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endocrinology Flashcards

1
Q

Give 5 causes of thyrotoxicosis.

A

Thyrotoxicosis - excess thyroid hormone due to any cause:
1. Increased production e.g. Grave’s, toxic adenoma.

  1. Leakage of T3/4 due to follicular damage.
  2. Ingestion of excess hormone.
  3. Thyroiditis (de quervain’s).
  4. Drug induced.
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2
Q

Grave’s disease vs gestational thyrotoxicosis?

A
  • Grave’s: symptoms predate pregnancy; symptoms are severe during pregnancy; goitre and TSH-R antibodies present.
  • Gestational thyrotoxicosis: symptoms do not predate pregnancy; lots of N/V - hyperemesis gravidarum associated. No goitre or TSH-R antibodies.
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3
Q

epidemiology of thyroid disorders?

A

Commonest endocrine disorder

Females (5-10x more)>males

Hyperthyroidism 2.5% prevalence

Hypothyroidism 5%

Most common clinical presentation of thyroid disease is Goitre 5-15%

2% of women will get Graves’ disease or autoimmune hypothyroidism (5-10 times the frequency in men)

5% will have postpartum thyroiditis and up to 20% will have positive thyroid antibodies

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4
Q

causes of hyperthyroidism?
(get main 2)

A
  1. Grave’s disease.
  2. Toxic adenoma. (benign) (causes 5% of cases of hyperthyroidism)
  3. Toxic multi nodular goitre (nodules that secrete thyroid hormones, seen in elderly and in iodine-deficient areas)
    • Ectopic thyroid tissue (metastases)
  5. Exogenous (iodine/T4 excess) - * eg w amiodarone medication (used to treat hypothyroidism)* bc its iodine rich
  6. De quervain’s thyroiditis (post-viral)

(hCG can activate TSH receptors (bc HCG and TSH are glycoprotein hormones with very similar structure) and cause hyperthyroidism)

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5
Q

Give 5 causes of hypothyroidism.

A
  1. Autoimmune thyroiditis e.g. Hashimoto’s and atrophic thyroiditis.
  2. Post-partum thyroiditis.
  3. Iatrogenic - thyroidectomy.
  4. Drug induced e.g. drug induced eg anti thyroid drugs (carbimazole, amiodarone, lithium.) or amiodarone (its used to treat hyperthyroidism)
  5. Iodine deficiency.
  6. hypopituitarism
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6
Q

primary hypothyroidism vs secondary hypothyroidism?

A

Primary hypothyroidism: thyroid gland itself producing LESS/reduced T4 and thus T3

Secondary hypothyroidism:

ANTERIOR PITUITARY is releasing LESS TSH
reduced TSH from anterior pituitary:
Thus not wnough T3 and T4

Hypopituitarism

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7
Q

Hypothyroidism: name 3 anti-bodies that may be present in the serum in someone with autoimmune thyroiditis.

A
  1. TPO (thyroid peroxidase).
  2. Thyroglobulin.
  3. TSH receptor.
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8
Q

What is the treatment for thyroid hypopituitarism?

A

Levothyroxine.

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9
Q

Give 5 symptoms of hypothyroidism.

A
  1. Menorrhagia – heavy bleeding.
  2. Obesity/weight gain.
  3. Malar flush.
  4. Tiredness.
  5. Intolerance to cold.
  6. Energy levels fall/eyebrow loss.
  7. Depression/dry skin and hair.
  8. GOITRE!
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10
Q

Give 5 signs of hypothyroidism.

A
  1. Mental slowness.
  2. Dry thin hair.
  3. Bradycardia. (mnemonic in oxford handbook)
  4. Anaemia.
  5. Hypertension.
  6. Loss of eyebrows.
  7. Cold peripheries.
  8. Carpal tunnel syndrome.
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11
Q

What 1st line investigation might you do in someone who you suspect has hypothyroidism?

A
  • TFT’s - serum TSH will be raised and T3/T4 will be low in primary hypothyroidism.
  • Thyroid antibodies.
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12
Q

in the 1st line investigation of suspected primary hypothyroidism - what are the results of the TFTs?
and why (pathophysiology)

A

TFT’s - serum TSH will be raised and T3/T4 will be low.

  1. Less T4 and T3 are produced due to the thyroid’s reduced capacity to produce hormone or respond to TSH.
  2. As a result, there is reduced negative feedback on the pituitary and hypothalamus.
  3. The reduction in negative feedback results in increased production of TRH (which we don’t typically measure) and TSH.
  4. The end result is low T4 and T3 and a raised TSH.
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13
Q

in the 1st line investigation of suspected secondary hypothyroidism - what are the results of the TFTs?
and why (pathophysiology)

A

Normal/low TSH: due to a lack of production.
Low T4: due to the absence of any positive feedback from TSH.

  1. Decreased production or secretion of TRH and TSH results in decreased stimulation of the thyroid gland.
  2. The thyroid gland, therefore, produces less T3 and T4.
  3. The low T3 and T4 would normally stimulate the pituitary and hypothalamic glands to increase TRH and TSH production, however, they are unable to increase production.
  4. The end result is low T4 and T3 and a normal/low TSH.
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14
Q

Give 3 potential consequences of untreated hypothyroidism in pregnancy.

A
  1. Gestational hypertension.
  2. Placental abruption.
  3. Post partum haemorrhage,
  4. Low birth weight.
  5. Neonatal goitre.
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15
Q

What is the effect of hyperthyroidism on TSH and T4 levels?

