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Phase 2A extra > Extra Endocrinology > Flashcards

Extra Endocrinology Flashcards

1
Q

DIABETES MELLITUS

A

/////

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2
Q

What are normal blood glucose levels?

A

3.5-8.0mmol/L

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3
Q

Why is glucose important for the brain?

A
  • The brain is a major consumer of glucose
  • The brain cannot use free fatty acids to be converted to ketones which then can be converted to Acetyl-CoA and used in Kreb’s cycle for energy production
  • This is because FREE FATTY ACIDS CANNOT PASS THE BLOOD BRAIN BARRIER
  • Glucose uptake by the brain is OBLIGATORY and is not dependant on insulin
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4
Q

Describe the biphasic release of insulin

A
  • B cells can sense the rising of glucose and want to metabolism it by releasing insulin
  • The first phase is the RAPID RELEASE of STORED INSULIN
  • If the glucose levels remain high then the second phase is initiated, this takes longer due to the fact that more insulin needs to be SYNTHESISED.
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5
Q

Describe insulin the molecule, how is it made?

A
  • Proinsulin made up of alpha and beta chains held together by C peptide.
  • The proinsulin is cleaved from the C peptide»insulin and packaged into vesicles.
  • Synthetic insulin does not have C peptide so the presence of C peptide in the blood determines whether the insulin is natural or not.
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6
Q

GLUT 1 receptors

A

Enables basal non-insulin stimulated glucose uptake into many cells.

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7
Q

GLUT 2 receptors

A

Found in the beta cells of the pancreas and renal tubules and hepatocytes.

  • They transport the glucose into the beta-cell, this allows the cells to sense glucose levels.
  • low-affinity receptor that only allows glucose in when there is a high conc of glucose
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8
Q

GLUT 3 receptors

A

Enables non-insulin mediated glucose uptake into brian neurones and placenta.

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9
Q

GLUT 4 receptors

A

Mediates much of the peripheral action of insulin. Channel through which glucose is taken up into muscle and adipose tissue cells following stimulation of the insulin receptor by insulin binding to it.

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10
Q

What conditions might diabetes be secondary to?

A
  • Pancreatic pathology
  • Endocrine diseases
  • Drug-induced
  • MODY
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11
Q

Maturity onset diabetes of youth

A
  • Autosomal dominant form of type 2 diabetes
  • Gene defect altering the beta-cell function
  • Tends to present <25 yrs with a positive family history
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12
Q

Pathophysiology of Type 1 Diabetes

A
  • Result of autoimmune destruction by autoantibodies of the pancreatic beta cells in the Islets of Langerhans
  • This causes insulin deficiency and thus a continued breakdown of liver glycogen»> increase in glucose and ketones.
  • This leads to glycosuria and ketonuria as more glucose is in the blood.
  • In skeletal muscle and fat there is impaired glucose clearance, when the blood glucose reaches 10mmol/L the body can no longer absorb glucose so you become thirsty and get polyuria (body’s attempt to remove glucose).
  • Eventual complete Beta-cell destruction results in the absence of serum C-peptide.
  • Risk of diabetic ketoacidosis
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13
Q

Describe the mechanism of action of ORLISTAT

A

Given in obese patients as it is an intestinal lipase inhibitor and reduces the absorption of fat from the diet hence promotes weight loss

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14
Q

Describe the effects of biguanides e.g. METFORMIN

A

1) Reduces the rate of gluconeogenesis in the liver
2) Increases cells sensitivity to insulin
3) Helps with weight issues
4) Reduces CVS risk in diabetes

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15
Q

State 4 S/E of METFORMIN

A

1) Anorexia
2) Diarrhoea
3) Nausea
4) Abdominal pain

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16
Q

When is METFORMIN contraindicated?

A

In heart failure, liver disease or renal disease, it can induce lactic acidosis.

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17
Q

Describe the mechanism of action of sulfonylurea e.g. ORAL GLICAZIDE

A

Promotes insulin secretion by binding to beta-cell receptors, therefore ineffective in patients without a functional beta-cell mass.

