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Phase 2A revision > Endocrine to work on COPY > Flashcards

Endocrine to work on COPY Flashcards

1
Q

Name 3 causes of hypocalcaemia

A 
Hypoparathyroidism
Vitamin D deficiency
Hyperventilation
Drugs
Malignancy
Toxic shock
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2
Q

Describe the treatment pathway for T2DM

A
  1. Lifestyle changes - lose weight, exercise, healthy diet and control of contributing conditions
  2. Metformin
  3. dual therapy of Metformin + one of the following:
    i) DPP4 inhibitor
    ii) sulphonylureas (gliclazide)
    iii) pioglitazone
  4. triple therapy
  5. insulin
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3
Q

what are the side effects of Sulfonylurea?

A

Hypoglycaemia
weight gain
hyponatraemia

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4
Q

what are the features of addisonian crisis?

A 
Vomiting
abdominal pain
profound weakness
hypoglycaemia 
hypovolemic shock
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5
Q

Name 5 risk factors for Graves disease

A
  1. Female
  2. Genetic association
  3. E.coli
  4. Smoking
  5. Stress
  6. High iodine intake
  7. Autoimmune diseases
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6
Q

Name 5 autoimmune diseases associated with thyroid autoimmunity

A
  1. T1DM
  2. Addison’s disease
  3. Pernicious anaemia
  4. Vitiligo
  5. Alopecia areata
  6. Rheumatoid arthritis
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7
Q

what are the causes of hyperthyroidism?

A
  • Grave’s disease
  • Toxic multinodular goitre
  • Solitary toxic nodule/adenoma - benign
  • De Quervarians thyroiditis
  • Postpartum thyroiditis
  • Drug induced
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8
Q

Give 5 side effects of anti-thyroid drugs

A
  1. Rash
  2. Arthralgia
  3. Hepatitis
  4. Neuritis
  5. Vasculitis
  6. Agranulocytosis - very serious
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9
Q

What is the treatment for a thyroid crisis?

A

Large doses of oral carbimazole, oral propranolol, oral potassium iodide and IV hydrocortisone

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10
Q

Name 4 causes of primary hypothyroidism

A
  1. autoimmune thyroiditis
  2. postpartum thyroiditis
  3. iatrogenic
  4. drug induced
  5. iodine deficiency
  6. congenital
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11
Q

Name 4 drugs that can cause hypothyroidism

A
  1. Carbimazole (used to treat hyperthyroidism)
  2. Amiodarone
  3. Lithium
  4. Iodine
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12
Q

Name 3 triggers of Hashimoto’s thyroiditis

A
  1. Iodine
  2. Infections
  3. Smoking
  4. Stress
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13
Q

what are the causes of cranial DI?

A 
Idiopathic 
Congenital defects in ADH gene 
Disease of hypothalamus 
Tumour – metastases, posterior pituitary 
Trauma – neurosurgery
Infiltrative disease
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14
Q

what are the causes of nephrogenic DI?

A
  • Hypokalaemia
  • Hypercalcaemia
  • Drugs
    - lithium chloride
    - Demeclocycline
    - glibenclamide
  • Renal tubular acidosis
  • Sickle cell disease
  • Prolonged polyuria of any cause
  • Familial (mutation in ADH receptor)
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15
Q

Give 3 possible differential diagnosis’s of DI

A
  1. DM
  2. Hypokalaemia
  3. Hypercalcaemia
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16
Q

What is the treatment for nephrogenic DI?

A
  • treat cause
  • thiazide diuretics - (BENDROFLUMETHIAZIDE) - Produces hypovolaemia which will encourage the kidneys to take up more Na+ and water in proximal tubule
  • NSAIDs - IBUPROFEN - Lower urine volume and plasma Na+ by inhibiting prostaglandin synthase. Prostaglandins locally inhibit the action of ADH
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17
Q

Give 4 causes of polyuria

A
  1. Hypokalaemia
  2. Hypercalcaemia
  3. Hyperglycaemia
  4. Diabetes insipidus
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18
Q

what are the clinical features of SIADH?

