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Phase 2a Green Conditions > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

T1DM - what is it? Epidemiology?

A
  • autoimmune destruction of pancreatic beta cells → complete insulin deficiency
  • usually presents aged 5-15
  • 10% of all diabetes
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2
Q

Risk Factors of T1DM

A
  • family history of HLA DR3-DQ2 or HLA DR4-DQ8
  • Northern European
  • other autoimmune diseases eg autoimmune thyroid, coeliac, Addison’s
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3
Q

Pathophysiology of T1DM

A
  • autoantibodies attack beta cells in the islets of Langerhans
  • causes insulin deficiency → hyperglycaemia
  • continuous breakdown of glycogen from liver (glucogenesis) → glycosuria
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4
Q

Signs and Symptoms of T1DM

A
  • classic triad = polydipsia, polyuria, weight loss (BMI <25)
  • usually short history of severe symptoms
  • may present with ketosis
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5
Q

Diagnostic Criteria of T1DM

A

random plasma glucose >11

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6
Q

Treatment of T1DM

A
  • insulin
  • short-acting insulin/insulin analogues → 4-6hrs
  • longer-acting insulin → 12-24hrs
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7
Q

What is T2DM?

A
  • non-insulin dependent
  • patients gradually become insulin resistant AND/OR
  • pancreatic beta cells fail to secrete enough insulin
  • progresses from impaired glucose tolerance
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8
Q

Causes of T2DM

A
  • gestational diabetes
  • steroids
  • Cushing’s
  • chronic pancreatitis
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9
Q

Risk Factors of T2DM

A
  • lifestyle factors
  • Asian men
  • > 40yrs
  • HTN
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10
Q

Signs and Symptoms of T2DM

A
  • polydipsia
  • polyuria
  • glycosuria
  • central obesity
  • blurred vision
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11
Q

Investigations for T2DM

A
  • fasting plasma glucose >7
  • random plasma glucose >11
  • HbA1c >48
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12
Q

1st Line Management for T2DM

A

LIFESTYLE

  • dietary advice
  • smoking cessation
  • decrease alcohol intake
  • encourage exercise
  • regular blood glucose and HbA1c monitoring
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13
Q

2nd Line Management for T2DM

A

MEDICATIONS
1. metformin → increased insulin sensitivity → 1st choice if overweight
2. add either DPP4 inhibitor, sulphonylurea (increased insulin secretion) or pioglitazone
3. triple therapy
4. then add insulin
use HbA1c levels to monitor

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14
Q

What is DKA

A
  • diabetes ketoacidosis
  • complete lack of insulin → high ketone production
  • medical emergency
  • serious complication of T1DM
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15
Q

Causes of DKA

A
  • untreated/undiagnosed T1DM
  • infection
  • illness
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16
Q

Pathophysiology of DKA

A
  • absence of insulin → hyperglycaemia
  • hyperglycaemia → osmotic diuresis → dehydration
  • peripheral lipolysis for energy → increased circulating free fatty acids → oxidised to acetyl CoA → ketone bodies (acidic) → acidosis
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17
Q

Symptoms of DKA

A
  • extreme diabetes symptoms plus
  • N&V
  • weight loss
  • confusion and reduced mental state
  • lethargy
  • abdominal pain
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18
Q

Signs of DKA

A
  • Kussmaul’s breathing
  • ‘pear drop’ breath
  • hypotension
  • tachycardia
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19
Q

Investigations of DKA

A
  • random plasma glucose >11
  • plasma ketones >3
  • blood pH <7.35
  • bicarb >15
  • urine dipstick → glycosuria, ketonuria
  • raised urea and creatinine
  • decreased total K+ and increased serum K+
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20
Q

Treatment of DKA

A
  • ABCDE management
  • replace fluid → 0.9% saline IV
  • IV insulin
  • restore electrolytes → K+
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21
Q

What is ABCDE management?

A
  • Airway
  • Breathing
  • Circulation
  • Disability
  • Exposure
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22
Q

What is HHS?