A

TSH will be low.T4 will be high.

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16
Q

Symptoms/signs of hyperthyroidism? COMPLETE THIS

A
  • Palpitations
  • Diarrhoea
  • Weight loss & increase appetite
  • Oligomenorrhea (infrequent periods) +/- infertility
  • Heat intolerance i.e. sweating a lot
  • Irritability/behavioural change
  • Tremor
  • Hyperkinesis muscle spasm
  • Warm - vasodilator peripheries
  • Proximal myopathy & muscle wasting
  • Lymphadenopathy and splenomegaly can occur
  • Anxiety
  • Hands:
    • Palmar erythema, warm moist skin and fine tremor
  • Diffuse goitre
  • Lid lag & ‘stare’ can occur in any hyperthyroidism
  • Elderly:
    • Atrial fibrillation
    • **Other tachycardias and/or heart failure
  • Children:
    • Excessive height or excessive growth rate
    • Behavioural problems like hyperactivity
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17
Q

Investigations of hyperthyroidism?

A

TFTs
- low serum TSH
- raised T3 and T4

And autoantibody status

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18
Q

management of hyperthyroidism?

A
  1. carbimazole 2. propylthiouracil
    (+ radioactive iodine)
    (+also beta blockers!!!!)

First-line pharmacological management of thyrotoxicosis involves the use of ablock (carbimazole) and replace (levothyroxine) regime. Anti-thyroid drugs

Beta-blockers(e.g. propranolol) are used to manage the adrenergic clinical features of thyrotoxicosis (e.g. tachycardia, tremor).

Other management options includeradioiodineandthyroidectomy.

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19
Q

complications of hyperthyroidism?

A

Main side effect is AGRANULOCYTOSIS (with carbimazole) - results in a severely low white blood cell count (leukopenia) - most commonly neutropenia:
- If they get sore throat, mouth ulcers and fevers then STOP DRUG
ASAP
- Other S/E; rash (common), arthralgia, hepatitis and vasculitis (in bold less common)

thyroid storm
Aka thyrotoxic crisis - excessive adrenergic activity secondary to thyrotoxicosis. Rapid T4 increase
- Management
Treated with LARGE DOSES of:
- ORAL CARBIMAZOLE
- ORAL PROPRANOLOL
- ORAL POTASSIUM IODIDE (to block acutely the release of thyroid hormone from gland)
- IV HYDROCORTISONE (to inhibits peripheral conversion of T4 to T3)
Thyroid storm is associated with high mortality.

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20
Q

grave’s disease: pathophysiology?

A

circulating IgG autoantibodies (aka TSH receptor stimulating antibodies TSHR-Ab) binding to and activating G-protein-coupled thyrotropin receptors, (TSH receptors in thyroid) which cause smooth thyroid enlargement and increased hormone production (esp. T3),

aka Autoimmune disease. TSH receptor antibodies stimulate thyroid hormone production -> hyperthyroidism.

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21
Q

grave’s disease: aetiology?

A
  • FEMALE - biggest risk factor (onset is common postpartum)
  • Genetic - association with HLA-B8, DR3 & DR2
  • E.coli and other gram-NEGATIVE organisms contain TSH-binding sites so may initiate pathogenesis via ‘molecular mimicry’
  • Smoking
  • Stress
  • High iodine intake
  • Autoimmune disease:
  • Vitiligo (pale white patches on skin)
  • Addison’s disease
  • Pernicious anaemia
  • Myasthenia gravis
  • Type 1 DM
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22
Q

Give 5 signs of Grave’s disease that don’t include opthalmopathy signs.

A
  1. Tachycardia.
  2. Arrhythmias e.g. AF.
  3. Warm peripheries.
  4. Muscle spasm.
  5. Pre-tibial myxoedema (raised purple lesions over the shins).
  6. Thyroid acropachy (clubbing and swollen fingers).
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23
Q

Give 5 symptoms of Grave’s disease that don’t include opthalmopathy signs.

A
  1. Weight loss.
  2. Increased appetite.
  3. Irritable.
  4. Tremor.
  5. Palpitations.
  6. Goitre.
  7. Diarrhoea.
  8. Heat intolerance.
  9. Malaise.
  10. Vomiting.
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24
Q

With what disease would you associated pre-tibial myxoedema and thyroid acropachy?

A

Grave’s disease.

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25
Q

Describe the treatment for Grave’s disease.

A
  1. Anti-thyroid drugs e.g. carbimazole. (blocks so targets thyroid peroxidase and so prevents the formation of T3/4.)
  2. Radioiodine drugs. ((blocks so targets thyroid peroxidase and so prevents the formation of T3/4.)
  3. Surgery - partial thyroidectomy.
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26
Q

De Quervain’s thyroiditis:
definition?

signs?

treatment?

A

Transient hyperthyroidism sometimes results from acute inflammation of the thyroid gland, probably due to viral infection

Usually accompanied by fever, malaise and pain in the neck

Treat with aspirin and only give prednisolone for severely symptomatic cases

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27
Q

Amiodarone:
function?

side-effects?

A

anti-arrythmia drug

can cause hypo/hyperthyroidism because it is iodine rich.
(can cause hypothyroidism alongside lithium and carbimazole)

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28
Q

Hashimoto’s thyroiditis
key presentation?

management of this?

A

Produces atrophic changes with regeneration that results in GOITRE FORMATION due to lymphocytic and plasma cell infiltration

LEVOTHYROXINE THERAPY may shrink the goitre, even when the patient is not hypothyroid

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29
Q

thyroid cancer:
risk factor?

pathophysiology?

