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Belle Phase 2a > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

Parathyroid hormone function

A

Raises calcium levels

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2
Q

Secondary hyperparathyroidism

A

Low calcium triggers > High PTH > still Low calcium (due to secondary cause)
High phosphate

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3
Q

Tertiary hyperparathyroidism

A

High PTH
High calcium
High phosphate

(Tertiary = 3)

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4
Q

Primary hyperparathyroidism

A

High PTH
High calcium
Low phosphate

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5
Q

Symptoms:
Low mood and energy
Constipation + abdominal pain
Dysuria

A

Hyperparathyroidism

hypercalcaemia = stones (urinary symptoms), bones (bone pain), moans (depression), groans (constipation)

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6
Q

URGENT complication of CKD

A

HYPERKALAEMIA: arrhythmias (VT and VF)

Tx:
calcium gluconate (IF heart arrhythmias)
insulin + dextrose (1st line if no heart arrhythmias)

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7
Q 
43 year old man 
symptoms over last 3 months
Polyuria 
Polydipsia 
Nocturia
Unexplained weight loss
A

Diabetes Type II

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8
Q

Diagnostic tests in DM2

A

NEED TWO ABNORMAL TESTS:
HbA1c >48
Fasting >7
Random >11

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9
Q

Monitoring test in DM

A

HbA1c

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10
Q

First line Mx in DM2

A

LIFESTYLE

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11
Q

Sulfonylurea most dangerous side effect

A

hypoglycaemia

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12
Q

Diabetes complications

A

Microvascular = OPATHY (retinopathy, peripheral neuropathy, nephropathy)

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13
Q

First line in DKA after ABCs

A

IV fluids

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14
Q

Diabetic ketoacidosis > Tx with high dose Insulin = fatigue, muscle cramping

Diagnosis? ECG pattern?

A

Insulin moves potassium into cells > HYPOKALAEMIA > U waves

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15
Q

Most significant ECG pattern in HYPERKALAEMIA

A

Tall Tented T waves

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16
Q

Diarrhoea not related to food intake + no blood/mucus
Facial flushing precipitated by stress
Intermittent palpitations

O/E: Hepatomegaly

A

Carcinoid tumour

GOLD STANDARD Ix: urinary 5-hydroxyindolecetic acid

Symptoms only appear when the tumour has metastasised to the liver (gets broken down elsewhere)

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17
Q

Fatigue
Weight gain
Bitemporal hemianopia
PMH: DM T2

Diagnosis? Ix?

A

Acromegaly

1st line: IGF-1
GOLD STANDARD: OGTT

Growth hormone inhibits insulin from working (so you eventually develop insulin resistance) and increases gluconeogenesis

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18
Q

Anxiety
Tremors
Palpitations
Weight loss

ECG: absent P waves, AF

Ix?

A

Hyperthyroidism: thyroid function test

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19
Q

Young onset hypertension

Non responsive to medication

A

Conns syndrome

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20
Q

Phaeochromocytoma Ix

A

Plasma free metanephrines

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21
Q 
Neck pain radiating to the jaw
Palpitations
Sweating
Recently recovered from viral infection 
Raised ESR 
Normal TFT
No weight loss
A

De Quervains thyroiditis

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22
Q

Graves triad

A

opthalmopathy, dermopathy (pretibial myoexedema), acropachy (clubbing)

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23
Q

Causes of drug induced Hyperthyroidism

A

Amiodarone + lithium

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24
Q

Hyperthyroidism Tx principles

A

TITRATE + BLOCK (slowly increase dose of carbimazole)

BLOCK AND REPLACE (carbimazole > levothyroxine)

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25
Q

Signs of agranulocytosis from carbimazole

A

Sore throat
fevers
Ulcers

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26
Q

Most common cause of Cushing’s

A

EXOGENOUS STEROIDS

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27
Q

Endogenous causes of Cushing’s

A

Corticotropin dependent:
Pituitary adenoma
SCLC

Corticotropin independent:
Adrenal adenoma

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28
Q

Complications of Cushing’s

A

CVD
Hypertension
Type 2 Diabetes
Osteoporosis +/- fractures

Courtney Has Ten Owls🙄🦉

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29
Q

Addisons patho

A

Autoimmune damage of the adrenal glands

Not enough cortisol = RAISED ACTH = pigmentation

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30
Q

Risk factors Addisons

A 
FHx autoimmune 
Female
TB
HIV (opportunistic infection) 
Sarcoidosis
Adrenal haemorrhage
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31
Q

