Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Core Conditions > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

T1 diabetes definition

A

Metabolic disorder characterised by hyperglycaemia due to absolute insulin deficiency

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

How common is T1 diabetes

A

Accounts for about 5-10% of all patients with diabetes

Most commonly diagnosed in childhood/ puberty

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Who does T1 diabetes affect

A

Mostly young people <20

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Risk factors of T1 Diabetes

A

Geographical region

Weak: genetic predisposition, infectious agents, dietary factors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Symptoms and signs of T1 diabetes

A

Presence of risk factors
Polyuria
Polydipsia - getting up at night to drink
Young age, weight loss, blurred vision, nausea and vomiting, abdominal pain, tachypnoea, lethargy, coma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Differentials of T1 diabetes

A

Monogenic diabetes: maturity onset diabetes of the young
Neonatal diabetes
Latent autoimmune diabetes in adults (LADA)
Type 2 diabetes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Investigations to confirm T1 diabetes ,

A

1st line:
Random plasma glucose: >11mmol/L confirms diagnosis in the presence of symptoms of polyuria, Polydipsia and unexplained weight loss.

Fasting plasma glucose: > 6.9mmol/L

2 hour plasma glucose: >11mmol/L plasma glucose is measured 2 hours after 75g oral glucose load

Plasma or urine ketones: medium or high quantity

Hb1Ac: >48mmol/mol- ref,eats degree of hyperglycaemia over the preceding 3 months

Consider: fasting c-peptide -> low or undetectable
Autoimmune markers -> glutamic acid decarboxylase,
Insulin, is,et cells etc. -> positive

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Management of T1 diabetes

A

1st line: basal bolus insulin e.g. insulin glargine: injected subcutaneously once daily
If pregnant- give insulin isophane human (NPH) subcut twice daily

2nd line: fixed dose insulin e.g. isophane human/ insulin neutral, injected subcut twice daily

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Prognosis of T1 diabetes

A

Dependant on whether it is treated
Untreated can be fatal due to DKA
Poorly controlled T1 diabetes is a risk factors for chronic complications e.g. CKD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Complications of T1 and T2 diabetes

A

Macrovascular - CAD, strokes, PVD

Microvascular - CKD, Retinopathy, Neuropathy

Metabolic- DKA, HHS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

T2 diabetes definition

A

Progressive disorder defined by deficits in insulin secretion and action that leads to abnormal glucose metabolism related metabolic derangements

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

How common is T2 diabetes

A

Global prevalence is 2.8%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Causes of T2 diabetes

A

Combination of insulin resistance/ insensitivity and insulin deficiency
This balance of the two varies between people

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Risk factors for T2 diabetes

A 
Older age 
Overweight/ obese 
Gestational diabetes 
Pre- diabetes 
Family history of T2 diabetes 
African, Hispanic, south Asian or Native American ancestry 
Hypertension 
Dyslipidaemia 
CVD 
Physical inactivity
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Symptoms of T2 diabetes

A

Presence of risk factors
Asymptomatic
Candida infections: most commonly vaginal, penile or in skin folds
Skin infections e.g. cellulitis or abscesses
UTIs e.g? Cystitis or pyelonephritis
Fatigue
Blurred vision

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Signs/ examination of T2 diabetes

A

Often no physical signs, although lymphadenopathy signs of a pleural effusion, lobar collapse or unresolved pneumonia may be present

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Differential diagnosis of T2 diabetes

A 
Pre- diabetes 
Diabetes mellitus 
LADA
Monogenic diabetes 
Ketosis prone diabetes 
Diabetes gestational
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

T2 diabetes investigations

A

1st line

  • Hb1Ac: confirm with a repeat Hb1Ac or another diagnostic test, also used to monitor glycemic control, usually every 3 months
  • fasting plasma glucose: order after a minimum 8 hour fast
  • 2 hour post load glucose after 75g glucose: more costly and inconvenient than fasting plasma glucose or Hb1Ac
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Management of T1 diabetes