A
  • hyperosmolar hyperglycaemic state
  • marked hyperglycaemia, hyperosmolality, mild/no ketosis
  • medical emergency
  • serious complication of T2DM
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23
Q

Pathophysiology of HHS

A
  • low insulin → increased glucogenesis
  • hyperglycaemia but enough insulin to inhibit ketogenesis
  • hyperglycaemia → dehydration
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24
Q

Signs and Symptoms of HHS

A
  • extreme diabetes symptoms plus
  • confusion and reduced mental state
  • lethargy
  • severe dehydration
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25
Q

Investigations for HHS

A
  • random plasma glucose >11
  • urine dipstick = glycosuria
  • plasma osmolality = high
  • decreased total K+ and increased serum K+
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26
Q

Treatment of HHS

A
  • replace fluids → 0.9% saline IV
  • low rate infusion of insulin
  • restore electrolytes → K+
  • LMW heparin
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27
Q

What is Hyperthyroidism

A
  • clinical effect of excess thyroid hormone
  • primary = abnormal increased thyroid function
  • secondary = abnormal increased TSH production
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28
Q

Causes of Hyperthyroidism

A
  • Graves disease
  • toxic multinodular goitre
  • toxic adenoma
  • metastatic follicular thyroid cancer
  • iodine excess eg IV contrast
  • secondary causes = TSH secreting pituitary tumour
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29
Q

Epidemiology of Hyperthyroidism

A
  • mainly young women → 20-40yrs

- Graves disease

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30
Q

Risk Factors of Hyperthyroidism

A
  • smoking
  • stress
  • HLA-DR3
  • other autoimmune diseases eg T1DM, Addison’s, vitiligo
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31
Q

Pathophysiology of Hyperthyroidism

A
  • increased T3
  • increased metabolic rate, CO, bone resorption
  • also activates sympathetic NS
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32
Q

Signs and Symptoms of Hyperthyroidism (9)

A
  • hot and sweaty
  • diarrhoea
  • hyperphagia
  • weight loss
  • palpitations
  • tremor
  • irritability/anxiety/restlessness
  • oligomenorrhoea
  • goitre
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33
Q

Investigations for Hyperthyroidism

A
  • TFTs → increased T4/T3
  • primary = decreased TSH
  • secondary = increased TSH
  • anti-TSHR
  • US/CT head
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34
Q

Treatment for Hyperthyroidism

A
  1. carbimazole → blocks synthesis of T4
  2. propylthiouracil → prevents conversion of T4 to T3
    - beta-blockers for symptom relief
    - radioiodine
    - thyroidectomy
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35
Q

Pathophysiology of Graves

A
  • IgG autoantibodies (anti-TSHR-Ab) bind to TSH receptors
  • increased T3/T4 production
  • also react with orbital autoantigens
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36
Q

Symptoms of Graves

A
  • hyperthyroid symptoms
  • thyroid eye disease → eyelid retraction, periorbital swelling, proptosis
  • pretibial myxoedema
  • thyroid acropachy → clubbing, painful finger and toe swelling
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37
Q

What is Hypothyroidism

A
  • clinical effect of lack of thyroid hormone
  • primary = abnormal decreased thyroid function
  • secondary = abnormal decreased TSH production
  • not enough T3 to increase metabolic rate for normal body functions
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38
Q

Epidemiology of Hypothyroidism

A
  • > 40yrs

- female

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39
Q

Causes of Hypothyroidism

A
  • autoimmune diseases eg hashimotos, primary atrophic hypothyroidism
  • primary iodine deficiency
  • drugs eg antithyroid, lithium
  • secondary cause = hypopituitarism
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40
Q

Signs and Symptoms of Hypothyroidism (9)

A
  • fatigue
  • weight gain
  • loss of appetite
  • cold
  • lethargy
  • constipation
  • low mood
  • menorrhagia
  • goitre
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41
Q

Investigations for Hypothyroidism

A
  • TFTs → decreased T3 and T4
  • primary = increased TSH
  • secondary = decreased TSH
  • autoantibodies → anti-TPO
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42
Q