Diagnostic test Addisons

A

SynACTHen

Other Ix: 9am cortisol

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32
Q

Addisons U&Es

A

Low sodium
High potassium
- due to FALL IN ALDOSTERONE

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33
Q

Addisons treatment

A

Hydrocortisone

Fludrocortisone (corrects glucocorticoids)

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34
Q

Carpal tunnel in acromegaly

A

Due to excess growth of hands

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35
Q

Complications of acromegaly

A

Diabetes T2
Cardiomyopathy
HTN

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36
Q

Severe abdo pain and weakness
Tachycardia, Low BP, Low urine output (hypovolaemic shock)
Hypoglycaemia
Deep pigmentation in buccal mucosa and skin creases

A

ADDISONIAN CRISIS

Tx: IV hydrocortisone + saline to correct dehydration and hypotension

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37
Q

SIADH

Diagnostic criteria:

A

Euvolemic hyponatraemia, High urine osmolality, Low plasma osmolality

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38
Q

Causes of SIADH

A 
SCLC 
Infection (pneumonia) 
Abscess 
Drugs e.g. SSRIs, sulfonylureas, carbamazepine
Head injury
Alcohol withdrawal
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39
Q

Diabetes insipidus

A

Neurogenic: Lack of production to ADH
Nephrogenic: Lack of response to ADH

Px: Polyuria, polydipsia without weight loss

Diagnostic test: water deprivation test (desmopressin stimulation test)

  • neurogenic: decreased urine output
  • nephrogenic: continued high urine output
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40
Q

Chvosteks sign

A

Clinical finding in HYPOCALCAEMIA

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41
Q

ADH MOA

A

Insertion of aquaporin channels

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42
Q

ADH effect on Na+ levels

A

Hyponatraemia: dilutes the level of Na+ in the blood

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43
Q

Causes of SIADH

A
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44
Q

Gold standard Ix in acromegaly

A

Oral glucose tolerance test (OGTT)

Measure glucose + GH
75g glucose 
Measure GH response to glucose 
- normal: GH decreases in response to glucose
- acromegaly: GH remains high
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45
Q

1st line screening test for acromegaly

A

Serum IGF-1

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46
Q

Hypercalcaemia ECG changes

A

Shortening of the QT interval (due to reduction in the calcium plateau of the action potential)

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47
Q

Hypercalcaemia Tx

A

Fluids

Calcitonin + IV Bisphosphonates

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48
Q

Calcitonin

A

Hormone secreted by parafollicular cells in the thyroid to REDUCE CALCIUM LEVELS

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49
Q

Child on second level of asthma treatment ladder

Weight gain but not height gain

A

ICS

Iatrogenic Cushing’s syndrome

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50
Q

T1DM risk factors

A

HLA DR3/DQ2
HLA DR4/DQ8
Northern European
Other autoimmune diseases (90%)

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51
Q

T1DM epidemiology

A

Usually presents ages 5-15

10% of diabetes = T1

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52
Q

Processes STIMULATED by insulin

A

GLUT4 uptake into cells
Glycogenesis into glycogen (for storage in hepatocytes)
Additional glucose > converted to fatty acids (exported from hepatocytes as lipoproteins > storage in adipocytes)

53
Q

Processes SUPPRESSED by insulin

A

Glycogenolysis (glucose from glycogen stores)
Gluconeogenesis (glucose from non-carb)
Lipolysis (release of free fatty acids from adipocytes) > Ketogenesis (acetyl coA to acidic ketone bodies)
= PATHOGENESIS OF DKA (LACK OF INSULIN IN T1DM)

54
Q

T1DM diagnostic test

A

Random plasma glucose >11mmol/L

55
Q 
Polydipsia
Polyuria
Ketosis
Rapid weight-loss
Young
BMI <25 
Personal or family history of autoimmune disease
A

T1DM

56
Q

Pathological causes of T2DM

A

Increased insulin resistance +/- Reduced insulin secretion

Gestational diabetes
Steroids/Cushing’s
Chronic pancreatitis

57
Q

T2DM risk factors

A

Lifestyle: obesity, sedentary, high calorie or alcohol excess
Higher prevalence in Asian men
Above 40 years old (late onset)
Hypertension