A

1st line - lifestyle, diet changes
Acute:
- hyperglycaemia: 1st line - basal bolus insulin + cardiovascular risk reduction / lifestyle measures
- HbA1c above goal at diagnosis: 1st line - metformin + cardiovascular risk reduction/ lifestyle measures
- pregnant: 1st line: diet + basal bolus insulin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Prognosis of T2 diabetes

A

Increases the likelihood of major cardiovascular events and death but varies between pts

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Definition of primary hypothyroidism

A

A clinical state resulting from underproduction of the thyroid hormones T3 and T4

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

How common is primary hypothyroidism

A

More common in the developing world due to iodine deficiency is a major cause of hypothyroidism

Autoimmune thyroiditis (Hashimoto’s disease) is the most common cause of primary hypothyroidism —> lymphocytic infiltration and destruction of thyroid tissue with secondary antibodies to thyroid peroxidase, thyroglobulin, and other thyroid antigens

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Prevalence of primary hypothyroidism

A

Higher in woman and increased with age

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Causes of primary hypothyroidism

A
  • T4 is the main hormone produced by the thyroid gland
  • It is converted to T3 in target tissues
  • T3 mediates the amin actions of thyroid hormone, which includes stimulation of cellular oxygen consumption and energy generation, by binding to nuclear receptors and modulating gene expression
  • Through a negative feedback mechanism, failure of the thyroid to produce its hormones stimulates the pituitary to increase production of TSH
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Risk factors for primary hypothyroidism

A 
Iodine deficiency 
Female 
Middle age 
Fx of autoimmune thyroiditis 
Autoimmune disorders 
Graves’ disease
Radiotherapy 
Aminodarone use 
Lithium use 
MS
Primary pulmonary hypertension
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Symptoms/ signs of primary hypothyroidism

A 
Presence of risk factors 
Weakness
Lethargy 
Cold sensitivity
Constipation 
Weight gain 
Depression 
Menstrual irregularity 
Myalgia 
Dry or coarse skin 
Eyelid and facial oedema 
Thick tongue 
Coarse hair 
Bradycardia 
Deep voice 
Diastolic hypertension 
Goitre 
Delayed relaxation of tendon reflexes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Differential diagnosis of primary hypothyroidism

A

Central or secondary hypothyroidism
Depression
Alzheimer’s dementia
Anaemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Investigations for primary hypothyroidism

A

1st line - serum TSH: normal is 0.5 to 5 - levels are elevated

Consider
Free serum R4, serum cholesterol, FBC, fasting blood glucose, serum CK, serum sodium, anti thyroid peroxide antibodies

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Management of primary hypothyroidism

A

1st line: levothyroxine e.g. 1.6micrograms/kg/day orally

Adjust dose in increments of 12.5or 25 micrograms to normalise TSH, start on full replacement dose

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Prognosis of primary hypothyroidism

A

Generally excellent with full recovery upon adequate replacement of thyroid hormones

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Complications of primary hypothyroidism

A

Angina, complications in pregnancy, AF, osteoporosis, myxoedema coma, resistant hypothyroidism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Secondary/ tertiary hypothyroidism definition

A
  • It results from a deficiency of thyroid hormones, which results in a generalised slowing of metabolic processes
  • Results of anterior pituitary hypofunction or thalamic hypofunction
  • It is characterised by decreased thyroid-stimulating hormone secretion in turn causing decreased thyroid hormone synthesis and release
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

How common is secondary/ tertiary hypothyroidism

A

Rare, only accounts for less than 1% of hypothyroid cases

Pituitary adenomas are the most common cause of secondary hypothyroidism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Causes of secondary/ tertiary hypothyroidism

