Endocrinology Flashcards
What are the features of DKA?
Abdo pain
Polyuria, polydipsia, dehydration
Kussmaul respiration (deep hyperventilation)
Pear drop breath
Confusion
High glucose, ketones ++
Low pH and bicarb
What is the diagnostic criteria for DKA?
Glucose >11mmol/L or known diabetic
pH <7.3
Ketones >3mmol/L or ++ in urine
What is the management of DKA?
IV 0.9% NaCl Insulin infusion 0.1 unit/kg/hr (usually 5-8L depleted)!!
5% dextrose once BM <15 to prevent hypoglycaemia
Correct hypokalaemia
Continue LONG acting insulin, STOP SHORT acting
Causes of primary hyperparathyroidism
Adenoma
Hyperplasia
Carcinoma
Features of hyperparathyroidism
Features of hypercalcaemia!
Polydipsia, polyuria
Peptic ulceration/constipation/pancreatitis
Bone pain/fracture
Renal stones
Depression
HTN
Blood results in primary hyperparathyroidism
Normal/High PTH
High Ca
Low phosphate
Pepperpot skull is characteristic of
Hyperparathyroidism
Management of primary hyperparathyroidism
Total parathyroidectomy- definitive
Conservative if Ca <0.25, patient >50yrs and no end-organ damage
Calcimimetic agents e.g. cincalet if unfit for surgery
Causes of Addisonian crisis
Sepsis
Surgery
Adrenal haemorrhage (Waterhouse-Friderichsen syndrome)
Steroid withdrawal
Management of Addisonian crisis
IV 0.9% saline
Hydrocortisone IV/IM 100mg
If hypoglycaemic give 20% dextrose
Symptoms/signs of Addisonian crisis
Nausea/vomiting
Severe fatigue
Severe headache
Mental confusion
Hypotension causing postural hypotension
Hyponatraemia
Hyperkalaemia
Hypoglycaemia
Investigations for Addisonian crisis
FBC U&Es, LFT, glucose, lipase
Capillary glucose
Venous blood gas
If suspected NEW dx take random cortisol and ACTH
Investigations for Addison’s disease
ACTH stimulation test (short synacthen test)
No response = hypoadrenalism
- Take basal sample for cortisol
- Give 250mcg Synacthen IV or IM
- Sample for cortisol taken @ 30 mins & 60 mins
Features of Addisons
Fatigue
Hyperpigmentation (sun-exposed areas, pressure points, mucous membranes, palmar creases, areas of friction, recent scars)
GI Sx- weight loss/anorexia/premature saiety/N/V/abdo pain
Muscle weakness, cramps, joint pain
Postural dizziness
Headache, fever, increased thirst/urination, loss of axillary/pubic hair in women, delayed puberty
Raised cortisol
Cushing’s
Cushings disease vs Cushings syndrome
Cushings syndrome = raised cortisol due to either raised cortisol alone or raised ACTH causing the raised cortisol.
A pituitary tumour causing raised cortisol is Cushing’s Disease
Cushing’s features
Central obesity/Cervical fat pads/Collagen weakness/Comedones (acne)
Urinary free cortisol + glucose ↑
Striae/Supressed immunity
Hypercortisolism/Hypertension/Hyperglycaemia/Hirsutism
Neoplasms
Glucose ↑
Metabolic acidosis and hyperkalaemia + hyperpigmentation if raised ACTH
Investigations for Cushing’s
ACTH (↑or↓) and cortisol (↑)
Dexamethasone suppression test (low dose then high dose).
- Cortisol decreased at high dose= Cushing’s Disease.
- Not reduced= Cushing’s syndrome.
Urinary free cortisol 24hr (↑) CT/MRI to establish cause
Treatment for Cushing’s
Depends on the cause
Remove cause- stop steroids/surgery if tumour/remove adrenal gland
Metyrapone (inhibits cortisol synthesis)
Ketoconazole
Causes of hyperthyroidism
Primary:
- Graves- most common cause. TSH-R Abs, autoimmune. Goitre. Eye signs in 30% (proptosis, lid lag)
- Toxic multinodular goitre - associated with iodine deficiency, more common in >60s. Benign folliclular adenoma.
- Toxic thyroid nodule (adenoma)
- Drugs e.g. iodine in amiodarone or contrast medium
Secondary:
- Raised hCG (pregnancy)
- Pituitary adenoma secreting excess TSH (rare)
- Thyroid hormone resistance
Causes of thyrotoxicosis without hyperthyroidism:
- Drugs- levothyroxine excess gives TSH <0.1
-
Thyroiditis:
- Postpartum
- Acute (bacterial infection)
- Subacute (DeQuervains)- painful thyroid, fever, viral infection.
Clinical features of thyroid storm
Tachycardia
Fever
AF
Heart failure
Diarrhoea
Vomiting
Dehydration
Jaundice
Agitation
Delirium
Coma
Treatment of thyroid crisis
Treat precipitating cause e.g. infection
O2, IV access, 0.9% saline, NG tube if vomiting
Antithyroid treatment:
carbimazole or propylthiouracil
Beta blockers (propanolol 5mg IV) or diltiazem
Hydrocortisone
Treatment for hyperthyroidism
- Drug treatment:
- carbimazole 1st line- titration block (titrate dose depending on T4), or block and replace (levothyroxine added when T4 normal)
- Radioiodine treatment
- Total or near-total thyroidectomy
Management of subclinical hyperthyroidism
+ what would TFTs show?