58
Q

Why is weight loss characteristic of T1DM and not T2DM

A

Weight loss = muscle breakdown from loss of insulin (occurs later in most cases of T2DM, insulin resistance occurs first)

59
Q

Second line Mx T2DM

A

Metformin (increases insulin sensitivity)

60
Q

Metformin dual therapy options

A

DPP4 (depeptidyl peptidase) inhibitor
Sulfonylurea (gliclazide) - increases insulin SECRETION
Pioglitiazone

61
Q

Why does hyperglycaemia cause dehydration

A

Osmotic diuresis

62
Q

Signs of DKA

A

Kussmauls breathing
Pear drop breath
Hypotension
Tachycardia

63
Q

DKA Ix

A 
Random plasma glucose >11
Plasma ketones >3
Blood pH <7.35 or Bicarbonate <15 
Urine dipstick: glucosuria, ketonuria
Serum U&E: raised urea + creatinine, decreased total K+, increased serum K+
64
Q

DKA Tx

A
  1. ABC management
  2. IV fluids
  3. IV insulin
  4. restore electrolytes (e.g. K+)
65
Q

Hyperosmolar hyperglycaemic state

A

Serious complication of T2DM
Hyperglycaemia = osmotic diuresis/high plasma osmolality
Enough insulin to prevent ketogenesis/DKA
Px: severe dehydration, confusion and reduced mental state

66
Q

HSS Tx

A

IV fluids
Insulin (at low rate of infusion)
Restore electrolytes
LMWH

67
Q

Hyperthyroidism epidemiology

A

Mainly young women 20-40 yrs (F > M 9:1)

Graves’ disease = 65-75% of cases

68
Q

Hyperthyroidism risk factors

A

Smoking
Stress
HLA-DR3
Other autoimmune diseases: T1DM, Addison’s, Vitiligo

69
Q

Effects of increased T3

A 
Increased:
metabolic rate
cardiac output 
bone resorption
activation of sympathetic nervous system
70
Q

Px of hyperthyroidism

A

EVERYTHING GOES FAST

71
Q

Second line treatment in hyperthyroidism

A

Propylthiouracil (prevents T4 > T3 conversion)

72
Q

Mechanism of action of carbimazole

A

Blocks synthesis of T4

73
Q

Hyperthyroidism Tx options

A
  1. Drug management: carbimazole, propylthiouracil; beta blockers for symptoms
  2. Radioiodine
  3. Thyroidectomy
74
Q

Pathophysiology of Graves’ disease

A

IgG autoantibodies (anti-TSHR-Ab) bind to TSH receptors and increase T4/T3 production

Interaction with orbital autoantigens = thyroid eye disease

75
Q

Graves specific symptoms

A

Thyroid eye disease (25-50%):

  • eyelid retraction
  • preorbital swelling
  • proptosis/exopthlamos

Pretibial myxoedema

Thyroid acropachy

76
Q

Hypothyroidism epidemiology

A

Mainly >40 years old

F > M 6:1

77
Q

Aetiology of hypothyroidism

A 
Primary:
Autoimmune: Hashimotos, Atrophy 
Iodine deficiency 
Drugs
Post thyroidectomy

Secondary:
Hypopituitarism

78
Q

Autoantibodies in Hashimotos

A

Anti-TPO

79
Q

Signs of hypothyroidism

A 
BRADYCARDIC
Bradycardia
Reflexes
Ataxia
Dry hair/skin
Yawning
Cold hands
Ascites
Round face (puffy)
Defeated demeanour 
Immobile
Congestive cardiac failure
80
Q

Cushing’s aetiology

A

ACTH dependent

  • Cushing’s disease (pituitary adenoma)
  • Ectopic ACTH (SCLC)

ACTH independent

  • Iatrogenic
  • Adrenal adenoma
81
Q

Cushing’s Px

A

+ mood change, acne

82
Q

Cushing’s Ix

A

Multiple investigations:

  • Random plasma cortisol
  • Overnight dexamethasone suppression test
  • Urinary free cortisol (24 hour)
  • Plasma ACTH
83
Q

Dexamethasone suppression test

A
84
Q

Causes of acromegaly

A 
Pituitary adenoma (MOST COMMON = 99%) 
Secondary to malignancy that secrets ectopic GH (SCLC)
85
Q