A

radiation

Over 90% secrete thyroglobulin which can be used as a tumour marker after thyroid ablation

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30
Q

thyroid cancer:
key presentations?

A
  • In 90% they present as thyroid nodules
  • Occasionally (5%) they present with cervical lymphadenopathy or with lung, cerebral, hepatic or bone metastases

If thyroid gland increases in size, becomes hard and is irregular in shape - think carcinoma

Patients may complain of dysphagia or hoarseness of voice due to tumour compression on surrounding structures i.e. oesophagus and laryngeal nerve

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31
Q

thyroid cancer:
investigations?

A
  • Fine needle aspiration cytology biopsy:
  • **To distinguish between benign or malignant nodules
  • Blood test to check TFTs (TSH, T4 & T3):
  • To check if hyperthyroid or hypothyroid needs to be treated before carcinoma surgery
  • Ultrasound of thyroid:
  • Can differentiate between benign or malignant
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32
Q

management of thyroid cancer?

A
  • Thyroid LOVES iodine so will readily take up radioactive iodine which in turn

will locally irradiate and destroy cancer - providing very little radiation damage to other surrounding structures

  • Administer lots of LEVOTHYROXINE (T4) to keep TSH reduced as this is a

growth factor for the cancer!

extra or treatments for each diff type of thyroid carcinoma → kp

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33
Q

hypothyroidism: management?

A

levothyroxine for adults, children and young people with primary hypothyroidism.

(am on empty stomach)

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34
Q

Give 5 metabolic changes that occur in pregnancy.

A
  1. Increased EPO, cortisol and NAd.
  2. High CO.
  3. High cholesterol and triglycerides.
  4. Pro thrombotic and inflammatory state.
  5. Insulin resistance.
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35
Q

Is hypothyroidism or thyrotoxicosis more common in pregnancy?

A

Hypothyroidism is more common in pregnancy.

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36
Q

Give 3 potential consequences of untreated hypothyroidism in pregnancy.

Give 3 potential consequences of untreated hyperthyroidism in pregnancy.

A
  1. Gestational hypertension.
  2. Placental abruption.
  3. Post partum haemorrhage,
  4. Low birth weight.
  5. Neonatal goitre.
  6. Intra-uterine growth restriction.
  7. Low birth weight.
  8. Pre-eclampsia.
  9. Risk of still birth/miscarriage.
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37
Q

Give 5 signs and symptoms of diabetes insipidus.

A
  1. Excessive urine production (>3L/24h).
  2. Very dilute urine - <300 mOsmol/Kg.
  3. Severe thirst.
  4. Hypernatraemia.
  5. Dehydration.

(6. incontinence [secondary to chronic bladder distension).)

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38
Q

What investigations might you do to determine whether someone has diabetes insipidus?

A
  1. Measure 24-hour urine volume - >3L/24h = suggests DI.
  2. Plasma biochemisty - hypernatraemia.
  3. Water deprivation test - urine will not concentrate when asked not to drink.
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39
Q

Treatment for cranial DI vs nephrogenic DI

A

cranial DI = Desmopressin. (man-made form of ADH)

nephrogenic = treat the cause

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40
Q

Give 4 causes of polyuria.

A
  1. Hypokalaemia.
  2. Hypercalcaemia.
  3. Hyperglycaemia.
  4. Diabetes insipidus.
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41
Q

causes of cranial diabetes insipidus vs nephrogenic DI

A

Cranial DI =
1. Tumours.
2. Trauma.

  1. Infections.
  2. Idiopathic. (<50%)
  3. Genetic - AR.

nephrogenic diabetes insipidus =
1. Osmotic diuresis - diabetes mellitus.
2. Drugs. (lithium, demeclocycline )

  1. CKD.
  2. Metabolic e.g. hypercalcaemia and hypokalaemia.
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42
Q

Give 3 potential consequences of a pituitary adenoma

and give eg of diseases

A
  1. Pressure on local structures e.g. optic chiasm. -> eg Bitemporal hemianopia
  2. Pressure on normal pituitary
    -> hypopituitarism.
  3. Functioning tumour e.g. Cushing’s, gigantism/acromegaly, prolactinoma.
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43
Q

Cushing’s syndrome: definition

A

A set of signs/symptoms/ a clinical state

resulting from chronic glucocorticoid excess with a
- loss of normal feedback mechanisms.
- and loss of circadian rhythm of cortisol secretion (normally highest on waking).

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44
Q

Cushing’s syndrome: aetiology?

A
  1. Adrenal Tumour (adenoma or carcinoma).(tumor on the adrenal gland itself makes too much cortisol)
  2. Pituitary adenoma/tumour (would secrete too much ACTH) - (Cushing’s disease).
  3. Exogenous steroids.
  4. Ectopic ACTH syndrome.(tumors that develop outside the pituitary gland)
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45
Q

Cushing’s syndrome:
signs/symptoms

A
  1. Central obesity.
  2. Moon face.
  3. Hypertension.
  4. Skin thinning.
  5. Abdominal striae.
  6. Mood change.
  7. Osteoporosis.
  8. Muscle thinning.
  9. Weight gain.
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46
Q

Cushing’s syndrome:
investigations?

