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PA Conditions > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

what is hypothyroidism?
what are the hormone levels in primary and secondary?

A

Decreased levels of circulating thyroid hormones T3 and T4 due to thyroid underactivity

Primary- low T3/T4 and high TSH (raised TSH due to pituitary gland trying to stimulate thyroid (thyroid gland dysfunction) gland to make more T3/T4)

Secondary- low TSH and T3/T4 (low TSH as there is a fault with the pituitary gland/ hypothalamus results in deficiency of TSH)

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2
Q

causes of primary and secondary hypothyroidism?

A

Primary causes:
Majority are autoimmune
Hashimoto thyroiditis
Atrophic thyroiditis

Secondary causes:
Thyroidectomy/ ablations
TSH deficiency
Congenital
Iodine deficiency

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3
Q

investigations for hypothyroidism?

A

History and thyroid exam
Bloods- FBC, U&E, LFT, calcium, potassium
TFT- high TSH but low T3/T4
Thyroid peroxidase antibodies- TPO
CK levels
Cholesterol- hypercholesteremia
Short Synacthen test
ECG- pericardial effusion
CXR- pericardial effusion

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4
Q

management of primary and secondary hypothyroidism?

A

Primary
50mcg Levothyroxine: form of T4 (start at a lower does for 65+ with IHD)
Annual blood test to assess TSH and ensure correct dose of levothyroxine
Avoid T3 and T4 management together

Secondary
Levothyroxine + addressing underlaying cause
Due to failure of pituitary gland itself TSH replacement cannot be used and TSH production is the problem

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5
Q

complications of hypothyroidism?

A

Goitre
Heart disease- low levels of thyroxine -> high levels of cholesterol
Infertility
Birth defects in babies who’s mother is hypothyroid.

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6
Q

define hyperthyroidism and the hormone levels?

A

Elevated levels of thyroid hormones (T3/T4) due to thyroid gland overactivity

Low TSH
High T3/T4

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7
Q

causes of hyperthyroidism?

A
  • Grave’s disease- autoimmune 80%
  • Nodular goitre (benign nodules within thyroid secreting T3/T4)
  • Thyroiditis- inflammation of thyroid commonly after pregnancy or via biologic/ cancer meds (TRAbs -ve)
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8
Q

investigations for hyperthyroidism?

A
  • Bloods- TFT (low TSH, high T3/T4)
  • Autoantibodies- TPOAb/ TSH-receptor stimulating Abs
  • Radioisotope screening- increased uptake of iodine in Grave’s
  • Thyroid US
  • US/ CT (nodular goitre)
  • ECG- if AF
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9
Q

symptoms of hyperthyroidism?

A

Weight loss
Diarrhoea + frequent
Heat intolerance
Nervousness
Sweating
Palpitations
Tremor

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10
Q

management of hyperthyroidism?

A
  1. propranolol + carbimazole

Carbimazole (block and replace)- high does to completely block action of thyroid with carbimazole and replace thyroid hormones with thyroxine

  1. Stop at 18 months and reassess
    If relapse -> radioactive iodine -> thyroidectomy
    If euthyroid -> may be treated but may later develop hypothyroidism
  2. Nodular goitre- BB-blocker -> carbimazole -> radioactive iodine
  3. Thyroiditis- BB-blocker -> usually resolves on its own/ post-pregnancy or when meds stopped
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11
Q

complications of hyperthyroidism?

A

Thyroid storm
AF
Eye problems
Cardiac problems

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12
Q

what is a thyroid storm?
symptoms?
treatment?

A

Medical emergency that requires immediate attention. Underlaying cause of Grave’s disease. can be caused by poor medication compliance. 30-50% mortality

Symptoms:
* Hyperpyrexia
* Altered mental state
* N&V + diarrhoea
* Tachycardia/ AF

Treatment: hydration + cooling -> BB-blockers (propranolol) -> anti-thyroid agent (propylthiouracil) -> iodine solution 4hrs after anti-thyroid agent

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13
Q

what is grave’s disease?

causes?

A

Autoimmune condition causes hyperthyroidism due to thyroid gland overactivity and release of excess of T3/T4. Confirmed by presence of thyroid-receptor Abs

  1. Autoimmune condition cause by activity against the TSH receptor
  2. Men > women
  3. > if Addisons disease, T1DM, vitiligo
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14
Q

investigations for grave’s disease?

