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nicks phase 2a flaschards > endocrine > Flashcards

endocrine Flashcards

1
Q

what is Cushing’s disease?

A

Cushings disease is caused by a pituitary gland tumour that over-secretes the hormone ACTH, thus overstimulating the adrenal glands’ cortisol production.

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2
Q

what are the signs and symptoms of Cushing’s disease?

A
  • signs- moon face, central obesity, hypertension

- symptoms- mood change and weight gain

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3
Q

how is Cushing’s disease diagnosed?

A
  • MRI to locate adenoma

- overnight dexamethasone suppression test

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4
Q

what is Cushing’s syndrome?

A

Refers to the signs and symptoms associated with excess cortisol in the body, regardless of the cause

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5
Q

what can cause Cushing’s syndrome?

A
  • exogenous administration of steroids
  • Cushing’s disease
  • adrenal nodular hyperplasia
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6
Q

what can cause hyperthyroidism?

A
  • Graves disease
  • Toxic multinodular disease
  • Toxic adenoma
  • Ectopic thyroid tissue
  • Exogenous- iodine excess
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7
Q

how does hyperthyroidism present?

A
  • symptoms- diarrhoea, weight loss, increased appetite

signs- warm skin, palmar erythema, irregular pulse

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8
Q

how is hyperthyroidism diagnosed?

A
  • low TSH

- T4 and T3 raised

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9
Q

how is hyperthyroidism treated?

A
  • beta blockers
  • carbimazole- anti-thyroid medication
  • radioiodine
    thyroidectomy
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10
Q

what can cause hypothyroidism?

A
  • Iodine deficiency
  • Post-thyroidectomy
  • Drug-induced- e.g. antithyroid
  • primary hypothyroidism- disease of the thyroid gland
  • secondary- hypothalamic or pituitary disease
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11
Q

clinically how does hypothyroidism present?

A
  • symptoms- tired, lethargic, weight increase, constipation

- signs- bradycardia, dry hair, ascites, goitre

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12
Q

how is hypothyroidism treated?

A

levothyroxine (T4)

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13
Q

what is Grave’s disease?

A

circulating IgG autoantibodies bid to and activate G coupled thyrotropin receptors, resulting in hyperplasia and hypertrophy of the thyroid gland- producing excess thyroid hormones

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14
Q

how does Grave’s disease present clinically?

A
  • pretibial myxoedema, thyroid acropachy

- signs of hyperthyroidism- e.g. weight loss and diarrhoea

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15
Q

how is Grave’s disease treated?

A

carbimazole and thyrozine

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16
Q

what is Hashimoto’s thyroiditis?

A

an autoimmune condition where a low colloid content in the cells results in hypothyroidism

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17
Q

what are the 5 types of thyroid carcinoma?

A
  • papillary
  • follicular
  • anaplastic
  • lymphoma
  • medullary cell
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18
Q

how is a thyroid carcinoma treated?

A
  • radioactive iodine
  • levothyroxine
  • chemotherapy
  • thyroidectomy
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19
Q

what is Conn’s syndrome?

A

Conns syndrome is the autonomous secretion of excess aldosterone

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20
Q

what zone of the adrenal gland is aldosterone produced in?

A

zona glomerulosa

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21
Q

clinically how does Conn’s syndrome present?

A

hypokalaemia and hypertension!

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22
Q

on an ECG how is Conn’s syndrome diagnosed?

A
  • flat T waves
  • ST depression
  • long QT interval
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23
Q

apart from an ECG, how else can Conn’s be diagnosed?

A

plasma aldosterone must be raised while renin is low

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24
Q

how is Conn’s syndrome treated?

A
  • laparoscopic adrenalectomy

- spironolactone

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25
Q

what is the aetiology of hypocalcaemia?

A
  • osteomalacia
  • high phosphate levels due to hypoparathyrodism
  • chronic kidney disease
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26
Q

how does hypocalcaemia present?

A 
SPASMODIC
Spasms
Perioral paraesthesiae
Anixous
Siezures
Muscle tone increased in smooth muscle
Orientation impaired
Dermatitis
Impetigo herpetiformis
Chovstek’s sign
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27
Q

what is the etiological basis of hypercalcaemia of malignancy?

A
  • Commonly of squamous cell tumours of the lung and breast
  • Bone metastases common
  • Lytic bone metastases
  • Myeloma
  • Production of osteoclast activating factor or PTH- like hormones by the tumour
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28
Q

what are the symptoms of a patient with hypercalcaemia of malignancy?

A

lethargy, anorexia, nausea, polydipsia, polyuria, dehydration, confusion

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29
Q

what can cause primary hyperparathyroidism?

A
  • solitary adenoma
  • hyperplasia
  • parathyroid cancer
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30
Q

what are the clinical manifestations of primary hyperparathyroidism?

A
  • Asymptomatic
  • Raised calcium
  • Weak, tired, depressed, renal stones, abdo pain
  • Bone pain, fractures, osteopenia/ osteoporosis
  • Raised blood pressure
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31
Q

what is the aetiology of secondary hyperparathyroidism?