A
  1. Overnight dexamethasone suppression test
    In Cushing’s syndrome there will be no suppression
  2. Late night salivary cortisol - loss of circadian rhythm.
  3. Urinary free cortisol is raised.
  4. Loss of circadian rhythm.
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47
Q

Cushing’s syndrome:
treatment?

A
  1. Surgical removal of pituitary tumours.
    (eg Bilateral adrenalectomy (remove both adrenal glands)) or Surgical selective removal of pituitary adenoma trans-sphenoidal approach
  2. Drugs to inhibit cortisol synthesis e.g. metyrapone, ketoconazole.
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48
Q

Acromegaly:
Aetiology?

A

A benign pituitary adenoma producing excess GH.

(In rare cases is due to hyperplasia e.g. ectopic GH-releasing hormone from a carcinoid tumour)

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49
Q

Symptoms vs signs of acromegaly?

A

Symptoms:
1. Change in appearance.
2. Increase in size of hands and feet.
3. Excessive sweating.
4. Headache.
5. Tiredness.
6. Weight gain.
7. Amenorrhoea.
8. Deep voice.
9. Goitre.

Signs:
1. Prognathism - jaw protrusion.
2. Interdental separation.
3. Large tongue.
4. Spade like hands and feet.
5. Tight rings.
6. Bi-temporal hemianopia.

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50
Q

What co-morbidities are associated with acromegaly?

A
  1. Arthritis.
  2. Cerebrovascular events.
  3. Hypertension and heart disease.
  4. Sleep apnea. (due to excess soft tissue in larynx - pauses in breathing whilst sleeping)
  5. T2 DM.
  6. Impaired glucose tolerance (40%)
    Colon Cancer
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51
Q

Acromegaly: investigations?

A
  1. Plasma GH levels can exclude acromegaly - not diagnostic!
  2. Serum IGF-1 levels raised.
  3. Oral glucose tolerance test - diagnostic! - (Oral glucose tolerance test - failure of glucose to suppress serum GH.)
  4. MRI of pituitary.
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52
Q

What test is diagnostic for acromegaly?

A

Oral glucose tolerance test - failure of glucose to suppress serum GH.

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53
Q

Acromegaly: treatment?

Also name 2 drugs that can be used to treat acromegaly. What class of drugs do they belong to?

A
  1. Trans-sphenoidal surgical resection.
  2. Radiotherapy.
  3. Medical therapy: somatostatin analogues, dopamine agonists e.g. cabergoline.

Cabergoline - dopamine agonist.
Octreotide - somatostatin analogue.

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54
Q

Prolactinoma: Aetiology?

A
  1. Pituitary adenoma.
  2. Anti-dopaminergic drugs.
  3. Physiological - pregnancy, breast feeding, stress
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55
Q

Prolactinoma: signs and symptoms?

A
  1. Infertility.
  2. Golactorrhoea.
  3. Amenorrhoea.
  4. Loss of libido.
  5. Visual field defects and headaches due to local effect of tumour.
  6. Erectile dysfunction and reduced facial hair in men
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56
Q

What investigation would you do on someone presenting with difficulty getting pregnant, golactorrhoea, amenorrhoea, loss of libido and headaches?

A

You would measure serum prolactin.

These are symptoms of prolactinoma.

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57
Q

Prolactinoma: treatment?

A
  1. Dopamine agonist e.g. oral cabergoline.
    (Result is massive shrinkage of tumour)
58
Q

Pathophysiology behind Prolactinoma?

A

Dopamine regulates prolactin production so:
- more dopamine = less prolactin produced from pituitary

Prolactin acts on the mammary glands to produce milk.

59
Q

Normal blood glucose levels between?

A

between 3.5-8.0mmol/L under all conditions

60
Q

Describe the pathophysiology of diabetic ketoacidosis.

A

No insulin -> lipolysis -> FFA’s -> oxidised in liver -> ketone bodies -> ketoacidosis.

61
Q

DKA: 5 symptoms?

A
  1. Polyuria.
  2. Polydipsia.
  3. Weight loss.
  4. Nausea/vomiting. (-> dehydration)
  5. Confusion.
  6. Weakness.
62
Q

DKA: aetiology

A
  1. Unknown.
  2. Infections.
  3. Treatment errors - not administering enough insulin.
  4. Having undiagnosed T1DM.
63
Q

DKA: blood test results?
(Triad of DKA?)

A
  1. Acidaemia – blood pH < 7.3
  2. Hyperglycaemia – blood glucose > 11mmol/L.
  3. Ketonaemia.
64
Q

DKA: complications if untreated?

A
  1. Oedema. (Cerebral oedema from rapid lowering of blood glucose and thus osmolality of blood )
  2. Adult respiratory distress syndrome.
  3. Aspiration pneumonia.
  4. Thromboembolism.
  5. Death.
  • Hypotension
  • Hypothermia
65
Q

DKA: 5 signs?

A

Hypotension
8. Tachycardia
9. Kussmaul’s respiration. (deep rapid breathing) may be present - sign of respiratory compensation by hyperventilating
10. Breath smells of ketones (pear drops)
11. Dehydration
12. Eyes sunken

66
Q

DKA: treatment?

A
  1. ABCDE.
  2. IV normal saline.
  3. IV soluble insulin via syringe driver and sliding scale.
  4. Restore potassium levels.
  5. Look for underlying cause.
67
Q

A man presents with a history of weight loss, polyuria and nocturia. He is very unwell. The GP performs a capillary blood glucose which is found to be 17.2mmol/l. What is the most likely diagnosis of this mans symptoms?

