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Medicine Year 2 2 > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

Specific Cutaneous Signs of Endocrinology Disorders:

What are the Specific Cutaneous Signs of Hyperthyroidism?

A
  • Hair loss
  • Onycholysis (when your nail separates from the skin underneath it)
  • Bulging eyes (stare)
  • Pretibial Myxedema (orange peel on anterior leg)
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2
Q

Specific Cutaneous Signs of Endocrinology Disorders:

What are the Specific Cutaneous Signs of Hypothyroidism?

A
  • Hair and eyebrow loss
  • Cold, pale skin
  • Characteristic ‘toad-like’ face
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3
Q

Specific Cutaneous Signs of Endocrinology Disorders:

What are the Specific Cutaneous Signs of Cushing’s Syndrome (hypercortisolism)?

A
  • Central obesity and wasted limbs (lemon on sticks)
  • Moon face
  • Buffalo hump
  • Supraclavicular fat pads
  • Striae (red stretch marks)
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4
Q

Specific Cutaneous Signs of Endocrinology Disorders:

What are the Specific Cutaneous Signs of Addison’s Disease (adrenal insufficiency)?

A
  • Hyperpigmentation (face, neck, palmar creases)
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5
Q

Specific Cutaneous Signs of Endocrinology Disorders:

What are the Specific Cutaneous Signs of Acromegaly?

A
  • Distal + soft tissue overgrowth
  • Large jaw, hands and feet
  • Thick skin and coarse facial features
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6
Q

Specific Cutaneous Signs of Endocrinology Disorders:

What are the Specific Cutaneous Signs of Hypopituitarism?

A
  • Pale/ yellow tinged thin skin

- Fine wrinkling round eyes and mouth (looks old)

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7
Q

Specific Cutaneous Signs of Endocrinology Disorders:

What are the Specific Cutaneous Signs of Hypoparathyroidism?

A
  • Dry, scaly, puffy skin

- Brittle nails and coarse hair

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8
Q

DIABETES MELLITUS

What is the primary cause of DM?

A

DM results from a lack of or reduced effectiveness of endogenous insulin and chronic hyperglycaemia.

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9
Q

DIABETES MELLITUS
Hyperglycaemia cause microvascular and macrovascular problems.

Name examples of microvascular problems.

A
  • Retinopathy
  • Nephropathy
  • Neuropathy
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10
Q

DIABETES MELLITUS
Hyperglycaemia cause microvascular and macrovascular problems.

Name examples of macrovascular problems.

A
  • Stroke
  • Heart disease
  • Limb ischaemia
  • Renovascular disease
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11
Q

DIABETES MELLITUS

Name some symptoms of hyperglycaemia.

A
  • Polyuria (excessive urine)
  • Polydipsia (excessive thirst)
  • Weight loss
  • Visual blur
  • Genital thrush
  • Lethargy
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12
Q

DIABETES MELLITUS

How is DM diagnosed

A
  • Hyperglycaemia symptoms
  • Fasting glucose of 7 mmol/L
  • normal glucose of over 11 mmol/L
  • HbA1c over 48 mmol/L (6.5%)
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13
Q

DIABETES MELLITUS

what is type 1 DM

A

it is insulin deficiency from autoimmune destruction of insulin-secreting pancreatic beta cells.

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14
Q

DIABETES MELLITUS

What is type 2 DM

A

it is decreased insulin secretion +- increased insulin resistance

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15
Q

DIABETES MELLITUS

Name some features that would suggest type 1 DM

A
  • Weight loss
  • Persistent hyperglycaemia despite diet/medication
  • ICA and GAD antibodies
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16
Q

DIABETES MELLITUS

name the difference in causes between type 1 and type 2

A

Type 1 is autoimmune beta cell DESTRUCTION.

Type 2 is beta cell DYSFUNCTION/ insulin resistance.