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18
Q

Describe the negative/ contraindications of ORAL GLICAZIDE

A

1) Avoided in pregnancy
2) Effect wears off as bet-cell mass declines
3) Does not prevent the gradual failure of insulin secretion
4) S/E: hypoglycaemia, weight gain
5) People with renal impairment should use sulfonylurea’s primarily excreted by the liver

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19
Q 
What class of drugs are ORAL NATEGLINIDE? 
How do they work?
A

Sulfonylurea receptor binders that increase beta-cell insulin release, taken 1/2 hour before a meal.

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20
Q 
What class of drugs are SC EXENATIDE? 
How do they work?
A

Glucagon-like peptide analogues, such as incretins which mimic the effect of two peptide hormones GIP, GLP-1, that are released from the pancreas and promote insulin release after an oral glucose load.

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21
Q

Name the main 3 types of insulin

A

1) Short-acting soluble insulin
2) Short-acting insulin analogues
3) Long-acting insulins

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22
Q

Describe the pathophysiology of DKA

A

Ketoacidosis is a state of uncontrolled catabolism associated with insulin deficiency.

1) In the absence of insulin peripheral lipolysis occurs leading to an increase in circulating free fatty acids which are then broken down to acetyl-coenzyme A within the liver cells and this, in turn, is converted to ketone bodies within the mitochondria.
2) Ketone bodies are acidic pH 3.5 therefore the pH of the blood decreases and produces a metabolic acidosis.
3) This impairs Hb ability to bind to O2, compensation for this leads to hyperventilation.
4) Dehydration leads to impaired renal excretion of H+ ions and ketones»> aggravating the acidosis.
5) pH falls below 7, the pH dependant enzyme system starts to fail, stress hormones also accelerate this process.

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23
Q

Describe the pain associated with diabetic neuropathy.

A
  • Allodynia (triggered by stimuli that usually doesn’t cause pain).
  • Paraesthesia (pins and needles type)
  • Burning and pain worse at night
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24
Q

What is hypoglycaemia defined as?

A

When the plasma glucose falls <3mmol/L

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25
Q

What is the cause commonly of hypoglycaemia in diabetics?

A

Due to insulin or sulphonylurea treatment

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26
Q

What are the causes of hypoglycaemia in non-diabetics?

EXPLAIN

A

EX- exogenous drugs (insulin, alcohol with no food)
P-Pituitary insufficiency
L- Liver failure
Addison’s disease
I- Islet cell tumour (insulinoma) and immune hypoglycaemia
N- Non-pancreatic neoplasm e.g. fibrosarcomas and haemangiopericytomas

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27
Q

Name 5 risk factors of hypoglycaemia

A
  • Female sex
  • Middle age
  • Long duration of diabetes
  • Insulinoma
  • Exogenous insulin
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28
Q

Name the Autonomic presentations of hypoglycaemia

A
  • Diaphoresis (Sweating)
  • Anxiety
  • Hunger
  • Tremor
  • Palpitations
  • Dizziness
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29
Q

Name the Neuroglycopenic presentations of hypoglycaemia

A
  • Confusion
  • Drowsiness
  • Visual trouble
  • Seizures
  • Coma
  • Nausea
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30
Q

Describe the first line diagnostics for hypoglycaemia

A
  • Fingerprick blood during the attack and sent to a lab
  • Take drug history and LFT to exclude liver failure
  • Bloods: glucose, insulin, C-peptide, plasma ketones
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31
Q

Treatment for Hypoglycaemia

A

1) Oral sugar and long-acting starch
2) If cannot swallow give iv 50% GLUCOSE
3) If no IV access give IM GLUCAGON
4) In diabetics re-educate them on insulin use and safety.

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32
Q

THYROID DISORDERS

A

//////

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33
Q

Describe the basic anatomy of the thyroid gland

  • location
  • blood supply
  • innervation
A
  • Located in the anterior neck between C5-T1 vertebrae
  • Divided into two lobes connected by the isthmus
  • Straddles the trachea
  • Blood supply:
    - Superior thyroid artery – arises as to the first
    branch of the external carotid artery.
    - Inferior thyroid artery – arises from the
    thyrocervical trunk (a branch of the subclavian
    artery).
    - In 10% of people extra artery thyroid ima artery
  • Innervation: The thyroid gland is innervated by branches derived from the sympathetic trunk.
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34
Q

Describe the pathogenesis of Graves’ Disease

A
  • Serum IgG antibodies known as TSH receptor stimulating antibodies bind to TSH receptors in the thyroid.
  • Therefore stimulating thyroid hormone production.
  • Results in excess secretion of the thyroid hormones and hyperplasia of thyroid follicular cells
  • Leads to a diffuse goitre
  • Similar autoantigen can also result in retro-orbital inflammation- graves ophthalmology
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35
Q

What is diplopia?