A

T1DM

68
Q

T1DM: aetiology?

A

Beta cells express HLA antigens. Autoimmune destruction -> beta cell loss -> impaired insulin secretion.

69
Q

T1DM: Pathophysiology?

A

…

70
Q

T1DM: key presentations?
Signs?
Symptoms?

A

Polyuria, polydipsia, blurred vision, fatigue or tiredness.

Signs:
Young age <50, weight loss, low BMI, FHx of autoimmune disease, ketoacidosis

Symptoms:
Thirst, dry mouth, lack of energy, blurred vision, hunger, weight loss

71
Q

T1DM: 1st line investigations?
Gold standard?

A

1st line:
Random glucose tolerance test if presenting to GP. >11.1mmol/L
-> Fasting plasma glucose, 2-hour plasma glucose, plasma or urine ketones can all be measured.

Gold standard:
Glycated haemoglobin A1C test: average blood sugar for past 2-3 months, measures % glucose attached to Hb. >6.5% =diabetes.

72
Q

T1DM: 1st line treatment?
2nd line?
Side effects of treatment?

A
  • Basal-bolus insulin (insulin glarginae s/c)
  • Pre-meal insulin correction dose
  • Amylin analogue (pramlintide)

2nd line:
- fixed insulin dose

Side effects:
hypoglycaemia, weight gain, lipodystrophy

73
Q

T1DM: monitoring?

A

Check BP at each visit and treat to a goal of <140/90mmHg. When not on statins, check lipid profile in adults with diabetes at the time of first diagnosis, at initial medical evaluation, then 5-yearly.

74
Q

T1DM: complications?

A
  • DKA
  • Microvascular – retinopathy, nephropathy, neuropathy.
  • Macrovascular – CAD, cerebrovascular disease, PAD

Untreated type 1 is fatal due to diabetic ketoacidosis. Poorly controlled type 1 is a RF for: blindness, renal failure, foot amputations, and MIs.

75
Q

T2DM: aetiology?

A

Genetic predisposition and environmental factors e.g. obesity and lack of exercise.

76
Q

T2DM: Pathophysiology?

A
  • Impaired insulin secretion and resistance -> IGT -> T2DM -> hyperglycaemia and high FFA’s.
  • Impaired insulin secretion is thought to be due to lipid deposition in the pancreatic islets.

(T1DM usually develops as a result of autoimmune pancreatic beta-cell destruction. Up to 90% will have autoantibodies to at least one of 3 antigens: glutamic acid decarboxylase; insulin; and islet auto-antigen-2.
→ insulin deficiency and also continued breakdown of liver glycogen (into glucose and ketones) → leading to glycosuria and ketonuria
More in notion)

77
Q

What happens to insulin resistance, insulin secretion and glucose levels in T2DM?

A
  • Insulin resistance increases.
  • Insulin secretion decreases.
  • Fasting and post-prandial glucose increase.
78
Q

Why do you rarely see diabetic ketoacidosis in T2DM?

A

Insulin secretion is impaired but there are still low levels of plasma insulin. Even low levels of insulin can prevent muscle catabolism and ketogenesis.

79
Q

T2D: management?
And side-effects of treatments?

A
  1. Lifestyle changes: lose weight, exercise, healthy diet.
  2. Metformin.
  3. Metformin + sulfonylurea.
  4. Metformin + sulfonylurea + insulin.
  5. Increase insulin dose as required.
  • Metformin increases insulin sensitivity and inhibits glucose production.
  • Sulfonylurea stimulates insulin release - thus a side effect is Hypoglycaemia.
80
Q

Give one way in which the presentation of diabetic nephropathy differs between T1 and T2DM.

A

T1 DM: microalbuminuria develops 5-10 years after diagnosis.

T2 DM: microalbuminuria is often present at diagnosis.

81
Q

Hyperosmolar hyperglycaemic state: definition?

A

life-threatening emergency characterised by marked hyperglycaemia, hyperosmolality and mild or no ketosis

Hyperosmolar Hyperglycaemic State (HHS) occurs in people with Type 2 diabetes who experience very high blood glucose levels (often over 40mmol/l). It can develop over a course of weeks through a combination of illness (e.g.infection) and dehydration

82
Q

Hyperosmolar hyperglycaemic state: symptoms/signs?

A

HHS symptoms can frequently include:

urination,
thirst
nausea
dry skin
disorientation and, in later stages, drowsiness and a gradual loss of consciousness.
- Severe dehydration (secondary to osmotic diuresis)
- Hyperglycaemia
- Hyperosmolality - which may predispose to stroke, MI or arterial
- No ketones in blood or urine (acidosis is absent as insulin is still present for uptake of glucose into cells. )

83
Q

Hyperosmolar hyperglycaemic state: management?

A
  1. Insulin infusion - These patients are more sensitive to insulin so give a lower rate of infusion (Only use insulin if blood glucose not falling by 5mmol/L/h with rehydration.)
  2. Fluid replacement (rehydrate slowly) with 0.9% saline over 48h
  3. Low molecular weight heparin e.g. SC ENOXAPARIN to reduce risk of Thromboembolism
  4. Restore electrolyte loss (K+) when urine starts to flow
84
Q

Hyperosmolar hyperglycaemic state: test results?

A
  • Hyperglycaemia blood glucose > 11mmol/L
  • Urine stick testing shows heavy glycosuria
  • Plasma osmolality is extremely high
  • Total body K+ is low as a result of osmotic diuresis - but serum K+ is often raised due to the absence of insulin which allows K+ to shift out of cells
85
Q

Hypoglycaemia: define?

