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3rd yr clinical > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

What are the main CAUSES of hyperthyroidism

A
  1. primary - thyroid makes too much TH
    2.Secondary- pathology in hypothalamus or pituitary - too much TSH
  2. Grave’s disease- autoimmune- TSH receptor antibodies cause primary hyperthyroidism
    4.Toxic multi nodular goitre- Plummers disease- over 50s
  3. Thyroiditis
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2
Q

What is a thyroid storm/ how do you manage it ?

A

Thyrotoxic crisis - usually due to surgery or infection etc- fever, tachy and delirium

Treat with: Fluid rhesus, anti arrhythmic meds and beta blockers

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3
Q

What is the management of hyperthyroidism ?

A

1st line- Carbimazole for 12-18 months
Once levels are normal continue maintenance

Higher doses of carbimazole will block all TH and levothyroxine will need to be given

2nd line- Propythiouracil- but high risk of liver damage

Both meds cause agranulocytosis - pt’s vulnerable to infection- BE AWARE OF SORE THROATS

Radioactive iodine- no pregnant 6 months , limit contact with children and pregnant women

B blockers for symptoms
Surgery

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4
Q

What are the main causes of hypothyroidism ?

A
  1. Primary hypo- thyroid doesn’t make enough T3/T4 - negative feedback so high TSH
  • Hashimoto’s thyroiditis (Autoimmune) - primary

-Iodine deficiency (most common) - primary

  • Treatment for hyperthyroidism
  • Lithium/ amiodarone medications
  1. Secondary hypo- pituitary not enough TSH- low T3/T4

-Pituitary adenoma
-Surgery to pituitary
-Radiotherapy
-Sheehans syndrome
-Trauma

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5
Q

What is the treatment for hypothyroidism?

A

Oral levothyroxine (synthetic T4)
-Dose titrated every 4 weeks based on TSH level

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6
Q

What is the difference between Cushing’s disease and syndrome and what are the main presentations?

A

Cushing’s syndrome= too much cortisol produced in the body for some reason

Cushing’s disease- = specific Pituitary adenoma secreting adrenocorticotrophic hormone stimulating excess cortisol from adrenal glands

High levels of glucocorticoids (cortisol)

-Moon face -Central obseity -Abdominal striae -Buffalo hump -Proximal limb muscle wasting
-hirsutism (male facial hair) -easy bruising poor skin healing -Hyperpigmentation of the skin

Metbolix effects
HTN Cardiac hypertrophy Type 2 diabetes Dyslipidaemia Osteoporosis

Mental health effects
Anxiety Depression Insomia

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7
Q

What are the causes of Cushing’s syndrome

A

-Cushings disease - pituitary adenoma
-Adrenal adenoma
-Paraneoplastic syndrome (Small cell lung cancer)
-Exogenous steroids

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8
Q

How do you test for Cushing’s

A

Dexamethasone suppression test - tells you when the problem is inside the body and not from exogenous steroids

Normal response is suppressed cortisol when dexamethasone given due to negative feedback

Low dose overnight - given to exclude Cushing’s
Low dose 48 hr- in suspected cushings
High dose in 48hrs - determines cause of cushing’s

Or 24hr urinary free cortisol

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9
Q

What would the findings be in a Dexamethasone suppression test for
1. Normal
2. Pituitary adenoma
3. Adrenal Adenoma
4.Ectopic Steroids

A
  1. Cortisol suppressed in all tests and ACTH normal
  2. Pituitary adenoma Low dose test not suppressed but high dose of dex will surprise cortisol - Cortisol but ACTH will still be high as pituitary tumour is producing this
  3. Adrenal adenoma- cortisol will not be suppressed in either doses as tumour is secreting cortisol but ACTH will be low as pituitary won’t be producing much
  4. No suppression for either doses and high ACTH
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10
Q

What are the two main types of hyperaldosteronism

A
  1. Primary- adrenal glands make too much aldosterone, low renin as high blood pressure surprises it - due to bilateral hyperplasia of adrenal glands, adrenal adenoma (Conn’s syndrome) or familial
  2. Secondary- high renin stimulating excessive adolsterone release- due to low BP in kidneys- Renal artery stenosis, HF, liver cirrhosis and ascites
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11
Q

What is the screening test for hyperaldosteronism

A

Aldosterone to renin ratio

High aldosterone to low renin= primary

High aldosterone to high renin = secondary

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12
Q

What is the management of hyperaldosteronism

A
  1. Treat underlying cause - percutaneous renal artery angioplasty via fem artery / remove adrenal adenoma

Aldosterone antagonists - spironolactone

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13
Q

What are the 3 types of Adrenal insufficiency

A

Low cortisol
1. Addison’s disease- when the adrenal glands are damaged - autoimmune

