checks for CVD, diabetic retinopathy, nephropathy, neuropathy etc done annually

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10
Q

What is LADA?

A

Latent Autoimmune diabetes in adults
‘Slow burning’ variant of DMT1 - slower progression to insulin deficiency, occurs in later life
∴ can be difficult to differentiate from DMT2

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11
Q

RF DMT1

A

Genetic susceptibility -
HLA-DR3-DQ2 or HLA-DR4-DQ8

Other autoimmune diseases
Vit D def
Enteroviruses e.g. Coxsackie B4

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12
Q

Why does polydipsia occur in DMT1?

A

Results of fluid and electrolyte loss

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13
Q

Why does polyuria occur in DMT1?

A

Result of osmotic diuresis
When blood glucose levels > renal tubular reabsorptive capacity

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14
Q

Why must DMT1 Px have insulin?

A

They are more prone to diabetic ketoacidosis

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15
Q

Key presentation of DMT1

A

2-6 week history of :
Unexplained weight loss, polyuria, polydipsia

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16
Q

State 1 other signs of DMT1

A

Breath may smell of ‘pear drops’ (KETONES)

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17
Q

Ix DMT1

A

Fasting plasma glucose (no food for 8hrs)
Random plasma glucose
Oral glucose tolerance test

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18
Q

Diagnostic values for DM

A

In symptomatic patient :
Symptoms + raised plasma glucose detected ONCE

If Asymptomatic, must show raised glucose on TWO SEPARATE occasions

–
Fasting glucose ≥ 7mmol/L (6mmol/L)
Random glucose ≥ 11.1 mmol/L
HbA1c ≥ 48 mmol/mol (41 mmol/mol)

If between normal and fasting, PRE-DIABETIC (T2)

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19
Q

What is the most common way children present with new T1DM?

A

Diabetic ketoacidosis

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20
Q

Tx DMT1

A

Patient education!!
BASAL BOLUS INSULIN

SC insulin - combo of long acting insulin (basal) od
& short acting insulin (bolus) injected 30 mins before meals

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21
Q

Define DMT2

A

Relative insulin def due to combination of insulin resistance and less severe insulin def

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22
Q

4 non-modifiable RF DMT2

A

> 40 years
Ethnicity - Black, Chinese, South Asian
FHx
Male

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23
Q

4 modifiable RF DMT2

A

Obesity
Sedentary lifestyle
High carbohydrate diet
HTN

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24
Q

Key presentation of DMT2

A

Usually asymptomatic and found incidentally on routine blood tests

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25
Q

Symptoms of a Px w/ severe T2DM

A

acanthosis nigricans

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26
Q

GS Ix DMT2

A

HbA1c test ! (tells us avg. BG for last 3 months)

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27
Q

State some complications of insulin treatment

A

Hypoglycaemia!
Lipohypertrophy (at injection site)
Insulin resistance
Weight gain - bc insulin makes people feel hungry

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28
Q

Tx DMT2

A

Lifestyle modifications first !!

  1. Metformin
  2. If HbA1c rises to 58 mmol/mol, dual therapy :
    Metformin + sulphonylurea e.g. gliclazide
    Metformin + DPP4 inhibitor e.g. sitagliptin
    Metformin + pioglitazone
    Metformin + SGLT-2i (glifazon)
  3. If STILL remains at 58 mmol/mol, triple therapy :
    Metformin + SU + DPP4 inhibitor
    Metformin + SU + pioglitazone
    Metformin + SU/pioglitazone + SGLT-i

–
IF symptomatic, SU or insulin until BG stable

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29
Q

Name some macrovascular complications of diabetes mellitus

A

Stroke
Ischaemic heart disease
Peripheral vascular disease

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30
Q

Which sex is at more risk of macrovascular complications of DM?

A

Neither - DM removes vascular advantage that females have

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31
Q

What can be given to DM patients to reduce the risk of macrovascular complications?

A

Statin
ACE-I

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32
Q

What are some microvascular complications of DM?