A

Defined as plasma glucose < 3mmol/L

86
Q

Hypoglycaemia: aetiology?

A

In diabetics: Due to insulin or sulphonylurea treatment -

In non-diabetics = EXPLAIN
- Ex -Exogenous drugs insulin, oral hypoglycaemic, alcohol binge with no food
- P - Pituitary insufficiency
- L Liver failure
- A - Addison’s disease
- I - Islets cell tumour (insulinoma) & immune hypoglycaemia
- N - Non-pancreatic neoplasm e.g. fibrosarcomas and haemangiopericytomas

87
Q

Hypoglycaemia: Pathophysiology?

A

Excess insulin in the bloodstream causescells in your body to absorb too much glucose (sugar) from your blood. It also causes the liver to release less glucose. These two effects together create dangerously low glucose levels in your blood. This condition is called hypoglycemia.

88
Q

Hypoglycaemia: key presentation?

A

autonomic:
Sweating, anxiety, hunger, tremor, palpitations, dizziness

Neuroglycopenic: (a shortage of glucose(glycopenia) in the brain, usually due to hypoglycemia)
Confusion, drowsiness, visual trouble, seizures, coma
Rarely there are focal symptoms such as transient hemiplegia, mutism, personality change, restlessness and incoherence

89
Q

Hypoglycaemia: 1st line investigations?

A
  1. Fingerprick blood during attack (on filter-paper at home) - and then can be sent for analysis
  2. Take drug history and exclude liver failure
  3. Bloods - glucose, insuline, C-peptide, plasma ketones
90
Q

Hypoglycaemia: management?

A
  1. Oral sugar and long-acting starch e.g. toast
  2. If cannot swallow then give 50% GLUCOSE IV
    3.
91
Q

Carcinoid syndrome: define?

A

Carcinoid syndrome occurswhen a rare cancerous tumor called a carcinoid tumor secretes certain chemicals into your bloodstream, causing a variety of signs and symptoms.
due to the release of serotonin and other vasoactive peptides into the systemic circulation from a carcinoid tumours

92
Q

Serotonin syndrome: define?

A

Serotonin syndrome occurs when you take medications that cause high levels of the chemical serotonin to accumulate in your body.

For example, serotonin syndrome may occur if you take an antidepressant with a migraine medication.

93
Q

conn’s syndrome: definition?

(where are these hormones synthesised?)

A

Excess production of aldosterone, (high aldosterone levels) independent of the renin-angiotensin system

Resulting in increased sodium and thus water retention (resulting in increased BP), and decreased renin release

(baso increased aldosterone and reduced renin)

(aldosterone -> synthesised in the zona glomerulosa.
and renin -> synthesised by the juxta-glomerular cells.)

94
Q

conn’s syndrome: aetiology?

A
  • 2/3rds - Adrenal adenoma that secretes aldosterone - Conn’s syndrome
  • 1/3rd - Bilateral adrenocortical hyperplasia
95
Q

conn’s syndrome: signs?
(2 main ones?)

A

Hypertension
and hypokalaemia
(Sodium will be normal or slightly raised.)

96
Q

conn’s syndrome: symptoms?

A deficiency in which electrolyte causes these symptoms?

A

muscle weakness
tiredness
Nocturia and polyuria
Mood disturbance
Difficulty concentrating

Due to potassium deficiency - hypokalaemia.

97
Q

conn’s syndrome: investigations?

A
  1. Bloods - U+E, renin (low) and aldosterone (high).
  2. Plasma aldosterone renin ratio can be used as an initial screening test - raised ratio indicates the need for further tests.
98
Q

conn’s syndrome: Give 4 ECG changes that you might see in someone with Conn’s syndrome.

A

Hypokalaemic ECG:

  1. Increased amplitude and width of P waves.
  2. Flat T waves.
  3. ST depression.
  4. Prolonged QT interval.
  5. U waves.
99
Q

conn’s syndrome: management?

A
  1. Laparoscopic adrenalectomy.
  2. Spironolactone (aldosterone antagonist)
    (for 4 wks pre-op to control BP and K+).
100
Q

hypokalaemia: aetiology?

A
  1. Diuretics.
  2. D+V.
  3. Conn’s syndrome.
  4. Insulin.
101
Q

Give 5 primary causes of adrenal insufficiency?

A
  1. Addison’s disease (autoimmune destruction of the adrenal cortex).
  2. Congenital adrenal hyperplasia (CAH).
  3. TB.
  4. Adrenal metastases.
  5. Drugs.
  6. Haemorrhage.
  7. Infection.
102
Q

adrenal insufficiency: define?

A

Adrenocortical insufficiency resulting in a reduction of mineralocorticoids, glucocorticoids and androgens.

103
Q

adrenal insufficiency: symptoms and signs?

A
  1. Tanned - pigmentation - only in Addison’s.
  2. Tired.
  3. Tearful.
  4. Thin - weight loss.
  5. Headaches.
  6. Abdominal cramps.
  7. Myalgia.
  8. Throwing up.
  9. Weakness.
104
Q

suspected adrenal insufficiency investigations?

(results of bloods?)

A
  1. Bloods - FBC, U+E (↓Na+ and ↑K+ - due to ↓ aldosterone - ↑Ca2+, ↑Urea).
  2. ↓ Glucose.
  3. ACTH stimulation test - Addison’s will not respond.

