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Endocrine > Pathophysiology of endocrine tissues > Flashcards

Pathophysiology of endocrine tissues Flashcards

1
Q

eicosanoids, catecholamines and peptide hormones all act at what kind of receptor?

A

membrane receptor as they are water soluble

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2
Q

What kind of receptor do steroid hormones and thyroid hormone work at?

A

Intracellular receptor as they are lipid soluble and can cross the plasma membrane

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3
Q

What is primary hypofunction?

A

Failure of the gland itself to produce the hormone

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4
Q

What are the three main causes of hypofunction? (broadly)

A

destruction of the gland tissue e.g. abscess, granuloma etc embryonic failure of tissue development Defective synthesis eg lambs with congenital dishormogenic goitre

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5
Q

what is secondary hypofunction?

A

hypofunction of the gland sue to lack of stimulation by trophic hormones (may be abnormal or lacking). eg inactive pituitary –> hypofunction of adrenal and thyroid glands and hypoplasia of gonads

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6
Q

What is primary hyperfunction?

A

Hyperfunction of the gland usually due to hormone secreting tumour, e.g. hyperthyroidism in cats

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7
Q

What is secondary hyperfunction?

A

increased hormone production in response to increased trophic hormone e.g. ACTH-secreting pituitary adenomas leading to hypertrophy and hyperplasia of the adrenal cortex and cushings disease

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8
Q

Where is the hypothalamus situated?

A

In the basal part of the diencephalon beneath the thalamus

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9
Q

What is secreted from the anterior pituitary in response to GnRH?

A

FSH & LH

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10
Q

What is secreted from the anterior pituitary in response to GHRH?

A

Growth hormone

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11
Q

What is secreted from/inhibited at the anterior pituitary in response to Somatostatin?

A

Inhibits Growth hormone and TSH

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12
Q

What is secreted from/inhibited at the anterior pituitary in response to TRH?

A

TSH and Prolactin stimulated

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13
Q

What is secreted from/inhibited at the anterior pituitary in response to DA?

A

prolactin inhibited

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14
Q

What is secreted from/inhibited at the anterior pituitary in response to CRH?

A

ACTH

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15
Q

What is the connection between the hypothalamus and the anterior pituitary?

A

Portal blood vessel system

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16
Q

How are the hypothalamus and the posterior pituitary connected?

A

nerve fibres from the paraventricular and supraoptic nuclei of the hypothalamus run to the posterior pituitary

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17
Q

What hormones are produced by the posterior pituitary?

A

Oxytocin and Vasopressin (ADH)

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18
Q

What is the sella turcica?

A

the bony cavity at the base of the skull in which the pituitary sits

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19
Q

What are the five main cell types in the anterior pituitary?

A

Gonadotroph

Lactotroph

Somatotroph

Corticotroph

Thyrotroph

Lucy Cheetham Sucked Tilly’s Gonads

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20
Q

what are the three parts of the anterior pituitary?

A

pars tuberalis

pars distalis

pars intermedia

(pars nervosa is in posterior)

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21
Q

What are the three types of cells in the pars distalis?

A

Acidophils (lactotrophs,somatotrophs)

Basophils (thyrotrophs, gonadotrophs, corticotrophs)

Chromophobes

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22
Q

Where is ACTH secreted from in the dog?

A

Pars intermedia and pars distalis

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23
Q

How do you get pituitary cysts?

A

failure of the oropharyngeal ectoderm to differerntiate into hormone secreting cells of the pars distalis

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24
Q

What breeds are commonly effected by pituitary cysts?

A

GSDs, spitz, minpin

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25
Q

What are the signs seen with pituitary cysts?

A

Relatable to reduced trophic hormones

dwarfism (noticeable around 2m of age)

Puppy coat retention –> alopecia and hyperpigmentation

Delayed growth plate closure in long bones

Delayed dentition

Hypoplasia of thyroid and adrenals

Infantile reproductive organs/genitalia

Life span short if severely affected

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26
Q

Which species do pituitary adenomas occur in?

