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1
Q

what is hypethyroidism

A

occurs when there is too much circulating thyroid hormone in the body.

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2
Q

what are the sx and signs of hyperthyroidism

A 
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
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3
Q

what are the causes of hyperthyroidism

A

graves
toxic multi nodular goitre
toxic solitary nodule goitre
de quervain’s thyroiditis

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4
Q

what Lx are required in hyperthyroidism

A

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

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5
Q

what are the complications of hyperthyroidism

A

AF
High output HF
cardiomyopathy
osteoporosis

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6
Q

describe grave’s disease, what are its distinguishing features and associations

A

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

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7
Q

a single nodule is suggestive of

A

thyroid neoplasia

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8
Q

describe de quervain’s thyroiditis

A

transient hyperthyroid that develops after viral infection

goitre often painful

a period of hypothyroidism may follow

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9
Q

describe how hyperthyroidism is managed

A
  1. Conservative: patient education, smoking cessation.
  2. symptomatic control = palpitations and tremor = beat blockers. eye sx = eye drops for lubrication
  3. antithyroid meds = carbimazole, prophylthiouracil
  4. radioactive idoine ablation = definitive retreat but pt must be euthyroid before it
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10
Q

what are the SE of anti thyroid meds

A

agranulocytosis

monitor bloods carefully

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11
Q

what is the surgical treatment for hyperthyroidism, what should you give pt before it and why

A

subtotal thyroidectomy

patients must be euthyroid before procedure

give pt potassium iodide before surgery as it decreases thyroid gland vascularity

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12
Q

what is hypothyroidism

A

where too little circulating thyroid hormone in the body

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13
Q

what are the causes of hypothyroidism category

A

primary vs secondary

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14
Q

what are the causes of primary hypothyroidism

A

Iodine deficiency

  • Hashimoto’s autoimmune thyroiditis
  • Post-thyroidectomy/radioactive iodine therapy
  • Drug induced, e.g. lithium, overtreatment of hyperthyroidism
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15
Q

what are the causes of secondary hypothyroidism

A

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

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16
Q

what are the complications of hypothyroidism

A

hypercholesterolaemia

complications in pregnancy = pre eclampsia

hyperthyroidism from treatment of hypothyroidism

myxoedema coma

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17
Q

describe the treatment of hypothyroidism

A

conservative = patient education

medical = lifelong replacement of thyroid hormone with levothyroxine

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18
Q

what lx are required in hypothyroidism

A 
TFTs (- TSH,  ̄ T3 and  ̄ T4). •Thyroid antibodies.
• FBC (anaemia)
Us and Es
LFTs
Creatinine 
Cholesterol 
Guthrie test for congenital screening
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19
Q

what are the signs and sx

A 
Weight gain.
• Cold skin/cold intolerance. • Constipation.
• Dry skin.
• Thinning of hair.
• Bradycardia.
• Depression.
• Delayed reflexes
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20
Q

what is diabetes insipidus

A

disorder caused by low levels of or insensitivity to antidiuretic hormone (ADH) leading to polyuria. This can be cranial or nephrogenic in origin.

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21
Q

what are the cranial causes of diabetes insipidus

A

CIVIT:

○ Congenital defect in ADH gene.
○ Idiopathic.
○ Vascular.
○ Infection: meningoencephalitis.
○ Tumour(e.g. pituitary adenoma), Tuberculosis and Trauma.
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22
Q

what are the causes of nephrogenic DI

A

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.

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23
Q

what are signs and sx of DI

A

Polydypsia
• Polyuria.
• Dehydration

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24
Q

what is cranial DI

A

Cranial: decreased ADH is released by the posterior pituitary gland.