A

CENTRAL HYPOTHYROIDISM: caused by a deficiency of TSH because of hypothalamic and/or pituitary dysfunction, can occur as a result of deficient stimulation of the anterior pituitary by TRH, deficient synthesis and secretion of TSH by the anterior, or secretuib of biologically ineffective TSH as in some genetic diseases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

T3 and T4 mechanism

A
  • TSH is glycoprotein that is produced and secrered by the anterior pituitary
  • TASH stimulates thyroidal biosynthesis and secretion of thyroid hromones T3 and T4
  • TSH secretion is regulated by the TRH as well as by thyroid hormones
  • TRH is a tripeptide released into the hypothalamic-pituitary portal vessels and transported to the anterior piruitarym where it promotes synthesis and secretion of TSH
  • T3 and T4 act on the anterior pituitary in a ngetaive feedback loop, inhibiting the synthesis and secretion of TSH
  • T3 and T4 also act at the hypothalamic level to inhibit the secretion of TRH
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Risk factors for secondary/ tertiary hypothyroidism

A

Multiple endocrine neoplasia (MEN) type 1
Head and neck irradiation
Traumatic brain injury (TBI)
Weak: sarcoidosis, histiocytosis, haemochromatosis, pregnancy, Fx of central hypothyroidism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Symptoms / signs of secondary/ tertiary hypothyroidism

A 
Presence of risk factors 
Weakness
Fatigue 
Cold intolerance 
Decrease memory 
Muscle cramps 
Weight gain 
Depression 
Dry coarse skin 
Bradycardia 
Reduced body and scalp hair
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Differential diagnosis of secondary/ tertiary hypothyroidism

A 
Primary hypothyroidism 
Non-thyroid also illness 
Iodine deficiency 
Chronic fatigue syndrome 
De Quervain’s thyroiditis 
Depression 
Fibromyalgia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Investigations for secondary/ tertiary hypothyroidism

A

1st line
TFTs
- serum free thyroxine (T4): low
- serum TSH: inappropriately low to normal TSH in the setting of low serum free T4

Consider: MRI of brain, Ct head, prolactin (PRL), 9a.m, serum cortisol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Management of secondary/ tertiary hypothyroidism

A

1st line - levothyroxine

If adrenal hormone deficiency -> add corticosteroids e.g. hydrocortisone orally

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Prognosis of secondary/ tertiary hypothyroidism

A

Risk for recurrent pneumothoraces

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Complications of secondary/ tertiary hypothyroidism

A

Re-expansion pulmonary oedema

Talc plaurodesis- related ARDS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Hyperthyroidism definition

A

Also known as thyrotoxicosis

The clinical effect of excess thyroid hormone, usually from gland hyperfunction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Causes of hyperthyroidism

A

Graves’ disease

  • The most common cause
  • Thyroid stimulating antibodies (IgG) bind to TSH receptors and stimulate the thyroid
  • Thyroid gland hypertrophies and becomes diffusely enlarged
  • The autoimmune process leads to mucopolysaccharide infiltration of the extra-ocular muscles and may lead to exophthalmos

TSH secreting pituitary adenoma
- T3 T4 secreting site in the thyroid (nodule in a multinodular goitre, adenoma or (very rarely) carcinoma

Thyroiditis
- Large amounts of preformed hormones are released after the destruction of follicles, with transient thyroid toxicosis

Exogenous intake of thyroid hormones (factitious thyrotoxicosis)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Risk factors for hyperthyroidism

A

Female
Tobacco use
Weak: high iodine intake, lithium therapy, biological agent and cytokine therapies, radiation, radioiodine therapy for benign modular goitre, stress

46
Q

Symptoms of hyperthyroidism

A 
Diarrhoea 
Weight loss 
Increased appetite 
Sweats 
Heat intolerance 
Palpitations 
Tremor 
Irritability
Labels emotions 
Oligomenorrhoea +/- infertility
47
Q