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17
Q

DIABETES MELLITUS

Risk factors for type 2 diabetes

A
  • obese
  • Asian
  • age >40
  • family history
  • gestation diabetes
  • diet in high fat/sugar
  • high cholesterol
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18
Q

DIABETES MELLITUS

Acute signs of DM

A

type 1- weight loss, polydipsia, polyuria

type 2- mainly asymptomatic but still complications

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19
Q

DIABETES MELLITUS

general treatment for DM

A
  • Address risk factors (quit smoking, start statin, control BP)
  • Inform DVLA
  • foot care
  • exercise
  • low fat/ sugar diet
  • Avoid alcohol
  • educate on what to do if they hypo (sugar drinks)
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20
Q

DIABETES MELLITUS

Treatment for type 1

A

Insulins.

1) ultra fast at start of meal- Novorapid
2) Isophane insulin- peaks at 4-12hrs
3) mixture-Novomix
4) long acting- insulin determir (bedtime)

vary injection site between thigh/abdomen

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21
Q

DIABETES MELLITUS

Treatment for type 2

A

1) Lifestyle changes
2) metformin

3) add gliptin or sulfonylurea or pioglitazone
4) triple therapy of metformin plus 2 above
5) triple therapy of metformin, sulfonylurea and GLP-1 mimetic

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22
Q

DIABETES MELLITUS

How is diabetes monitored

A
  • Fingerprick glucose

- HbA1c- mean glucose over past 8 weeks

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23
Q

Hypoglycaemia
symptoms?
plasma glucose reading?
treatment?

A
  • sweating, hunger, dizzy, confusion, tired, visual issues
  • < 3mmol/L
  • oral/ IV glucose depending if they can swallow
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24
Q

DIABETEIC KETOACIDOSIS

symptoms?

A
  • Drowsiness
  • Pear drop breath (due to acetones)
  • Kussmaul Breathing- trying to get rid of acid by respiratory compensation
  • Dehydration and vomiting
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25
Q

DIABETEIC KETOACIDOSIS

what can trigger DK

A
  • Infection, surgery, MI, wrong insulin dose
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26
Q

DIABETEIC KETOACIDOSIS

diagnosis?

A
  • Acidaemia blood pH < 7.3

- Hyperglycaemia and Ketonaemia

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27
Q

DIABETEIC KETOACIDOSIS

Treatment?

A

-Fluids and IV insulin

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28
Q

Hyperglycaemic, hyperosmolar non- ketotic (HONK) coma

what is it?

A

Long history of dehydration and glucose is > 35mmol/L

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29
Q

what is the treatment for a HONK coma

A
  • Rehydrate slowly with IV saline, replace K+ when urine starts to flow
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30
Q

THYROID

What does the thyroid gland secrete?

A

hormones T3 and T4. (thyroxine is T4, triiiodothyronin is T3)`

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31
Q

THYROID

How is T3 produced and what does it do

A

T3 is produced by the peripheral conversation of T4 and it acts to control metabolism/ increase BMR.

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32
Q

HYPERTHYROIDISM

signs and symptoms?

A
  • Diarrhoea
  • weight loss
  • increased appetite
  • irritability and over-active
  • Fast irregular pulse
  • warm, moist skin
  • fine tremor
  • Lid lag (eyelid lags behind eyes as it descends to follows finger)
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33
Q

HYPERTHYROIDISM

What tests would be done and what would they show?

A
  • TSH low
  • increased T3 and T4
  • Mild anaemia
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34
Q

HYPERTHYROIDISM

how is it treated

A
  • beta blockers (propranolol- rapid symptom relief)
  • anti thyroid meds ( carbimazole)
  • thyroidectomy if severe
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35
Q

GRAVE’S DISEASE

What is it?

A

Circulating IgG autoantibodies bind to and activate G-protein thyrotropin receptors, this causes thyroid enlargement and increased production of T3.

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36
Q

GRAVE’S DISEASE

what may trigger graves disease and what age/ gender is most likely to get it

A

triggers: stress, childbirth infection
age: 40-60 years
F:M 9:1

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37
Q

GRAVE’S DISEASE

Signs?