Repeat TFTs 3-6 months if other causes of low TSH ruled out and asymptomatic
Low TSH <0.4, normal T3/T4
Causes of hypothyroidism
Primary:
-
Overt (Raised TSH, low T4):
- Autoimmune e.g. Hashimotos (goitre), atrophic (no gotire)- Thyroid peroxidase antibodies
- Iodine deficiency
- Drugs e.g. carbimazole, propylthiouracil
- Subclinical (raised TSH, normal T3/4)
Secondary:
Due to pituitary/hypothalamic disorder= insufficient production of bioactive TSH
Treatment for hypothyroidism
(incl. dose and timing)
Levothyroxine 50-100mcg taken at least 30 mins before breakfast/caffeine/other drugs
Features of myoedema coma
(incl. blood results)
Features of hypothyroidism
Hyperthermia
Coma
Seizures
Bloods: Raised TSH, low T3/4, hyponatraemia, raised CK
Treatment of myxoedema coma
IV T4
IV hydrocortisone 100mg
Fluids
Correct electrolyte disturbances
Antibiotics if likely infection
Management of T1DM
DAFNE
Insulin- 1st line is multiple injection basal bolus regimen- basal twce daily detemivir plus bolus of rapid acting insulin analogue before meals
(alternative is twice daily human mixed insulin regimen e.g. humulin)
Monitor for complications
Complications of T1DM
Microvascular
- Nephropathy- kidney damage causing CKD
- Retinopathy
- Painful neuropathy
- Autnomic neuropathy (sweating, postural hypotension, gastroparesis, diarrhoea, erectile dysfunction)
Macrovascular
- Cardiovascular disease
- Cerebrovascular disease
- Peripheral arterial disease
Metabolic
- DKA
- Dyslipidaemia
Psychologyical
Infections
Skin complications
Other autoimmune conditions e.g. thyroid disease, autoimmune gastritis/pernicious anaemia, coeliac, vitiligo, Addisons.
Symptoms and definition of hypoglycaemia
Blood glucose <3.5mmol/L
Symptoms:
Mild- hunger, anxiety, irritability, palpitations, sweating, tingling lips
Weakness, lethargy, impaired vision, confusion, irrational behaviour
Severe- convulsions, LOC, coma
Treatment of hypoglycaemia
Able to swallow:
- 10-20g fast-acting carb e.g. sugary drink, glucose tablets, 4 jelly babies, 7 jelly beans, dextrogel
- Recheck BM after 10-15 mins- if no response repeat above
- When sx improve/normoglycaemia, increase carb at next meal (if meal due) or eat long acting starchy carb e.g. bread/pasta/potatoes
Unable to swallow:
- IM glucagon (1mg)
- Then oral carbohydate if responds and able to swallow within 10mins
- Otherwise needs ambulance
Cause of T2DM
a combination of insulin resistance (where the body is unable to respond to normal levels of insulin) and insulin deficiency (where the pancreas is unable to secrete enough insulin to compensate for this resistance)
Complications of T2DM
- Microvascular complications — retinopathy, nephropathy, and neuropathy.
- Macrovascular complications — cardiovascular disease (CVD), cerebrovascular disease, and peripheral arterial disease (PAD).
- Metabolic complications — dyslipidaemia and diabetic ketoacidosis (DKA, uncommon).
- Psychological complications — including anxiety and depression.
- Reduced quality of life.
- Reduced life expectancy.
Type 2 diabetes is likely in a person who presents with:
- Hyperglycaemia — the characteristic features (thirst, polyuria, blurred vision, weight loss, recurrent infections, and tiredness) are not usually severe and may be absent.
- Risk factor(s) for type 2 diabetes.
- Evidence of insulin resistance (for example acanthosis nigricans).
- No additional features of type 1 diabetes (such as rapid onset, often in childhood, insulin dependence, or ketoacidosis).
- No features of monogenic diabetes or diabetes secondary to a pathological condition or disease, drug treatment, trauma, or pancreatic surgery.
To dx T2DM need
HbA1c of 48+mmol/L (on 2 occasions if asymptomatic or 1 if symptomatic)
Random plasma glucose >11mmol/L
Management of T2DM
Education- DESMOND programme, provide info
Lifestyle- healthy diet, exercise, stop smoking, avoid alcohol on empty stomach
Drugs:
1) Metformin
2) Add a gliptin/pioglitazone/sulfonuylurea/SGLT2i
3) metformin + 2 other anti-diabetic drugs, or start insulin
4) consider adding GLP-1 mimetic if BMI >35
Fetaures and investigations for diabetes insipidus
Features
- polyuria
- polydipsia
- high plasma osmolality, low urine osmolality
(a urine osmolality of >700 mOsm/kg excludes diabetes insipidus)
water deprivation test- deprive of fluids then give demsopressin
If responds to desmopressin is cranial DI
What causes diabetes insipidus and what are the 2 major forms?
A condition caused by hyposecretion of, or insensitivity to the effects of, antidiuretic hormone
There are two major forms of DI:
Cranial DI: decreased secretion of ADH. Decreased secretion of ADH reduces the ability to concentrate urine and so causes polyuria and polydipsia.
Nephrogenic DI: decreased ability to concentrate urine because of resistance to ADH in the kidney.
Management of diabetes insipidus
Cranial: desmopressin
Nephrogenic: rehydration, correct electrolyte abnormalities, stop drugs which may be causing problem/ DDAVP. Combo of thiazide diuretic + NSAID may reduce urine volume.