Complications of acromegaly

A

Erectile dysfunction

Diabetes Mellitus

86
Q

Treatment of acromegaly

A

1st line: transsphenoidal resection surgery
2nd line: somatostatin analogue eg ocreotide
3rd line: GH receptor antagonist
4th line: dopamine agonist

87
Q

Prolactinoma

A

Benign adenoma of pituitary gland producing excess prolactin

88
Q

Galactorrhoea

A

Prolactinoma stimulates milk production from mammary gland as well as inhibiting FSH and LH

89
Q

Prolactinoma Ix

A

Prolactin levels

CT head

90
Q

Gold standard Prolactinoma Tx

A

Transsphenoidal resection surgery of pituitary

91
Q

1st line Prolactinoma Tx

A

Dopamine agonists (bromocriptine/carbergoline) - dopamine has an inhibitory effect on prolactin

92
Q

Conns syndrome

A

Primary hyperaldosteronism due to an aldosterone producing adenoma = high sodium and water retention and increase potassium excretion independent of RAAS

93
Q

Conns syndrome Px

A 
HTN
Hypokalaemia
Nocturia 
Polyuria
Mood disturbance 
Difficulty concentrating
94
Q

Conns syndrome Ix

A

Aldosterone:Renin ratio: increased

U&Es (plasma potassium: decreased)

95
Q

Conns syndrome Tx 1st line + gold standard

A 
1st line (pre-operative) 
Spironolactone (aldosterone antagonist) - controls HTN and K+

Gold standard: laparoscopic adrenalectomy

96
Q

Addison’s disease

A

Primary adrenal insufficiency = destruction of adrenal cortex leads to decreased production of glucocorticoids (cortisol) and mineralocorticoids (aldosterone)

(opposite of Cushing’s and Conn’s)

97
Q

Causes of Addison’s disease

A

Autoimmune destruction (80% of UK cases)
TB (most common cause worldwide)
Adrenal metastases

98
Q

Presentation of Addison’s disease

A 
Tanned
Lean
Fatigue
Pigmented palmar creases 
Postural hypotension
99
Q

Addison’s disease Ix 1st line + gold standard

A

1st line: U&E (hyponatraemia, hyperkalaemia, hypoglycaemia)

Gold standard: Short synACTHen test (high ACTH, low cortisol)

Plasma renin and aldosterone (high renin, low aldosterone)

Other tests:
Adrenal CT/MRI
21-hydroxylase adrenal autoantibodies (80% +)

100
Q

Addison’s disease Tx

A

Steroid replacement dependent on Px:

  • Hydrocortisone (cortisol replacement)
  • Fludrocortisone (aldosterone replacement)

Treat underlying cause
STEROID WITHDRAWAL ADVICE

101
Q

SIADH causes + Tx

A

Post-operative from major surgery
Infection (atypical pneumonia + lung abscess)
Head injury
Medications (thiazide diuretics) - MOST COMMON CAUSE

Tx = treat underlying cause e.g. stop medication

102
Q

SIADH Px

A 
Headache 
Nausea 
Fatigue
Muscle cramps
Confusion
Severe hyponatraemia
103
Q

Tolvaptan

A

ADH receptor blocker, can be used in SIADH

104
Q

Potassium normal range (mmol/L)

A

3.5-5.5

105
Q

Causes of hyperkalaemia

A
  1. IMPAIRED EXCRETION
    - AKI/CKD
    - Iatrogenic (ACEi, NSAIDs, Beta-blockers)
    - Addison’s disease
  2. INCREASED INTAKE
    - IV K+ therapy
    - dietary
  3. SHIFT TO EXTRACELLULAR
    - tumour lysis syndrome
    - decreased insulin
    - metabolic acidosis (H+/K+)
106
Q

Px of potassium imbalance

A 
Fatigue 
Weakness
Cramping 
Palpitations 
Arrythmias 
Hypotonia
Hyporeflexia
Paralysis

Hypo: constipation, Hyper: diarrhoea

107
Q

Hyperkalaemia Tx

A

ABC
Cardiac monitoring
- if cardiac problems = calcium gluconate 1st line to protect myocardium
No cardiac problems = insulin + dextrose 1st line (or nebulised salbutamol) = drive K+ intracellularly
Treat underlying cause