Signs of hyperthyroidism

A 
Bradycardia
Irregular pulse 
Warm moist skin 
Fine tremor 
Palmar erythema 
Thin hair 
Lid lag 
Lid retraction 
Exophthalmos 
May be a goitre, thyroid nodules or bruit depending on the cause
48
Q

Differential diagnosis of hyperthyroidism

A

Pleural thickening
Pulmonary collapse and consolidation
Elevated hemidiaphragm
Pleural tumours/ extrapleural fat

49
Q

Investigations for hyperthyroidism

A

1st line: TFTs - TSH suppressed and T4 & T3 increased
2nd line: autoantibodies - most commonly seen in Graves’ disease e.g. anti micro Somali antibodies against thyroid peroxidase, anti- thyroglobulin antibodies, TSH receptor antibodies
3rd line: thyroid USS and thyroid uptake scans when cause is unknown
Consider: CRP and ESR (raised)

50
Q

Management for hyperthyroidism

A

Thyroid storm: high dose antithyroid drugs, corticosteroids, beta blockers and iodine solution with supportive care

Symptomatic but not pregnant: prolonged antithyroid drug therapy (carbimazole, orally) OR radioactive iodine + hydrocortisone OR surgery ( patients need to be returned to euthyroid state before surgery)

Pregnant: propylthiouracil (causes liver failure so only give 1st line in pregnancy and thyroid storm)

51
Q

Prognosis for hyperthyroidism

A

• Relaspes and remittances, spontenous remission is seen in <10%

52
Q

Complications of hyperthyroidism

A

• Heart failure, angina, AF, osteoporosis, ophthalopathy, gynaecomastia

53
Q

Thyroid lump (goitre and thyroid nodule) definition

A

Goitre - enlargement of the thyroid gland
Thyroid nodule - lump in an otherwise normal thyroid gland
Goitres may consist of many nodules (multi-modular goitre) and solitary nodules may exist within a goitre
Nodules may be cystic, colloid, hyperplastic, adenomatous or cancerous

54
Q

How common is Thyroid lump (goitre and thyroid nodule)

A

24.8 cases per 100,000 adults

Affects mainly adults

55
Q

What causes Thyroid lump (goitre and thyroid nodule)

A

Can be physiological or pathological in origin
Diffuse:
- physiological (puberty or pregnancy)
- autoimmune (graves or hashimotos)
- acute viral thyroiditis (de Quervains thyroiditis)
- Iodine deficiency (endemic goitre) -> most common, dyshormonogenesis
- goitrogens e.g. sulphonylureas

Nodular:

  • multinodular goitre
  • solitary nodule
  • fibrotic (Riedell’s thyroiditis)
  • Cysts

Tumours - adenoma, carcinoma, lymphoma

Miscellaneous - sarcoidosis, TB

56
Q

Characteristics of thyroid cancer

A
  • Papillary (70%): young people, spreads locally, good prognosis
  • Follicular (20%): middle age, spreads to the lung/bone. Prognosis usually good
  • Medullary cell (5%): often familial (MEN1), spreads locally and via mets. Poor prognosis
    Anaplastic <5%, aggressive, spreads locally, very poor prognosis
57
Q

Symptoms of Thyroid lump (goitre and thyroid nodule)

A

Often asymptomatic and noticed by family members or seen in the mirror
Sometimes can cause pain and rarely present with features of compression of the trachea
Ask about previous radiation

58
Q

Signs of Thyroid lump (goitre and thyroid nodule)

A

• Ask the patient patient to drink some water and note the thyroid moves as the pt swallows
• Note enlargement or asymmetry
• Stand behind a seated pt and use the second and third fingers of both hands to eamine the gland as they swallow again
• Note lumps, asymmetry, size and tenderness
- check for regional lymphadenopathy

Red flags
Stridor associated with a thyroid mass
Unexplained hoarseness or voice changes associated with goitre
Painless thyroid mass enlarging rapidly over a period of a few weeks
Palpable cervical lymphadenopathy