A

Diabetic neuropathy
Diabetic retinopathies
Diabetic nephropathy

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33
Q

Describe the pathophysiology of Diabetic neuropathy

A

Occlusion of vasa nervorum and accumulation of fructose and sorbitol
Disrupts structure and function of nerves

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34
Q

How can diabetic foot ulceration occur/get so bad?

A

Diabetic neuropathy increases risk of Px not noticing ulceration.
Also, causes skin dryness of foot ∴ more susceptible to cracking and ulcers

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35
Q

Describe some symptoms of diabetic neuropathy

A

Numbness, ↓ ability to feel pain/temp changes
Tingling/burning sensation
Sharp pain/cramps
Hypersensitivity
Muscle weakness
Loss of balance/coordination
diabetic foot - ulcers!!

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36
Q

Diabetic foot ulcer management

A

FOOT SCREENING!

Patient education! - Check feet daily, tie laces for enough room, keep feet away from heat

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37
Q

State a common consequence of childhood diabetes relating to skin and how to demonstrate this

A

Skin contractures
Ask Px to join hands in prayer - MCP and IP joints cannot be opposed

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38
Q

Describe pathophysiology of diabetic retinopathy

A

XS glucose in blood
∴ glucose uptake into lens and blockage of retinal blood supply
∴ eye attempts to grow new blood vessels but don’t develop properly and can leak

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39
Q

State and describe the two types of diabetic retinopathy

A
  1. Non-proliferative
    new blood vessels not growing
  2. **Proliferative
    Damaged blood vessels close off ∴ new abnormal vessels grow, will leak
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40
Q

Ix diabetic retinopathy

A

Fundoscopy
Cotton wool spots and flare haemorrhages

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41
Q

Early indication of diabetic nephropathy

A

Microalbuminuria

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42
Q

Other types of diabetes

A

MODY
LADY (latent autoimmune diabetes of young)
Gestational diabetes - usually in 3rd trimester

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43
Q

Tx diabetic nephropathy

A

Aggressive BP control (ACE-I, angiotensin-II antagonists etc)

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44
Q

Causes of hypoglycaemia

A

EXPLAIN

Exogenous drugs - insulin, alcohol binge w/ no food
Pituitary insufficiency
Liver failure
Addison’s disease
Islet’s cell tumour & Immune hypoglycaemia
Non-pancreatic neoplasm e.g. fibrosarcoma

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45
Q

Key presentation of hypoglycaemia

A

Odd behaviour (aggression), sweating, tachycardia

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46
Q

Ix Hypoglycaemia

A

1st - Whipple’s triad !
1. Signs/symptoms of hypoglycaemia
2. Low BG
3. Resolution of symptoms w/ correction of BG

GS 48-72 hr fast w/ serial BG

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47
Q

Tx hypoglycaemia

A

In Community -
Oral glucose (10-20g) - liquid, gel, tablet
Px might have ‘hypokit’ w/ IM or SC glucagon

In Hospital Setting
If Px alert, quick acting carb
If unconscious/unable to swallow, SC or IM glucagon
OR IV 20% glucose solution

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48
Q

How does the presentation of hypoglycaemia change and at what blood glucose level?

A

< 3.3 mol/L - sweating, shaking, hunger, anxiety, nausea

< 2.8 mol/L - weakness, vision change, confusion

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49
Q

What is diabetic ketoacidosis characterised by?

A
  1. Hyperglycaemia > 11 mmol/L
  2. ↑ Plasma ketones > 3 mmol/L
  3. Metabolic acidosis - pH < 7.3
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50
Q

Causes/RF Diabetic ketoacidosis

A

Untreated DMT1 or stopping insulin therapy
Undiagnosed DM
Infection/illness
MI

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51
Q

What is a big and preventable cause of diabetic ketoacidosis?

A

When patients stop/reduce insulin suddenly (bc Px is vomiting or not eating).