A
  • eye disease
  • pretibial myxoedema (swelling above lateral malleoli)
  • thyroid acropachy
  • clubbing and swlling of fingers/toes
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38
Q

GRAVE’S DISEASE

Tests?

A

test for the signs and also may have mild neutropaenia

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39
Q

GRAVE’S DISEASE

Treatment?

A
  • propranolol
  • Carbimazole +- thyrozine
  • 50% will relapse and need radioiodine/ surgery
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40
Q

HYPOTHYROIDISM

Causes?

A
  • Hashimotos Thyroiditis (goitre due to lymphocytic and plasma cell infiltration)
  • F:M 6:1
  • iodine deficiency
  • post thyroidectomy
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41
Q

HYPOTHYROIDISM

associations?

A

pregnancy problems ( Eclampsia, anaemia, prematurity, low birth weight, postpartum haemorrhage)

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42
Q

HYPOTHYROIDISM

signs?

A 
Bradycardic
Reflexes relax slowly
Ataxia (cerebellar)
Dry skin/hair
Yawn/drowsy
Cold hands/ low temp
Ascites
Round face/obese
Defeated demeanour
Immobile
CCF (congestive cardiac failure)
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43
Q

HYPOTHYROIDISM

Tests?

A
  • high TSH
  • low T4
  • high cholesterol
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44
Q

HYPOTHYROIDISM

treatment?

A
  • Levothyroxine (T4)
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45
Q

THYROID CANCERS

What are the types of thyroid cancer?

A
  • Papillary 60%
  • Follicular 25%
  • Medullary 5%
    Lymphoma 5%
    -Anaplastic (rare)
46
Q

THYROID CANCERS

what is the treatment for the cancers?

A
  • thyroidectomy
  • radiotherapy
  • node clearance/excision
  • thyroxine to suppress TSH in papillary
47
Q

THYROID CANCERS

how many more women have this than men?

A

F:M 3:1

48
Q

What is the function of the ADRENAL CORTEX?

A

Production of:

  • Glucocorticoids (cortisol, carb,fat,protein metabolism)
  • steroids
  • Mineralocorticoids (aldosterone, Na+ and K+ balance)
  • Androgens (sex hormones, e.g. convert to testosterone)
49
Q

What does corticotrophin releasing factor (CRF) do?

A

CRF from the hypothalamus stimulates ACTH from pituitary, this initiates cortisol and androgen production.

50
Q

CUSHING’S SYNDROME

What is it?

A

• Clinical state produced by chronic glucocorticoid excess + loss of normal feedback mechanisms of the hypothalamo-pituitary-adrenal axis and loss of circadian rhythm of cortisol secretion

51
Q

CUSHING’S SYNDROME

what is Cushing’s disease?

A

Bilateral adrenal hyperplasia from an ACTH-secreting pituitary adenoma

52
Q

CUSHING’S SYNDROME

What may cause Cushing’s syndrome?

A 
it may be caused by:
- oral steroids
- Cushing's Disease
- Ectopic ACTH production
- Decreased ACTH due to  –ve feedback
•	Adrenal adenoma/cancer
53
Q

CUSHING’S SYNDROME

symptoms?

A
  • weight gain
  • acne
  • Recurrent achilles rupture
  • mood change
  • ED
  • irregular menstruation
54
Q

CUSHING’S SYNDROME

signs?

A
  • central obesity
  • plethoric moonface
  • skin/muscle atrophy
  • osteoporosis
55
Q

CUSHING’S SYNDROME

Tests?

A
  • the overnight dexamethasone test (DST). Dexamethasone suppresses the production of cortisol, if there is no suppression then this patient has Cushing’s.
56
Q

CUSHING’S SYNDROME

Treatment for Cushing’s is cause dependant. what are they?

A

Iatrogenic- stop meds

Cushing’s Disease- bilateral adrenalectomy

Ectopic ACTH production- surgery, metyrapone

Adrneal adenoma- adrenalectomy+ radiotherapy

57
Q

ACROMEGALY

what is acromegaly caused by?