59
Q

Differential diagnosis of Thyroid lump (goitre and thyroid nodule)

A

Non- toxic (simple) goitre - non functioning nodules, TFTs are normal
Toxic multi nodular goitre - functioning nodules, abnormal TFTs
Retrosternal goitre (usually multi nodular)
Hyperplastic nodule. ( single nodule or part of a multinodular goitre)
Colloid nodule
Thyroid adenoma
Thyroid cyst
Thyroid carcinoma
Graves - diffusely overactive thyroid gland
Hashimoto’s thyroiditis- autoimmune destruction of the gland may cause diffuse enlargement

60
Q

Investigations for Thyroid lump (goitre and thyroid nodule)

A

1st line: TFTs • 1st LINE: TFTs – those with abnormal TFTs and no suspicious features should be referred to an endocrinologist
• 2ND LINE: USS – highly sensitive for detection and characterisation of thyroid nodules
• 3RD LINE: FNA – fine needle aspiration  gives tissue for cytology

61
Q

Management of Thyroid lump (goitre and thyroid nodule)

A
  • Usually not required  apart from introducing euthyroidism if necessary
  • Surgical intervention is required for the cosmetic effects of large goitres, pressure effects on the trachea or oesophagus, or confirmed or possible malignancy
62
Q

Prognosis and complications of Thyroid lump (goitre and thyroid nodule)

A

Dependant on cause

63
Q

Cushing’s syndrome definition

A

Clinical manifestation of pathological hypercortisolism from any cause

64
Q

How common is Cushing’s syndrome

A

Occurs 4 times more commonly in women than men

Relatively uncommon in the general population

65
Q

Causes of Cushing’s syndrome

A

ATH secreting pituitary tumours by autonomous adrenal cortisol overproduction and, rarely by ectopic ACTH secreting tumours

66
Q

Risk factors for Cushing’s syndrome

A 
Exogenous corticosteroid use 
Pituitary adenoma 
Adrenal adenoma 
Adrenal carcinoma 
WEAK: neuroendocrine tumours, thoracic or bronchogenic carcinoma
67
Q

Symptoms / signs for Cushing’s syndrome

A

Presence of risk factors
Facial plethora
Moon face
Pathological fractures ( especially vertebrae and ribs)

Supraclavicular fullness 
Violaceous striae 
Absence of pregnancy 
Menstrual irregularities 
Absence of malnutrition, alcoholism and of physiological stress 
Linear growth deceleration in children 
Decreased libido 
Acne 
Facial rounding
68
Q

Differential diagnosis of Cushing’s syndrome

A

Obesity

Metabolic syndrome

69
Q

Investigations for Cushing’s syndrome

A
  • urine pregnancy test
  • serum glucose : elevated
  • late night salivary cortisol: elevated
  • 1mg overnight dexamethasone suppression test: morning cortisol > 50 nanomol/L
  • 24 hour 2mg (low dose) dexamethasone suppression test: morning cortisol >50nanomol/L
70
Q

Management for Cushing’s syndrome

A

1st line: transsphenoidal pituitary adenomectomy - removes the causative pituitary adenoma
2nd line: repeat transsphenoidal pituitary adenomectomy
3rd line: pituitary radiotherapy
4th line: bilateral adrenalectomy

71
Q

Prognosis for Cushing’s syndrome

A

Without treatment, hypercortisolism persist and in many patients worsens
Untreated disease carries a dismal survival rate at 50% at 5 years

72
Q

Complications for Cushing’s syndrome

A 
Adrenal insufficiency 
CVD
Hypertension
Osteoporosis 
Diabetes mellitus
73
Q

Definition for Addison’s Disease (Primary Adrenal Insufficiency)

A

Disorder that affects the adrenal glands causing decreased production of adrenocrotical hormones (cortisol, aldosterone, and dehydroepiandrosterone)

