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Deck 1 > 3E > Flashcards

3E Flashcards

1
Q

What is Addison’s disease?

A

chronic adrenal insufficiency due to destruction of the adrenal cortex

UK prevalence is about 4/100,000

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2
Q

What is the main aetiology of Addison’s disease in affluent countries?

A

autoimmune adrenalitis

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3
Q

What is the main aetiology of Addison’s disease in developing countries?

A

tuberculosis

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4
Q

Explain why a patient with Addison’s disease may have a low baseline cortisol level and not respond to a synacthen test.

A

In the case of infection, the patient will be using cortisol at a greater rate than usual. If the patient fails to increase their cortisol dosage to account for this, it will result in reduced basal cortisol levels.

The patient fails to respond to synacthen because the Addison’s disease has caused significant adrenal atrophy.

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5
Q

How is the short synathen test performed?

A

take a basal serum cortisol reading
administer 250 micrograms of synacthen intravenously at time 0
measure blood cortisol at 30 and 60 minutes

in healthy individuals, basal plasma cortisol should exceed 170nmol/l and rise to at least 580nmol/l on stimulation.

Patients with insufficient adrenal function are unable to raise their serum cortisol in response to synacthen.

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6
Q

What often separates the kidney and adrenal gland?

A

a thin layer of adipose tissue. Appears as a light gap on MRI

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7
Q

Name the three zones of the adrenal gland and the hormone produced in each zone

A

Z. glomerulosa - aldosterone/mineralocorticoids

Z. fasciculata - cortisol/glucocorticoids

Z. reticularis - adrenal androgens

NB: cortisol and adrenal androgens are thought to be produced by both the fasciculata and reticularis

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8
Q

Which autoantibodies are commonly found with IDDM?

A

ICA (islet cell antibody)
I-A2 (insulinoma associated antigen 2)
GAD 65 (glutamic acid decarboxylase 65)

Others:
AII (insulin autoantibody)
ZnT8 (zinc transporter)

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9
Q

Define MODY (Maturity-onset Diabetes of the Young)

A

hereditary forms of diabetes mellitus caused by mutations in an autosomal dominant gene disrupting insulin production

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10
Q

embryology of the adrenal glands

A

cortex - mesodermal. derived from urogenital ridge

medulla - neural crest cells

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11
Q

Which area of the adrenal cortex is the largest?

A

zona fasciculata (forms 80% of cortex)

Lipid rich layer

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12
Q

Phaeochromocytoma

A

tumour of adrenal medulla

causes secondary hypertension

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13
Q

What are the effects of Glucagon & Adrenaline on enzymes regulating gluconeogenesis?

A

stimulate gluconeogenesis in the liver:

  • stimulate glucose 6 phophatase
  • stimulate PEPCK
  • inhibit glucokinase
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14
Q

Which Tissues are dependent on a constant supply of glucose?

A

1) brain - fatty acids cannot cross blood-brain barrier
2) RBC - no mitochondria
3) Testes - testis blood barrier prevents entry of FA
4) Retina

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15
Q

Glucagon receptor

A

Found on hepatocytes
GPCR
binding activates cAMP dependent protein kinase A

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16
Q

Insulin receptor

A

Fuond on adipocytes, striated muscle and liver
tyrosine kinase receptor
binding causes autophosphorylation of intracellular tyrosine residues. This activates protein kinase B (akt)

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17
Q

What are the effects of Glucagon & Adrenaline on enzymes regulating glycogen synthesis/breakdown?

A

stimulate glycogenolysis in the liver:

  • stimulate G6Pase
  • stimulate glycogen phosphorylase
  • inhibit glucokinase
  • inhibit glycogen synthase

Glucagon has no direct effect on muscle or adipose tissue because they have no glucagon receptors

NA - stimulates glycogen phosphorylase in muscle

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18
Q

what is the effect of Insulin on enzymes regulating glycogen synthesis/breakdown?

A

Insulin stimulates glycogenesis (glycogen synthesis)

  • stimulates GK/HK
  • stimulate glycogen synthase
  • inhibits G6Pase (liver)
  • inhibits glycogen phosphorylase
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19
Q

what is the effect of Insulin on enzymes regulating gluconeogenesis?

A

Insulin inhibits gluconeogenesis:

  • inhibits PEPCK
  • inhibits G6Pase
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20
Q

What are the Principal actions of Insulin on the liver?

A

Stimulates:

1) glycolysis
2) glycogen synthesis
3) fatty acid synthesis

Inhibits:

1) gluconeogenesis (PEPCK & G6Pase)
2) glycogen breakdown

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21
Q

What are the Principal actions of Insulin on striated muscle?

A

1) increased glut 4 mobilisation to the membrane (increased glucose uptake)
2) glycogen synthesis
3) fatty acid synthesis

Inhibits glycogen breakdown

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22
Q

What are the Principal actions of Insulin on adipose tissue?

A

1) increased glut 4 mobilisation to the membrane (increased glucose uptake)
2) increased FA synthesis (LPL and ACC stimulated)

3) inhibits lipolysis (breakdown of cAMP prevents HSL activation)

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23
Q

What is the effect of adrenaline on adipose tissue?

A

stimulates lipolysis by upregulating hormone sensitive lipase

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24
Q

which molecule directly inhibits PFK1 activity?

A

ATP

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25
Q

Which enzyme is activated by insulin in skeletal muscle after a meal?

A

Glycogen synthase

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26
Q

Mutations in which gene(s) account for the highest proportion (~50%) of the genetic risk of Type 1 diabetes?

A

HLAs

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27
Q

What is the baseline population risk of Type 1 diabetes in North America and Europe?

A

0.4%

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28
Q

what are the 3 features of DKA?