108
Q

Causes of hypokalaemia

A
  1. INCREASED EXCRETION
    - Renal disease
    - Iatrogenic (thiazide, loop diuretics)
    - GI loss (D+V)
    - Conns syndrome (aldosterone)
  2. DECREASED INTAKE
    - dietary
  3. SHIFT TO INTRACELLULAR
    - metabolic alkalosis
    - Iatrogenic (insulin, B2 agonists - SABA/LABA)
109
Q

Hypokalaemia ECG changes

A

Prolonged PR interval
ST depression
Flat T waves
Prominent U waves

110
Q

Causes of cranial diabetes insipidus

A

[DISRUPTED ADH SECRETION]

Idiopathic
Congenital
Tumour 
Trauma 
Infection
111
Q

Causes of nephrogenic diabetes insipidus

A

[DISRUPTED ADH RESPONSE]

Inherited/genetic mutation
Metabolic
Iatrogenic (lithium)
Chronic renal disease

112
Q

Gold standard diagnostic test for DI

A

8 hour water deprivation test

  • measure plasma and urine osmolality
  • end of 8h: desmopressin + measure plasma osmality (nephrogenic won’t react to ADH analogue)
113
Q

Tx of Diabetes insipidus

A

Treat underlying cause
Conservative management - rehydration
Cranial: desmopressin to replace ADH
Nephrogenic: bendroflumethiazide

114
Q

Ix to establish cranial vs nephrogenic DI

A

Desmopressin test
Nephrogenic: urine osmolality, urine output
Cranial: urine osmalility, urine output

115
Q

Primary hyperPTH

Patho
Aetiology
Ix
Tx

A

1 PTH gland produces excess PTH

Adenomas (80%) or hyperplasia of all glands

Raised calcium

Surgical removal of adenoma, bisphosphonates

116
Q

Secondary hyperPTH

Patho
Aetiology
Ix
Tx

A

Increased secretion of PTH to compensate hypocalcaemia

CKD/Low Vit D

Low serum calcium

Calcium correction, treat underlying cause

117
Q

Tertiary hyperPTH

Patho
Aetiology
Ix
Tx

A

Autonomous secretion of PTH even after correction of calcium deficiency (due to CKD)

Prolonged secondary hyperparathyroidism

Raised calcium

Cinacalcet (calcium mimetic - reduces PTH levels), total/part parathyroidectomy

118
Q

Hyperparathyroidism Px

A 
Bones (bone pain) 
Stones (renal calculi)
Moans (psychiatric)
Groans (abdominal) 
Hypercalcaemia
119
Q

Primary hypoPTH

A

= gland failure
Autoimmune destruction
Congenital (DiGeorge syndrome)

120
Q

Secondary hypoPTH causes

A 
Surgical removal
Decreased magnesium (required for PTH secretion)
121
Q

HypoPTH symptoms

A

= neurones become more excitable

CATS go numb
Convulsions
Arrythmias 
Tetany
Spasm
Numbness
122
Q

HypoPTH signs

A 
Chvosteks sign (facial nerve tap induces spasm)
Trousseaus sign (BP cuff causes wrist flexion and fingers to pull together)
123
Q

Primary hypoPTH Ix

A

Decreased calcium, increased or normal phosphate, decreased PTH
ECG: prolonged QT + ST segments

124
Q

Causes of hypercalcaemia

A 
CHIMPANZEES
Calcium supplements 
Hydrochlorothiazide
Iatrogenic/Immobilisation
Multiple Myeloma/Medication (lithiuM)
Parathyroid hyperplasia (primary) 
Alcohol
Neoplasm 
Zollinger Ellison syndrome 
Excessive Vit D
Excess Vit A
Sarcoidosis
125
Q

Triad of carcinoid symptoms

A

Palpitations
Diarrhoea
Flushing

126
Q

Carcinoid syndrome patho

A

Enterochromoffin cell tumour producing 5-HT
Most commonly found in terminal ileum or appendix
Hepatic involvement = carcinoid SYNDROME
Excess secretion of substance P, insulin, 5-HTm ACTH, bradykinin etc - wide range of symptoms

127
Q

Most common cause of secondary adrenal insufficiency

A

Long term corticosteroid use

128
Q

Carcinoid immediate treatment

A

Somatostatin analogue + surgery

Belle Phase 2a (14 decks)

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