INSULIN SHOULD NEVER BE STOPPED IN T1DM

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52
Q

Pathophysiology diabetic ketoacidosis

A

Complete absence of insulin results in unrestrained hepatic gluconeogenesis
∴ ↑ circulating glucose
∴ osmotic diuresis
∴ dehydration

Peripheral lipolysis occurs ∴ ↑ circulating FFAs
Oxidised to Acetyl CoA ∴ ↑ ketones
∴ metabolic acidosis

Process is accelerated by “stress hormones e.g. catecholamines, glucagon, cortisol
Secreted in response to dehydration and intercurrent illness

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53
Q

Why is insulin def necessary for diabetic ketoacidosis?

A

Because even a small elevation will inhibit hepatic ketogenesis

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54
Q

DKA prognosis

A

Medical emergency!
If untreated, can be fatal!

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55
Q

DKA key presentation

A

Dehydration, vomiting, abdominal pain, ↓ tissue turgor

56
Q

DKA is rare in T2DM, more common in T1 !!

A

dont forget

57
Q

DKA signs/symptoms

A

Kussmaul’s sign
‘Pear drop’ breath
Low BP
Low body temp - even in presence of infection
Sunken eyes
-
Drowsiness/confusion

58
Q

DKA Ix

A

Usually recognised from clinical features and confirmed w/ Ix

Blood glucose measurement (BG > 11 mmol/L)
ABG ( ph < 7.3 and/or bicarbonate < 15 mmol/L)
Finger prick sample and near-patient meter (measures Beta-hydroxybutyrate) - to measure plasma ketones ( > 3 mmol/L)

–
Urine dipstick - heavy glucosuria and ketonuria
Serum U+E

59
Q

DKA Tx

A

Immediate ABCDE management if unconscious!

Fluid replacement w/ IV 0.9% saline (NaCl)

Replace deficient insulin - IV insulin (+ glucose to prevent hypoglycaemia)

Electrolytes! K+
monitor closely and treat if necessary!

60
Q

Complications of DKA & why does this occur?

A

Cerebral oedema

Blood is initially v conc w/ corresponding hypernatraemia.
W/ Tx, blood becomes hyponatraemic
∴ osmotic shift -> water moves from blood into tissues
In the brain, can cause swelling in enclosed space (skull). This causes rapid deterioration/coma/can be fatal.

∴ Fluid should be undertaken SLOWLY ! Over 48 hours

61
Q

Describe how fluid replacement in DKA should be given

A

Slowly!! Over 48 hours!

62
Q

Why can insulin treatment for DKA cause hypokalaemia? Why is this dangerous?

A

Insulin decreases K+ in blood
bc redistributes K+ into cells via ↑ Na+/K+ pump activity
∴ low serum K+

63
Q

Describe the action of biguanide and give an example

A

Increases peripheral insulin sensitivity and hepatic glucose uptake
e.g. Metformin

64
Q

Describe the action of Sulfonylurea and give an example

A

e.g. Gliclazide
Depolarises islet cells in pancreas ∴ ↑ insulin release

65
Q

Describe the action of Thiazolidinedione and give an example

A

e.g. Pioglitazone
↑ Peripheral insulin sensitivity

66
Q

Describe the action of SGLT-2i and give an example

A

e.g. Dapglifozin
↑ Urinary glucose loss

67
Q

Describe the action of DPP4-i and give an example

A

e.g. Sitagliptin
Inhibits GLP1 breakdown

68
Q

Describe the action of GLP1 analogue and give an example

A

e.g. Exenatide
↑ Insulin secretion and sensitivity

69
Q

Describe the action of Intestinal Alpha-Glucosidase Inhibitors and give an example

A

e.g. Acarbose
Delays intestinal carbohydrate absorption

70
Q

S/E biguanide

A

Lactic acidosis, GI disturbance

71
Q

S/E Sulfonylurea

A

Hypoglycaemia, weight gain

72
Q

S/E Thiazolidinediones

A

Fluid retention, weight gain, worsening heart failure

73
Q

S/E SGLT-2i

A

DKA when used w/ insulin
↑ Risk of UTI

74
Q

S/E DPP4-i

A

Hypoglycaemia, GI upset

75
Q

S/E GLP1 analogues

A

Hypoglycaemia, GI upset
May increase risk of pancreatitis when used with DPP4-i

76
Q

S/E Intestinal alpha-glucosidase inhibitors

A

Flatulence, GI disturbance

77
Q

Define Hyperosmolar Hyperglycaemic State

A

Medical emergency!

