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Flashcards in Endocrine Deck (91)
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1
Q

Type 1 Diabetes

A

Syndrome of chronic hyperglycaemia due to relative insulin deficiency

2
Q

Type 2 Diabetes

A

Syndrome of chronic hyperglycaemia due to relative insulin resistance

3
Q

Gestational Diabetes

A

When pregnant women without previous DM develop high blood sugar

4
Q

Cause of Type 1 Diabetes

A

Insulin deficiency due to autoimmune destruction of insulin-secreting pancreatic B-cells. Destruction of B-cells causes hyperglycaemia and metabolic acidosis.

5
Q

Causes of Type 2 Diabetes

A

Decreased insulin secretion and insulin resistance due to B-cell dysfunction. Insulin resistance primarily occurs in liver, muscle and fat tissue. Typically progresses from impaired glucose tolerance or impaired fasting-glucose

6
Q

How common is Type 1 DM

A

Younger usually <30 yo
Usually leand
Increased in Northern Eastern ancestry

7
Q

How common is Type 2 DM

A

Older usually > 30 yo
Often overweight
All racial groups. Increase in peoples of Asian, African Polynesian ancestry
Higher concordance in identical twins

8
Q

Risk factors for Type 2 DM

A

Obesity, increasing age, male, low exercise, alcohol, high calorie intake, poor diet, family Hx, Hx of gestational diabetes, polycystic ovary syndrome, HTN, dyslipidaemia

9
Q

Symptoms for Diabetes Mellitus

A

Polyuria, polydipsia (increased thirst), polyphagia (increased hunger), lethargy, frequent infections, weight loss, psychosocial implications, blurred vision for type 2

10
Q

Symptoms for Type 1 Diabetes

A

Dehydration, ketonuria, hyperventilation, abdominal pain, vomiting, fetor hepaticus (breath smells like pear drops)
all due to ketoacidosis

11
Q

Symptoms for Type 2 Diabetes

A

Candida infections, skin infections, UTIs, fatigue, blurred vision, polydipsia and polyuria, acanthosis nigricans

12
Q

Investigations for Type 1 Diabetes

A
Random Plasma glucose >11mmol/L
fasting plasma glucose >6.9
2-hour plasma glucose >11
Plasma or urine ketones
HbA1C >48
Fasting C-peptide low or undectable
13
Q

Investigations for Type 2 Diabetes

A

Fasting plasma glucose >6.9
HbA1C of 48 or greater
Abnormal glucose tolerance tests
Random plasma glucose of >11.1 plus symptoms of hyperglycaemia

14
Q

Investigations for Pre-diabetes

A

Single fasting plasma glucose of 5.6-6.9

HbA1c of 39-46

15
Q

Differentials for Type 1 Diabetes

A

Maturity onset diabetes of the young

Type 2 Diabetes

16
Q

Differentials for Type 2 Diabetes

A

Pre-diabetes
Type 1 diabetes
Latent autoimmune diabetes in adults (LADA)

17
Q

Treatment plan for treating Diabetes

A
1. Lifestyle changes
\+ Glycaemic management
\+ BP management
\+ Lipid management
\+ Antiplatelet therapy
2. Metformin
18
Q

Treatment for Type 1 Diabetes

A

Patient will always need insulin
Short-acting insulin in twice daily regimen
Long-acting insulin works well for those who dislike injecting
Inhaled forms also available

19
Q

Treatment for Type 2 Diabetes

A

3 drugs:

  • Biguanide (metformin)
  • Sulfonylureas (tolbutamide, glibenclamide, glipzide, glicazide, chlopropamide)
  • Thiazolidinediones

Others: intestinal enzyme inhibitors, orlistat, rimonbant
Bariatric surgery for some

20
Q

Complications of Diabetes

A
Stroke, MI
Amputation for foot gangrene
Diabetic retinopathy, nephropathy, neuropathy
Diabetic foot ulcers
Diabetic ketoacidosis
Cataracts
Dehydration
Coronary artery disease, cerebrovascular disease, peripheral vascular disease
Diabetic Kidney Disease
21
Q

Prognosis of Type 1 Diabetes

A

Untreated Type 1 is fatal due to DKA.

22
Q

Prognosis of Type 2 Diabetes

A

When diagnoses at age 40:
men lose 5.8 years of life
women lose 6.8 years of life

23
Q

Primary and Secondary Hypothyroidism

A

Hypothyroidism is underproduction of T3 and T4. Primary hypothyroidism (95% of cases) is failure of the thyroid gland to produce thyroid hormones. Secondary hypothyroidism is underproduction of TSH by the pituitary gland.