A

Double vision

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36
Q

What is pretibial myxedema?

A

Raised, purple-red symmetrical skin lesions over the anterolateral aspects of the shin.

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37
Q

What is thyroid acropathy?

A

Clubbing, swollen fingers and periosteal bone formation

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38
Q

THYROID CANCER

A

/////

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39
Q

Pathophysiology of thyroid cancer

A
  • Thyroglobulin secreted by 90% which can be used as a tumour marker after thyroid ablation
  • Derived from thyroid epithelium
  • Maybe undifferentiated/ differentiated
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40
Q

HYPOTHYROIDISM

A

/////

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41
Q

Name 4 drugs that can cause hypothyroidism.

A

1) Carbimazole
2) Lithium
3) Amiodarone
4) Interferon

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42
Q

CUSHING’S SYNDROME/DISEASE

A

/////

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43
Q

What are the functions of cortisol

A

1) Increased carbohydrate and protein catabolism
2) Increased deposition of fat and glycogen
3) Na+ retention
4) Increased renal K+ loss
5) Diminished host response to infection

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44
Q

In what pattern is cortisol released?

A

CRH and hence cortisol are released according the circadian rhythm and in stress
Highest levels in the morning 7/9am and lowest at midnight

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45
Q

Name 2 ACTH independent causes of Cushing’s disease

A

1) Adrenal adenoma
- tumour of the adrenal gland that releases cortisol
2) Iatrogenic
e. g. prednisolone

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46
Q

ACROMEGALY

A

///////

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47
Q

Which two hypothalamus hormones are the growth hormone controlled by?

A
  • Growth hormone-releasing hormone (STIMULATES)

- Somatostatin (INHIBITS)

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48
Q

What two other factors can inhibit/stimulate the release of GH?

A
  • High glucose levels can inhibit GH

- Ghrelin, which is synthesised in the stomach also stimulates GH secretion.

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49
Q

Describe two ways in which GH exerts its actions

A

1) Indirectly through the induction of insulin-like growth factor (IGF-1), which is synthesised in the liver and other tissues.
2) Directly on tissues such as liver, muscle, bone or fat to induce metabolic changes

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50
Q

What is growth hormone?

A
  • Somatotropin
  • Peptide hormone
  • Synthesised, stored and secreted by somatotropic cells within the lateral wings of the anterior pituitary gland.
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51
Q

Name 4 functions of growth hormone

A

1) Stimulates growth and protein synthesis
2) Stimulates glucogenesis and inhibits insulin resulting in an increase in glucose. It is a stress hormone
3) Works on adipose tissue to break down fat
4) Stimulates the production of IGF-1 which acts on the skeleton to increase cartilage proliferation

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52
Q

Gigantism

A

Excessive GH production in children before the fusion of the epiphyses of the long bones

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53
Q

Acromegaly

A

Excess GH in adults.

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54
Q

Describe the 2 main aetiology behind Acromegaly

A
  • Benign GH-producing pituitary tumour

- Rarer hyperplasia e.g. ectopic GH-releasing hormone from a carcinoid tumour.

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55
Q

Pathophysiology of Acromegaly

A
  • Increased GH secreted by a pituitary tumour or due to ectopic carcinoid tumour travels to tissues such as the liver where it binds to receptors»>increased IGF-1
  • This stimulates skeletal and soft tissue growth giving rise to a “giant-like” appearance and symptoms
  • Local tumour expansion in the pituitary can result in compression of surrounding structures resulting in headaches and visual field loss
56
Q

Why is the plasma GH levels not diagnostic?

A

GH is released in pulsatile secretions. It also increases in times of pregnancy, puberty, stress and sleep. If it is detected then you proceed to a glucose tolerance test.

57
Q

How do Somatostatin analogues like IM OCTREOTIDE/IM LANREOTIDE work? What are the side effects?

A
  • Inhibits GH release

- S/E: GI and abdominal cramps, flatulence (farting), loose stools

58
Q

How do dopamine agonists e.g. CABERGOLINE work for acromegaly?
Dis/Advantages?