Treatment for Hypothyroidism

A

levothyroxine T4

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43
Q

What is Hashimoto’s thyroiditis

A
  • most common cause of hypothyroidism
  • cause = autoimmune inflammation of thyroid gland
  • associated with anti-TPO and antithyroglobulin antibodies
  • goitre then atrophy of gland
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44
Q

What is Cushing’s

A

long term exposure cortisol → released by adrenal glands

45
Q

Causes of Cushing’s

A
  • ACTH secreting from pituitary adenoma (Cushing’s disease)
  • ectopic ACTH production from small cell lung cancer
  • iatrogenic → steroids
  • adrenal adenoma
46
Q

Signs and Symptoms of Cushing’s (7)

A
  • moon face
  • central obesity
  • buffalo hump
  • acne
  • HTN
  • striae
  • hirsutism
47
Q

Investigations for Cushing’s

A
  • raised random plasma cortisol
  • overnight dexamethasone suppression test → cortisol will not be suppressed
  • urinary free cortisol
  • plasma ACTH
48
Q

Treatment for Cushing’s

A
  • depends on underlying cause
  • Cushing’s disease → remove pituitary adenoma → transsphenoidal surgery
  • adrenal adenoma → adrenalectomy
  • cortisol synthesis inhibition → metyrapone, ketoconazole
49
Q

What is Acromegaly?

A
  • release of excess GH causing overgrowth of all systems
  • GH acts directly on tissues eg liver, muscle, bone, fat
  • GH acts indirectly through induction of insulin-like GF
50
Q

Causes of Acromegaly

A
  • pituitary adenoma

- secondary to malignancy that secretes ectopic GH eg lung cancer

51
Q

Complications of Acromegaly

A
  • erectile dysfunction

- DM

52
Q

Signs and Symptoms of Acromegaly (7)

A
  • prominent forehead and brow
  • increased jaw size
  • large hands, nose, tongue, feet
  • visual field defect
  • profuse sweating
  • lower pitch of voice
  • obstructive sleep apnoea
53
Q

Investigations for Acromegaly

A
  1. insulin-like GF 1 test = raised
    GOLD STANDARD = oral glucose tolerance test
    - random serum GH = raised
    - MRI pituitary fossa
54
Q

Treatment for Acromegaly

A
  1. transshpenoidal resection surgery (for adenoma)
  2. somatostatin analogue eg octreotide
  3. GH receptor antagonist eg pegvisomant
  4. dopamine agonist eg cabergoline
55
Q

What is Prolactinoma?

A
  • benign pituitary adenoma producing excess prolactin

- thought to have a genetic association

56
Q

Causes of Hyperprolactinaemia

A
  • non-functioning pituitary tumour → compresses pituitary stalk → no inhibition of prolactin release
  • prolactinoma
  • antidopaminergic/antipsychotic drugs
57
Q

Pathophysiology of hyperprolactinaemia

A
  • galactorrhea (stimulates milk)

- inhibits FSH and LH

58
Q

Signs and Symptoms of Prolactinoma (5)

A
  • visual field defect
  • menstrual irregularity
  • infertility
  • galactorrhoea
  • secondary hypogonadism (rediced libido, sexual dysfunction)
59
Q

Investigations for Prolactinoma

A
  • prolactin levels

- CT head

60
Q

Treatment for Prolactinoma

A
  1. dopamine agonists → bromocriptine/cabergoline

GOLD STANDARD = transsphenoidal resection surgery of pituitary gland

61
Q

What is Conn’s?