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25
what is nephrogenic DI
Nephrogenic: the kidney does not respond to ADH.
26
what are the complications of DI
Electrolyte imbalance | • Dehydration.
27
what are the Lx required in DI
1. plasma osmolality -increases 2. urine osmolality =decreases 3. plasma sodium = increases 4. 24hr urine volume = greater than 2L 5. water deprivation test = urine does not concentrate 6. after desmopressin = in cranial urine becomes concentrated, nephrogenic urine does not concentrate 7. MRI scan to look for pituitary gland e.g tumour
28
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
29
how does desmopressin work
ADH analogue/ vasopressin synthetic replacement = increases number of aquaporin 2 channels in DCT and CD = increases water reabsorption
30
how is nephrogenic DI managed
conservative medical = high dose desmopressin, correct electrolytes, thiazide diuretics, prostaglandin synthase inhibitors
31
what is cushing's syndrome
collection od signs and sx that occur when patient has long term exposure to cortisol
32
what are the exogenous causes of cushing's
iatrogenic = presciprtion of glucocorticoids for asthma
33
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 ```
34
what are the endogenous cause ACTH dependent of cushing's
1. cushing's disease | 2. ectopic ACTH production from SCLC
35
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.
36
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. ```
37
what the diagnostic Lx are required for cushing's
Diagnostic tests: urinary free cortisol, low-dose and high-dose dexamethasone suppression test.
38
other dx for cushings
bloods = FBC, US, LTFs, glucose, lipid radiology CXR look for lung cancer and vertebral collapse other = DEXA scan
39
what is the conservative treatment for cushing's
Conservative:educationaboutthecondition. Advise patient to decrease alcohol consumption since alcohol increases cortisol levels.
40
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.
41
what are the complications related to cushing's
``` Osteoporosis. • Diabetes mellitus. • Hypertension. • Immunosuppression. • Cataracts. • Striae formation. • Ulcers. ```
42
what is adrenal insufficiency
ccurs when the adrenal glands fail to produce sufficient steroid hormone. The causes of adrenal insufficiency
43
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
44
what are the secondary causes of addisons disease
Prolonged prednisolone use. • Pituitary adenoma. | sheehans syndrome
45
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 ```
46
what are the dx Lx required in addisons
ACTH and cortisol measurements insulin tolerance test short synacthen test
47
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
48
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
49
complications for adrenal insufficiency
``` adrenal crisi hyperK hypoglycaemia eosinophilia alopecia ```
50
anatomy of adrenal cortex abd adrenal medulla
page 91
51
what is hypoparathyroidism
when too little PTH is produced from the parathyroid gland
52
what are the causes of hypoparathyroidism
1. congenital = DiGeorge syndrome 2. acquired = complication of parathyroidectomy or thyroidectomy 3. transient = neonates born prematurely 4. inherited = pseudo and pseudopseudo
53
sx and signs of hypoparathyroidism
``` abd pain myalgia muscle spasm seizures fatigue trousseau's sign ```
54
Lx of hypoparrthyroism
PTH level reduced Serum calcium reduced serum phosphate increased for pseudo = PTH level increased
55
other lx for hypoparathyroid
Bloods:FBC,U&Es,LFTs,creatinine,urea. • ECG:arrhythmias. • ECHO: cardiac structural defects (DiGeorge syndrome
56
treatment for hypoparathyroidism
Conservative: diet high in calcium and low in phosphate. Support for parents. Medical: calcium and vitamin D supplements
57
complications of hypoparathyroisim
renal calculi. • Arrhythmias. • Cataract formation. • Dental problems.
58
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.
59
what are the primary causes of hyperparathyroidism
Parathyroid adenoma Parathyroid hyperplasia Parathyroid carcinoma Drug induced, e.g. lithium
60
what are the secondary causes of hyperparathyroidism
vit d defieciency | ckd
61
what is the cause of tertiary hyperthyroidism
prolonged secondary hyperparathyroidism
62
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
63
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
64
other lx in hyperparathyroidism
``` bloods - FBC, UE, LFT, creatinine urine calcium DEXA Radiology - USS Kidneys and neck parathyroid gland biopsy ```
65
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
66
complications of hyperparathyroidism
renal calculi acute pancreatitis peptic ulceration calcification of the cornea
67
what is DM
metabolic condition in which the patient has hyperglycaemia due to insulin insensitivity or decreased insulin secretion.
68
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
69
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.
70
sx and symptoms of DM
polyuria, polyphagia, polydipsia, blurred vision, glycosuria, signs of macrovascular and microvascular disease.
71
sx more common in T1DM
acetone breath, weight loss, Kussmaul breathing, nausea and vomiting.
72
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)
73
other tests for DM
1. 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) 2. Impaired fasting glucose: plasma glucose: 5.6–6.9 mmol/L (110–126 mg/dL).
74
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
75
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 ```
76
complications of DM
Macrovascular: hypertension, increased risk of stroke, myocardial infarction, diabetic foot. Microvascular: nephropathy, peripheral neuropathy (glove and stocking distribution), retinopathy, erectile dysfunction.

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