Characterised by :
1. Marked hyperglycaemia
2. Hyperosmolality
3. Mild/No ketosis

78
Q

Hyperosmolar hyperglycaemic state usually presents in whom?

A

Elderly w/ poorly controlled T2DM

79
Q

Hyperosmolar hyperglycaemic state - RF

A

*Infection! esp pneumonia
Consumption of glucose rich fluids
Concurrent medication - thiazide diuretic or steroids

80
Q

Pathophysiology of Hyperosmolar Hyperglycaemic State

A

↓ Endogenous insulin
Enough to inhibit hepatic ketogenesis
but not enough to inhibit hepatic glucose production

81
Q

Key presentation of Hyperosmolar Hyperglycaemic State

A

Severe dehydration
↓ Levels of consciousness

82
Q

Other signs/symptoms of Hyperosmolar Hyperglycaemic State

A

General : Fatigue, N+V

Neurological : Headaches, papilloedema, weakness

Haematological : Hyperviscosity - could result in MI, stroke, periph arterial thrombosis etc

Cardiovascular : dehydration, hypotension, tachycardia

83
Q

Bicarbonate level in Hyperosmolar Hyperglycaemic State

A

NORMAL

84
Q

Diagnostic values for Hyperosmolar Hyperglycaemic State

A

Hyperglycaemia (> 30 mmol/L)
Hypotension
Hyperosmolality (usually > 320 mosmol/kg)

Unlike DKA, NOT accompanised w/ acidosis or ketosis

85
Q

Ix Hyperosmolar Hyperglycaemic State

A

Blood glucose
Plasma osmolality
Urine stick test

86
Q

K+ levels in Hyperosmolar Hyperglycaemic State

A

Total body K+ is low (osmotic diuresis)
BUT serum K+ is often high bc low insulin
∴ K+ shifts out of cells

87
Q

Tx of Hyperosmolar Hyperglycaemic State

A

Fluid replacement w/ 0.9% saline

Insulin (only if high levels of ketones/glucose don’t decrease after fluid replacement) - patients more sensitive to insulin ∴ lower rate of infusion

VTE prophylaxis (venous thromboembolism) - high risk bc severe dehydration
∴ give LMWH e.g. SC enoxaparin

88
Q

Complications of Hyperosmolar Hyperglycaemic State

A

Cerebral oedema - from rapid lowering GB from insulin Tx (bc Px vv sensitive)

89
Q

Epidemiology of Hyperthyroidism

A

F > M
Presents between 20 - 40 (not Graves’)

90
Q

Causes of Hyperthyroidism

A

**Graves’ Disease
Toxic multinodular goitre (elder women)
De Quervain’s
Toxic thyroid adenoma
Drug induced - iodine, amiodarone

91
Q

How does De Quervain’s usually present?

A

W/ fever, neck pain, malaise

92
Q

At what age does Graves’ disease present?

A

40-60 years
Earlier if maternal FHx

93
Q

Define Thyrotoxicosis

A

Increase in T3 and T4 levels in circulation

94
Q

Define hyperthyroidism

A

Increased synthesis of T3 and T4 in the thyroid gland

95
Q

Signs/symptoms of hyperthyroidism

A

Weight loss
Heat intolerance
Palpitations
DIFFUSE GOITRE
Increased sweating
Diarrhoea
Oligomenorrhoea
Anxiety
Onycholysis

96
Q

What are some Graves’ disease specific signs/symptoms?

A

Orbitopathy
Exophthalmos
Ophthalmoplegia
Thyroid acropachy
Pretibial myxoedema

97
Q

What is thyroid acropachy?