A 
SYMPTOMS:
Nausea and vomiting
Headache
Lethargy
Cramps
Weakness
Confusion / irritability

SIGNS
raised JVP
oedema
ascites

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19
Q

what are the causes of SIADH?

A 
brain injury
infection
hypothyroidism
cancers
lung diseases
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20
Q

what are the investigations for SIADH?

A
  • ADH levels
  • U and Es (low sodium normal potassium),
  • fluid status

distinguish SIADH from salt & water depletion - test with 1-2L of
0.9% saline:
• Sodium depletion will respond
• SIADH will NOT RESPOND

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21
Q

Describe the treatment for SIADH

A
  1. Restrict fluid - <1L/day
  2. Give salt
  3. Loop diuretics - furosemide
  4. Demeoclocycline - inhibitor of ADH
  5. ADH-R antagonists - vaptans - primate water excretion with no loss of electrolytes
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22
Q

Give 4 local effects a pituitary adenoma

A
  1. Headaches
  2. Visual field defects - bitemporal hemianopia
  3. Cranial nerve palsy and temporal lobe epilepsy
  4. CSF rhinorrhoea
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23
Q

Give 4 potential complications of untreated DKA

A
  1. Cerebral oedema
  2. Adult respiratory distress syndrome
  3. Aspiration pneumonia
  4. Thromboembolism
  5. Death
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24
Q

Name 3 other types of diabetes other than T1DM, T2DM and DI

A
  1. Maturity onset diabetes of the young (MODY)
  2. Permanent neonatal diabetes
  3. Maternal inherited diabetes and deafness
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25
Q

Name 3 exocrine causes of Diabetes

A
  1. Inflammatory - actue/chronic pancreatitis
  2. Hereditary haemochromatosis
  3. Pancreatic neoplasia
  4. Cystic fibrosis
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26
Q

what are the clinical features of pheochromocytoma?

A 
SYMPTOMS
Headache
Profuse Sweating
Palpitations
Tremor 
SIGNS
Hypertension
Postural hypotension
Tremor
hypertensive retinopathy
Pallor
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27
Q

Describe the treatment for diabetic nephropathy

A
  1. Glycaemic and BP control
  2. Angiotensin receptor blockers/ACE inhibitors - RAMIPRIL or CANDESARTAN
  3. Proteinuria and cholesterol control
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28
Q

Give 5 risk factors for diabetic neuropathy

A
  1. Poor glycaemic control
  2. Hypertension
  3. Smoking
  4. High HbA1c
  5. Overweight
  6. Long duration DM
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29
Q

Why do isolated mononeuropathies result from in diabetic neuropathy?

A

Occlusion of vasa nervorum - small arteries that provide blood supply to peripheral nerves

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30
Q

what infections can poorly controlled diabetes lead to?

A
  1. UTIs
  2. Staphylococcal infection of skin
  3. Mucocutaneous candidiasis
  4. Pyelonephritis
  5. TB
  6. Pneumonia
  7. rectal abscess
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31
Q

How do incretin based agents treat diabetes?

A

Influence glucose homeostasis via:

  • glucose dependent insulin secretion
  • postprandial glucagon suppression
  • slowing gastric emptying
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32
Q

What diseases are associated with polycystic ovary syndrome?

A
  1. Insulin resistance - T2DM
  2. Hypertension
  3. Hyperlipidaemia
  4. CV disease
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33
Q

Give 5 symptoms of polycystic ovary syndrome

A
  1. Amenorrhoea
  2. Oligomenorrhoea
  3. Hirsutism
  4. Acne
  5. Overweight
  6. Infertility
34
Q

What criteria can be used to make a diagnosis of polycystic ovary syndrome?