(- Hyponatraemia.
- Hyperkalaemia.
Lack of aldosterone and so less sodium is reabsorbed and less potassium is excreted.)

105
Q

adrenal insufficiency: management?
specifically for addison’s?

A

Hormone replacement - any steroids e.g. hydrocortisone.

In addison’s disease replace aldosterone with fludrocortisone.

(Glucocorticoids and Mineralocorticoids to correct postural hypotension, Na+/K+ Adjust both on clinical grounds.)

106
Q

adrenal insufficiency: pathophysiology?
(cortisol and ACTH levels)

A
  • Cortisol is low.
  • ACTH is high.
107
Q

adrenal insufficiency: aetiology?

A
  1. Hypopituitarism.
  2. Withdrawal from long term steroids.
  3. Infiltration.
  4. Infection.
  5. Radiotherapy.
108
Q

An adrenal crisis is a common presentation of adrenal insufficiency. Give 3 features of an adrenal crisis.

A
  1. Hypotension.
  2. Fatigue.
  3. Fever.
  4. Hypoglycaemia.
  5. Hyponatraemia.
  6. Hyperkalaemia.
109
Q

Adrenal Crisis: management?

A

Hydrocortisone and IV saline.

110
Q

SIADH: definition?

A

Syndrome of inappropriate ADH secretion.

Too much ADH = very concentrated urine and hyponatreamia.

This hormone helps the kidneys control the amount of water your body loses through the urine. SIADH causes the body to retain too much water.

111
Q

SIADH: Symptoms?

A
  1. Anorexia.
  2. Nausea.
  3. Malaise.
  4. Headache.
  5. Confusion.

(symptoms vary depending upon both the severity of the hyponatraemia and the rate at which it develops:
- Mild hyponatraemia: nausea, vomiting, headache, anorexia and lethargy.
- Moderate hyponatraemia: muscle cramps, weakness, confusion and ataxia.
- Severe hyponatraemia: drowsiness, seizures and coma.)

112
Q

SIADH: aetiology?

A
  1. Malignancy. (e.g. small-cell lung cancer)
  2. CNS disorders/primary brain injury e.g. meningitis, brain tumour, cerebral haemorrhage.
  3. TB.
  4. Pneumonia.
  5. Drugs.
  6. Hypothyroidism
113
Q

SIADH: management?

management of asymptomatic
SIADH vs symptomatic SIADH of acute onset?

A
  1. Restrict fluid!
  2. Give salt.
  3. Loop diuretics e.g. furosemide.
  4. ADH-R antagonists e.g. vaptans - can be used when people find fluid restriction challenging.

asymptomatic
SIADH:
fluid restriction

vs symptomatic SIADH of acute onset:
give 3%saline

114
Q

Hyponatraemia: aetiology?

A
  1. SIADH.
  2. Sodium deficiency.
  3. Renal failure.
  4. Malignancy.

Medications (most commonly thiazide diuretics).

115
Q

Describe 5 features of the essential criteria for SIADH.

A
  1. Hyponatreamia (<135mmol/L).
  2. Plasma hypo-osmolality.
  3. High urine osmolality. (Inappropriately elevated urine osmolality (i.e. greater than plasma osmolality))
  4. Clinical euvolaemia.
  5. Increased urinary sodium excretion with normal salt and water intake.(Urine [Na+] >40 mmol/L despite normal salt intake)
  6. Normal thyroid and adrenal function
116
Q

SIADH - differential diagnosis/ diseases that you must exclude in someone who you suspect could have SIADH.

A
  1. Renal disease.
  2. Hypothyroidism.
  3. Hypocortism.
  4. Recent diuretic use.
117
Q

Hyperkalaemia: definition?
and aetiology?

A

> 5.5mmol/L
- Mild – 5.5-5.9 mmol/L
- Moderate – 6.0-6.4 mmol/L
- Severe – >6.5 mmol/L

aetiology:
1. AKI (acute kidney injury) - renal .
2. NSAIDs - iatrogenic - many meds can cause

  1. Metabolic acidosis.
  2. K+ sparing diuretics.
    - Addison’s (adrenal insufficiency)
118
Q

Hyperkalaemia: symptoms?

A
  1. Weakness.
  2. Palpitations.
  3. Tachycardia.
  4. Chest pain.
    fatigue
119
Q

What ECG changes might you see in someone with hyperkalaemia?

A
  1. Tall tented T waves.
  2. Wide QRS.
  3. Small P waves.

below are all investigations done:
- U&Es
- FBC
- capillary blood gas
- ABG
- serum cortisol
- digoxin level
- ECG

120
Q

Hyperkalaemia: management?

A
  • Prevent further accumulation of potassium
  • stop any fluids/meds etc that inc K+
  • Stabilise the cardiac membrane - Administer intravenouscalcium gluconate(10mls of 10% solution)
  • Shift potassium intracellularly -> Insulin-glucose infusion: insulin helps to shift potassium from the extracellular to the intracellular compartment
    -> Salbutamol: promotes the movement of potassium into cells and therefore out of the serum.

Remove potassium from the body - Calcium polystyrene sulfonate resin (Calcium resonium) - used to remove potassium via the gastrointestinal tract.
Correction of the underlying cause:
(haemodialysis as last resort)

121
Q

Polyuria: aetiology?

A
  1. Hypokalaemia.
  2. Hypercalcaemia.
  3. Hyperglycaemia.
  4. Diabetes insipidus.
122
Q

Hypokalaemia: definition?