A

TRIAD OF :
1. Digital clubbing
2. Soft tissue swelling of hands and feet
3. Periosteal new bone formation

98
Q

RF Graves’ disease

A

Female - common postpartum
Genetics - HLA-B8, DR3 & DR4
E.coli & other GRAM-NEG
Stress
Amiodarone (AF), Alemtuzumab (MS)
Autoimmune diseases

99
Q

Why are E.coli and other GRAM-NEG organisms a risk factor for Hyperthyroidism?

A

Contain TSH-binding sites
∴ molecular mimicry may occur

100
Q

Key presentation of Hyperthyroidism

A

Weight loss
Irritability
Heat intolerance

101
Q

Key presentation of Hyperthyroidism

A

Weight loss
Irritability
Heat intolerance

102
Q

Thyroid hormone plays a major role in …

A

… Metabolism, growth and development

103
Q

1st Ix Hyperthyroidism (Graves’)

A

Thyroid function tests (TFTs) - ↑ T4, ↓ TSH

104
Q

In TFT, how can you differentiate between 1º and 2ºhyperthyroidism? Why is this difference shown?

A

1º - high T3/T4, low TSH
2º - high T3/T4, high TSH

bc in 2º, problem with pituitary ∴ TSH not suppressed

105
Q

Give some examples of 2º hyperthyroidism

A

Pituitary resistance
Pituitary secreting adenoma

106
Q

If thyroid peroxidase antibodies (TPO Abs) are found in blood, what does this indicate?

A

Thyroid disease due to autoimmune disorder
e.g. Graves’, Hashimoto’s

107
Q

GS Ix Hyperthyroidism

A

TSH-receptor Ab - if pos = Graves’
TPO-Ab - to confirm Graves’

diagnosis made in addition to TFT results

108
Q

Tx Hyperthyroidism

A

1ST LINE -
Propranolol - used at diagnosis, to rapidly treat symptoms (e.g. tremor)
–
Anti-thyroid drug - Carbimazole OR Propylthiouracil (PTU)

Radioiodine treatment - Radioactive I(131)

Surgery - thyroidectomy

109
Q

What treatment should be given to patients with active moderate-severe and sight-threatening orbitopathy with Graves’ disease?

A

IV corticosteroids e.g. methylprednisolone

110
Q

Describe the mechanism of Carbimazole in the treatment of Hyperthyroidism

A

Blocks thyroid peroxidase
∴ reduces thyroid levels

111
Q

What is a common S/E of Carbimazole?

A

AGRANULOCYTOSIS

112
Q

Describe the mechanism behind radioiodine treatment for Hyperthyroidism?

A

Emits beta particules
∴ ionisation of thyroid cell

113
Q

S/E of radioiodine treatment for Hyperthyroidism

A

May exacerbate thyroid eye disease

114
Q

Describe the 4 phases of De Quervain’s thyroiditis

A

Phase 1 - last 3-6 weeks
hyperthyroidism, painful goitre, ↑ ESR

Phase 2 - lasts 1-3 weeks
Normal thyroid function

Phase 3 - weeks-months
Hypothyroidism

Phase 4 -
Thyroid structure and function goes back to normal

115
Q

Key presentation of De Quervain’s thyroiditis

A

Neck pain (which may move to jaw and ears)
Difficulty eating
Tender, firm, enlarged thyroid
Fever
Palpitations

116
Q

When is radioiodine treatment contraindicated when treating Hyperthyroidism?

A

Pregnancy
Breast-feeding

117
Q

Describe the process of thyroidectomy in reference to treating hyperthyroidism

A

Removal of thyroid gland, leaving small part
so thyroid function maintained

118
Q

Conditions of thyroidectomy when treating hyperthyroidism

A

Anti-thyroid drugs stopped 10-14 days prior
Replaced w/ oral potassium iodide

119
Q

Complications of thyroidectomy when treating hyperthyroidism

A

Hypocalcaemia
Hypothyroidism
Hypoparathyroidism
Recurrent laryngeal palsy (laceration)
Recurrent hyperthyroidism

120
Q

Key presentation of Thyroid Crisis (Thyroid Storm)

A

Hyperpyrexia
Tachycardia
Extreme restlessness
Maybe delirium, coma, death

121
Q

What is Thyroid Storm precipitated by?