A

Rotterdam diagnostic criteria

  1. Menstrual irregularity
  2. Clinical or biochemical evidence of hyperandrogenism
  3. Polycystic ovaries on USS
35
Q

What investigations might you do in someone to confirm a diagnosis of Conn’s syndrome?

A
  • first line = aldosterone renin ratio - high
  • increased plasma aldosterone levels that aren’t suppressed with 0.9% saline infusion or fludrocortisone administration - DIAGNOSTIC
  • Bloods - plasma potassium = low
    4. ECG - flat T waves, ST depression and long QT
36
Q

Give 4 ECG changes you might see in someone with Conn’s syndrome

A
  1. Increased amplitude and width of P waves
  2. Flat T waves
  3. ST depression
  4. Prolonged QT interval
  5. U waves
37
Q

What is adrenal hyperplasia?

A

Defective enzymes mediating the production of adrenal cortex products - low levels of cortisol and high levels of male hormones

38
Q

How does adrenal hyperplasia present?

A

Salt loss
Females - ambiguous genitalia with common urogenital sinus
Males - no signs at brith, subtle hyperpigmentation and possible penile enlargement

39
Q

What diagnostic test would be done to confirm adrenal hyperplasia?

A

Serum 17-hydorxyprogesterone (precursor to cortisol) = high

40
Q

what are the clinical features of hyperkalaemia?

A 
SYMPTOMS
Fatigue
Generalised weakness
Chest pain
Palpitations
SIGNS
Arrhythmias
Reduced power
Reduced reflexes
Signs of underlying cause
41
Q

what are the causes of hyperkalaemia

A

IMPAIRED EXCRETION

  • AKI and CKD
  • drug effect
  • renal tubular acidosis (T4)

INCREASED INTAKE

  • IV therapy
  • increased dietary intake

SHIFT TO EXTRACELLULAR

  • metabolic acidosis
  • rhabdomyolysis
42
Q

what are the clinical features of hypokalaemia?

A 
SYMPTOMS:
Asymptomatic
Fatigue
Generalised weakness
Muscle cramps and pain
Palpitations

SIGNS:
Arrhythmias
Muscle paralysis and rhabdomyolysis

43
Q

Give 3 causes of hypokalaemia

A
  • INCREASED EXCRETION
    • drugs e.g. thiazide, loop
    • renal disease
    • GI loss
    • increased aldosterone

REDUCED INTAKE
- dietary deficiency

SHIFT TO INTRACELLULAR
- drugs e.g. insulin, salbutamol

44
Q

What ECG changes might you see in someone with hypokalaemia?

A
  1. Increased amplitude and width of P waves
  2. ST depression
  3. Flat T waves
  4. U waves
  5. QT prolongation
45
Q

How does a medullary cancer of the thyroid present?

A

Diarrhoea
Flushing episodes
Itching

46
Q

what are the side effects of metformin?

A

GI upset

lactic acidosis

47
Q

what is the mechanism of action for SGLT-2 inhibitors?

A

inhibits resorption of glucose in the kidney

48
Q

what are the side effects of SGLT-2 inhibitors?

A

UTI

49
Q

what is the mechanism of action for glitazones?

A

Activate PPAR-gamma receptor in adipocytes to promote adipogenesis and fatty acid uptake

50
Q

what are the side effects of glitazones?

A

Weight gain

Fluid retention

51
Q

what are the risk factors for hyperosmolar hyperglycaemic state?

A
  • infection
  • consumption of glucose rich fluids
  • concurrent medication (thiazides or steroids)
52
Q

what are the investigations for hyperosmolar hyperglycaemic state?

A

Random plasma glucose >11mmol/L
Urine dipstick: glucosuria
Plasma osmolality - high
U+E - ↓ total body K+, ↑serum K+

53
Q

what is the treatment for hyperosmolar hyperglycaemic state?

A
  • Replace fluid - 0.9% saline IV
  • Insulin - At low rate of infusion!
  • Restore electrolytes - e.g. K+
  • LMWH
54
Q

what are the side effects of levothyroxine?