24
Q

How common is hypothyroidism

A

More common in women and white people.

Increases with age

25
Q

Pathophysiology of Hypothyroidism

A

T4 is produced in the thyroid gland and converted to T3 in target tissues. Failure of the thyroid to produce T4 and T3 stimulates the pituitary to increase production of TSH.

26
Q

Causes of Hypothyroidism

A
  • Hashimoto’s Disease (Autoimmune thyroiditis)
  • Iodine deficiency
  • Damage to thyroid gland from Thyroidectomy, radioactive iodine therapy
  • Infiltrative diseases: Sarcoidosis, Haemochromotosis
  • Primary atrophic hypothyroidism (Thyroid infiltrated with lymphocytes)
27
Q

Risk factors for Hypothyroidism

A
Iodine deficiency 
Female
Middle Age
Autoimmune disorders
Graves disease
Radiotherapy
28
Q

Symptoms of Hypothyroidism

A

Constipation, weight gain, decreased appetite, cold intolerance, tiredness and lethargy, difficulty concentrating, menorrhagia, dry skin, loss of outer 3rd of eyebrows, alopecia, loss of libido, hoarse voice, cramps, dementia, weakness

29
Q

Signs of Hypothyroidism

A

Myxoedema (puffy hands, face and feet), dry coarse skin, cold peripheries, bradycardia, delayed tendon reflex relation, cavity effusion e.g. pleural effusion, pericarditis, goitre, pretibial myxoedema, exophthalmos, ophthalmopegia (paralysis of muscles around eyes)

30
Q

Differentials for Hypothyroidism

A

Phaechromocytoma

Depression

31
Q

Investigations for Hypothyroidism

A

TFTs: Elevated TSH, low T3 and T4

Anti-thyroid peroxidase antibodies (anti-TPO)

32
Q

Treatment for Hypothyroidism

A

Levothyroxine (T4)

Lower dose for pre-existing CAD or > 60 yo and some with subclinical hypothyroidism TSH > 10

33
Q

Complications of Hypothyroidism

A
Angina due to Levothyroixine, AF, Osteoporosis
Myxoedema coma  (severe form of hypothyrodism with multi-organ failure, decreased mental status, hypothermia)
34
Q

Hyperthyroidism aka Grave’s Disease

A

Hyperfunction and over-activity of the thyroid gland

35
Q

Pathophysiology

A

Anti-TSH receptor antibodies cause thyroid hormone overproduction as well as thyroid hypertrophy and hyperplasia of thyroid follicular cells

36
Q

How common is Hyperthyroidism

A

More common in women
40-60yo
Lower prevalence in black people

37
Q

Causes of Hyperthyroidism

A
Grave's disease
Toxic Thyroid Adenoma
Toxic Multinodular Goitre
Ectopic Thyroid Tissue
Struma Ovarii
38
Q

Secondary Hyperthyroidism

A

TSH, T3 and T4 are all high
Caused by TSH-secreting pituitary adenoma, thyroid hormone-resistance syndrome, HCG-secreting tumour, gestational thyrotoxicosis

39
Q

Risk Factors for Hyperthyroidism

A

High Iodine Intake
Female
Smoking

40
Q

Symptoms and signs of Hyperthroidism

A

Diarrhoea, weight loss despite overeating, increased appetite, sweating, heat intolerance, palpitations, resting tremor, irritability, mood swings, oligomenorrhoea (infrequent period), psychosis, itch, alopecia, urticaria, loss of libido, palmar erythema, tachycardia, goitre, gynaecomastia, lid lag

41
Q

Signs of Grave’s Disease

A

Exopthalmos, opthalmoplegia, pretibial myxoedema, thyroid acropachy, thyroid bruit

42
Q

Differentials for Hyperthyroidism

A

Phaeochromocytoma
Toxic nodular goitre
Painless and postnatal thyroiditis
TSH-producing pituitary adenoma

43
Q

Investigations for Hyperthyroidism

A
TFTs: Low TSH, High T3 and T4
Mild normocytic anaemia 
Mild neutropenia
High ESR, CPR
Raised LFTs
Thyroid Antibodies
Isotope Scan
44
Q

Treatment for Hyperthyroidism

A
  • Anti-thyroid drug e.g. Carbimazole
    + corticosteroids, beta blockers, iodine solution
  • Radioactive iodine
  • Thyroid surgery
45
Q

Complications of Hyperthyroidism

A

Hypothyroidism due to radio-iodine treatment

Hoarse voise, heart failure, Angina, AF, Osteoporosis, Opthalmopathy, gynaecomastia