A

They bind to D2 receptors on the GH producing cells and this weakly controls IGF-1. It is not as effective as the other two however since it is ORAL ADMINISTRATION there are a rapid onset and no hypopituitarism

59
Q

PITUITARY ADENOMAS

A

/////

60
Q

Name 5 diseases that can present in the pituitary

A

1) Benign pituitary adenoma
2) Craniopharyngioma
3) Trauma
4) Sheenans- pituitary infarction after labour
5) Sarcoid/ TB

61
Q

What is Rathke’s pouch?

A

It is an evagination at the roof of the developing mouth in front of the buccopharyngeal membrane. It gives rise to the anterior pituitary (adenohypophysis).

62
Q

3 vital presentation points of pituitary tumour

A

1) Pressure on local structures
2) Pressure on the normal pituitary- hypopituitarism
3) Functioning tumour- hyperpituitarism

63
Q

What can the pressure of the pituitary tumour on local structures give rise to? What symptoms would this lead to?

A

It can put pressure on the optic chiasm resulting in bitemporal hemianopia. It can also cause hydrocephalus and get a CSF leak. This can give rise to:

  • visual defects
  • headaches
  • 3rd nerve palsy (down, outward, pupillary dilatation)
64
Q

Hypopituitarism —— cortisol deficiency

How does it present in male and females?

A

Males: pale, no body hair, central obesity, effeminate skin
Females: loose body hair, sallow complexion

65
Q

What is functioning tumour?

A

One that is producing too much hormones

66
Q

What are lentigines?

A

Harmless hyperplasia of melanocytes which present as smaller pigmented spot on the skin with a clear defined edge.

67
Q

CARCINOID SYNDROME

A

/////

68
Q

What is carcinoid syndrome?

A

Carcinoid syndrome occurs due to the release of serotonin (5-hydroxytryptamine) and other vasoactive peptides into the systemic circulation from a carcinoid tumour.

69
Q

Where can they occur?

A
  • Appendix (most common)
  • Terminal illeum (most common)
  • GI tract
  • Ovary
  • Testis
  • Bronchi
70
Q

Effects of serotonin

A

1) Bowel function
2) Mood
3) Clotting
4) Nausea
5) Bone denisty
6) Vasoconstriction
7) Increased force of contraction and heart rate

71
Q

Are carcinoid tumours benign or malignant?

A

Consider all carcinoid tumours as malignant

72
Q

Carcinoid syndrome

A

Called this when there is hepatic involvement, i.e. hepatic metastases. This happens in 5% of carcinoid tumours.

73
Q

ADRENAL INSUFFICIENCY

A

//////

74
Q

Autoimmune adrenalitis is the most common cause of primary adrenal insufficiency in the UK. What is it?

A

Destruction of the adrenal cortex by organ-specific antibodies with 21-hydroxylase as the common antigen.

75
Q

Pathophysiology of Addison’s disease

A

1) Destruction of the entire adrenal cortex resulting in reduced glucocorticoid (cortisol), mineralocorticoid (aldosterone) and androgen production.
2) All steroids are reduced which differs from a hypothalamic-pituitary disease in which mineralocorticoid and androgen secretion remain largely intact due to their relative independence from the pituitary.
3) In Addison’s the reduced cortisol leads to negative feedback causing increased CRH and ACTH production, being later responsible for hyperpigmentation.

76
Q

Myalgia

A

Pain in a muscle or a group of muscles

77
Q

What causes the pigmentation of skin in Addison’s disease?

A

Increase in ACTH which cross-reacts with melanin receptors especially in new scars and palmar creases.

78
Q

What causes the postural hypotension in Addison’s disease?

A

Due to loss of aldosterone resulting in hypervolaemia as there is less sodium and water retention.

79
Q

What is postural hypotension?

A

Postural hypotension (also called orthostatic hypotension) is a condition in which a person’s blood pressure drops abnormally when they stand up after sitting or lying down.

80
Q

HYPO/HYPERKALAEMIA

A

/////

81
Q

What controls serum levels of potassium?