A
  • increased GH from a pituitary tumour OR

- hyperplasia ectopic GH releasing hormone from a carcinoid tumour

58
Q

ACROMEGALY

What does growth hormone do?

A

GH stimulates bone& tissue growth by the secretion of IGF-1

59
Q

ACROMEGALY

how many people in the UK have acromegaly?

A

3 per million a year

60
Q

ACROMEGALY

symptoms?

A
  • paraesthesia ( pins and needles in extremities)
  • amenorrhea
  • low libido
  • Arthralgia (joint pain)
61
Q

ACROMEGALY

Signs?

A
  • large hands, feet and jaw
  • wide nose
  • macroglossia (large tongue)
  • Acantosis nigricans- hyperpigmentation in folds of skin
62
Q

ACROMEGALY

complications?

A
  • DM
  • vascular (HTN,CCF,LVH, IHD, arrhythmias, cardiomyopathy)
  • Neoplasia ( increased risk of colon cancer)
63
Q

ACROMEGALY

Tests?

A
  • MRI

- OGTT (high glucose suppresses GH so if GH still high then= acromegaly)

64
Q

ACROMEGALY

treatment?

A
  • excising lesion

- reduce GH and IGF-1 by: surgery, GH antagonist, somatostatin analogues

65
Q

HYPERALDOSTERONISM

what is it?

A

excess aldosterone independent of RAAS, increased Na+ and water retention, decreased renin.

66
Q

HYPERALDOSTERONISM

symptoms?

A
  • signs of hypokalaemia ( weakness, polydipsia, polyuria, paraesthesia)
67
Q

HYPERALDOSTERONISM

Causes?

A

2/3- Conn’s syndrome (solitary aldosterone producing adenoma)
1/3- bilateral adrenal hyperplasia

68
Q

HYPERALDOSTERONISM

what tests would you carry out?

A
  • U+E, renin, aldosterone
69
Q

HYPERALDOSTERONISM

Treatments?

A

conn’s- laproscopic adrenalectomy, spironolactone pre-op

Hyperplasia- spironolactone, amiloride, eplerenone

70
Q

ADDISON’S DISEASE (ADRENAL INSUFFICIENCY)

What is it?

A

glucocorticoid and mineralocorticoid deficiency due to destruction of the adrenal cortex. Not enough cortisol or aldosterone.

71
Q

ADDISON’S DISEASE (ADRENAL INSUFFICIENCY)

What is it caused by?

A
  • 80% due to autoimmunity.
  • Worldwide TB is the most common cause.
  • Adrenal metastases
  • Lymphoma
72
Q

ADDISON’S DISEASE (ADRENAL INSUFFICIENCY)

Symptoms and signs?

A
  • Depression/ low self esteem
  • Tanned, tired, tearful, weak, faint, flu, myalgias, arthralgias
  • GI, (nausea, diarrhoea/ constipated)
  • postural hypotension
73
Q

ADDISON’S DISEASE (ADRENAL INSUFFICIENCY)

Tests?

A

Na+ low and K+ high due to less aldosterone

Low glucose due to less cortisol

ACTH stimulation test- measure plasma cortisol 30 mins before/after tetracosactide, Addison’s excluded if over 550nmol/L

21- hydroxylase autoantibodies positive in autoimmune disease

74
Q

ADDISON’S DISEASE (ADRENAL INSUFFICIENCY)

Treatment?

A
  • replace steroids with oral hydrocortisone

- mineralocorticoids to correct postural hypotension (fludrocortisone oral)

75
Q

ADDISON’S DISEASE (ADRENAL INSUFFICIENCY)

Common differential diagnosis?

A

Commonly misdiagnosed with anorexia, viral infection.

however, in anorexia K+ DECREASES, in Addison’s, K+ INCREASES.

76
Q

ADDISON’S DISEASE (ADRENAL INSUFFICIENCY)

What may occur after long term steroid therapy?

A

Suppression of pituitary- adrenal axis

77
Q

DIABETES INSIPIDUS

What is it?