A

Infection
Stress
Surgery
Radioactive iodine therapy

122
Q

Tx Thyroid Storm

A

Large doses of carbimazole
Propanolol
Potassium iodide
Hydrocortisone

123
Q

How does potassium iodide help to manage thyroid storm?

A

Blocks release of thyroid hormone from gland

124
Q

What does hydrocortisone do when used to treat Thyroid storm?

A

Inhibits peripheral conversion of T4 to T3

125
Q

What is Thyroid Crisis/Thyroid Storm?

A

Rare, life-threatening disease!!
Rapid deterioration of thyrotoxicosis

126
Q

Tx De Quervain’s

A

If hyperthyroidism phase - NSAIDs and corticosteroids (for pain)
If hypothyroidism phase - Normally no Tx but if severe, small dose of levothyroxine

127
Q

What can pituitary adenomas cause?

A

Cushing’s Syndrome/Disease
Acromegaly
Prolactinoma

128
Q

Define Cushing’s syndrome
What differentiates it from Cushing’s Disease?

A

XS CORTISTOL
(chronic, free circulating)

Cushing’s disease - results from pituitary adenoma

129
Q

Causes of Cushing’s

A

ACTH independent : ACTH = normal, cortisol = high
Oral steroid use !! e.g. prednisolone - most common!!
Adrenal adenoma/carcinoma

ACTH dependent ACTH and cortisol = high
*Cushing’s disease (ant. pituitary adenoma)
Ectopic ACTH production e.g. SCLC producing ACTH

130
Q

Key presentation of Cushing’s syndrome

A

*Round moon face
*Truncal obesity
*Thin skin/bruising

Buffalo hump - fatty hump on upper back
Acne
Hirsutism
Osteoporosis

CUSHING
Cataracts
Ulcers
Striae
HTN and Hyperglycaemia
Increased risk of infection
Necrosis
Glucosuria

131
Q

What gland secretes ACTH?

A

Pituitary

132
Q

What gland secretes cortisol?

A

Adrenal gland

133
Q

Describe the relationship between ACTH and cortisol

A

ACTH stimulates adrenal gland to produce cortisol
∴ ↑ ACTH = ↑ Cortisol

134
Q

Ix Cushing’s

A

1st line - raised plasma cortisol

GS : DEXAMETHASONE SUPPRESSION TEST
Low dose - 1mg
Failure to suppress over 24 hrs

OTHER :
24 hr urinary free cortisol - alternative to GS but doesn’t indicate underlying cause
MRI brain - pituitary adenoma
Chest CT - SCLC
Adbo CT - adrenal tumour

135
Q

Tx Cushing’s

A

Treat underlying cause :
Iatrogenic - stop steroids !!!
Adrenal adenoma - adrenalectomy
Cushing’s disease - trans-sphenoidal surgery to remove pituitary adenoma
Ectopic ACTH production - surgery to remove neoplasm if can be located and hasn’t metastasised

If cannot surgically remove cause, remove both adrenal glands and give Px replacement steroids - lifelong

136
Q

Describe the Dexamethasone Suppression Test

A

Given at night (10pm), measured in morning (9am)

Low dose test :
1mg dexamethasone

Results :
if low cortisol = normal
if high/normal = cushing’s syndrome (POS)
–
High dose test
8mg dexamethasone

Results :
if low cortisol = Cushing’s disease
If high/normal w LOW ACTH - Adrenal adenoma
if high/normal w HIGH ACTH - Ectopic ACTH

137
Q

What inhibits the release of GH?

A

Somatostatin
High levels of glucose
Dopamine (not as potent as Somatostatin)

Phase 2 (24 decks)

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