A

1) Uptake of K+ into cells
2) Renal excretion
3) Extrarenal losses

82
Q

Pathophysiology behind hyperkalaemia

A
  • The amount of K+ in the blood determines the excitability of nerve and muscle cells, including the heart muscle or myocardium
  • When the K+ levels rise in the blood, this reduces the difference in the electrical potential between cardiac myocytes and outside of the cells meaning the threshold for the AP is significantly decreased
  • Resulting in abnormal AP and abnormal heart rhythms that can result in ventricular fibrillation and cardiac arrest.
83
Q

Name some increased renal excretion causes of hypokalemia

A

1) Thiazide diuretics e.g. Bendroflumethiazide
2) Loop diuretics e.g. furosemide
3) Increased aldosterone secretion (k+ exchanged for na+, in liver/heart failure, cushing’s, conns and nephrotic syndrome)
4) Exogenous mineralocorticoids
5) Renal disease

84
Q

Name the causes of hypokalaemia

A

1) Increased renal excretion
2) Reduced dietary intake
3) GI losses (vomiting, severe diarrhoea, laxative abuse)
4) Redistribution to cells.

85
Q

What is tetany?

A

Intermittent muscle cramps/ spasms

86
Q

Describe the thirst axis

A
  • Vasopressin or ADH is synthesised in the hypothalamus
  • It migrates in neurosecretory granules along axonal pathways to the posterior pituitary
  • Large falls in BLOOD PRESSURE or BLOOD VOLUME detected by the osmoreceptors or baroreceptors stimulate vasopressin release.
  • Secretion of vasopressin/ADH is determined principally by plasma osmolality. i.e. blood conc
  • Once released ADH acts on the principal cells of the collecting ducts of the kidney.
  • Here it binds to V2R (adenyl-cyclase couple vasopressin receptor) where kinase action results in the insertion of aquaporin 2 channels into the apical membrane of the collecting duct.
87
Q

What effect does the insertion of more aquaporin 2 channels have

A

1) Increase water permeability of the collecting duct resulting in increased water absorption and very concentrated urine.
2) Widespread arteriolar vasoconstriction»increase BP

88
Q

Cranial DI causes:

A
  • Idiopathic
  • Congenital defects in the ADH gene
  • Disease of the hypothalamus
  • Tumour (metastases, posterior pituitary tumour)
  • Trauma
  • Infiltrative diseases e.g. sacrcoidos
89
Q

Nephrogenic DI causes:

A
  • Hypokalaemia
  • Hypercalcemia
  • Drugs: lithium chloride, glibenclamide
  • Renal tubular acidosis
  • Sickle cell disease
  • Post obstructive uropathy
  • Prolonged polyuria
  • Familial- mutation of ADH receptor
90
Q

How does HYPOkalaemia cause DI?

A

One of the renal impairments caused by hypokalemia is a reduction in urinary concentrating ability and a lack of response to the antidiuretic hormone arginine vasopressin (AVP), resulting in nephrogenic diabetes insipidus.

91
Q

Where would you find each one of these G-protein coupled 7 transmembrane domain receptors?

  • V1a
  • V2
  • V1b
A 
V1a= vasculature 
V2= renal collecting tubules - reabsorption of water 
V1b= pituitary release controlled by osmoreceptors in the hypothalamus.
92
Q

DIABETES INSIPIDUS

A

/////

93
Q

What does the water deprivation test involve?

A

It aims to determine whether the kidneys continue to produce dilute urine despite dehydration.

  • Serum and urine osmolality, urine volume, body weight are measured hourly during fasting and without fluids.
  • Normally you would get serum osmolality remains within the normal range while urine osmolality rises.
94
Q

SYNDROME OF INAPPROPRIATE ADH

A

/////

95
Q

Pathophysiology behind SIADH

A
  • Excess release of ADH due to different causes results in the increased insertion of aquaporin 2 channels in the apical membrane of the collecting duct.
    This results in excess water retention which in turn will dilute blood plasma thereby resulting in hyponatraemia as the Na+ concentration will decrease. The Euvoleamic
96
Q

HYPERCALCAEMIA AND HYPERPARATHYROIDISM

A

/////

97
Q

What two things regulate serum Ca2+?