A
  • low vitamin D intake
  • hypertrophy of parathyroid resulting in excess PTH
  • chronic renal failure
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32
Q

how does tertiary hyperparathyroidism occur?

A

Occurs after prolonged secondary hyperparathyroidism- glands act autonomously having undergone hyperplastic or adenomatous change

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33
Q

what is SiADH?

A

Continued secretion of ADH despite plasma being very dilute leading to retention of water and excess blood volume- results in hyponatraemia (Na+ becomes less concentrated)

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34
Q

what can cause SiADH?

A
  • Malignancy- small cell carcinoma of the lung
  • Drugs
  • CNS disorder- meningoencephalitis, abscess, stroke
  • Pneumonia
  • Meningitis
35
Q

how would a patient with SiADH present clinically?

A
  • Confusion
  • Anorexia
  • Nausea
  • Concentrated urine
36
Q

what values of concentrated urine and osmolality must be present to diagnose SiADH?

A

Concentrated urine- Na+ > 20mmol/L and osmolality >100mOsmol/kg in the presence of hyponatraemia and low plasma osmolality

37
Q

What can cause acromegaly?

A
  • Increased secretion of GH from pituitary tumour

- Hyperplasia

38
Q

clinical manifestations of acromegaly

A
  • Symptoms- acroparaesthesia, amenorrhoea, low libido, headache, increased sweating, arthralgia, backache
  • Signs- massive growth of hands, feet and jaw, wide nose, macroglossia, widely spaced teeth, sclap folds, skin darkening, acanthosis nigricans, laryngeal dyspnoea, obstructive sleep apnoea, goitre
39
Q

what diagnostic test can be done to confirm an initial diagnosis of acromegaly?

A

oral glucose 24 hour test

40
Q

what is a prolactinoma?

A

a benign tumour of lactotroph cells of the anterior pituitary gland which causes excess production of prolactin

41
Q

what is the clinical presentation of males and females who have a prolactinoma?

A
  • Symptoms in both genders- vision problems, headaches, decreased libido, infertility, galactorrhoea
  • Female symptoms- amenorrhoea, vaginal dryness, brittle bones in old age
  • Male symptoms- gynecomastia, erectile dysfunction
42
Q

what are carcinoid tumours?

A

a diverse group of tumours of enterochromaffin cell origin, capable of producing serotonin

43
Q

where can carcinoid tumours commonly occur?

A

Appendix
Ileum
Rectum
Elsewhere in GI tract, ovary, testis, bronchi

44
Q

what are the signs and symptoms of carcinoid syndrome?

A

Bronchoconstriction
Paroxysmal flushing of upper body
Diarrhoea
CCF (congestive cardiac failure)

45
Q

what is diabetes inspidus?

A

passage of large volumes (over 3L a day) of dilute urine due to impaired water reabsorption of the kidney

46
Q

what are the causes of diabetes insipidus?

A
  • cranial- defects in ADH gene, posterior pituitary tumour

- nephrogenic- impaired response of the kidney to ADH due to hypokalaemia, hypercalcaemia or sickle cell

47
Q

how does diabetes insipidus present clinically?

A
  • Polyuria
  • Polydipsia
  • Dehydration
  • Symptoms of hypernatraemia- lethargy, thirst, weakness, irritability, confusion, coma, fits
48
Q

what is the pharmacological treatment of diabetes insipidus?

A
  • cranial- desmopressin

- nephrogenic- benzoflumethiazide

49
Q

what is Addison’s disease?

A

destruction of the adrenal cortex leads to glucocorticoid (cortisol) and mineralocorticoid (aldosterone) deficiency

50
Q

what is the aetiology of Addison’s disease?

A
  • Autoimmune
  • TB
  • Adrenal metastases
  • Lymphoma
  • Opportunistic infection- HIV
  • Adrenal haemorrhage
  • Congenital
51
Q

what is the commonest cause of secondary adrenal insufficiency?

A

iatrogenic due to Lon term steroid therapy surpressing the pituitary

52
Q

what are the symptoms of hyperglycaemia?

A 
polyuria
polydipsia
unexplained weight loss
visual blurring
lethargy
53
Q

what are the stages of diabetic retinopathy?

A
  • background- micro-aneurysms
  • pre-proliferative- occluded vessels, venous loops
  • proliferative- ischaemia, new blood vessels form
54
Q

what are the microvascular complications of hyperglycaemia?

A

retinopathy
nephropathy
neuropathy

55
Q

why does diabetic ketoacidosis occur?

A

glucose is not taken up by cells due to lack of insulin, therefore ketoacidosis must occur to produce energy, however this produces acetone as a by-product

56
Q

what are the fasted and random glucose levels used to diagnose diabetes?

A

fasting greater than 7mmol/L

random greater than 11 mol/L

57
Q

what can cause type 1 diabetes?

A

insulin deficiency from autoimmune destruction of insulin secreting pancreatic beta cells

58
Q

how is hypoglycaemia diagnosed?