A
  • usually due to excessive doses

- GI disturbance, cardiac arrhythmias and neurological tremors

55
Q

what is the mechanism of action for carbimazole?

A

prevents thyroid peroxidase from producing T3 and T4

56
Q

what are the side effects of GH receptor antagonists e.g. pegvisomant?

A
  • reactions at injection site
  • GI disturbance
  • hypoglycaemia
  • chest pain
  • hepatitis
57
Q

what is the mechanism of action for vasopressin antagonists e.g. tolvaptan?

A
  • inhibits vasopressin-2 receptor -> increases fluid excretion
  • causes aquaresis (excretion of H2O with no electrolyte loss) -> increased Na+
58
Q

what are the side effect of vasopressin antagonists e.g. tolvaptan?

A
  • GI disturbance
  • headache
  • increased thirst
  • insomnia
59
Q

what is the mechanism of action for vasopressin analogues e.g. desmopressin?

A

binds to V2 receptors -> aquaporin 2 inserted in collecting duct which increases water reabsorption

60
Q

what are the side effects of vasopressin analogies e.g. desmopressin?

A
  • headache
  • facial flushing
  • nausea
  • seizures
61
Q

what is the mechanism of action for metyrapone?

A
  • blocks cortisol synthesis by irreversibly inhibiting steroid 11 beta-hydroxide
62
Q

what are the side effects of metyrapone?

A
  • GI disturbance
  • headache
  • dizziness
  • drowsiness
  • hirsutism
63
Q

how would cortisol levels react to the synacthen test if there was secondary adrenal insufficiency?

A

short ACTH = no change

long ACTH = increase

64
Q

what are the most common sites for carcinoid tumours?

A 
appendix (45%)
terminal ileum (30%)
65
Q

what is the clinical presentation of carcinoid tumours?

A
  • bluish-red flushing of face and neck(bradykinin release)
  • appendicitis/GI obstruction
  • RUQ pain (hepatic mets)
  • bronchoconstriction/bronchospasm with cough (bradykinin release)
  • congestive heart failure
  • diarrhoea
66
Q

what are the investigations for carcinoid tumours?

A
  • liver USS - confirms liver mets
  • urinalysis - high conc of 5-hydroxyindolacetic acid
  • CXR chest/pelvis
  • MRI/CT
67
Q

what is carcinoid crisis?

A
  • tumour outgrows blood supply/handled too much in surgery
    LIFE-THREATENING
  • vasodilation, hypotension, tachycardia, bronchoconstriction, hyperglycaemia
68
Q

what are the clinical features of Conn’s syndrome?

A
  • hypertension
  • nocturia and polyuria
  • mood disturbance
  • difficulty concentrating
  • hypokalaemia
69
Q

give an example of a water soluble hormone

A

peptides - TRH, LH, FSH

70
Q

are water soluble hormones stored in vesicles or synthesised on demand?

A

stored in vesicles

71
Q

how do water soluble homrones get into cells

A

bind to cell surface receptors

72
Q

give an example of a fat soluble hormone

A

steroids - cortisol

73
Q

are fat soluble hormones stored in vesicles or synthesised on demand?

A

synthesised on demand

74
Q

give an example of an amine hormone

A

noradrenaline and adrenaline

75
Q

give the pathway for noradrenaline synthesis

A

phenylalanine -> L-tyrosine -> L-DOPA -> dopamine -> NAd and Ad

76
Q

where are peptide hormone receptors located?

A

om cell membrane

77
Q

where are steroid hormone receptors located?

A

in the cytoplasm

78
Q

where are thyroid/vitamin A and D receptors located?

A

nucleus

79
Q

what cells does FSH act on?

A 
ovaries = granulosa cells
testes = sertoli cells
80
Q

what cells does LH act on?

A 
ovaries = theca cells
testes = leydig cells

Phase 2A revision (38 decks)

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