A

1) metabolic acidosis
2) ketosis
3) hyperglycaemia

State of cellular starvation in the midst of plenty
o Hyperglycaemia, but access to substrate for fuel is denied due to a lack of insulin
 Characterised by uncontrolled catabolism as cells seek alternative sources of fuel

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29
Q

Explain how Diabetic ketoacidosis causes osmotic diuresis

A

o Glucose (and ketones) are freely filtered at glomerulus
o As blood glucose rises, the maximal reabsorption threshold of glucose is exceeded
o This means that there is an elevation of solute content in the tubules
o Increased solute concentration in tubular lumen generates an osmotic gradient
o This results in increased water loss in urine

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30
Q

HYPEROSMOLAR HYPERGLYCAEMIC STATE

A

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

Occurs in Type 2 DM

o Insulin action is enough to suppress the production of ketones
o However, the low level of insulin action cannot suppress persistent hyperglycaemia and osmotic
diuresis

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31
Q

Which lobe of the pituitary is connected to the hypothalamus by blood vessels? what are the blood vessels called?

A

adenohypophysis, hypophysial portal veins

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32
Q

Which hormones travel to the pituitary gland via nerve fibres?

A

oxytocin

ADH

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33
Q

Which hormones are produced by the anterior pituitary?

A

1) growth hormone
2) LH/FSH
3) TSH
4) ACTH
5) Prolactin

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34
Q

where is melanocyte-stimulating hormone produced?

A

adenohypophysis (intermediate lobe)

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35
Q

What are the main effects of cortisol in the body?

A

1) METABOLIC
- stimulates gluconeogenesis
- glycogenesis
- lipolysis
- opposes insulin (raises blood glucose)

2) IMMUNOSUPPRESSION
- decreases lymphoid tissue (volume and activity)
- decreases antibodies and lymphocytes
- anti-inflammatory, blocks recruitment of eosinophils

3) SYSTEMIC
- increased apetite
- decreased vitamin D, therefore decreased calcium absorption
- increased bone resorption
- promotes effects of adrenaline -> increased BP/vascular tone

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36
Q

Explain how taking daily oral corticosteroids affects the normal production of hormones from all layers in the adrenal glands.

A

corticosteroid use increases serum cortisol, increasing negative feedback on the hypothalamus and anterior pituitary. This in turn decreases production of CRH and ACTH, causing understimulation of the adrenal glands, which atrophy.

Atrophy means that supplementation with glucocorticoids and possibly mineralocorticoids is a necessity

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37
Q

Explain the cause of pigmentation patches in primary hypoadrenalism.

A

in primary hypoadrenalism there is increased ACTH release from the anterior pituitary due to the lack of negative feedback. ACTH contains a sequence similar to melanocyte-stimulating hormone, which causes pigementation on the skin and buccal surfaces with excess ACTH

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38
Q

In which layer of the skin are melanocytes found?

A

stratum basale and underlying dermis.

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39
Q

Why does adrenal insufficiency cause hypoglycaemia?

A

cortisol normally increases gluconeogenesis and increases plasma glucose

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40
Q

What is fludrocortisone?

A

aldosterone replacement therapy

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41
Q

Which cells secrete insulin and which group of cells in the pancreas do they belong to?

A

beta cells belong to islets of langerhans

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42
Q

How do beta cells react to increasing concentrations of circulating glucose?

A

glucose enters beta cells via GLUT 2 receptors and is metabolised to ATP. ATP inhibits ATP-sensitive K+ channels, preventing K+ efflux. This depolarises the cell, opening voltage-gated calcium channels. Calcium influx stimulates insulin secretion.

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43
Q

What is the general structure of insulin in the blood stream?

A

two polypeptide chains linked by a disulphide bond

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44
Q

What protein can be used as a marker for insulin production?

A

C peptide

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45
Q

Describe the transduction of insulin signal in the effector cell.

A

Insulin receptor has alpha and beta subunits. binding of insulin causes autophosphorylation of the beta subunit, activating tyrosine kinase.
enzyme cascades are activated, including PIP3 kinase
glut 4 receptors are translocated to the cell membrane, allowing glucose entry

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46
Q

Which form of diabetes is usually an HLA-associated autoimmune disease?

A

type 1

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47
Q

What would be an appropriate adjustment to an insulin regimen during a period of intercurrent illness and why?

A

increase insulin. illness causes increase in cortisol, which counters the action of insulin

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48
Q

Which three ketones are produced in DKA?

A

1) acetoacetate
2) betahydroxybutyrate
3) acetone

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49
Q

Explain how insulin deficiency results in ketone production

A

deficiency of insulin causes excessive lipolysis. FA are broken down to acetyl CoA, which enters TCA. Excess acetyl CoA is converted to acetoacetyl CoA, which is metabolised by the liver to produce acetoacetate and betahydroxybutyrate. Production of ketones exceeds their metabolism

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50
Q

What is the normal anion gap?

A

<18 mmol/L

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51
Q

What anion gap is seen in DKA?

A

high anion gap due to addition of organic acids.

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52
Q

What does a normal anion gap indicate?

A

retention of HCl or loss of bicarbonate. Plasma bicarbonate decreases but electroneutrality is maintained by retaining chloride

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53
Q

What is the first line of treatment with DKA?

A

IV saline to correct dehydration. The life-threatening aspect is dehydration, not hyperglycaemia.

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54
Q

What endocrine emergency can occur in type 2 diabetes?

A

hyperglycaemic hyperosmolar state.
Onset tends to be insidious. Marker dehydration and hyperglycaemia but no ketosis/acidosis (no switch to ketone metabolism).

NB: patients are given heparin to prevent coaguation and hyperosmolar state increases the risk of coagulation.

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55
Q

What is the normal relationship of the upper lid to the cornea?