A

primary hyperaldosteronism due to an aldosterone producing adenoma

62
Q

Pathophysiology of Conn’s

A
  • excess production of aldosterone, independent of RAAS
  • high Na+ and H2O retention
  • increased K+ excretion in kidneys
  • low renin release
63
Q

Signs and Symptoms of Conn’s (5)

A
  • HTN
  • hypokalaemia
  • nocturia, polyuria
  • mood disturbance
  • difficulty concentrating
64
Q

Investigations for Conn’s

A
  • aldosterone-renin ratio blood test = increased
  • plasma K+ = reduced
  • U&E
65
Q

Treatment for Conn’s

A
  1. spironolactone → if hyperplasia
    GOLD STANDARD = laporascopic adrenalectomy → if adenoma
    aim = lower BP, decrease aldosterone, resolve electrolyte imbalance
66
Q

What is Addison’s

A
  • primary adrenal insufficiency

- destruction of adrenal cortex → decreased production of cortisol and aldosterone

67
Q

Causes of Addison’s

A
  • autoimmune destruction = most common in UK
  • TB → most common cause worldwide
  • adrenal metastases
68
Q

Signs of Addison’s

A

Signs

  • 4T’s = thin, teary, tired, tanned
  • pigmented palmar creases
  • postural hypotension
69
Q

Investigations for Addison’s

A
  1. U&E → hyponatraemia, hyperkalaemia, blood glucose (high)

GOLD STANDARD = short synACTHen test = ACTH stimulation test

70
Q

Treatment for Addison’s

A
  • glucocorticoids → oral hydrocortisone/prednisolone to replace cortisol
  • mineralocorticoids → fludrocortisone to replace aldosterone
  • double dose of steroid when there is infection, trauma, surgery, nightshift work
71
Q

What is SIADH?

A
  • syndrome of inappropriate ADH

- high ADH secretion → increased water reabsorption in CD

72
Q

Causes of SIADH

A
  • post-op from major surgery
  • infection → atypical pneumonia, lung abscess
  • head injury
  • thiazide diuretics = most common
73
Q

Signs and Symptoms of SIADH

A
  • muscle cramps
  • confusion
  • severe hyponatraemia
74
Q

Investigations for SIADH

A
  • diagnosis of exclusion
  • U&E = hyponatraemia
  • urine Na+ and osmolality = high

exclude causes of hyponatraemia

  • -ve short synACTHen test
  • no D&V
  • no history of diuretic use
  • no AKI/CKD
75
Q

What is Hyperkalaemia?

A

high K+

>5.5

76
Q

Causes of Hyperkalaemia

A

impaired excretion

  • AKI/CKD
  • drugs eg ACEi, NSAIDs, beta blockers
  • renal tubular acidosis
  • addisons → decreased aldosterone

increased intake

shift to EC

  • metabolic acidosis
  • rhabdomyolysis
  • decreased insulin
  • tumour lysis syndrome
77
Q

Symptoms of Hyperkalaemia

A
  • lightheadedness
  • weakness
  • chest pain
  • palpitations
78
Q

Signs of Hyperkalaemia

A
  • arrhythmias
  • reduced power and reflexes
  • flaccid paralysis
79
Q

Investigations for Hyperkalaemia

A
  • ECG
  • bloods
  • urine osmolality and electrolytes
80
Q

Treatment for Hyperkalaemia

A
  • cardiac monitoring
  • calcium gluconate → protects myocardium
  • insulin/dextrose/nebulised salbutamol → drive K+ IC
81
Q

What is Hypokalaemia?

A

low K+

<3.5

82
Q

Causes of Hypokalaemia

A

increased excretion

  • renal disease
  • drugs eg thiazide/loop diuretics, laxatives
  • GI loss → D&V
  • Conns → increased aldosterone

decreased intake

  • dietary deficiency/fasting
  • liquorice abuse

shift to IC

  • metabolic alkalosis
  • drugs eg insulin, SABA/LABAs
83
Q

Investigations for Hypokalaemia

A
  • ECG
  • bloods
  • urine osmolality and electrolytes
84
Q

Treatment for Hypokalaemia

A
  • K+ → PO/IV

- other electrolytes as required

85
Q

What are the two types of DI?

A

cranial and nephrogenic

86
Q

Pathophysiology of DI

A
  • impaired water resorption from kidneys
  • large volumes of dilute urine due to reduced ADH
  • impaired ADH secretion from posterior pituitary = cranial
  • impaired response of the kidney to ADH = nephrogenic
87
Q

Symptoms of DI

A
  • polyuria
  • polydipsia
  • dehydration
88
Q

Causes of Cranial DI

A
  • idiopathic
  • congenital
  • tumour
  • trauma
  • infection
89
Q

Causes of Nephrogenic DI

A
  • inherited
  • metabolic → low K, high Ca
  • drugs → Li
  • chronic renal disease
90
Q

Diagnosis of DI

A

GOLD STANDARD = 8hr water deprivation test

  • then desmopressin test → establish cranial or nephrogenic
  • cranial MRI
91
Q

Treatment of DI

A
  • mild = manage conservatively → rehydration
  • cranial = desmopressin (synthetic ADH)
  • nephrogenic = if cause persists → bendroflumethazide
92
Q

What is Primary Hyperparathyroidism?

A
  • excessive secretion of PTH

- 1 PTH gland produces excess PTH

93
Q

What is Secondary Hyperparathyroidism?

A
  • excessive secretion of PTH

- increased secretion of PTH to compensate for hypocalcaemia

94
Q

What is Tertiary Hyperparathyroidism?

A
  • excessive secretion of PTH

- autonomous secretion of PTH even after corrrect of Ca2+ deficiency due to CKD

95
Q

How does PTH raise Ca2+ levels?

A
  • bone resorption
  • gut/renal absorption
  • activates vitamin D
96
Q

Causes of Hyperparathyroidism

A
  1. adenomas = main, hyperplasia of all glands
  2. CKD, low vitamin D
  3. develops from prolonged secondary hyperPTH
97
Q

Signs and Symptoms of Hyperparathyroidism

A
  • bones = bone pain
  • stones = renal calculi
  • moans = psychic moans
  • groans = abdominal groans
  • hypercalcaemia
98
Q

Investigations for Hyperparathyroidism

A
  • PTH/bone profile → high PTH/Ca2+, low phosphates
    1. raised Ca2+
    2. low serum Ca2+, high PTH
    3. raised Ca2+ and PTH
  • DEXA scan
  • xray → salt and pepper degradation
  • US for stones
99
Q

Management of Hyperparathyroidism

A
  • watchful waiting
    1. surgical removal of adenoma, bisphosphonates
    2. Ca2+ correction, treat underlying cause
    3. Cinacalet (Ca2+ mimetic), total/part parathyroidectomy
100
Q

What is Primary Hypoparathyroidism? Causes?

A
  • reduced pTH production due to gland failure
  • autoimmune destruction
  • congenital = DiGeorge syndrome → 22q11 del
101
Q

What causes Secondary Hypoparathyroidism?

A
  • surgical removal

- decreased Mg+ → required for PTH secretion

102
Q

Risk Factors for Hypoparathyroidism

A
  • other autoimmune disorders
103
Q

Pathophysiology of Hypoparathyroidism

A
  • low PTH - hypocalcaemia and hyperphosphataemia

- neurons become more excitable

104
Q

Symptoms of Hypoparathyroidism

A

CATS go numb

  • convulsions
  • arrhythmias
  • tetany
  • spasm
  • numbness
105
Q

Signs of Hypoparathyroidism

A
  • Chvostek’s sign → facial nerve induces spasm

Trousseau’s → BP cuff causes wrist flexion and fingers to pull together → carpopedal spasm

106
Q

Investigations for Hypoparathyroidism

A

bone profile = decreased Ca2+/PTH, increased/normal phosphate

107
Q

Treatment for Hypoparathyroidism

A
  • IV Ca2+
  • D3 = calcitriol
  • synthetic PTH is required
108
Q

ECG abnormalities in hypokalaemia

A
  • flat T waves
  • ST depression
  • long QT interval
  • prominent U waves
109
Q

ECG abnormalities in hyperkalaemia

A
  • tall tented T waves
  • ST elevation
  • short QT interval
  • small/absent P waves

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