46
Q

Goitre

A

A goitre is a swelling in the neck caused by an enlarged thyroid gland. May be due to hypo/hyper thyroidism

47
Q

Types of Goitre

A

Uninodular
Multinodular
Diffuse

48
Q

Risk Factors for Goitre

A
  1. Excess iodine
  2. Iodine insufficiency
  3. Family History
  4. Autoimmune deficiency
49
Q

Causes of Goitre

A

Iodine deficiency (hyperplasia)
Hashimoto’s (infiltration of lymphocytes)
Pituitary adenoma (hypersecretion of TSH)
Graves (Autoantibodies activating the TSH receptor)
Thyroid cancer

50
Q

Symptoms and signs of Goitre

A

Heat intolerance and weight loss, depression, nervousness, palpitations, tachycardia, resting tremor
Large goitre= oesophageal compression, dysphagia, tracheal compression

51
Q

Investigations for Goitre

A

TSH suppressed
T3, T4 elevated
Thyroid USS
TSH receptor antibodies. : negative but positive in Graves

52
Q

Treatment for Goitre

A

Radioactive iodine therapy
Anti-thyroid drugs i.e. thiamazole
Thyroid surgery

53
Q

Cushing’s Syndrome

A

Condition in which the pituitary gland releases excess adrenocorticotrophic hormone (ACTH) causing excess cortisol release from adrenal glands. Involves abnormal feedback of HPA axis

54
Q

How common is Cushing’s syndrome

A

More common in women

20-50yo

55
Q

Cushing’s Syndrome

A

Condition involving hypercortisolism. Can
either be ACTH-dependent Cushing’s syndrome or ACTH-independent hypercortisolism.

Cushing is when the adrenal glands secrete excess cortisol and involves abnormal feedback of the HPA axis.

56
Q

How common is Cushing’s Syndrome

A

More common in women

20-50yo

57
Q

Cushing’s Syndrome

A

Condition in which the adrenal glands secrete excess cortisol and involves abnormal feedback of the HPA axis.

58
Q

Causes of Cushings

A
  • Increased ACTH secretion from anterior pituitary
  • Ectopic ACTH production i.e. small cell lung carcinoma
  • Ectopic CRH production
  • Adrenal adenomas
  • Adrenal nodular hyperplasia
59
Q

Causes of hypercortisolism where HPA axis is not involved

A
Pregnancy
Malnutrition
Alcoholism
Obesity, Diabetes
Stress, anxiety, depression
60
Q

3 Zones of the Adrenal Cortex and the steroids they make

A

Zona Glomerulosa - mineralocorticoids (aldosterone)
Zona Fisculate - glucocorticoids (cortisol)
Zona Reticularis - sex steroids (androgens)

61
Q

Effect of High and Low Cortisol

A

High cortisol causes gluconeogenesis, glycogen depostion

Low cortisol causes protein synthesis and initiation of host response to infection

62
Q

Risk factors for Cushing’s Syndrome

A
Obestity
Diabetes
Hypertension
Osteoporosis
Iatrogenic steroid use
Female
63
Q

Symptoms and signs of Cushing’s Syndrome

A

Facial plethora and rounding, weight gain and central obesity, acne, striae, amenorrhoea, oligomenorhoea, depression, HTN, diabetes, osteoporosis, easy bruising, muscle weakness, insomnia, psychosis, hirsutism

64
Q

Investigations for Cushing’s Syndrome

A
  1. Dexamethasone suppression test: Give dexamethasone at midnight then measure cortisol levels at 8am. If cortisol levels arn’t suppressed, then Cushing’s.
  2. Midnight cortisol test. Elevated cortisol at night if Cushing’s.
  3. Urine pregnancy test
  4. Serum glucose
65
Q

Differentials for Cushing’s

A

Obesity

Metabolic Syndrome

66
Q

Treatment for Cushing’s Syndrome

A
  1. If iatrogenic cause- stop medication when possible
  2. Adrenal adenoma- requires resection of tumour or adrenalectomy
  3. Adrenal carcinoma- adrenalectomy + radiotherapy
  4. Ectopic ACTH -surgery
  5. Metyrapone - 11B-hydroxylase blocker used to reduce cortisol levels
67
Q

Complications of Cushing’s Syndrome

A
Metabolic Syndrome
Hypertension
Diabetes
Obesity
Hyperlipidaemia
Thrombophilia
Osteoporosis
68
Q

Addison’s disease

A

Adrenal insufficiency leading to glucocorticoid and mineral corticoid deficiency. 90% of the adrenal cortex needs to be destroyed to produce adrenal insufficiency