Characterised by hyponatreamia, hypercalcaemia, and hyperkalaemia

74
Q

How common is Addison’s Disease (Primary Adrenal Insufficiency)

A

5-10% of all patients with diabetes
Most commonly diagnosed under 20 years of age
Affects mostly young people <20 years

75
Q

What causes Addison’s Disease (Primary Adrenal Insufficiency)

A

Decreased production of adrenalcortical hormones as a result of either destruction of the 3 layers of the adrenal cortex (the glomerulosa, fasciculate, and reticularis or destruction of hormone synthesis

Infiltrating diseases such as TB or metastasis can also cause destruction of the adrenal medulla

Primary: destruction or dysfunction of the adrenal gland
Secondary: inadequate pituitary adrenocroticotophic hormone (ACTH) and subsequent cortisol production
Tertiary: inadequate hypothalamic corticotropin- releasing hormone and subsequent ACTH release

76
Q

Risk factors for Addison’s Disease (Primary Adrenal Insufficiency)

A 
Female 
Adrenocortical abs 
Adrenal haemorrhage 
TB 
Non-TB bacterial infection
77
Q

Symptoms for Addison’s Disease (Primary Adrenal Insufficiency)

A 
Presence of risk factors 
Fatigue 
Anorexia 
Weight loss
Hyperpigmentation - present in mucosa and sun-exposed areas, more pronounced in cloak are creases, areas of friction and scars
78
Q

Signs for Addison’s Disease (Primary Adrenal Insufficiency)

A

Hyponatreamia
Hypercalcaemia
Hyperkalaemia

79
Q

Differential diagnosis for Addison’s Disease (Primary Adrenal Insufficiency)

A 
Adrenal suppression due to corticosteroid therapy 
Haemochromatosis 
Hyperthyroidism 
Occult malignancy 
Anorexia nervosa
80
Q

Investigations for Addison’s Disease (Primary Adrenal Insufficiency)

A

1st line:
- SERUM ELECTROLYTES: not routinely required for diagnosis but findings are typical -> low sodium, elevated potassium, elevated calcium
- BLOOD UREA: may be elevated
- FBC: anaemia, eosinophilia
- MORNING SERUM CORTISOL: blood should be drawn between 8am and 9am when cortisol levels leak -> of <83 nanomols/ L
- ACTH STIMULATION TEST: should be ordered when morning serum cortisol does not confirm or exclude adrenal insufficiency -> serum cortisol <497 nanomols/L
- ADRENAL CRISIS- GLUCOCORTICOID AND SUPPORTIVE THERAPY: hydrocortisone sodium succinct IV
- ONGOING- GLUCOCORTICOID PLUS MINERALCORTICOID: cortisone or hydrocortisone or prednisone + fludrocortisone
With use of orenusolone it avoids the peaks and troughs which may occur with hydrocortisone

81
Q

Prognosis for Addison’s Disease (Primary Adrenal Insufficiency)

A

Patients should receive treatments for life

82
Q

Complications of Addison’s Disease (Primary Adrenal Insufficiency)

A

Secondary Cushing’s syndrome
Osteopenia/ osteoporosis
Treatment related hypertension

83
Q

Parathyroid adenoma definition

A
  • Benign tumour on one your parathyroid glands
  • These are 4 very small glans located near or at the back of your thyroid gland
  • Generally causes hyperparathyroidism
84
Q

How common is parathyroid adenoma

A

1% incidence rate

85
Q

Who does parathyroid adenoma affect

A

Prevalence is highest among post menopa women, with 1:500 possible being affected

86
Q

Causes of parathyroid adenoma

A

Associated with the overexpression of cyclic D1 gene and MEN syndromes

87
Q

Risk factors for parathyroid adenoma

A

MEN gene

Cyclin D1 gene

88
Q

Symptoms of parathyroid adenoma

A
  • Bone fractures
  • Urinary calculi
  • Mental changes: depression, lethargy or confusion
  • Nausea
  • Vomiting
  • Pain in your muscles or abdomen
89
Q