A

serum concentration of potassium <3.5mmol/L
(normal range 3.5-5.3mmol/L).

Severity of hypokalaemia is further classified into
- Mild= 3.1 – 3.5mmol/L
- Moderate= 2.5 – 3.0mmol/L
- Severe= < 2.5mmol/L

123
Q

Hypokalaemia: symptoms?

A
  1. Muscle weakness.
  2. Hypotonia.
  3. Hyporeflexia.
  4. Palpitations.
  5. Arrhythmia.
  6. Nausea and vomiting.
  7. Cramps.

Hypokalaemiaisgenerallyasymptomatic in mild cases. but see above in more severe cases

124
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. Prominent U waves.
  5. QT prolongation. (Elongated PR interval)
125
Q

Hypokalaemia: investigations?

A
  • ECGIf any changes relating to hypokalaemia are noted (or the patient requires aggressive IV potassium replacement), the patient may need to be put on a cardiac monitor
  • Bloods, especially FBC, U&Es, Caand PO, and Mg
    • Low magnesium levels are often associated with hypokalaemia; and low magnesium levels can often be found in patients refractory to potassium replacement therapy
  • A venous blood gas(VBG) can be useful for an immediate potassium check following intervention
126
Q

Hyperparathyroidism: definition?

define primary, secondary and tertiary?

A

Hyperparathyroidism is a condition in which one or more of your parathyroid glands become overactive and release (secrete) too much parathyroid hormone (PTH). This causes the levels of calcium in your blood to rise, a condition known ashypercalcemia

primary: hypercalcaemia abnormally active pt glands

secondary: HYPOcalcaemia results in reactive over[rpduction of PTH

tertiary: hypercalcaemia results from untreated sHPT with continuously elevated PTH levels

127
Q

Hyperparathyroidism: symptoms?

A

The majority of patients are asymptomatic.

“Stones, bones, abdominal groans, thrones, and psychiatric overtones!”
/Stones,bones, groans, thrones, moans.

Hyperparathyroidism -> hypercalcaemia

  1. Renal/biliary stones.
  2. Bone pain.
  3. Abdominal pain.
  4. Polyuria.
  5. Depression, anxiety, malaise.
128
Q

Hyperparathyroidism: aetiology?

A
  1. Primary: parathyroid adenoma - ↑PTH ↑Calcium ↓Phosphate.
  2. Secondary: physiological hypertrophy in an attempt to correct low calcium.
  3. Prolonged uncorrected hypertrophy.
129
Q

Hyperparathyroidism: management?

A
  1. High fluid intake, low calcium diet.
  2. Excision of adenoma.
  3. Correct underlying cause.
  4. Parathyroidectomy.
130
Q

Give 2 ECG changes that you might see in someone with hyperparathyroidism.

A

Hyperparathyroidism -> hypercalcaemia and so:
1. Tall T waves.

  1. Shorted QT interval.
131
Q

Give 3 causes of hypercalcaemia.

A
  1. Hyperparathyroidism.
  2. Hypercalcaemia of malignancy.
  3. Vitamin D toxicity.
  4. Myeloma.
132
Q

Hypoparathyroidism: Definition

A

Hypoparathyroidism is an uncommon condition in which your body produces abnormally low levels of parathyroid hormone (PTH).

Hypoparathyroidism -> hypocalcaemia.
133
Q

Hypoparathyroidism: Symptoms?

A

Hypoparathyroidism -> hypocalcaemia:
1. Spasm.

  1. Paraesthesia around mouth and lips.
  2. Anxious/irritable.
  3. Seizures.
  4. Increased muscle tone.
  5. Confusion.
  6. Dermatitis.
  7. Impetigo herpetiformis.
  8. QT prolongation.

SPASMODIC

134
Q

Hypoparathyroidism: treatment?

A

Calcium supplements.

135
Q

Give 5 causes of hypocalcaemia.

A
  1. Dietary insufficiency.
  2. Anticonvulsant therapy.
  3. CKD.
  4. Vitamin D deficiency.
  5. Osteomalacia.
  6. Hypoparathyroidism.
136
Q

Hypercalcaemia:- Management

A
  1. IV normal saline.
    1. IV furosemide.
    2. IV calcitonin.
137
Q

Phaeochromocytoma: definition?

A

A rare catecholamine secreting tumour in the adrenal medulla.

138
Q

Phaeochromocytoma: symptoms?

A

Classic triad of:
1. Headache.
2. Sweating.
3. Tachycardia.

Also:
4. Hypertension.
5. Palpitations.
6. Tremor.
7. Arrhythmia.
8. Confusion.

139
Q

Phaeochromocytoma:
Investigations

.
A

Bloods - raised WCC, increased plasma metadrenaline and normetadrenaline

140
Q

Phaeochromocytoma: management?

A
  1. Non-competitive Alpha blocker e.g. phenoxybenzamine.
  2. Beta blockers.
  3. Surgical resection of tumour.
141
Q

17 year old man presents with intermittent headaches and anxiety. He is sweating and vomiting. His BP is 223/159 and his pulse is 115. What is the likely cause?

A

Phaeochromocytoma crisis!

Hypertension and tachycardia = phaeochromocytoma until proved otherwise; especially in younger patients.

142
Q

graves’ disease: investigations?

A

bc its an autoimmune condition - gold standard = autoantibodies
TSH-Ah are present in high titres in grave’s

(tpo-ab can be present but more specific to hypothyroidism)

med 2a (13 decks)

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