A

plasma glucose less than 3 mol/L

59
Q 
how would you treat:
-vascular disease
- nephropathy
- diabetic retinopathy
in diabetes?
A
  • vascular disease- address risk factors, statins
  • nephropathy- renal dialysis, control hypertension vi ACE/ ARB
  • diabetic retinopathy- laser photo coagulation
60
Q

what value must Hb1Ac be above to diagnose diabetes?

A

greater than 48mmol/L (6.5%)

61
Q

what value must the oral glucose tolerance test be above to diagnose diabetes?

A

2 hour value greater than 11.1mmol/L

62
Q

how would you treat diabetic ketoacidosis?

A

fluids, IV insulin and potassium replacement

63
Q

what are the marcovascular problems associated with hyperglycaemia?

A 
stroke
MI
renovascular disease
limb ischaemia 
heart disease
64
Q

what are the clinical features of type 1 diabetes?

A

weight loss
persistent hyperglycaemia despite diet and medication
islet cell antibodies
ketonuria on dipstick
anti-glutamic acid decarboxylase antibodies

65
Q

what are some common insulin regimens used in type 1 diabetes?

A
  • disposable pens
  • vary injection site
    BD biphasic regimen- twice daily pre mixed
    QDS- ultra fast before meals and bed time long acting analogue
66
Q

complications of diabetic ketoacidosis

A 
cerebral oedema
aspiration pneumonia
hypokalaemia
hypomagnesaemia
hypophosphataemia
thromboembolism
67
Q

how would you treat a patient with type 2 diabetes?

A 
metformin
then add sulfonylurea
then add glitazone
add sulfonylurea receptor binders
glucagon-like peptide analogues
alpha glucosidase inhibitors
68
Q

what different types of sub-cutaneous insulin injections can be offered to a patient?

A
  • ultra-fasting acting (nororapid)- 30 mins before meal
  • isophate insulin- peaks at 4-12 hours
  • pre-mixed insulins
  • long term recombinant human insulin analogues to use before bed
69
Q

what can cause hypokalaemia?

A
  • Diuretics
  • Vomiting and diarrhoea
  • Pyloric stenosis
  • Rectal villous adenoma
  • Intestinal fistula
  • Cushings
  • Conns
  • Alkalosis
  • Liquorice abuse
  • Renal tubular failure
70
Q

clinically how does hypokalaemia present?

A 
muscle weakness
hypotonia
hyporeflexia
cramps
tetany
constipation
71
Q

what appearance would hypokalaemia give on an ECG?

A

small/ inverted T waves
prominent U waves
long PR interval
ST depression

72
Q

what can cause hyperkalaemia?

A
  • Drug interference with potassium excretion
  • Combination of ACE inhibitors with NSAIDS
  • Oliguric renal failure
  • K+-sparing diuretics
  • Rhabdomyolysis – due to crush injury
  • Metabolic acidosis
  • Excess K+ therapy
  • Addison’s disease
  • Massive blood transfusion
  • Burns
73
Q

how does hyperkalaemia present?

A

fast irregular pulse
chest pain
weakness
palpitations

74
Q

how does hyperkalaemia present on an ECG?

A

tall T waves
small P waves
wide QRS complex

75
Q

how can hyperkalaemia be diagnosed?

A

serum potassium greater than 5.5mmol/L

76
Q

how would you treat a patient with hyperkalaemia?

A
  • treat underlying cause

- IV calcium gluconate and IV actrapid

77
Q

what is the hyperosmolar hyperglycaemic state?

A

Complication of diabetes mellitus in which high blood sugar results in high osmolarity without significant ketoacidosis

78
Q

what clinical features would suggest a diagnosis of type 1 diabetes?

A
  • weight loss
  • persistent hyperglycaemia despite diet
  • autoantibodies
  • islet cell antibodies
  • anti-glutamic acid decarboxylase (GAD) antibodies
  • ketonuria on dipstick
79
Q

what can cause diabetes mellitus?

A
  • drugs- anti-HIV, thiazides, steroids
  • pancreatic- surgery, trauma, haemochromatosis, cancer
  • Cushing’s disease
  • acromegaly
  • phaemochromocytoma
  • hyperthyroidism
80
Q

what is the typical type 2 DM patient?

A

asian background, male, over 40

81
Q

how does diabetic ketoacidosis present clinically?

A
  • drowsiness, vomiting and dehydration
  • pear drop smell on breath
  • triggers- infection, surgery, MI, chemotherapy, pancreatitis
82
Q

how is diabetic ketoacidosis diagnosed?

A
  • acidaemia
  • hyperglycaemia
  • ketonaemia
83
Q

how is Addison’s disease diagnosed?

A

Na+ decreased, K+ increased due to reduced aldosterone

  • hypoglycaemia- low cortisol
  • short ACTH stimulation test
84
Q

how is Addison’s disease treated?

A

replace steroids with oral hydrocortisone

nicks phase 2a flaschards (15 decks)

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