  1. Secondary- inadequate ACTH doesn’t stimulate the adrenal glands - damage to pituitary gland (adenoma/ sheehans syndrome)
  2. Tertiary- inadequate CRH from the hypothalamus - from patients taking long term oral steroids
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14
Q

What is the presentation of adrenal insufficiency

A

Fatigue, muscle cramps/ weakness, dizzy/fainting/ thirst/ craving salt, weight loss, abdominal pain, depression, low libido, bronze hyperpigmentation (excess ACTH stimulates melanocytes to produce melanin)

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15
Q

What investigations/ findings are present in adrenal insufficiency

A

High potassium and low sodium
Hypoglycaemia
High creatinine and urea
Hypercalcaemia

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16
Q

What is the test used to diagnose Adrenal insufficiency?

A

Short synthacthen test - JFK was short - check blood cortisol 30 and 60 mins

  • In healthy adrenal glands the extra ACTH will stimulate high cortisol

-Primary adrenal insufficiency (Addison’s)- cortisol will not increase- Adrenal glands not working- won’t be stimulated by ACTH

Long synacthen test - used to choose between primary and secondary - in secondary insufficiency- ACTH will be low as not being produced normal so only the amount given in the fake dose is there

17
Q

Management of adrenal insufficiency

A

-hydrocortisone (glucocorticoid)- replaces cortisol and fludrocortisone (mineralocorticoid) - Replaces aldosterone

Patients given steroid card and ID tag
Family members taught how to give IM hydrocortisone

18
Q

Why are steroid doses important in Adrenal insufficiency

A

Doses should not be missed and if sick doses should be doubled

19
Q

What is Addisonian/ Adrenal crisis/ How is it treated

A

Hypotension. LOC, hypoglycaemia, hyperkalaemia caused by infection trauma or acute illness in patients

Do not perform investigations treat if suspected

ABCDE approach
-IM/IV hydrocortisone (100mg then infusion of 6hrly doses)
-IV fluid resus
-Correct hypoglycaemia with dextrose
-Monitor electrolytes and fluid balance

20
Q

What is the main presentation of DKA

A

-Hyperglycaemia -Dehydration -ketosis -Metabolic acidosis (low bicarb) -Potassium imbalance

Polyuria/dipsia -N&V -Dehydration -Weight loss -Hypotension

Criteria
Hyperglycaemia HB>11mmol/L

Ketosis- Ketones >3mmol/L

Acidosis pH below 7.3

21
Q

How is DKA treated

A

Escalate

FIG-PICK

Fluids-IV fluid resus - 1L normal saline for 1st hr then 1L every 2 hrs

Insulin- Fixed rate infusion - act rapid 0.1 units/kg/hr

Glucose-monitor and only add glucose to infusion when it goes below 14mmol/L

Potassium- Add potassium to IV fluids every hr initially - do not exceed 10mmol/Hr

Chart fluid balance

Ketones- monitor blood ketones, pH and bicarb

*Don’t stop insulin infusion and fluids until patient is eating and drinking and has restarted subcut insulin

22
Q

What is pre- type 2 diabetes and type 2 diabetes

A

Pre-diabetes- HbA1c- 42-47mmol/L

Diabetes HbA1c over 48mmol/L

23
Q

What are the treatment options of type 2 diabetes

A
  1. First line- weight loss and exercise with diet
  2. First line mediation- Metformin

If QRISK is over 10% add an SGLT2 inhibitor (dapagliflozin) ** this one most likely in second line but potential side effect is DKA

  1. Second line medication- add to metformin a sulfonurea, pioglitazone, DPP-4 inhibit or SGLT2 inhibit
  2. Third line- triple therapy- metformin and two second line drugs

Insulin therapy by specialist diabetic nurse

If triple therapy fails and BMI over 35 can give GLP-1 mimetic

24
Q

What does metformin do

A

Increase insulin sensitivity and decrease glucose production by liver

No weight gain

25
Q

What do SGLT2- inhibitors do

A
  • all end in gliflozin
    -Block the sodium glucose transporter protein in proximal tube of kidneys - less glucose absorbed and more in urine

Can cause hypoglycaemia, urine infections, glucose in urine , weight loss, DKA

Putting a patient on this then counsel them for DKA

26
Q

What is a sulfonurea

A

Gliclazide- stimulates release of insulin from the pancreas

Cause weight gain and hypoglycaemia

27
Q

What are DDP-4 inhibitors or GLP-1 mimetics

A

GLP1 is an incretin which reduces blood sugar

DDP-4 inhibits incretins
So a DDP-4 inhibitor med will allow incretins to work

GLP-1 mimetics - exenatide etc are subcut injections and can be used for weight loss

3rd yr clinical (22 decks)

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