69
Q

Types of Addison’s disease

A
  1. Primary - adrenal pathology
  2. Secondary - hypothalamic/ pituitary pathology
  3. Autoimmune (most common) destruction of the adrenal cortex
70
Q

How common is Addison’s disease

A

Most common in women- 90% of cases

71
Q

Cause of Addison’s disease

A
  • Destruction of the 3 layers of the adrenal cortex.
  • Disruption of hormone synthesis
  • Dysfunction of the autoimmune system with antibodies against the adrenal cortex
    ,
72
Q

Risk factors to Addison’s Disease

A
TB
Adrenal metastases
Lymphoma
Infections: HIV, meningoccocal infection, systemic fungal infection
Adrenal Haemorrhage
Coealiaac disease
Female
73
Q

Symptoms and Signs of Addison’s Disease

A
Fatigue, weakness
Nausea and vomiting
Abdominal pain
Anorexia 
Weight loss
Diarrhoea
Constipation
Dizziness
Personality change/ Irritability
Amenorrhoea
Skin pigmentation
Postural hypotension
74
Q

Investigations for Addison’s Disease

A
  1. Bloods
    - Low Na/high K+- low aldosterone
    - Low glucose, low cortisol levels
    - Anaemic
  2. Synacthen test- ACTH stimulation test: serum cortisol <497
  3. U&E: Elevated Blood Urea nitrogen (BUN) and creatinine
75
Q

Treatment for Addison’s Disease

A

Daily hydrocortisone tablets:
Glucocorticoid replacement (cortisol)
Fludrocortisone (mineralocorticoid replacement)

76
Q

Complications of Addison’s Disease

A

Acute Adrenal Insufficiency –> Emergency –> requiring IV hydrocortisone

77
Q

Hyperparathyroidism

A

Overproduction of PTH results in derangement of calcium metabolism

78
Q

Types of Hyperparathyroidism

A

Primary: solitary adenoma, gland hyperplasia
Secondary: Low calcium levels, high parathyroid
Tertiary: Low calcium, very high parathyroid hormone
Malignant hyperparathyroidism

79
Q

Pathophysiology of Hyperparathyroidism

A
  1. PTH is released by parathyroid glands in response to low ionised calcium levels
  2. When calcium levels are high, parathyroid gland excretion stops
  3. Effects of parathyroid hormone:
    - increased osteoclast activity- to release calcium and phosphate from bones
    - Increased kidney reabsorption of calcium + decreasing phosphate reabsorption
    - Activate 1,25 dihyrdroxy-vitamin D3 production is to increase absorption of calcium
80
Q

Risk Factors for Hyperparathyroidism

A
Female > Male
Age > 45
Radiation therapy
Currently on Lithium treatment for Bipolar Disorder
Female
81
Q

Symptoms and signs for Hyperparathyroidism

A

Stones: renal stones, polyuria, polydipsia
Bones: Osteoporosis, osteomalacia, arthritis
Moans: depression, fatigue, memory loss
Throans: polyuria, constipation

82
Q

Investigations for Hyperparathyroidism

A
  1. Blood: raised calcium and PTH, reduced phosphate,

2. DEXA scan

83
Q

Differentials for Hyperparathyroidism

A
Familial hypocalciuric hypercalcaemia
Humoral hypercalcaemia of malignancy
Multiple myeloma
Thyrotoxicosis
Leukaemia
Thiazide use
84
Q

Treatment for Hyperparathyroidism

A

Parathyroid excision (lead to hypoparathyroidism)
Vitamin D supplementation
Bisphosphonate

85
Q

Complications for Hyperparathyroidism

A
Osteoporosis
Bone fractures
Nephrolithiasis
Hypocalcaemia following surgery
Recurrent and superior laryngeal nerve injury following surgery
86
Q

Parathyroid adenoma

A

Benign tumour of the parathyroid gland causing hyperparathyroidism.

87
Q

How common are Parathyroid adenomas

A

Most common cause of hyperparathyroidism (85%)

88
Q

Cause of Parathyroid adenomas

A

MEN genes inactivate tumour suppressor genes and activate RET proto-oncogenes

89
Q

Symptoms and signs of Parathyroid adenomas

A

Stones, Bones, Moans, Thrones

90
Q

Investigation for Parathyroid Adenomas

A
  1. Bloods: raised PTH, low calcium

2. Sestamibi Parathyroid Scintigraphy: scan to localise parathyroid adenoma

91
Q

Treatment for Parathyroid Adenomas

A

Parathyroidectomy