e n d o + d i a b e t e s Flashcards
what is hypethyroidism
occurs when there is too much circulating thyroid hormone in the body.
what are the sx and signs of hyperthyroidism
Weight loss. • Warm skin/heat intolerance. • Diarrhoea. • Exophthalmos (Graves’ disease). • Lid lag • Palpitations. • Anxiety. • Tremor. • Goitre +/– bruit. • Brisk reflexes. arrhythmias loss of weight sweating infrequent periods diarrhoea clubbing
what are the causes of hyperthyroidism
graves
toxic multi nodular goitre
toxic solitary nodule goitre
de quervain’s thyroiditis
what Lx are required in hyperthyroidism
TFT = reduced TSH, increased T3, T4
USS scan of nodules
fine needle aspiration of solitary nodules to rule out malignancy
isotope scan to assess hot and cold thyroid nodules
what are the complications of hyperthyroidism
AF
High output HF
cardiomyopathy
osteoporosis
describe grave’s disease, what are its distinguishing features and associations
commonest cause of hyperthyroidism
autoimmune condition
may be distinghied from other causes of hyperthyroid by ocular changes, e.g. exophthalmos,
and other signs, e.g. pretibial myxoedema
assorted with autoimmune conditions like pernicious anaemia
a single nodule is suggestive of
thyroid neoplasia
describe de quervain’s thyroiditis
transient hyperthyroid that develops after viral infection
goitre often painful
a period of hypothyroidism may follow
describe how hyperthyroidism is managed
- Conservative: patient education, smoking cessation.
- symptomatic control = palpitations and tremor = beat blockers. eye sx = eye drops for lubrication
- antithyroid meds = carbimazole, prophylthiouracil
- radioactive idoine ablation = definitive retreat but pt must be euthyroid before it
what are the SE of anti thyroid meds
agranulocytosis
monitor bloods carefully
what is the surgical treatment for hyperthyroidism, what should you give pt before it and why
subtotal thyroidectomy
patients must be euthyroid before procedure
give pt potassium iodide before surgery as it decreases thyroid gland vascularity
what is hypothyroidism
where too little circulating thyroid hormone in the body
what are the causes of hypothyroidism category
primary vs secondary
what are the causes of primary hypothyroidism
Iodine deficiency
- Hashimoto’s autoimmune thyroiditis
- Post-thyroidectomy/radioactive iodine therapy
- Drug induced, e.g. lithium, overtreatment of hyperthyroidism
what are the causes of secondary hypothyroidism
Dysfunction of the hypothalamic–pituitary axis
• Pituitary adenoma
• Sheehan’s syndrome (ischaemic necrosis of the
hyperthyroidism
pituitary gland after childbirth)
• Infiltrative disease, e.g. tuberculosis and
haemochromatosis
what are the complications of hypothyroidism
hypercholesterolaemia
complications in pregnancy = pre eclampsia
hyperthyroidism from treatment of hypothyroidism
myxoedema coma
describe the treatment of hypothyroidism
conservative = patient education
medical = lifelong replacement of thyroid hormone with levothyroxine
what lx are required in hypothyroidism
TFTs (- TSH, ̄ T3 and ̄ T4). •Thyroid antibodies. • FBC (anaemia) Us and Es LFTs Creatinine Cholesterol Guthrie test for congenital screening
what are the signs and sx
Weight gain. • Cold skin/cold intolerance. • Constipation. • Dry skin. • Thinning of hair. • Bradycardia. • Depression. • Delayed reflexes
what is diabetes insipidus
disorder caused by low levels of or insensitivity to antidiuretic hormone (ADH) leading to polyuria. This can be cranial or nephrogenic in origin.
what are the cranial causes of diabetes insipidus
CIVIT:
○ Congenital defect in ADH gene. ○ Idiopathic. ○ Vascular. ○ Infection: meningoencephalitis. ○ Tumour(e.g. pituitary adenoma), Tuberculosis and Trauma.
what are the causes of nephrogenic DI
Nephrogenic: the kidney does not respond to ADH. Remember this as DIMC:
○ Drugs, e.g. lithium.
○ Inherited.
○ Metabolic ̄ reduced potassium, increased calcium.
○ Chronic renal disease.
what are signs and sx of DI
Polydypsia
• Polyuria.