A

Passage of large volumes (>3L a day) of dilute urine due to impaired water retention of the kidneys

78
Q

DIABETES INSIPIDUS

What are the two types of DI and what is the difference?

A

Too little ADH from posterior pituitary gland (cranial DI)

OR

Kidney not responding to ADH (nephrogenic DI)

79
Q

DIABETES INSIPIDUS

What are the causes for each type of DI?`

A

Cranial DI: Head trauma, pituitary tumour

Nephrogenic DI: Drugs (eg: Lithium), CKD

80
Q

DIABETES INSIPIDUS

What are the signs and symptoms?

A
  • polyuria
  • polydipsia
  • dehydration
  • hypernatremia symptoms (lethargy, weak, thirst, irritated and confusion)
81
Q

DIABETES INSIPIDUS

How is it diagnosed and tested for?

A

Water Deprivation Test

1) deprive of fluids, measure osmolality and volume of urine every 2 hours
2) if still dilute, give DESMOPRESSIN (distinguish cranial or nephrogenic)
3) If there is a response and concentrated urine begins to be produced then it is CRANIAL DI

82
Q

DIABETES INSIPIDUS

Treatment?

A

Cranial DI- Desmopressin (synthetic ADH analogue), MRI to find cause

Nephrogenic DI-
Bendroflumethiazide
(causes more Na+ excretion -increased water lost makes body responds by reducing GFR, so treat DI)

NSAIDS- inhibit prostaglandin synthase (inhibits ADH), so reduced GFR and decreased volume of urine

83
Q

Syndrome of Inappropriate ADH Secretion (SIADH)

What is it?

A

Too much secretion of ADH despite hypertonicity and volume being normal.

Concentrated urine and hyponatraemia

84
Q

Syndrome of Inappropriate ADH Secretion (SIADH)

Causes?

A

Any neoplastic process

Any pulmonary process (pneumonia, chronic obstructive pulmonary disease, pulmonary hypertension, pulmonary embolism, etc)

CNS disturbances due to stroke, hemorrhage, or trauma

Metabolic- alcohol withdrawal

85
Q

Syndrome of Inappropriate ADH Secretion (SIADH)

Symptoms?

A
  • Nausea
  • Hyponatraemia ( anorexia, irritability, headache, confusion, weakness)
  • Malaise (feeling of general discomfort)
86
Q

Syndrome of Inappropriate ADH Secretion (SIADH)

Diagnosis and Tests?

A
  • Measure urine and plasma osmolality, both low

- continued Na+ secretion

87
Q

Syndrome of Inappropriate ADH Secretion (SIADH)

Treatment?

A
  • Treat underlying cause
  • Restrict fluids
  • Vasopressin receptor antagonists (‘vaptans’, block the action of ADH)
88
Q

PARATHYROID HORMONE

What is the action of PTH?

A

Increased bone resorption by osteoclasts

Increased intestinal calcium absorption

Actives 1,25-dihydroxyVD (calcitriol) in kidney

Increased calcium reabsorption and phosphate excretion in the kidney

OVERALL INCREASE CALCIUM AND DECREASE PHOSPHATE

89
Q

HYPERPARATHYROIDISM

Causes?

A 
80% = solitary adenoma
20% = parathyroid hyperplasia 
Rare = parathyroid cancer
90
Q

HYPERPARATHYROIDISM

Presentation?

A

hypercalcaemia: weak, tired, depressed, thirsty, renal stones

Bone resorption causes pain, fracture, osteoporosis

Hypertension

91
Q

HYPERPARATHYROIDISM

Investigation?`

A

Bloods:
Primary: ↑PTH, ↑Ca, ↓Phosph
Secondary: ↑PTH, ↓Ca, ↑Phosph
Tertiary: ↑everything (progression of secondary)

Increased 24hr urinary calcium excretion
DEXA bone scan for osteoporosis

92
Q

HYPERPARATHYROIDISM

Treatment?