Signs of parathyroid adenoma

A
  • Polyuria, polydipsia and nocturia are also common symptoms
  • More than half of patients report no specific symptoms and accept it as getting older
  • Hypercalcaemic crisis can occur in patients with PHPT exposed to severe dehydration (diarrhoea, vomiting)
  • In severe cases, patients can present in a coma
90
Q

Differential diagnosis of parathyroid adenoma

A

Monogenic diabetes: maturity onset diabetes of the young
Neonatal diabetes
Latent autoimmune diabetes in adults (LADA)
Type 2 diabetes

91
Q

Investigations for parathyroid adenoma

A

1st line

  • SERUM CALCIUM: increased corrected SC is highly suggestive if unexplained but not diagnostic
  • SERUM PTH: increased PTH in the presence of hypercalcaemia confirms the diagnosis (e.g. bone mets. (Breast renal, thyroid carcinoma) have a low PTH concs )
  • USS: high resolution may identify tumours
  • SESTAMIBI (Radioisotope): scanning used to localise adenomas and is accurate in 50% of cases
92
Q

Management for parathyroid adenomas

A

• 1st LINE:

  • PARATHYROIDECTOMY: if tumour location is known
  • IF UNKNOWN: bilateral neck exploration and removing the enlarged ones has been standard tx
93
Q

Prognosis and complications for parathyroid adenomas

A

Surgery cures 95% of patients

Complications include paralysis of the voice box, permanent low calcium levels in the blood

94
Q

Primary hyperparathyroidism definition

A
  • PHPT is an endocrine disorder in which autonomous overproduction of PTH results in derangement of calcium metabolism
  • In approx. 80% of cases, over-production of PTH is due to a single parathyroid adenoma
95
Q

How common is Primary hyperparathyroidism

A

• 1 in 500 women and 1 in 2000 men aged over 40

Affects post menopausal women

96
Q

What causes Primary hyperparathyroidism

A
  • Low serum calcium ordinarily stimulates PTH secretion, whereas high calcium levels suppress PTH secretion
  • In PHPT, PTH secretion is not suppressed (as would typically be expected) by high calcium levels
  • Excessive PTH leads to over-stimulation of bone resorption, with cortical bone affected more than cancellous bone
  • PTH also stimulates the kidneys to reabsorb calcium and to convert 25-hydroxyvitamin D3 to its more active form of 1,25-dihydroxyvitamin D3
  • This active vit d is responsible for GI absorption of calcium
  • Over-stimulation of PTH receptors, specifically type-2 PTH receptors is thought to play a role in the subjective neurocognitive and affective symptoms
  • Hypercalcuria may also lead to nephrolithiasis
97
Q

Risk factors for Primary hyperparathyroidism

A 
Female 
Over 59 
Treatment 
MEN 1,2A or 4 
Hyperparathyroidism- jaw tumour syndrome 
Hx of head and neck irradiation
98
Q

Symptoms for primary hyperparathyroidism

A
  • Hx of osteoporosis or osteopenia
  • Fx of PHPT
  • Nephrolithiasis
  • Bone pain
  • Fatigue, anxiety, depression, memory loss
  • Bones: Aches/pains localised in larger joints
  • Stones: Calcium based renal stones
  • Moans: Psychological/psychiatric symptoms (lethargy, depressed mood)
  • Groans: Non-specific GI symptoms (abdominal pain, constipation)
99
Q

DDx of primary hyperparathyroidism

A
  • Familial hypocalciuric hypercalaemia
  • Humoral hypercalcaemia of malignancy
  • Multiple myeloma
  • Milk-alkali syndrome
  • Sarcoidosis
  • Hypervitaminosis D
100
Q

Investigations for primary hyperparathyroidism

A

1st line:

  • SERUM CALCIUM: from high-normal to raised
  • SERUM INTACT PTH WITH IMMUNORADIOMETRIC OR IMMUNOCHEMICAL ASSAY: from high-normal to elevated
  • PARATHYROIDECTOMY: if asymptomatic with surgical indications or symptomatic  inc. over 50, inability to ensure appropriate follow-up, serum calcium >0.25 abover normal reage, creatinine clearance <60, T-score<2.5 at lumbar spine, total hip, femoral neck or distal third of radius
  • If asymptomatic with no surgical indications: monitor (1st), parathyroidectomy when indicated (2nd line)
101
Q

Prognosis for primary hyperparathyroidism

A

• Parathyroidectomy has a cure rate of over 95%

102
Q

Complications for primary hyperparathyroidism

A

Osteoporosis
Bone fractures
Nephrolithiasis
Pneumothorax and/ or hypocalcaemia following surgery, neck haematoma following surgery

103
Q

Secondary hyperparathyroidism definition

A

Manifestation of abnormalities of calcium, phosphorus, PTH or vit D metabolism, abnormalities in bone turnover, mineralisation, volume, linear growth or strength, vascular or other soft tissue calcification

104
Q

How common is secondary hyperparathyroidism

A

• Most commonly associated with CKD or vit d deficiency (which may arise from malabsorption syndromes or chronic lack of exposure to sunlight)
Commonly affects Caucasians

105
Q

Causes of secondary hyperparathyroidism

A
  • Any disorder that results in hypocalcaemia will elevated PTH levels and can serve as a cause of secondary hyperparathyroidism
  • 3 principal aetiologies that may lead to this situation are CKD, malabsorption syndromes or chronic inadequate exposure to sunglight
  • CKD: there is loss of 1-alpha-hydroxylase in the kidney, which results in a decreased conversion of 25-hydroxyvitamin D to the active 1,25-dihydroxyvitamin D, this then causes hyperphosphataemia and hypocalcaemia with a consequent rise in PTH
  • in conditions such as Crohn’s disease, coeliac disease, chronic pancreatitis or Whipple’s disease or following gastric bypass surgery there is fat malabsorption that contributes to reduced absorption of vit d and dietary calcium ultimately leading to hypocalcaemia and an increase in PTH
  • for most people, exposure to sunlight enables them to synthesis 90-95% of the vit d they require
106
Q

Risk factors for secondary hyperparathyroidism

A

Ageing
Chronic renal failure
Bit D deficiency: inadequate sunlight exposure or malabsorption
Nutritional deficiency ( especially absence of dairy products and fish)

107
Q

Symptoms of secondary hyperparathyroidism

A

Presence of risk factors
Features of chronic renal failure
Features of underlying malabsorption syndrome
Muscle cramps and bone pain

108
Q

Signs of secondary hyperparathyroidism

A
  • Chvostek’s sign: tapping on the face ant to the ear and seeing a twitching of muscles around the mouth
  • Trousseau’s sign: inflating blood-pressure cuff above diastolic for about 3 minutes causes muscular flexion of the wrist, hyperextension of the fingers and flexion of the thumb
109
Q

Differential for secondary hyperparathyroidism

A

Primary hyperparathyroidism

110
Q

Investigations for secondary hyperparathyroidism

A

• 1st LINE:

  • SERUM CALCIUM: first line for diagnosis <2.1 mmol/L
  • SERUM INTACT PTH: first line and definitive test  >88 nanograms/L
  • SERUM CREATININE
  • SERUM UREA NITROGEN
111
Q

Management for secondary hyperparathyroidism

A

• 1st LINE:

  • LACK OF SUNLIGHT: UV radiation exposure and vit d/calcium supplementation
  • MALABSOPRTION-RELATED: optimised management of underlying disease
112
Q

Prognosis and complications for secondary hyperparathyroidism

A

Dependant on cause

Complications include osteodystrophy, osteoporosis, uraemia

Core Conditions (13 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions