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e n d o + d i a b e t e s Flashcards

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
Q

what is nephrogenic DI

A

Nephrogenic: the kidney does not respond to ADH.

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26
Q

what are the complications of DI

A

Electrolyte imbalance

• Dehydration.

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27
Q

what are the Lx required in DI

A
  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
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28
Q

what is the treatment for cranial DI

A

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

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29
Q

how does desmopressin work

A

ADH analogue/ vasopressin synthetic replacement = increases number of aquaporin 2 channels in DCT and CD = increases water reabsorption

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30
Q

how is nephrogenic DI managed

A

conservative

medical = high dose desmopressin, correct electrolytes, thiazide diuretics, prostaglandin synthase inhibitors

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31
Q

what is cushing’s syndrome

A

collection od signs and sx that occur when patient has long term exposure to cortisol

32
Q

what are the exogenous causes of cushing’s

A

iatrogenic = presciprtion of glucocorticoids for asthma

33
Q

what are the endogenous cause ACTH independent of cushing’s

A

ACTH independent

CARS.
 Cancer: adrenal adenoma.
○ Adrenal nodular hyperplasia.
○ Rare causes: McCune–Albright syndrome.
○ Steroid us
34
Q

what are the endogenous cause ACTH dependent of cushing’s

A
  1. cushing’s disease

2. ectopic ACTH production from SCLC

35
Q

how is cushing’s disease confirmed in pituitary adenoma

A

this occurs when
ACTH is produced from a pituitary adenoma.

Use a low-dose dexamethasone test to confirm.

36
Q

what are the signs and sx of cushing’s disease

A 
Moon face.
• Central obesity.
• Buffalo hump.
• Acne.
• Hypertension.
• Hyperglycaemia.
• Striae.
• Vertebral collapse.
• Proximal muscle wasting.
 • Psychosis.
37
Q

what the diagnostic Lx are required for cushing’s

A

Diagnostic tests: urinary free cortisol, low-dose and high-dose dexamethasone suppression test.

38
Q

other dx for cushings

A

bloods = FBC, US, LTFs, glucose, lipid

radiology CXR look for lung cancer and vertebral collapse

other = DEXA scan

39
Q

what is the conservative treatment for cushing’s

A

Conservative:educationaboutthecondition. Advise patient to decrease alcohol consumption since alcohol increases cortisol levels.

40
Q

what is the medical and surgical management of cushings

A

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
Q

what are the complications related to cushing’s

A 
Osteoporosis.
• Diabetes mellitus.
• Hypertension.
• Immunosuppression.
 • Cataracts.
• Striae formation.
• Ulcers.
42
Q

what is adrenal insufficiency

A

ccurs when the adrenal glands fail to produce sufficient steroid hormone. The causes of adrenal insufficiency

43
Q

what are the primary causes of adrenal insufficiency/ addisons disease

A

MAIL:
○ Metastases from breast, lung and renal cancers.
○ Autoimmune.
○ Infections, e.g. tuberculosis (commonest) and opportunist infections
Lymphomas
Idiopathic
Post adrenalectomy

44
Q

what are the secondary causes of addisons disease

A

Prolonged prednisolone use. • Pituitary adenoma.

sheehans syndrome

45
Q

what are the signs and sx associated with addisons disease

A 
Unintentional weight loss. • Myalgia.
• Weakness.
• Fatigue.
adrenal Insufficiency
• Postural hypotension. 
• Abdominal pain.
Skin pigmentation. • Body hair loss.
• Diarrhoea.
• Nausea.
vomiting
depression
46
Q

what are the dx Lx required in addisons

A

ACTH and cortisol measurements

insulin tolerance test

short synacthen test

47
Q

other lx in adrenal insufficiency

A 
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
Q

treatment of addisons

A

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
Q

complications for adrenal insufficiency

A 
adrenal crisi 
hyperK
hypoglycaemia 
eosinophilia 
alopecia
50
Q

anatomy of adrenal cortex abd adrenal medulla

A

page 91

51
Q

what is hypoparathyroidism

A

when too little PTH is produced from the parathyroid gland

52
Q

what are the causes of hypoparathyroidism

A
  1. congenital = DiGeorge syndrome
  2. acquired = complication of parathyroidectomy or thyroidectomy
  3. transient = neonates born prematurely
  4. inherited = pseudo and pseudopseudo
53
Q

sx and signs of hypoparathyroidism

A 
abd pain 
myalgia 
muscle spasm
seizures 
fatigue 
trousseau's sign
54
Q

Lx of hypoparrthyroism

A

PTH level reduced
Serum calcium reduced
serum phosphate increased

for pseudo = PTH level increased

55
Q

other lx for hypoparathyroid

A

Bloods:FBC,U&Es,LFTs,creatinine,urea.
• ECG:arrhythmias.
• ECHO: cardiac structural defects (DiGeorge syndrome

56
Q

treatment for hypoparathyroidism

A

Conservative: diet high in calcium and low in phosphate. Support for parents.
Medical: calcium and vitamin D supplements

57
Q

complications of hypoparathyroisim

A

renal calculi.
• Arrhythmias.
• Cataract formation.
• Dental problems.

58
Q

what is hyperparathyroidism

A

occurs when too much parathyroid hormone (PTH) is produced from the parathyroid gland. It may be categorised into primary, secondary and tertiary causes.

59
Q

what are the primary causes of hyperparathyroidism

A

Parathyroid adenoma Parathyroid hyperplasia Parathyroid carcinoma Drug induced, e.g. lithium

60
Q

what are the secondary causes of hyperparathyroidism

A

vit d defieciency

ckd

61
Q

what is the cause of tertiary hyperthyroidism

A

prolonged secondary hyperparathyroidism

62
Q

what are the signs and sx of hyper parathyroidisim

A

asymptomatic

bones = pain, osteoporosis 
moans = depression and fatigue 
groans = myalgia 
stones = kidney stones

secondary = rickets, osteomalacia, renal osteodystrophy

63
Q

what are the Lx of hyperparathyroidism

A

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
Q

other lx in hyperparathyroidism

A 
bloods - FBC, UE, LFT, creatinine 
urine calcium 
DEXA
Radiology - USS Kidneys and neck 
parathyroid gland biopsy
65
Q

management of hyperparathyroidism

A

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
Q

complications of hyperparathyroidism

A

renal calculi
acute pancreatitis
peptic ulceration
calcification of the cornea

67
Q

what is DM

A

metabolic condition in which the patient has hyperglycaemia due to insulin insensitivity or decreased insulin secretion.

68
Q

what is T2DM

A

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
Q
A

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
Q

sx and symptoms of DM

A

polyuria, polyphagia, polydipsia, blurred vision, glycosuria, signs of macrovascular and microvascular disease.

71
Q

sx more common in T1DM

A

acetone breath, weight loss, Kussmaul breathing, nausea and vomiting.

72
Q

DX Lx for DM

A

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
Q

other tests for DM

A
  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)

  1. Impaired fasting glucose: plasma glucose: 5.6–6.9 mmol/L
    (110–126 mg/dL).
74
Q

describe the management for T2DM

A 
Dietary advice
BMI measurement 
Smoking cessation
 Decrease alcohol intake Regular blood glucose 
HbA1C monitoring 
encourage exercise

medical = anti diabetic agents

75
Q

management in T1DM

A 
diet = high in complex carbs, low in fat
BMI measurement 
smoking cessation 
decrease alcohol intake 
regular blood glucose and Hb1Ac monitoring 
encourage exercise
76
Q

complications of DM

A

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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