A

upper lid normally crosses the cornea so that the uppermost part of the iris is obscured

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56
Q

Name the thyroid hormones and indicate which is more potent

A

tri-iodithyronine = more potent

tetraiodothyronine (thyroxine)

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57
Q

Define basal metabolic rate

A

the calculated equivalent oxygen consumption or heat production by the body in a fasting subject at complete rest

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58
Q

outline two functions of thyroid follicular cells

A

1) transport iodide from the blood and trap it in the cytosol
2) synthesise thyroglobulin
3) resorption of thyroglobulin
4) release of thyroxine from follicles

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59
Q

Name the main protein that transports thyroid hormones in the plasma

A

thyroid binding globulin

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60
Q

Why does the thyroid gland move upwards on swallowing

A

larynx rises on swallowing

thyroid is attached to it by the pretracheal fascia

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61
Q

Name two components derived from the diet that are essential in thyroid hormone synthesis

A

1) iodine

2) tyrosine

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62
Q

Describe the regulation of thyroid hormone secretion

A

TRH is released from the hypothalamus in response to low T3/4 or low metabolic rate

TRH stimulates anterior pituitary to release TSH. TSH is released into circulation and stimulates thyroid follicular cells to secrete T3 and T4 into the blood strweam

Blood levels of T3/4 reach normal levels and inhibit TRH/TSH release

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63
Q

What results would you expect from the thyroid function tests to confirm a diagnosis of primary hyperthyroidism?

A 
low TSH (undetectable)
high T3/T4
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64
Q

Where is the pituitary gland located?

A

Lies beneath the third ventricle in a bony cavity of the sphenoid bone (sella turcica) in the base of the skull

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65
Q

Which part of the pituitary stains darker?

A

anterior

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66
Q

Embryology of the pituitary

A 
neurohypophysis = downgrowth from diencephalon
adenohypophysis = rathke's pouch (upgrowth from oral cavity)
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67
Q

chromophils

A

cells which take up stain

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68
Q

acidophils

A

lactotrophs and somatotrophs

pink cytoplasm and dark nuclei

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69
Q

basophils

A

corticotrophs, thyrotrophs, and gonadotrophs

darker cells with purple cytoplasm

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70
Q

chromophobes

A

resting/degranulated chromophils, stain weakly

non-secretory and serve as support cells or precursors to the acidophils and basophils.

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71
Q

Posterior Pituitary

A

contains non-myelinated axons which are the neurosecretory cells.
 cell bodies are located in the hypothalamus.
 Direct extension of the CNS
 Not strictly speaking an endocrine organ

Secretes two hormones, which are stored in vesicles:
o ADH
o oxytocin - acts on the uterus.

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72
Q

Embryology of the thyroid gland

A

develops as an endodermal downgrowth (the ‘thyroglossal duct’) from the floor of the developing pharynx.

The foramen caecum at the back of the tongue marks the site of the downgrowth.

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73
Q

Hashimoto’s thyroiditis

A

Autoimmune reaction against thyroid antigens:
 Anti-thyroid peroxidase
 Anti-TSH receptor antibodies
 Anti-thyroglobulin

o diffusely but asymmetrically enlarged
o Lymphocyte infiltration
o prominent fibrosis
o Oncocytic change in epithelium (Hürthle cells), fibrosis
o Paler, may resemble lymph node on section

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74
Q

Embryology of the parathyroid glands

A

o Upper pair from 4th branchial cleft - Descend with thyroid

o Lower pair from 3rd branchial cleft - Descend with thymus

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75
Q

What are the cell types found in the parathyroid glands?

A

1) chief cells - contain PTH granules, secrete PTH
2) Oxyphil cells - No secretory granules
3) water clear cells - chief cells with pools of glycogen in cytoplasm

Fat infiltration normal, increases with age to plateau in early adulthood

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76
Q

Which is the most abundant cell type in the anterior pituitary?

A

somatotrophs (50%)

Secrete growth hormone in response to growth hormone releasing hormone from the hypothalamus

77
Q

Which is the least abundant cell type in the anterior pituitary?

A

Thyrotrophs (5%)

78
Q

Describe the regulation of prolactin release

A

prolactin is under negative control; dopamine inhibits prolactin production (because it is only needed in the
context of pregnancy/breastfeeding)

High oestrogenic states overcome inhibition by dopamine

79
Q

Somatotroph axis

A

Hypothalamus alters its activity in response to external/environmental factors (stress, exercise, sleep, hypoglycaemia) –> secretes GHRH

Pituitary ssecretes growth hormone. secretion is pulsatile, mainly overnight

Effects are direct of mediated by insulin-like growth factor 1

growth hormone and IGF-1 are both involved in negative
feedback loop

Somatostatin released by the hypothalamus also inhibits growth hormone production by the anterior pituitary

80
Q

Clinical disorders of the posterior pituitary gland

A

1) Cranial diabetes insipidus - insufficient ADH

2) SIADH - syndome of inappropriate ADH secretion -> causes hyponatremia and hypo-osmolality

81
Q

Clinical disorders of the anterior pituitary gland

A

1) pituitary tumours - can result in overproduction or under function
2) Hypopituitarism - pituitary failure

82
Q

Diabetes insipidus

A

 lack of ADH and inability to reabsorb water
 Results in passage of large volumes (>3 L/day, sometimes >10L) of dilute urine

Clinical features:
o Polyuria, polydipsia, nocturia
o Low urine osmolality and high plasma osmolality (inability to concentrate urine)

83
Q

AVPR2

A

ADH receptor
basolateral membrane of kidney
GPCR
Binding causes PKA activation

84
Q

Types of diabetes insipidus

A

1) cranial DI - ADH deficiency
- Can be idiopathic or genetic (mutation in ADH gene)

2) nephrogenic DI - ADH resistance
- genetic, usually a mutation in AVPR2 gene, or secondary to drugs

85
Q

Diagnosis of DI

A

Water deprivation test
- first ask patient to keep a diary of urine production to
determine genuine polyuria
 Deprive patients of fluid for 8h
 Measure plasma and urine osmolality every 2-4h
 Then give synthetic ADH and reassess urine osmolality. Will correct cranial DI but not nephrogenic DI (due to resistance rather than deficiency)

86
Q

Treatment of DI

A

desmopressin = ADH analogue without vasoconstrictor effects

works for Cranial DI but not nephrogenic (maybe in high doses)

87
Q

incidentaloma

A

asymptomatic non-functioning pituitary tumour

88
Q

What is the most common Secretory pituitary adenoma?