• Dehydration
what is cranial DI
Cranial: decreased ADH is released by the posterior pituitary gland.
what is nephrogenic DI
Nephrogenic: the kidney does not respond to ADH.
what are the complications of DI
Electrolyte imbalance
• Dehydration.
what are the Lx required in DI
- plasma osmolality -increases
- urine osmolality =decreases
- plasma sodium = increases
- 24hr urine volume = greater than 2L
- water deprivation test = urine does not concentrate
- after desmopressin = in cranial urine becomes concentrated, nephrogenic urine does not concentrate
- MRI scan to look for pituitary gland e.g tumour
what is the treatment for cranial DI
conservative = patient education on how to monitor fluid levels, dietary salt levels. advise pt to wear a medic alert bracelet
desmopressin
surgical excision if tumour
how does desmopressin work
ADH analogue/ vasopressin synthetic replacement = increases number of aquaporin 2 channels in DCT and CD = increases water reabsorption
how is nephrogenic DI managed
conservative
medical = high dose desmopressin, correct electrolytes, thiazide diuretics, prostaglandin synthase inhibitors
what is cushing’s syndrome
collection od signs and sx that occur when patient has long term exposure to cortisol
what are the exogenous causes of cushing’s
iatrogenic = presciprtion of glucocorticoids for asthma
what are the endogenous cause ACTH independent of cushing’s
ACTH independent
CARS. Cancer: adrenal adenoma. ○ Adrenal nodular hyperplasia. ○ Rare causes: McCune–Albright syndrome. ○ Steroid us
what are the endogenous cause ACTH dependent of cushing’s
- cushing’s disease
2. ectopic ACTH production from SCLC
how is cushing’s disease confirmed in pituitary adenoma
this occurs when
ACTH is produced from a pituitary adenoma.
Use a low-dose dexamethasone test to confirm.
what are the signs and sx of cushing’s disease
Moon face. • Central obesity. • Buffalo hump. • Acne. • Hypertension. • Hyperglycaemia. • Striae. • Vertebral collapse. • Proximal muscle wasting. • Psychosis.
what the diagnostic Lx are required for cushing’s
Diagnostic tests: urinary free cortisol, low-dose and high-dose dexamethasone suppression test.
other dx for cushings
bloods = FBC, US, LTFs, glucose, lipid
radiology CXR look for lung cancer and vertebral collapse
other = DEXA scan
what is the conservative treatment for cushing’s
Conservative:educationaboutthecondition. Advise patient to decrease alcohol consumption since alcohol increases cortisol levels.
what is the medical and surgical management of cushings
ketoconazole, metyrapone, mitotane. Treat complications such as hypertension and diabetes mellitus
surgery = trans-sphenoidal surgery to remove pituitaryadenoma
or bilateral adrenalectomy to remove adrenal adenoma, if indicated.
what are the complications related to cushing’s
Osteoporosis. • Diabetes mellitus. • Hypertension. • Immunosuppression. • Cataracts. • Striae formation. • Ulcers.
what is adrenal insufficiency
ccurs when the adrenal glands fail to produce sufficient steroid hormone. The causes of adrenal insufficiency
what are the primary causes of adrenal insufficiency/ addisons disease
MAIL:
○ Metastases from breast, lung and renal cancers.
○ Autoimmune.
○ Infections, e.g. tuberculosis (commonest) and opportunist infections
Lymphomas
Idiopathic
Post adrenalectomy
what are the secondary causes of addisons disease
Prolonged prednisolone use. • Pituitary adenoma.
sheehans syndrome
what are the signs and sx associated with addisons disease
Unintentional weight loss. • Myalgia. • Weakness. • Fatigue. adrenal Insufficiency • Postural hypotension. • Abdominal pain. Skin pigmentation. • Body hair loss. • Diarrhoea. • Nausea. vomiting depression
what are the dx Lx required in addisons
ACTH and cortisol measurements
insulin tolerance test
short synacthen test
other lx in adrenal insufficiency
FBC, UE, reduced sodium and raised k glucose LFT lipid levels serum calcium
CXR for lung Ca
CT and mri for scan of adrenal glands
treatment of addisons
conservative = pt education. pt carry steroid alert card
medical = replace glucocorticoids and mineralocorticoids with hydrocortisone and fludrocortisone, treat complications
surgery = excision of tumour if needed
complications for adrenal insufficiency
adrenal crisi hyperK hypoglycaemia eosinophilia alopecia
anatomy of adrenal cortex abd adrenal medulla
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what is hypoparathyroidism
when too little PTH is produced from the parathyroid gland
what are the causes of hypoparathyroidism
- congenital = DiGeorge syndrome
- acquired = complication of parathyroidectomy or thyroidectomy
- transient = neonates born prematurely
- inherited = pseudo and pseudopseudo
sx and signs of hypoparathyroidism
abd pain myalgia muscle spasm seizures fatigue trousseau's sign
Lx of hypoparrthyroism
PTH level reduced
Serum calcium reduced
serum phosphate increased
for pseudo = PTH level increased
other lx for hypoparathyroid
Bloods:FBC,U&Es,LFTs,creatinine,urea.