A
  • Bloods- thyroid receptor Abs, FBC, U%E, LFT,
  • TFT- high T3/T4 low TSH
  • Radio-iodine uptake scans- thyroid activity regions
  • Fine-needle aspiration
  • ECG- AF
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15
Q

management for grave’s disease?

A
  1. Carbimazole + propranolol
    Block and replace (carbimazole + thyroxine)
    Titration (titrating drug does until lowest possible dose of drugs achieves euthyroid status)
  2. Radioactive iodine
    Can be used in refractory grave’s post initial treatment (may cause hypothyroidism)
  3. Surgery- thyroidectomy
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16
Q

complications of grave’s disease?

A

Refractory of condition post treatment- relapse
Treatment can cause hypothyroidism
Thyroid storm
AF
Osteoporosis
Vision impairment
Menstrual problems

17
Q

what is cushing’s syndrome?

causes/ risks?

A

Overproduction of cortisol from the adrenal gland
Multi-system condition
Cause by a pituitary adenoma secreting excess amounts of ACTH

Adrenal adenoma- ACTH low and cortisol high
Ectopic ACTH- both ACTH and cortisol are high

Causes:
Drug induce via steroids- most common
Pituitary microadenoma
Adrenal adenoma
Ectopic ACTH production- from preexisting cancers (lung)

Risks:
Diabetes
HTN
Osteoporosis

18
Q

investigations for Cushing’s syndrome?

A

Detailed drug history- if cause by steroids then stop
1. Confirm high cortisol via urinary free cortisol
2. High-dose dexamethasone suppression test- 1mg dexamethasone given at 11pm and levels measured at 8am

Normal= cortisol levels supressed/ decreased
Abnormal= cortisol levels remain high = Cushing’s -> confirm with 24hr free urinary cortisol excretion. (patients with Cushing’s will fail to supress cortisol and levels will
remain high in the morning)

> 50% suppression= Cushing’s of pituitary source
<50% suppression= ectopic ACTH secreting tumour

  1. MRI of pituitary
  2. CT thorax/ abdomen
19
Q

management of Cushing’s?

A
  1. Cushing’s caused by pituitary adenoma- trans-sphenoidal surgical resection + glucocorticoid support
  2. Ectopic tumour cause- surgical adrenalectomy
  3. Radiotherapy for pituitary- can affect other hormones and takes time work
  4. Medically- metyrapone- cortisol supressing tablets
  5. Chemotherapy/ radiotherapy for SCLC- if it’s the cause
20
Q

what is adrenal insufficiency?

A

Underproduction of hormones of the adrenal cortex- aldosterone and cortisol

Primary: Addison’s disease= adrenal glands unable to produce hormones usually secondary due to autoimmune destruction of the gland. Damage to the whole adrenal cortex.

Secondary: due to pituitary/ hypothalamic failure or pituitary ACTH deficiency. Adrenal cortex remains intact.

21
Q

what is an Addisonian crisis?

A

Addisonian crisis: patient with known Addison’s disease has a precipitating event (illness/ surgery) which causes increase in the demand of mineralocorticoids/ glucocorticoids. Life-threatening situation that results in low blood pressure, low blood levels of sugar and hyperkalaemia

22
Q

symptoms of acute and chronic adrenal insufficiency?

A

Acute/ Addisonian crisis
Shock/ confusion
Hypoglycaemia
Low BP
Severe abdominal pain
Hyponatraemia/ hypokalaemia

Chronic
Fatigue
Weight loss
Depression
Hypotension
Vitiligo
Hyperpigmentation

23
Q

causes of adrenal insufficiency?

A

Autoimmune- hyperthyroidism
Steroid medication
TB
Haemochromatosis

24
Q

investigations of adrenal insufficiency?

A
  1. Bloods- U&E, electrolytes, FBC, TFT, LFT
  2. Measure early morning cortisol levels
  3. Synacthen test
    Cortisol rises -> exclude Addison’s
    Cortisol fails to rise -> Addison’s
  4. Measure plasma ACTH
  5. Other investigations- autoimmune testing, TFT, haemochromatosis
  6. CXR- TB/ malignancy
  7. MRI/ CT pituitary fossa
25
Q

management of adrenal insufficiency?