A

prolactinoma (usually a microadenoma <1cm)

Clinical features result from suppression of gonadotrophic hormones, because prolactin inhibits GnRH secretion

 hypogonadrotrophic hypogonadism (negative feedback on gonadotropins)
o Galactorrhoea
o Menstrual disturbance and subfertility in women
o Rare in men, presents with reduced libido/erectile dysfunction

Managed with Dopamine agonists (cabergoline)

89
Q

Acromegaly

A

Excessive production of GH (and IGF-1) in adults (causes ‘gigantism’ in children)
o Growth plates have fused, and therefore cannot cause increase in height
o Cartilage, muscles and tendons can still grow

Usually due to a GH producing macroadenoma of the pituitary

Can be diagnosed with a glucose suppression test - glucose normally suppresses GH

90
Q

Hypopituitarism

A

 Failure of (usually anterior) pituitary function
 Can affect a single hormonal axis (FSH/LH most commonly) or all hormones (panhypopituitarism)
 Leads to secondary gonadal/thyroid/adrenal failure
 Need multiple hormone replacement (give cortisol first if all axes affected)
o Lack of cortisol is life threatening

Caused by tumours, radiotherapy, surgery, infarction, etc.

91
Q

What are the actions of growth hormone an cortisol on blood glucose?

A

increase blood glucose

counter-regulatory hormones for insulin - do the opposite

92
Q

Describe the state of thyroid follicular cells when active/suppressed

A 
Active = columnar cells, depleted colloid
Suppressed = squamous cells, colloid acumulates
93
Q

Describe thyroid hormone biosynthesis

A

orally ingested iodine is reduced to iodide in the GIT and absorbed.

Basolateral sodium-iodide pump transports iodide from the blood into follicular cells. The iodide diffuses to the apical membrane, where it is antiported with chloride by pendrin. Iodide is oxidised to I+ by thyroid peroxidase.

I+ combines with tyrosine residues in thyroglobulin (organification of thyroglobulin) forming mono or di-iodinated thyronine, which combine to form T3/T4.

94
Q

Describe thyroid hormone release

A

1) Stimulation by TSH causes follicle cells to remove thyroglobulin from the follicles by endocytosis.
2) Lysosomes in the cell fuse with the vesicles, and lysosomal enzymes break down thyroglobulin, releasing free T3 and T4 into the cytoplasm. amino acids are recycled and used to synthesise more thyroglobulin.
3) T3 and T4 diffuse across the basement membrane and into the bloodstream.
4) Most of the T3 and T4 are bound to thyroid-binding globulins (TBGs), and some are bound to transthyretin or albumin.

95
Q

Thyroglobulin

A

Polypeptide backbone for the synthesis and storage of thyroid hormones.

Iodinated glycoprotein with many tyrosine residues

96
Q

What is important to remember in Secondary hypothyroidism?

A

this is due to pituitary gland failure

other HP axes may be affect as well -> critical to check cortisol!

97
Q

Complications of Surgery for Graves’ Disease

A

haemorrhage - bleeding following surgery can lead to compression of the trachea and respiratory interruption.
RLN nerve palsy
hypocalcaemia
hypothyroidism

98
Q

Goitre

A

Swelling in the neck resulting from an enlarged thyroid gland.

99
Q

Which nerves must be preserved during neck surgery to ensure no voice hoarseness post operatively?

A

RLN and external branch of the superior laryngeal nerve

RLN lies in the groove between the oesophagus and the trachea and is closely associated with the inferior thyroid artery. Easily damaged by division, stretching or compression

100
Q

What symptoms are seen with unilateral RLN damage?

A

hoarseness

101
Q

What symptoms are seen with bilateral RLN damage?

A

complete voice loss and severe airway narrowing

102
Q

which muscle is supplied by the superior laryngeal nerve?

A

cricothyroid muscle

closely associated with superior thyroid arteries and may be damaged when vessles are ligated

103
Q

What symptoms are seen with superior laryngeal nerve damage?

A

weakness of phonation and impaired alteration of pitch due to loss of tension on vocal cords (usually achieved by action of cricothyroid muscle)

104
Q

How many parathyroid glands are there and why are they at risk in thyroid surgery?

A

4 glands, 2 on each side

Usually embedded in posterior part of the thyroid gland and can be inadvertently excised

105
Q

What is the effect of low PTH on calcium and bone?

A

hypocalcaemia, but little effect on bone.

Low serum calcium ca lead to tetany, tremor and convulsions

106
Q

Where are the enzymes involved in steroid hormone synthesis located?

A

mitochondria and SER

107
Q

Describe the blood supply of the adrenal glands

A

superior adrenal artery - branch of inferior phrenic artery
middle adrenal artery - branch of AA
inferior adrenal artery - branch of renal artery

  • The blood reaches the outer surface of the gland before entering and supplying each layer (centrepetal blood flow).
  • At the centre, it flows into the medullary vein.
108
Q

What regulates prduction of Adrenal Androgens?

A

ACTH

•Adrenal Androgens = DHEA, DHEA-S, androstenedione

109
Q

Which enzyme catalyses the first enzymatic step in steroid hormone synthesis and where is it located?

A

Step 1 = conversion of cholesterol -> pregnenolone

catalysed by cholesterol side chain cleavage enzyme (P450scc)
located on inner mitochondrial membrane

110
Q

What is the rate-limiting step in steroid hormone synthesis?