A

Fluids
surgically treat underlying cause
Bisphosphonates

93
Q

HYPOPARATHYROIDISM

A 
Aetiology:	Autoimmune destruction of PT glands
			Congenital
			Surgical removal (secondary)
			Mg deficiency, VD deficiency

Clinical: Signs and symptoms of hypocalcaemia

Tx: Ca supplement, calcitriol, synthetic PTH

94
Q

HYPERKALAEMIA

Investigations?

A

ECG-
Tall, tented T waves
Small/ no P wave
Wide QRS complex

95
Q

HYPERKALAEMIA

Treatment?

A

Non-urgent-
Polystyrene sulphonate resin= Binds K+ in the gut decreasing uptake

Urgent-
Calcium gluconate= decreases VF risk in the heart
Insulin= drives K+ into the cells

96
Q

HYPOKALAEMIA

Investigations?

A

ECG!
Rhyme- U have no Pot (K+) & no Tea but a Long PR & a long QT.

U waves
No T waves/ inversion
Long PR
Long QT

97
Q

HYPOKALAEMIA

Hypokalaemia is when K+ is <3.5mmol/L, what will this cause?

A

Low K+ in the serum (ECF) causes a water concentration gradient out of the cell (ICF)

Increased leakage from the ICF causing hyperpolarisation of the myocyte membrane decreasing myocyte excitability.

98
Q

HYPOKALAEMIA

Treatment? (easiest answer ever)

A

Mild- oral K+

Severe- IV K+

99
Q

What is calcium levels controlled by?

A

Calcium balance controlled by:
Parathyroid: PTH
Thyroid: Calcitonin

100
Q

What are the functions of PTH and Calcitriol?

A

Parathyroid hormone causes stimulation of kidneys and GI tract to increase absorption of calcium and causes stimulation of osteoclasts to break down bone and release calcium stored there.

Calcitriol (active vitamin D) levels are increased by PTH and cause increased GI and Kidney absorption of Calcium.

101
Q

HYPOCALCAEMIA

Causes?

A 
H- hypoparathyroidism
A- Acute pancreatitis
V- Vitamin D Deficiency 
O- Osteomalacia
C- Chronic Kidney Disease
102
Q

HYPOCALCAEMIA

Clinical Features?

A 
S – spasms 
P -  peripheral paraesthesia 
A - anxious
S - seizures
M – muscle tone increase in SM
O- Orientation impaired
D- Dermatitis
I- Impetigo herpetiformis (severe pustular psoriasis)
C- cataracts
103
Q

HYPOCALCAEMIA

Ix?

A

ECG- long QT interval

104
Q

HYPOCALCAEMIA

Treatment?

A

Mild= Adcal (oral calcium)
Severe= IV Calcium gluconate
In CKD- Alfacalcidol

105
Q

HYPERCALCAEMIA

Causes?

A

90% is due to primary hyperparathyroidism or cancer.

106
Q

HYPERCALCAEMIA

Symptoms?

A

Painful Bones
Renal Stones
Abdo Groans (nausea, constipation, indigestion)
Psychiatric Moans (lethargy, memory loss, depression)

107
Q

HYPERCALCAEMIA

Investigations?

A

Investigations-

1) find cause:
Corrected calcium levels
PTH

2) identify damage:
U&E (Renal damage)
XRay

108
Q

HYPERCALCAEMIA

Treatment?

A

rehydration
Saline (NaCl) (dilute blood of calcium)
Bisphosphonates (pamidronate) (encourage osteoclast apoptosis so bone resorption)

109
Q

What is Hashimoto’s Thyroiditis?

A

goitre due to lymphocytic and plasma cell infiltration

110
Q

When would you do the ACTH stimulation test and briefly describe it?

A

Addison’s- Adrenal Insufficiency

ACTH stimulation test- measure plasma cortisol 30 mins before/after tetracosactide (ACTH)

Addison’s excluded if over 550nmol/L (would mean its responsive to ACTH)

Medicine Year 2 2 (15 decks)

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