A
  • Parathyroid hormone

- Vitamin D

98
Q

The anatomy of the parathyroid:

  • Location
  • Blood supply
  • Innervation
A

LOCATION:
The parathyroid glands are usually located on the posterior aspect of the thyroid gland. They are flattened and oval in shape – situated external to the thyroid gland itself but within the pretracheal fascia.
Most people have 4 but you can have 2-6

99
Q

The anatomy of the parathyroid:

- Blood supply

A
  • Arterial supply is via the inferior thyroid artery (as this artery supplies the posterior aspect of the thyroid gland – where the parathyroids are located).
  • Collateral arterial supply is from the superior thyroid artery and thyroid ima artery.
  • Venous drainage is into the superior, middle, and inferior thyroid veins.
100
Q

The anatomy of the parathyroid:

- Innervation

A

The parathyroid glands have an extensive supply of sympathetic nerves derived from thyroid branches of the cervical ganglia.

Note: these nerves are vasomotor, not secretomotor – endocrine secretion of parathyroid hormone is under hormonal control.

101
Q

Where is PTH hormone secreted from?

A

Chief cells of the parathyroid glands

102
Q

What is PTH secreted in response to? What detects this change?

A

Decreased levels of Ca2+ plasma concentrations. The decrease in plasma Ca2+ is detected by specific G-protein coupled, calcium sensing receptors on the plasma membrane of the parathyroid glands.

103
Q

What is the function of calcium?

A

1) Normal blood clotting
2) Muscle contractility
3) Nerve function

104
Q

Describe the composition of calcium in the body

A

1) Ionised calcium (metabolically active, soluble, 40%)
2) Protein-bound (less active, bound to albumin, insoluble)
3) Complexed (e.g. citrate and phosphate)

105
Q

Why is it hard to get values for calcium levels in your blood?

A

The kidney filters ionised and complexed calcium but not protein-bound calcium, this makes it hard to get figures for the calcium in your blood, as if you have more albumin in your blood, then you will appear to have more calcium too, but your ionised calcium might actually be normal.

106
Q

What is the effect of higher pH on calcium?

A
  • At a higher pH, albumin binds strongly to calcium
    MORE of the IONISED CALCIUM become bound to albumin
  • Levels of IONISED CALCIUM DROPS
  • This triggers neurological irritability and presents itself as tingling around your mouth and fingers.
107
Q

Describe 5 ways in which PTH increases plasma Ca2+

A

1) Increasing osteoclastic resorption of bone
2) Increasing intestinal absorption of Ca2+
3) Activation of 1,25-dihydroxyvitamin D (calcitriol) in the kidney
4) Increasing renal tubular reabsorption of Ca2+
5) Increasing excretion of phosphate

108
Q

Calcitriol release is stimulated by what 3 factors?

A
  • Low plasma Ca2+
  • Low plasma phosphate (FGF-23)
  • Increase in PTH
109
Q

Describe the biosynthesis pathway for Vit D

A

1) In our skins we have precursors of Vit-D, 7-dehydrocholesterol. Under the influence of UV-B (from sun and food) , it gets transformed into a more active form of Vitamin D.
2) Vitamin D is hydroxylated in the liver to 25-hydroxy vitamin D
3) 25- hydroxyvitamin D then goes to the kidney where it is further hydroxylated to 1.25-hydroxyvitamin D
A.K.A CALCITRIOL

110
Q

What roles does Calcitriol have?

A

1) Increased Ca2+ and phosphate absorption in the gut
2) Inhibits PTH release
3) Enhanced bone turnover by increasing numbers of osteoclasts
4) Increased Ca2+ and phosphate reabsorption in the kidney’s

111
Q

What is calcitonin? What does it do?

A
  • Made in the C-cells of the thyroid

- Causes a decrease in plasma Ca2+ and phosphate

112
Q

What causes the bones, stones, groans and psychiatric moans in hypercalcemia?

A

Bones: due to excess bone resorption caused by PTH
Stones: due to excess Ca2+
Groans: Ca2+ deposition and high Ca2+ level

113
Q

Why is alkaline phosphatase elevated in hyperparathyroidism?

A

Bone ALP is secreted by osteoblast cells. It is involved in bone formation and skeletal mineralization. PTH stimulates osteoblast activity and thus increases the level of ALP in the blood.

114
Q

What is Chovostek’s sign?

A

Chvostek’s sign is the twitching of the facial muscles in response to tapping over the area of the facial nerve.

115
Q

What is Trousseau’s sign?

A

Trousseau’s sign is carpopedal spasm caused by inflating the blood-pressure cuff to a level above systolic pressure for 3 minutes.