A

Rate-limiting step is the transport of free cholesterol
from cytoplasm into mitochondria.

Carried out by Steroidogenic Acute Regulatory Protein (StAR)

111
Q

Where does the conversion of cholesterol to pregnenolone take place?

A

mitochondria

112
Q

Which domains are conserved in steroid receptors?

A

Domain C - DNA binding domain (Highly conserved) contains 2 zinc fingers which bind to specific sequences DNA (HREs)

Domain E - ligand binding domain.

113
Q

Where are MR receptors found?

A 
Mineralocorticoid Receptors (MR)
Distal Nephron, Salivary glands,
sweat glands, large intestine,
Brain, vascular tissue, heart
114
Q

Steroid Receptor Affinity

A

MR: aldosterone > cortisol

GR: aldosterone = cortisol

NB: Cortisol conc is much higher than aldosterone. Cortisol can bind to MR

115
Q

Which mechanism to protects mineralocorticoid receptor from illicit occupation by glucocorticoids?

A

11 beta hydroxysteroid dehydrogenase

catalyses the conversion of Cortisol (active) to Cortisone (inactive) in selective tissues e.g kidney, allowing aldosterone to function normally

116
Q

Action of ACTH

A

ACTH binds to GPCR and activates AC -> cAMP -> PKA

Stimulation of cholesterol delivery to the
mitochondria (rapid).

Increased transcription of genes coding for steroidogenic enzymes (long-term).

117
Q

Action of Angiotensin II (aldosterone)

A

binds to GPCR and activates phospholipase C -> PIP2 cleavage -> IP3 and DAG

stimulates transcription of StAR and cholesterol uptake into mitochondria

118
Q

Primary Aldosteronism

A

Conn’s syndrome

  • HTN
  • hypokalaemia
  • hypernataemia
  • low renin
  • alkalosis (due to H+ excretion stimulated by aldosterone)

Causes: Aldosterone producing adenoma (unilateral)
Bilateral adrenal hyperplasia

119
Q

Cushing’s Syndrome

A

Excess cortisol

  • weight gain (central obesity)
  • hyperglycaemia
  • moon face
  • high blood pressure
  • red ruddy face, extra fat around neck
  • striae
  • proximal muscle wasting (presents as weakness)

Causes:

  • ACTH producing adenoma (pituitary)
  • Cortisol producing adenoma (adrenal)
  • Iatrogenic
120
Q

Management of primary adrenal insufficiency

A

hydrocortisone (cortisol replacement) and fludrocortisone (aldosterone replacement)

do not delay treatment, treat empirically

121
Q

Differentiate clinically between primary and secondary adrenal insufficiency

A

Secondary insufficiency is similar to Addison’s EXCEPT:
o Skin pale (no elevated ACTH, therefore no pigmentation)
o No electrolyte abnormalities as aldosterone production is intact (regulated by RAAS)

Treat with hydrocortisone replacement (fludrocortisone unnecessary)

122
Q

Cushing’s Disease

A

cushing’s syndrome caused by a pituitary adenoma

123
Q

Diagnosis of Cushing’s syndrome

A

1) dexamethasone suppresion test to establish cortisol excess

2) measure ACTH.
- Low = ACTH-independent cause (e.g. adrenal adenoma)
- High = ACTH-dependent (ectopic tumour or cushing’s disease)

124
Q

What is the most common cause of cortisol excess?

A

Iatrogenic - Due to prolonged high dose steroid therapy

Cushingoid appearance but low plasma cortisol

Chronic suppression of pituitary ACTH production and adrenal atrophy

125
Q

What adrenal gland disorders cause HTN?

A
  • phaeochromocytoma (increased afterload as NA vasoconstricts)
  • primary aldosteronism (increased preload due to increased venous return)
126
Q

Commonest secondary cause of hypertension

A

Conn’s syndrome (primary aldosteronism)

127
Q

Clinical features of Conn’s

A 
o Significant hypertension
o Hypokalaemia (in up to 50%) 
o Alkalosis-> aldosterone increases H+ secretion in distal tubule
  • renin supressed
  • high aldosterone levels

Suppression testing
o Intravenous saline load -> should normally switch off RAAS

128
Q

phaeochromocytoma hallmark symptoms

A

episodes of headache (HTN), palpitations, pallor and sweating (due to +++ NA)

129
Q

Hyponatraemia

A

serum sodium <135 mmol/l

Almost always due to disorder of water balance, not sodium deficiency

130
Q

Causes of hyponatraemia

A

1) SIADH
2) renal impairment
3) diuretic effect

Excess water retention dilutes plasma sodium concentration

131
Q

SIADH diagnostic criteria

A

1) Hyponatraemia
2) urine osmolality > plasma osmolality
3) Urine sodium >20 mmol/l (inappropriate sodium excretion)
4) Absence of adrenal, thyroid, pituitary or renal insufficiency
5) no recent diuretic use

132
Q

What is the effect of Hyponatraemia on the brain?

A

Plasma dilution decreases serum osmolality, resulting in a higher osmolality in the brain compared
to the serum.

This creates an abnormal pressure gradient and movement of water into the brain, which can cause
progressive cerebral oedema,

133
Q

What is the risk of overly rapid correction of hyponatremia?

A

can cause central pontine myelinosis

withchronic hyponatremia, the brain compensates by decreasing the levels of osmolytes within the cells, so
that they can remain relatively isotonic with their surroundings and not absorb too much fluid.

With correction of the hyponatremia withintravenous fluids, the extracellular tonicity increases, followed by
an increase in intracellular tonicity.

When the correction is too rapid, not enough time is allowed for the brain’s cells to adjust to the new
tonicity (by increasing the intracellular osmoles)

Water will leave the brain

134
Q

Causes of HYPERNATRAEMIA

A

o Insensible/sweat losses (severe burns/sepsis)
o GI losses
o Diabetes Insipidus
o Osmotic diuresis due to hyperglycaemia (HHS/DKA)

Seen a lot in patients with dementia as they may have no intact thirst mechanisms

135
Q

Clinical features of hypercalcaemia

A

 Moans = depression/slowed down
 Bones = bone pain, muscle weakness, osteopaenia
 Stones = predisposed to nephrocalcinosis/nephrolithiasis
 Abdominal Groans = vomiting, constipation

136
Q

Causes of hypercalcaemia

A

1) primary hyperparathyroidism
2) ectopic PTHrP production (malignancy)

To differentiate between causes, measure the PTH
o If ↓ then malignancy is likely (PTHrP has negative feedback effect on PTH production)
o If ‘normal’ or ↑ then primary hyperparathyroidism

137
Q

What is the effect of Glucocorticoids on vitamin D?

A

inhibit vit D production

138
Q

What is the link between hyperventilation and calcium?

A

hyperventilation causes very mild and transient hypocalcaemia due to alkalosis –> tingling in hands

As the blood pH increases, blood transport proteins, such as albumin, become more ionized into anions. This causes the free calcium present in blood to bind more strongly with albumin.

139
Q

Causes of hypocalcaemia

A

1) hypoparathyroidism
2) vitamin D deficiency
3) chronic renal failure - reduced ability to hydroxylate vitamin D

140
Q

Ketone body formation

A

Occurs when there is an excess of acetyl CoA and not enough oxaloacetate for it to enter TCA

Acetyl CoA + acetyl CoA -> acetoacetate

can be convertate to acetone and betahydroxybutyrate

141
Q

Macrovascular complications of DM

A

DM is associated with CHD, CVD, peripheral vascular disease

Hyperglycaemia causes excessive uptake of glucose into endothelial cells. Glucose is converted to sorbitol via the polyol pathway. This depletes NADPH and NO, and leads to oxidative stress and ROS formation.

Sorbitol is converted to fructose, which glycosylates proteins, leading to a buildup of advanced glycated end products (AGEs), which cause structural changes (e.g. basement membrane thickening)

ROS also stimulate increased transcription of pro-inflammatory mediators -> increased permeability causing LDL and monocyte infiltration -> ATHEROMA formation

tight glycaemic control has little effect, all CVD risk factors must be targeted

142
Q

Microvascular complications of DM

A

Retinopathy
Neuropathy
Nephropathy

Two components:
1) capillary damage
Structurally and functionally abnormal small blood vessels receive increased blood flow and therefore increased BP. This leads to endothelial damage, causing leakage of albumin/other proteins

2) metabolic damage
Most tissues need insulin to take up glucose, but retina / kidney / nerves don’t
Hyperglycaemia causes excessive uptake of glucose into these cells. Glucose is converted to sorbitol via the polyol pathway. This depletes NADPH and NO, and leads to oxidative stress and ROS formation. CELL DAMAGE.

Sorbitol is converted to fructose, which glycosylates proteins, leading to a buildup of AGEs

143
Q

Diabetic Retinopathy

A

1) Early stages (non-proliferative)
- hyperglycaemia causes damage to small blood vessels walls, causing microaneurysms
- these rupture and form dot haemorrhages
- protein exudate is left behind, forming hard exudate
- cotton wool spots result from microinfarcts

2) late stages (proliferative)
- damage to veins causes ischaemia
- VEGF is produced, stimulating angiogenesis -> proliferative retinopathy
- new blood vessels are fragile and easily rupture, causing vitreous haemorrhage
- failure to clear fluid causes macular oedema

144
Q

Diabetic nephropathy

A

Hyperglycaemia causes damage to glomeruli - AGE cause GBM thickening and widening of filtration slits, causing proteinuria.

Kidney damage initially causes renal enlargement and hyperfiltration (afferent arteriole dilation and efferent arteriole constriction increases filtration pressure).

Systemic BP increases, and exacerbates disease progression. This leads to microalbuminuria, then macroalbuminuria.

progressive damage causes eventual decline in GFR, leading to end-stage kidney disease.

145
Q

Neuropathy

A

Capillary damage, including occlusion in the vasa
nervorum causes reduced blood supply to the neural tissue. This results in impairments in nerve signalling that affect both sensory and motor function.

Sorbitol accumulation causes metabolic damage

146
Q

Diabetic Foot

A

combination of peripheral neuropathy and peripheral vascular disease

Compromise of the blood supply + lack of sensation .

loss of sensation causes repetitive stress; unnoticed injuries and fractures, ulcer formation

-> reduced blood flow impairs healing, limits the access of phagocytic cells to the infected area

147
Q

What does macrocytosis mean?

A

Macrocytosis is the enlargement of red blood cells with near-constant hemoglobin concentration

microcytosis = RBC are unusually small

148
Q

What peritoneal fold connects the liver to the abdominal wall?

A

falciform ligament

149
Q

Does the relatively high concentration of insulin within the blood entering the post-Islet exocrine pancreas influence activity of any other biomechanisms apart from uptake of glucose by cells of the body?

A

YES- INCREASED PRODUCTION OF INSULIN BY BETA CELLS IN THE ISLETS STIMULATES/ UPREGULATES SYNTHESIS OF EXOCRINE PANCREATIC DIGESTIVE
ENZYMES FOR RELEASE INTO THE DUODENUM VIA THE PANCREATIC DUCT

150
Q

Why would a person with diabetes need to take

insulin even if they have not eaten?

A

To suppress glycogenolysis, lipolysis and gluconeogenesis

Illness can raise blood glucose levels (cortisol stimulates
gluconeogenesis – stress response), so people with diabetes may need
to increase their insulin dose.

151
Q

How do patients with diabetes self-manage their

condition and why is this important?

A
  • Insulin-dependent patients test blood glucose multiple times a day. May also test glucose and ketones in urine
  • Awareness of diet, exercise, and other factors (e.g. menstrual cycle); adjust insulin dose accordingly.
  • fixed dose insulin regime - diet/eating patterns much more restrictive
  • non-insulin-dependent patients monitor blood (urine) glucose levels regularly
  • T2DM: adherence to medication and lifestyle changes for other CV risk factors

T1DM: good blood glucose control helps minimise complications

• T2DM: healthy diet and exercise important to slow progress of diabetes and minimise complications

152
Q

From which tissue does this capsule surrounding the pituitary develop?

A

MENINGES- CONTIINUOUS WITH DURA

153
Q

Which substances do Corticotrophs secrete?

A

1) ACTH
2) MSH
3) β-lipotropin
4) β-endorphin.

154
Q

Which enzyme, synthesized by the follicle cell, enables iodide to be converted to iodine?

A

THYROID PEROXIDASE

155
Q

Synthesis of thyroid hormones involves both an exocrine and an endocrine stage. What are these?

A

exocrine - production and secretion of colloid into follicle lumen
endocrine - secretion of T3/T4 into blood capillaires

156
Q

Describe the control of T3/T4 synthesis

A

The synthesis and breakdown of thryoglobulin is controlled by the hypothalamus and
adenohypophysis.

TSH reaching the thyroid gland via the circulation binds to its receptor (Thyrotropin receptor (TSHr)) stimulates the cAMP pathway.

Activation of TSHr stimulates thyroid follicular cells to synthesise and breakdown thyroglobulin from thyroid follicles and result in an increased release of thyroxine into the thyroid capillaries.

157
Q

Summarise the function of calcitonin

A

LOWERS SERUM CALCIUM LEVELS- REDUCES RENAL CALCIUM REABSORPTION, promotes the absorption of calcium by bone and inhibits the action of osteoclasts.

158
Q

three features of hypothyroidism seen on the face

A

Periorbital oedema
Coarsening of skin and facial features
puffy face (myxoedema)
hair loss/thinning

159
Q

most common cause of secondary adrenal insufficiency

A

exogenous steroids

Negative feedback of endogenous steroids on CRH/ACTH -> no stimulus for adrenal gland, atrophy
Patients become steroid dependent

Implications:
o Unable to respond to stress (illness/surgery)
o Need extra doses of steroid when ill
o Cannot stop suddenly
o Gradual withdrawal of steroid therapy if >4-6 weeks

160
Q

How do you screen for cortisol excess?

A

dexamethasone suppression test

161
Q

How to differentiate between ectopic excess ACTH production vs pituitary excess production?

A

CRH stimulation test. no change in ACTH = ectopic source

162
Q

IATROGENIC CUSHING’S SYNDROME

A

COMMONEST CAUSE OF CORTISOL EXCESS

 Cushingoid appearance but low plasma cortisol
 Due to prolonged high dose steroid therapy

163
Q

Metabolic syndrome

A

cluster of conditions — increased blood pressure, high blood sugar, excess body fat around the waist, and abnormal cholesterol or triglyceride levels — that occur together, increasing your risk of heart disease, stroke and diabetes.

164
Q

In a patient who presents with central weight gain, which is the best screening test to exclude cortisol excess?

A

Overnight dexamethasone suppression test.
Plasma cortisol should be undetectable in normal
circumstances

OR:

  • Urinary free cortisol
  • Late night salivary cortisol (Should be undetectable or very low in normal)
165
Q

Explain how aldosterone influences Na, K and H

A

Aldosterone upregulates ENaC channels on the interstitial side and sodium-potassium ATPase channels on the basolateral side of renal tubular epithelial cells, resulting in [increased] resorption of sodium ions from the lumen in the collecting duct.

The increased negative charge in the luminal fluid causes increased potassium ion [secretion] from principle tubular cells and increased hydrogen ion secretion from tubular intercalated cells, aided by upregulation of the apical H+-ATPase and sodium-potassium ATPase channels by aldosterone and hypokalemia.

Overall, [more] potassium and hydrogen ions are lost in the urine.

166
Q

What is the link between type 2 diabetes and obesity?

A

The mechanism linking obesity and type 2 Diabetes Mellitus is poorly understood.

Inflammation is an important mediator that links Type 2 DM with atherosclerosis. Type 2 Diabetes is associated with [higher] levels of pro-inflammatory cytokines such as CRP, IL6, and TNF α.

Hormones released by adipose tissue ([adipokines]) can also [promote] inflammation. The [distribution] pattern of body fat is also important, with [central] obesity a significant risk factor for both Type 2 diabetes and [cardiovascular] disease.

167
Q

What is a clinical sign of hypoparathyroidism?

A

tetany due to hypocalcaemia

168
Q

Most common causes of thyrotoxicosis

A

Autoimmune (Grave’s disease) 70%
Toxic multinodular goitre 20%
Toxic adenoma 5%
Thyroiditis 3% (Inflammatory, drug induced, post-pregnancy)

169
Q

Graves’ disease

A

Autoimmune disorder
Seen most frequently in women (age 40-60y)
Thyroid antibodies often detectable
- TRAB (TSH receptor Ab) in 70-100%
- TPO in 70-80% (overlapping autoimmunity)

Symmetrical gland enlargement
Histologically = colloid depletion and columnar epithelial cells

Associated with other autoimmune diseases
- Type 1 DM, pernicious anaemia, vitiligo
Can be associated with eye disease

170
Q

Signs/symptoms of hyperthyroidism

A 
Irritability/hyperactivity
Heat intolerance and sweating
Weight loss with increased appetite
Diarrhoea
Amenorrhea/oligomenorrhea
Signs:
Sinus tachycardia/AF
Fine tremor
Warm, moist skin
Eye signs
Goitre, pre tibial myxoedema
171
Q

Graves’ Ophthalmopathy

A

due to oedema and inflammation of extra-ocular muscles

Occurs in 70% of graves patients

172
Q

What additional investigations should be performed in a patient with high levels of T3/T4?