A

Horses and to a lesser extent dogs

(older animals)

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27
Q

What is the disease you get associated with hormonally active pituitary adenomas in dogs?

A

Hyperadrenocorticism (as ACTH produced)

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28
Q

What might happen if the pituitary adenoma gows to the extent that you get obliteration of the gland?

A

Hypopituitarism, commonly expressed as diabetes insipidus

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29
Q

What is the appearance of adnomas of adenomas of the pars intermedia in horses?

A

Large, multinodular, yellow/brown/white and firm

May compress the pars nervosa (posterior pituitary) and the overlying thalamus

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30
Q

What happens to plasma cortisol levels in horses with PPID?

A

normally normal or slightly raised. Different precursor metabolism to in dogs (POMC)

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31
Q

What are the three hormones normally produced from POMC in the pars intermedia in horses?

A

CLIP, MSH, B-endorphin

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32
Q

What is mainly produced in the pars distalis in the horse from POMC?

A

ACTH

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33
Q

What parts of the pituitary can an ACTH secreting adenoma arise from in the dog?

A

distalis or intermedia

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34
Q

Which breeds are predisposed to ACTH secreting adenoma in dogs?

A

Boston Terrier

Boxer

Dachshund

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35
Q

What happens to the adrenal gland physically in cushings disease in dogs?

A

The adrenal cortex has bilateral enlargement, adrenals show yellow/orange coloured nodules of variable size which may compress the corticomedullary junction. Similar nodules in fat around the glands

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36
Q

What does an ACTH secreting adenoma in the dog look like on histology?

A

nests of chromophobe cells

Fine connective tissue stroma

No secretory granules seen on light microscopy

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37
Q

What are the four vague ststemic effects of ACTH secreting adenoma in the dog?

A

Gluconeogenesis

Lipolysis

Protein catabolism

Anti-inflammatory actions

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38
Q

What are the clinical signs seen with ACTH secreting adenoma in the dog?

A

Abdominal enlargement

Muscle wasting

Enlarged liver

Bilateral alopecia

Thin skin with hyperpigmentation

Fat pads around neck and shoulders

Poor wound healing

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39
Q

What are the two main hormones secreted by the pars nervosa?

A

Oxytocin

Vasopressin

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40
Q

Where are oxytocin and vasopressin synthesised (exactly)

A

Nerve cell bodies of the suproptic and paraventicular nuclei of the hypothalamus

41
Q

How long is the half life of oxytocin and vasopressin?

A

About 5 mins

Circulate at very low levels

42
Q

How do oxytocin and vasopressin act?

A

G protien coupled plasma membrane receptor

43
Q

How do you get central diabetes insipidus?

A

Inadequat production or release of ADH

44
Q

Which part of the pituitary needs to be damaged to cause central diabetes insipidus?

A

Pars nervosa needs to be obliterated or compressed by an expanding cyst or tumour

45
Q

Why does damage to the hypothalamus have the potential to cause central diabetes insipidus?

A

Can cause inadequate production as ADH made there (SON, PVN)

46
Q

What is the main clinical sign associated with diabetes insipidus?

A

Marked PU/PD, very hypotonic urine

47
Q

What is the main stay of diagnosis in diabetes insipidus?

A

Water deprivation test and assessment of response to exogenous ADH

48
Q

What is nephrogenic diabetes insipidus?

A

Unrelated to pituitary disease, is caused by an inability of the epithelium in the collecting ducts to utilise ADH

49
Q

What does the adrenal cortex secrete?

A

Glucocorticoids

Mineralocorticoids

small amount of sex steroids

50
Q

What does the adrenal medulla secrete?

A

Adrenaline and Noradrenaline (catecholamines)

51
Q

What are the zones of the adrenal cortex called?

A

glomerulosa

fasciculata

reticularis

(GFR)

52
Q

What is produced in the zona glomerulosa?

A

Mineralocorticoid e.g. aldosterone

53
Q

What is produced in the zona fasciculata?