• ECG:arrhythmias.
• ECHO: cardiac structural defects (DiGeorge syndrome
treatment for hypoparathyroidism
Conservative: diet high in calcium and low in phosphate. Support for parents.
Medical: calcium and vitamin D supplements
complications of hypoparathyroisim
renal calculi.
• Arrhythmias.
• Cataract formation.
• Dental problems.
what is hyperparathyroidism
occurs when too much parathyroid hormone (PTH) is produced from the parathyroid gland. It may be categorised into primary, secondary and tertiary causes.
what are the primary causes of hyperparathyroidism
Parathyroid adenoma Parathyroid hyperplasia Parathyroid carcinoma Drug induced, e.g. lithium
what are the secondary causes of hyperparathyroidism
vit d defieciency
ckd
what is the cause of tertiary hyperthyroidism
prolonged secondary hyperparathyroidism
what are the signs and sx of hyper parathyroidisim
asymptomatic
bones = pain, osteoporosis moans = depression and fatigue groans = myalgia stones = kidney stones
secondary = rickets, osteomalacia, renal osteodystrophy
what are the Lx of hyperparathyroidism
PTH level increase
serum calcium increase
serum phospate decrease
in secondary = PTH increase
serum Ca decrease
serum phosphate increase
in tertiary PTH is increase, calcium increase and phosphate decrease
other lx in hyperparathyroidism
bloods - FBC, UE, LFT, creatinine urine calcium DEXA Radiology - USS Kidneys and neck parathyroid gland biopsy
management of hyperparathyroidism
conservative = increase oral fluid intake
bisphophonates
surgical parathyroidectomy
secondary = diet low in phosphate and high in ca calcimimetics = cinacalcet
parathyroidectomy if unresponsive to tx
tertiary -= surgery removal of gland
complications of hyperparathyroidism
renal calculi
acute pancreatitis
peptic ulceration
calcification of the cornea
what is DM
metabolic condition in which the patient has hyperglycaemia due to insulin insensitivity or decreased insulin secretion.
what is T2DM
patients gradually become insulin resistant or when the pancreatic beta cells fail to secrete enough insulin or both.
Patients are at risk of developing a hyperosmolar state.
associated with obesity and sedentary lifestyle
autoimmune condition
destruction of the pancreatic beta cells resulting in no insulin production.
This condition has a juvenile onset and is associated with HLA-DR3 and HLA-DR4.
Patients are at risk of ketoacidosis.
sx and symptoms of DM
polyuria, polyphagia, polydipsia, blurred vision, glycosuria, signs of macrovascular and microvascular disease.
sx more common in T1DM
acetone breath, weight loss, Kussmaul breathing, nausea and vomiting.
DX Lx for DM
Fasting plasma glucose: >7 mmol/L (126 mg/dL)
- Random plasma glucose (plus DM symptoms); >11.1 mmol/L (200 mg/dL).
- HbA1c: >6.5% (48 mmol/mol)
other tests for DM
- impaired glucose tolerance test for borderline cases.
Fasting plasma glucose: <7 mmol/L (126 mg/dL) and at 2 h, after a 75 g oral glucose load, a level of 7.8–11 mmol/L (140–200 mg/dL)
- Impaired fasting glucose: plasma glucose: 5.6–6.9 mmol/L
(110–126 mg/dL).
describe the management for T2DM
Dietary advice BMI measurement Smoking cessation Decrease alcohol intake Regular blood glucose HbA1C monitoring encourage exercise
medical = anti diabetic agents
management in T1DM
diet = high in complex carbs, low in fat BMI measurement smoking cessation decrease alcohol intake regular blood glucose and Hb1Ac monitoring encourage exercise
complications of DM
Macrovascular: hypertension, increased risk of stroke, myocardial infarction, diabetic foot.
Microvascular: nephropathy, peripheral neuropathy (glove and stocking distribution), retinopathy, erectile dysfunction.