A

Thyroid autoantibodies (TRAB)

Radioiodine uptake scan (symmetrical in graves, will be localised to site of nodule/adenoma with toxic nodular goitre or adenoma)

173
Q

Outline management options for hyperthyroidism

A

Anti thyroid therapy (carbimazole/PTU)

Beta blockers for symptomatic relief

Radioiodine therapy

Surgery

174
Q

Patient presents with:

  • TSH 28 (0.04-5)
  • T4 6 (9-21)

Outline 3 causes of this pattern of thyroid hormone dysfunction.

A

1) Hashimoto’s thyroiditis (anti TPO antibody)
2) Severe iodine deficiency
3) Iatrogenic - Following radio iodine therapy or surgery, Amiodarone, lithium
4) Thyroiditis - Viral or post-partum, often temporary

175
Q

What symptoms are typical in hypothyroidism?

A 
Symptoms of hypothyroidism:
Weight gain
Depression
Lethargy
Constipation
Cold intolerance
Poor concentration
Hoarseness
Menorrhagia
176
Q

What clinical signs can be seen in hypothyroidism?

A 
Weight gain
Bradycardia
Dry skin
Coarse, thin hair
Anaemia
Slow relaxing reflexes
May have goitre
177
Q

A 22 year old woman complains of suddenly feeling very tired over the past 3 days.

On further questioning she reports that she is going to
the toilet almost every hour and passing lots of urine.

She has no significant past medical history.

You suspect she may have diabetes mellitus.

List 3 further questions you would ask her in order to support your hypothesis that she has diabetes

A

Thirst, excessive fluid intake

Weight loss

Lethargy/recurrent infections

178
Q

The patient is prescribed insulin therapy. You then
need to educate her about factors that can precipitate
hypoglycaemia. List 3 important factors of which she needs to be aware

A

Hypoglycaemia = Plasma glucose < 4 mmol/L

Main precipitants:

Exercise
Alcohol
Missed meal
Error
Sepsis
Hypoadrenalism
179
Q

She asks you what to look out for if she is becoming
hypoglycaemic. Give two clinical features she might
have in this situation

A 
Autonomic:
tremor
sweating
anxiety
nausea
Neuroglycopenic:
headache
dizziness
difficulty speaking
confusion
180
Q

Give 2 therapeutic methods of reducing the chance of

this patient developing diabetic nephropathy

A

GOOD GLYCAEMIC CONTROL

ACEi is treatment of choice to reduce risk of progression of nephropathy

NB: for neuropathy annual assessment of vibration and light touch

181
Q

3 causes of cushing’s syndrome

A

1) cushing’s disease - pituitary adenoma
2) iatrogenic
3) ectopic ACTH-producing tumour (e.g. lung cancer)
4) adrenal adenoma/carcinoma

182
Q

How would you distinguish between exogenous and endogenous excess steroid?

A

ENDOGENOUS SOURCE
- Increased urinary and plasma cortisol

EXOGENOUS SOURCE

  • May look normal or ‘Cushingoid’
  • Decreased urinary and plasma cortisol
183
Q

List potential causes of hyponatraemia (4)

A

Any cause of SIADH (infection/malignancy/drugs)
Loss of salt and water (diarrhoea/vomiting)
Retention of water and salt (heart failure/liver cirrhosis)1) With hypovolaemia (Na/water loss)

  • Loss of sodium via GI tract (vomiting/diarrhoea) or
    kidneys (diuretics/renal tubular disorders)

2) With normovolaemia (water gain)
- Syndrome of Inappropriate ADH (SIADH)
- Glucocorticoid deficiency

3) With hypervolaemia (Na/water gain)
- Heart failure, hepatic cirrhosis, nephrotic syndrome
- Pathological fluid retention lowers plasma sodium

184
Q

Hyponatraemia - What investigations should be performed? (4)

A 
Plasma osmolality
Urine osmolality
Urine sodium
TFT
Short synacthen test/ early am cortisol
185
Q

Management of hyponatraemia

A

Treat underlying cause
Fluid restrict
If acute or severe, consider IV hypertonic saline bolus

1) Severe and acute
- Unconscious or seizures
- Give infusion of hypertonic (3%) saline
- Can increase quickly

2) Less severe
- Try to establish cause- treat pneumonia
- Usually fluid restriction is correct management
- Increase slowly
- 2nd line treatment controversial -> Can consider AVPR2 antagonists (‘vaptans’)

186
Q

action of thyroid hormones

A

Increase basal metabolic rate:

  • upregulate metabolic enzymes -> upregulates all metabolic processes = CALORIGENIC EFFECT
  • increased HR/BP to facilitate increased O2 delivery
  • Increased rate/depth of respiration
  • vasodilation to eliminate heat
  • increased GI activity - motility/enzyme secretion/appetite
  • increased breakdown of fats/proteins
187
Q

causes of hyperthyroidism

A

Graves
Toxic adenomas (rarely thyroid carcinomas)
Multinodular goitre (abnormal swelling of the neck)
Thyroiditis
Excessive administration of thyroxine

188
Q

causes of hypothyroidism

A

Hashimoto’s Thyroiditis (anti-TPO antibodies).
Thyroiditis (viral) - inflammation of thyroid gland due to a viral cause
Thyroidectomy
Following Radioactive Iodine therapy
Pituitary/Hypothalamic disease - secondary hypothyroidism
Severe Iodine Deficiency - ‘endemic goitre’

189
Q

Radioactive iodine uptake scan

A

Usually ordered in the setting of thyrotoxicosis to help identify the underlying aetiology.
measures the amount of radioactive iodine (usually I-123) that is taken up by the thyroid gland.

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