A

Glucocorticoid e.g. cortisol

54
Q

What is produced in the zona reticularis?

A

Androgens e.g. oestradiol

55
Q

What kind of hormone is cortisol and what is its roll?

A

Cortisol is a glucorticoid (from adrenal zona fasciculata) and is for dealing with stressful events e.g. trauma, starvation, infection etc

56
Q

What are the effects on the body of cortisol?

A

Stress response - increased vascular tone

Immunosuppressive and antiinflammatory actions

Increased mobilisation of fatty acids from skeletal muscle

Liver has increased gluconeogenesis, glycogenesis, glycogen storage, and enzyme activity

Increased mobilisation of glycerol and fatty acids from dat cells

57
Q

What are mineralocortcoids regulated by?

A

RAAS

plasma sodium and potassium levels

58
Q

What does aldosterone do?

A

Conservation of body sodium by exchanging for potassium in the kidney

59
Q

Which species commonly get mineralisation of the adrenal glands?

A

adult cats and monkeys

60
Q

Which species commonly get amyloidosis of the adrenal glands?

A

old mice, rats and monkeys

61
Q

Name two diseases which can cause adrenalitis (abscesses/disseminated disease of adrenals)

NB adrenalitis really means inflammtion of one or both adrenal glands

A

Toxoplasmosis and Tuberculosis

62
Q

Which of the adrenal products is vastly increased in cushings disease?

A

excessive glucocorticoids (e.g. cortisol)

63
Q

What percentage of cushings syndrome cases in dogs are caused by a pituitary tumour?

A

80%

64
Q

Why do you get a pot bellied appearance in cushings?

A

Due to hepatomegaly and abdominal muscle weakness

65
Q

What is the appearance of nodular adrenocortical hyperplasia?

A
66
Q

What groups does nodular adrenocortical hyperplasia occur in?

A

older dogs cats and horses. Similar nodules in liver, spleen and pancreas

67
Q

What is the histological appearance of the nodules in adrenocortical nodular hyperplasia?

A

resemble the zona glomerulosa or fasciculata

68
Q

What is the appearance of diffuse adrenocortical hyperplasia?

A

adrenal cortex uniformaly enlarged

normally due to ACTH secreting pituitary tumour but can be idiopathic

69
Q

What does diffuse adrenocortical hyperplasia look like on microscopy?

A

hypertrophy and hyperplasia of the zona fasciculata and reticularis

cells are often vacuolated due to richness in lipids

70
Q

What is being described?

mainly old dogs

single pale yellow/red nodule, partially or completely encapsulated, surrounding tissue may be compressed, sometimes in both glands

A

adrenocortical adenoma

71
Q

What is the microscopic appearance of an adrenocortical adenoma?

A

Cells resemble either zona fasciculata or reticularis

Vacuolated, divided by fibrovascular stroma

Image shows capsule on the left

72
Q

How do you differentiate adrenocotrical adenoma from adrenocortical nodular hyperplasia?

A

Adenoma tends to be singular, encapsulated and compressive

73
Q

Which products of the adrenal cortex are decreased in primary hypoadrenocorticism?

A

both glucocorticoids and mineralocorticoids

74
Q

What is primary hypoadrenocorticism caused by and which groups are most often affected?

A

Destruction of the adrenals

Idiopathic bilateral adrenocortical atrophy

Autoimmune reaction or inflammatory disease

Young adults are mainly affected and all three layers of cortex are affected

Effects are mainly due to lack of mineralocorticoid, therefore altered mineral balance

75
Q

What are the effects of primary hypoadrenocorticism?

A

Increased excretion of Sodium, Calcium and Water

Haemoconcentration and dehydration

Increased potassium in the blood-DANGER slows the heart

Generalised tissue under perfusion

V & D

Reduction of glucocorticoids - susceptible to stressful events

76
Q

What are the three hormones secreted by the thyroid gland?

A

Thyroxine

Tri-iodothyronine

Calcitonin

77
Q

What are T3 and T4 attached to?