A

Acute
1. High-dose IV corticosteroids + 0.9% IV saline
2. Treat underlaying cause (autoimmune, TB, haemo)
3. Treat hypoglycaemia- IV dextrose

Normal first-line treatment
4. Patient education to wear medic alert bracelet
5. Replacement of mineralocorticoids/ glucocorticoids with oral hydrocortisone and fludrocortisone

26
Q

what is HHS?

A

A state of hyperglycaemia without presence of ketosis (ketones)- complication of T2DM

27
Q

signs to look out for with HHS?

HHS eqaution?

A

Dehydration
Hypovolemia (low blood volume) + hyperosmolarity (hyper concentrated blood)
Hyperglycaemia
Absence of ketoacidosis

2(Na + K) glucose + urea -> if more than 320 then suspect HHS

28
Q

investigations for HHS?

A
  1. Measure blood glucose >33mmol/L
  2. Check for glycosuria + ketones -> urine dipstick show glycosuria with absence of ketones
  3. Serum osmolality
  4. Other causes check bloods- FBC, U&E, LFT, CRP, cultures
  5. CXR- infections
  6. ECG- MI
  7. Troponin- MI
29
Q

management for HHS?

A
  • IV 0.9% saline
  • IV Actrapid insulin- started at a lower dose
  • Potassium replacement
  • Look for underlaying cause (MI, infection, poor adherence)
  • Monitor osmolarity
30
Q

what is hyperparathyroidism?

causes?

A

Excess serum levels of PTH hormone

Benign- hyperparathyroidism
Malignant- bone cancer MM (if presenting as severely sick)

  1. Primary hyperparathyroidism- one or more parathyroid gland contributes to excess PTH levels. Adenomas 80%, gland hyperplasia 20%, parathyroid carcinoma <1%
  2. Secondary- occurs as a result of any condition that cause hypocalcaemia (malabsorption syndromes/ lack of vit-D)
  3. Tertiary- prolonged secondary hyperparathyroidism lead to hyperplasia of parathyroid glands -> excess PTH levels
31
Q

hyperparathyroidism investigations?

A
  1. Bloods- FBC, U&E, LFT, calcium, phosphate, PTH, ALP
  2. Bone density scan/ XRAYs- osteopenia
    Measure PTH levels
    If PTH suppressed -> malignancy until proven otherwise
    If PTH inappropriately elevated -> benign/ primary hyperparathyroidism
  3. DHx- thiazide diuretics increase calcium levels
  4. Ensure adequate renal function- U&E, LFT
  5. Ensure patient does not consume excess calcium
  6. Check for end-organ damage (osteopetrosis, KS)
  7. US neck/ radio-isotope uptake scan- locate overactive gland
32
Q

management of hyperparathyroidism?

A

Emergency hypercalcemia/ hyperparathyroidism
1. ABCDE
2. Measure PTH and establish cause of hypercalcemia
3. IV bisphosphonates- reduce osteoclast activity
Primary hyperparathyroidism
1. Surgical removal of parathyroid gland
Secondary hyperparathyroidism- medical
1. Cinacalcet- lowers calcium and PTH levels (if unfit for surgery)

33
Q

complications of hyperparathyroidism?

A

End-organ damage: osteopetrosis, cardiovascular disease kidney stones, renal impairment

34
Q

what is hypoparathyroidism?

causes?

A

Decreased serum levels of PTH hormone
Mostly mild and detected on routine testing

  • Vitamin D deficiency- sunlight/ diet (most common)
  • Iatrogenic- head/ neck surgery, removal of parathyroid gland (thyroidectomy)
  • Congenital- DiGeorge Syndrome
  • Autoimmune- haemochromatosis

Pseudo-hypoparathyroidism: low calcium levels but high PTH due to end organ receptor insensitivity to PTH

35
Q

investigations and management for hypoparathyroidism?

A

Bloods- calcium, phosphate, PTH, ALP, FBC, U&E, LFT
Genetic testing- congenital
FBC- hemochromatosis

Severe hypocalcaemia
1. IV calcium gluconate
Normal first-line treatment
1. Calcium and vit-D replacement (supplements, diet, sunlight)

36
Q

what is volume depletion?
causes?

A

total loss of water and sodium in the body

Causes: vomiting, excessive sweating, diarrhoea, burns, diuretic use, and kidney failure.

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