116
Q

HYPOPARATHYROIDISM/ HYPOCALCAEMIA

A

/////

117
Q

Name some causes for hypocalcaemia

A

1) CKD
2) Vit D deficiency
3) Primary hypoparathyroidism (↓ PTH)
4) Secondary hypoparathyroidism (↓ PTH)
5) Pseudohypoparathyroidism (↓ Ca2+, ↑PTH)
6) Drugs

118
Q

How does increased phosphate levels in CKD lead to hypocalcemia?

A

Hypocalcemia in chronic renal failure is due to two primary causes - increased serum phosphorus and decreased renal production of 1,25 (OH)2 vitamin D. The former causes hypocalcemia by complexing with serum calcium and depositing it into the bone and other tissues.

119
Q

How does Vit D deficiency lead to mild /severe hypocalcemia?

A

It results in less Ca2+ absorption.

120
Q

Name 5 causes of Vit D deficiency

A

1) Reduced UV exposure
2) Malabsorption
3) Anti-epileptic drugs- induce enzymes that increase vitamin D metabolism
4) Vitamin D resistance- rare!

121
Q

How does primary hypoparathyroidism lead to hypocalcaemia?

A
  • Low PTH due to parathyroid gland failure

- Ca2+ is low and phosphate is high

122
Q

Name some causes for primary hypoparathyroidism

A

1) Autoimmune DiGeorge syndrome:
Congenital familial condition in which the parathyroid glands fail to develop.
2) Idiopathic hyperparathyroidism:
Rare autoimmune causes by parathyroid antibodies. k

123
Q

Name some causes of secondary hypoparathyroidism

A 
1) After parathyroidectomy/ thyroidectomy:
MOST COMMON CAUSE OF HYPOPARATHYROIDISM
2) Radiation 
3) Hypomagnesaemia
Mg required for PTH secretion
124
Q

How does pseudohypoparathyroidism lead to hypocalcaemia?

A

There is a failure of the target cell response to PTH.
A syndrome of end-organ resistance to PTH due to a mutation in the Gs alpha protein (GNAS1) which is coupled to the PTH receptor.

125
Q

Characteristics of pseudohypoparathyroidism

A
  • Short stature
  • Short metacarpals (esp. 4th and 5th)
  • Subcutaneous calcification
  • Intellectual impairment
  • Low Ca2+ and high PTH
126
Q

What is pseudopseudohypoparathyroidism? Does it ↑ or ↓ Calcium levels?

A

Inherited disorder from father. It has the same phenotypic defects as pseudohypoparathyroidism e.g. short stature. There are no abnormalities with Ca2+ levels. VERY RARE.

127
Q

What drugs cause hypocalcaemia and how?

A

1) Calcitonin : decreases plasma Ca2+ and phosphate

2) Bisphosphonates: reduce osteoclast activity resulting in ↓ Ca2+.

128
Q

What is impetigo herpetiformis?

A

Impetigo herpetiformis is a form of severe pustular psoriasis occurring in pregnancy which may occur during any trimester.

129
Q

What is tetany?

A

Intermittent muscle spasms/cramps

130
Q

PROLACTINOMAS

A

//////

131
Q

What does a raised prolactin lead to?

A
  • Lactation

- Inhibition of GnRH»> ↓ LH/FSH»»↓ testosterone or oestrogen

132
Q

Is hyperprolactinaemia more common in men or females?

A

Females. They present earlier in females than men.

133
Q

Name 4 causes/ risk factors of hyperprolactaemia

A

1) Prolactinoma
2) Pituitary stalk damage
3) Drugs
4) Physiological

134
Q

What is a microadenoma?

A

A microadenoma is a very small, noncancerous tumour that typically develops in the pituitary gland.
There are two kinds of microadenomas: functioning (which produce hormones) and nonfunctioning (which do not).

135
Q

What is a macroadenoma?

A

A macroadenoma is a usually benign tumour composed of glandular tissue growth larger than 10 mm in the pituitary gland. Macroadenomas can cause symptoms because they grow and press on nearby brain structures.

136
Q

What drugs can cause hyperprolactaemia?

A

Most common cause

Antidopaminergic drugs: metoclopramide or ecstasy

137
Q

What physiological factors can cause hyperprolactaemia?

A

Pregnancy, breastfeeding and stress

Phase 2A extra (7 decks)

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