A

Thyroglobulin

78
Q

Where are T3 and T4 stored? (bound to thyroglobulin)

A

In the colloid part

79
Q

What do the C cells/parafollicular cells do?

A

Secrete calcitonin

80
Q

What is the pathway by which T3 and T4 release is stimulated?

A

TRH from hyopthalamus

TSH from pituitary

acts on thyroid to cause release of T3 and T4

81
Q

Which is the more potent thyroid hormone? T3 or T4? Where is the less potent one converted into the more potent one?

A

T3 is the most potent

Target tissues have a deiodinase enzyme to covnert T4 to T3

Pituitary can also do this to facilitate negative feedback

82
Q

Which hypothalamic hormone inhibits TSH release?

A

Somatostatin

83
Q

What is the effect of thyroid hormones?

A

Caloregenic by increasing BMR

Increased cardiac output

Alterations in metabolism

84
Q

Iodide enters te thyroid epithelial cell by the ___a___ __a__ which is dependent on ___b___ and is situated on the _____c____ membrane

It then diffuses into the __d__ across the ___e___ membrane

A

a) iodide pump
b) cAMP
c) basolateral
d) colloid
e) apical

85
Q

The enzyme ____a___ then combines Iodide and tyrosine to form T3 and T4 which are bound to __b___

A

a) TPO-thyroid peroxidase
b) thyroglobulin

86
Q

T3 is made up of one__a__ and one __b__

T4 is made up of two __c__

A

a) monoiodothyronine
b) diiodothyronine
c) diiodothronine

87
Q

Colloid droplets are lysed in the ___a___ and MIT and DIT provide more iodide by the action of the enzyme ___b___

A

a) epithelial cell
b) deiodinase

88
Q

What is the definition of a goitre?

A
89
Q

What is a dyshormogenetic goitre?

A

congenital inability to make T3 T4 in certain breeds of sheep. Will have rough sparse coats and die quickly

90
Q

What are the four broad causes of a goitre?

A

Genetic enzyme defect (eg lambs dyshormogenetic goitre)

Iodine deficiency (calves least susceptible)

Iodine excess (foals from dams fed dried seaweed)

Goitrogenic substances-Brassica plants, some sulphonamides

91
Q

What is the microscopic appearance of a goitre?

A

Diffuse hyperplasia of the follicles

Rate of colloid excreted eventually slows down and follicular cells become flat and less active. Unused colloid becomes prominent, called an involuted colloid goitre (see pic)

92
Q

What are the three main causes of hyperthyroidism in cats?

A

Thyoird gland hyperplasia

Thyroid gland adenoma

autoimmune disease - Graves disease

93
Q

What are the symptoms of hyperthyroidism?

A

Weight loss

Polyphagia

Unkempt coat

Tremor

pos Goitre

Agitated and Nervous

Fast heart rate, pos atrial fibrillation

Muscle weakness

Dyspnea

Heat intolerance due to excess heat production

Staring eyes

V+ D+ (due to thyroid hormone stimulation of CRTZ)

PU/PD

94
Q

Info: multifocal nodular hyperplasia seen in cats dogs and horses (old)

Nocapsule and no compressino o adjacent tissue

Hyperplastic folicales seen histologically often with very little colloid

Can be hormonally active in cats

A

fg

95
Q

What are the two most common causes of hypothyroidism?

A

Idiopathic atrophy

Immune mediated thyroiditis

96
Q

What does idiopathic thyroid atrophy look like histologically?

A

Atrophy of the thyroid follicles (reduced in number and size), prominent connective tissue and fat cells

97
Q

what causes immune mediated thyroiditis?

A

autoantibodies binding to thyrogloblin

98
Q

what does immune mediated thyroiditis look like histologically?

A

infiltration of lymphocytes, plasma cells, macrophages

Degeneration of follicular cells

99
Q

Name three less common causes of hypothyroidism?

A

bilateral non functioning thyroid tumours

severe iodine deficiency

destructive lesions of pituitary gland

Endocrine (11 decks)

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