Brainscape's Knowledge GenomeTM

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


See full index

BVETMED2 > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

Describe the Development of the pituitary

A
  • Downgrowth of the neuroectoderm and Theres and outgrowth from the buccal ectoderm forming Rathkus pouch.
  • Rathkus pouch forms a vesicle
  • Vescicle fuses with the downgrowth from the neuroectoderm.

Rathkes pouch is the origin of the Anterior pituitary

Neuroectoderm is the origin of the Posterior pituitary

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

Describe the link between the hypothalamus and the pituitary

A
  • Anterior pituitary has NO neuronal link with hypothalamus. Hormones are deposited into the medial eminence, where they drain into the Hypothalamo - pituitary portal vessels.
  • Posterior pituitary receives blood from Inferior hypophyseal artery. No hormones are received this way. Has neuronal input from hypothalamus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Explain why pituitary tumours can often have no clinical signs or lead to loss of vision

A

Pituitary sits in a bony cavity known as the pituitary fossa. This means tumours have no where to grow except for upwards. Can lead to compression of the optic nerve

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

Describe the histology of the pituitary

A
  • Pars distalis - Makes up the AP.
  • Pars intermedia - Boundary between two areas.
  • Pars nervosa - Makes up PP
  • Pars tuberalis - Produces TSH, Also has high amount of melatonin receptors. After melatonin release big increase gene expression
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Name 2 possible transcription factors that could be mutated in the pituitary

A
  1. SF-1: Drives differention of the gonadotrophs. mutations can lead to failure to develop gonads
  2. PIT-1: Needed for the development of growth hormone secreting cells. mutations will cause growth disorders
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are the 5 cell types of the pituitary, what do they secrete and what are they regulated by

A
  1. Somatotrophs - Secrete Humane growth hormone (GH). GH acts via JAK-STAT pathway. causes the release of insulin like growth factor. This is caused by release of GHRH from hypothalamus in a pulsultile manner. Inhibited by somatostatin
  2. Lactotroph - Prolactin secreted for milk production. TRH (thyropin releasing hormone) promotes secretion. Dopamine release is the main control of PRL. Must decrease dopamine to increase PRL.
  3. Corticotroph - Adrenocorticotropic hormone (ACTH), stimulate release of glucocorticoids. Also releases MSH. Release of ACTH is due to corticotropin releasing hormone (CRH)
  4. Thyrotroph - secretes thyrtropin releasing hormone (TRH). Inhibited by somatostatin
  5. Gonadotrophs - FSH & LH secreted. Released due to stimulation by pulsultile release of GnRH.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Describe properties of protein & peptides

A
  • Synthesised as pre hormones & undergo post translational modification.
  • Stored in granules and released by exocytosis
  • Water soluble
  • Small difference in amino acid sequence causes big difference in physiological function
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Describe properties of steroidal hormones

A

Synthesised in adrenal cortex, testis & ovary. 3 six membered rings and 1 five membered ring. ALL derived from cholesterol. 4 classes:

  1. Corticosteroid - cortisol & aldosterone
  2. Pregnans - Progesterone
  3. Androgen - testosterone
  4. Oestrogens - Oestradiol-17
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What are the properties of amine hormones

A

Derived from tyrosine. Have a rapid onset and no species differentiation. Short half life. E.gs adrenaline and dopamine.

Can also be derived from tryptophan, same properties. E.g serotonin

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

What are the properties of eicosanoids

A

2 major classes both derived from arachidonic acids. Rate limiting step is amount of free amino acids from phospholipids by phopholipase A2.

  1. Leukotriens - 5-lipoxygenase converts arachidonic acid into leukotriens
  2. Prostaglandins - Converted by Cyclooxygenase (COX)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Why do some hormones bind to carrier proteins in blood

A
  1. Increases hormones aqueous solubility
  2. protects hormone against metabolism by proteolytic enzymes.

When bound hormones are biologically inactive. steroids and thyroid hormones

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

Describe structure of hypothalamus

A
  • Basal part of diencephalon
  • Hormones released into median eminence and then into hypophyseal portal system (anterior pituitary)
  • Medial hypothalamus has connections to amygdala (anxiety/mood)
  • afferent conncetions to the hippocampus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What hormones are released by the hypothalamus

A

GnRH

  • neurones are born in vomeronasal organ & migrate to hypothalamus.
  • Key regulator in reproduction, released in pultultile manner controlling LH & FSH secretions
  • Controlled by E2 in negative feedback loop
  • The GnRH receptor has no C-terminal tail, meaning it never switches off
  • Causes increase in cAMP

Somatostatin (SS)

  • 5 isoforms of receptor, inhibit cAMP production
  • potent inhibitor of GH secretions. used therapeutically for GH tumours
  • Neurones in the periventricular (Pev) hypothalamus

Thyrotrophin releasing hormone (TRH)

  • Neurones in Paraventricular nucleus.
  • Key regulator of TSH
  • Increases phosphoinositidase C production in pituirary

Dopamine

  • Produced from tyrosine residues by Tyrosine hydroxylase & DOPA decarboxylase
  • Neurones in hypothalamic tubero-infundibular system
  • Tonic inhibitor of PRL secretions from pituitary. Only way to increase PRL is to decrease dopamine

Corticotrophin releasing hormone (CRH)

  • Neurones in the Paraventricular nucleus & regulated by Glucocorticosteroids
  • Receptors stimulate cAMP production in pituitary to generate ACTH - stress response
  • CRH mutation = Imparied stress response
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Describe the structure of the adrenals

A
  • Medulla - Central, Synthesis of adrenaline
  • Cortex is comprised of 3 areas:
  1. Zona glomerulosa - Lies under capsule, cells arranged circularly. Makes aldosterone
  2. Zona fasciculata - makes up 60-70% of cortex. Large numbers of lipid droplets. syntheses cortisol
  3. Zona reticularis - Cells are intermediate in size between zf & zg. synthesis androgens
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Cholesterol is the precursor for progesterone, ostrediol, aldosteron & cortisol. What are the sources of cholesterol?

A
  • Cholesterol esters - In lipid droplets. Catalysed by cholesterol ester hydrolase ( activated by ACTH)
  • Cholesterol in lipoproteins in blood
  • Synthesised from acetate via HMG CoA reductase
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

How does cholesterol become pregnenolone

A
  • Cholesterol cant pass into the inner mitochondrial membrane Without the StAR protein.
  • Here is where the enzyme cholesterol side-chain cleavage (cscc) is located
  • Cscc cleaves 6 carbon side chain off cholesterol to form pregnenolone
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What carrier proteins are bound to cortisol in the blood

A

Transcortin

Corticosteroid binding protein

Biologically inactive

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What are the actions of the glucocorticoids

A
  • Raise plasma glucose
  • Protein breakdown & lipid lipolysis
  • glucogenesi & gluconeogenesis
  • Increased expression of gluconeogenic enzymes
  • Decrease in IGF-1
  • Increase anti inflammatory cytokines, IL-4, IL-10
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What are the maturational effects of glucocorticoid on the fetus

A

Lungs

  • Surfactant production
  • Beta adrenic receptors

Liver

  • Gluconeogenic enzymes
  • IGF gene expression

GIT

  • Acid secretions
  • Digestive enzymes
  • Mucosal growth

Kidney

  • Glomerular filtrate rate
  • Tubular Na reasbsorption
20
Q

What is the difference between cushings syndrome and cushings disease

A

Cushings syndrome - Excessive quantitites of glucocorticoids.

Cushings disease - Cortisol excess due to hypersecretion of pituitary or extra pituitary ACTH (tumour)

21
Q

What is the action of aldosterone

A

Causes the expression of new protein channels into the kidney which increases Na+ absorption and K+ secretion

22
Q

What is primary and secondary hyperaldosteronism

A

Primary hyperaldosteronism

  • Autonomous secretions of aldosterone due to presence of adrenal adenomas in zona glomerulosa
  • Results in hypertension, muscle weakness & cardiac arrythmias due to hypokalaemia

Secondary hyperaldosteronism

  • Increase in aldosterone due to increase in angiotensin II because of increased renin secretions
23
Q

Describe the causes, clinical signs and diagnosis of hypoadrenocorticism (addisons)

A

Causes:

  • Idiopathic bilateral adrenalcortical atrophy
  • Immune mediated
  • Pituitary lesion

Clinical signs:

  • Hypovalaemic shock (dehydration due to increased Na+ secretion decreased aldosterone)
  • Increase in K+ (decreased aldosterone) = bradycardia
  • increased negative feedback = Increased ACTH & MSH = hyperpigmentation

Diagnosis

  • ACTH stimulation test (no cortisol increase)
  • Hyperkalaemia
24
Q

Describe the causes, clinical signs and Diagnosis of hyperadrenocortism (cushings)

A

Causes

  • Active pituitary tumour (85%)
  • Active adrenal tumour
  • Iatrogenic due to glucocorticoid therapy

Clinical signs

  • Cortisol interfers with ADH to cause polyuria and thus polydypsia
  • Induces gluconeogenesis => hyperglycaemia can cause secondary D.melitus
  • stimulates protein catabolism => muscle weakness & poor wound healing
  • inhibits growth phase of hair = bilateral symmetric alopecia
  • Lipolysis and redistribution of fats in abdomen => pot belly

Diagnosis

  • Lymphocytopenia (low lyphocytes), cortisol is anti-inflammatory
  • Low dose dexamethasone test - pituitary dependant and normal animals will show suppression cortisol after 3 hours. Adrenal dependant cortisol remains high
25
Q

What enzyme converts T4 into T3

A

T4 converted into T3 in peripheral tissues by

5’-deiodinase

26
Q

Describe the synthesis of T4/T3

A
  1. TSH binds to cell surface receptor causing intracellular increase in cAMP => pKa
  2. pKa phosphorylates Iodine pump allowing I- into epithelial cell & it diffuses into colloid.
  3. Enzyme Thyroperoxidase allows addition of iodine to tyrosine residues from thyroglobulin
  4. Produces Monoiodotyrosin and diiodotyrosine. Combine to form either T4 or T3
  5. Products are endocytosed into epithium. Proteases later break down endosome allowin release into the blood
27
Q

How are thyroid hormones transported in blood

A

Bind to carrier proteins in blood.

  • Thyroxin binding globulin (TBG)
  • Thyroxin binding pre albumin
  • Albumin

Inactive while bound

28
Q

What are the actions of thyroid hormone and how is it metabolised

A

Actions

  • Calorigenesis - Increase BMR & produce heat
  • Increase hepatic gluconeogenesis & lipolysis
  • Increase amount of Beta adrenoreceptors - increase HR and contractility

Metabolism

  • Deiodinasation enzymes in liver/kidney.brain
  • 20% of T4 & 100% of T3 conjugated to sulphuric acid, then undergoes oxidative deamination & decarboxylation to be excreted
29
Q

What are the causes, clinical signs and diagnosis of hypothyroidism

A

Causes

  • Iodiopathic follicular collapse
  • Lymphocytic thyroiditis

Clinical features

  • Weight gain with a normal appetite
  • infertility
  • Bradycardia
  • Bilaterally symmetrical alopecia
  • myxoedema - deposition of mucinous material, causing thickened skin and tragic facial expression

Diagnosis

  • measure T4 levels (low)
  • Measure cholesterol which should be high (hypercholesterolaemia), due to decreased activity of lipoprotein lipase
30
Q

What are the causes, clinical signs & diagnosis methods for hyperthyroidism

A

Causes

  • Nodular hyperplasia / Thyroid adenoma
  • Thyroid carcinoma

Clinical signs

  • Tachycardia (increased 02 consumption)
  • Weight loss despite polyphagia
  • Polydypsia/polyuria

Diagnosis

  • T3 suppression test
  • Increased ALP or ALT
31
Q

What is goitre and what are its causes

A

Non neoplastic & no inflammatory enlargement of the thyroid

Causes:

  • Genetic enzymatic defect - inability to produce T3/T4
  • Iodine deficiency
  • Iodine excess
32
Q

What ways can you affect disorders of the thyroid therapeutically

A

Affect TSH secretion

  • Protirelin - synthetic TRH
  • T4/T3 - Inhibit TSH

Act on thyroid

  • Radioisotope of iodine - absorbed by thyroid mainly, destroys cells
  • thioureylenes - inhibit thyroidal peroxidase

Mimic thyroidal hormones

Beta blockers (propranolol) antagonise some CVS actions oh hyperthyroid cats.

33
Q

What drugs affect adrenals

A
  1. Affect hypothalamus to decrease CRF - Bromocriptine
  2. Affecting pituitary to affect ACTH secretions - Glucocorticoid Analogues
  3. Synacthen - ACTH analogue
  4. Inhibit cortisol biosynthesis - Aminoglutethimide

Drugs which mimic cortisol

  • Replacement therapy, anti inflammatory, immunosuppresive.
  • Side effects are it will suppress ACTH, Adrenal gland atrophy and iatrogenic cushings
34
Q

Explain how insulin is synthesised and explain its biphasic release

A

Synthesis

  • Synthesised initially as a pre-prohormone
  • Processed in thew ER into prohormone
  • Mature insulin then formed in gogli by Prohormone convertase enzymes.
  • C-peptide cleaved off

1st phase of release occurs in 3-5 mins from readily releasable granules close to plasma membrane. 2<strong>nd</strong> in 15mins-2hours. From newly synthesised granules

Insulin is a large Peptide, species specific

35
Q

Explain the secretion mechanism of insulin and the actions it has on the body

A

Secretion

  • Stimulated by high blood glucose
  • GLUT-2 transports glucose into B-cells
  • Glucokinase phosphorylates glucose to produce pyruvate making ATP.
  • Atp dependant K+ channels open =>outflux of K+
  • Depolarisation causes opening of Ca<strong>=2</strong> => exocytosis

Actions: Increased…

  • Glycogen synthesis
  • Glycolysis
  • Lipogensis
  • Protein synthesis

Relaxes smooth muscle of resistance vessels

36
Q

What are the actions of glucagon and how are these achieved

A
  • Lipolysis by the phosphorylation of hormone sensitive lipase to break downs TAG’s into free fatty acids
  • Phosphorylation of phosphorylase B to a promotes glycogenolysis
37
Q

What is the effects of somatostatin

A
  • Paracrine effects to inhibt insulin & glucagon secretions
  • Stimulated by nutrient ingestion & increased blood glucose. maintains a constant nutrient supply
38
Q

What is secreted from C cells of thyroid and what are its affects

A
  • Calcitonin
  • Secreted in responce to hyperkalcaemia
  • Inhibits osteoclast activity
  • Neoplasms can occur here, and if malignant spread to Lymph nodes
39
Q

What is the role of parathyroid hormone

A

Secreted by chief cells in responce to hypokalcaemia. Increases osteoclast activity, causing bone resorption, mobilising Ca+2 stores. Also increases phosphate excretion in kidney

40
Q

What is the causes & clinical signs of hypoparathyroidism

A

Causes

  • Lymphocytic parathyroidism - infiltration of lymphocytes destroying chief cells
  • Metastic neoplasm
  • Chronic hypercalcaemia - atrophy of parathyroid
  • Iatrogenic damage during surgery on thyroid

Clinical signs

  • Tachycardia
  • Decrease in Ca+2 increases permeability of Na+ in neuronal membranes causing depolarisation => tetany
41
Q

What are the causes of hyperparathyroidism, what are the different types and what are the clinical signs

A

Causes

  • Primary - Functional parathyroid hyperplasia or neoplasm (adenoma or carcinoma)
  • Tumours associated with paraneoplastic hyperparathyroidism are Lymphoma, Plasma cell tumour and anal sacapocrine gland adenocarcinoma.

Secondary

  • Due to chronic renal failure. imparied glomerular filtrate causes a hyperphosphotaemia. Phosphate binds to calcium forming salts which deposit in kidney. Decreased calcium causes increased PTH secretion=> hyperplasia. But kidney damaged therefore phosphate retained.
  • Nutritional. Due to increased Phosphorus intake, causing relative calcium deficiency by binding to calcium in the gut and decreasing its absorption.

_Fibrous osteodystophy_ - Breakdown of bone and removal of Ca+2 . Bone replaced by fibrous tissue in areas of mechanical stress. susceptible to lameness and fracture.

42
Q

What is the consequences of adenoma in the pituitary

A
  1. Paraneoplastic effects - Can be active producing hormones E.g Producing ACTH=>cushings or producing GH=> gigantism
  2. Compression & atrophy of adjacent pituitary - will cause a decrease in hormones secreted causing atrophy of distint glands e.g Adrenals. Compression of the Posterior pituitary can cause a decrease in ADH, causing polyuria and polydypsia
43
Q

What would occur if there was an adenoma of the Pars intermedia?

A

If its inactive can compress onto the pituitary and hypothalamus causing intermitten fevers, sweating and polydypsia & polyuria

If active can secrete MSH (hyperpigmentation), ACTH (cushings) and Beta endorphins

44
Q

What is the most common type of Diabetes melitus in domestic animals and what are the clinical signs

A

Type 1 is more common in domestic animals

Clinical signs

  • Weight loss despite Polyphagia - Inadequete uptake of glucose
  • Also weight loss due to decreased muscle mass due to gluconeogenesis
  • Polydypsia and polyuria because glucose exceed renal threshold
  • cateract as metabolism of lens altered to compensate for hyperglycaemia
  • Higher risk of infection because less glucose for leukocytes

High blood glucose and glycosuria common indecators

45
Q

What is diabtes insipidous

A

Characterized by inedaquate amounts of ADH. Occurs for two reasons

  1. Central - inedaquate release of ADH. No ablity to concentrate urine. Polydypsia and polyuria
  2. Nephrogenic - Failure of nephrons to respond to ADH.
  3. Phychogenic polydypsia - neurological disorder triggering excess thirst. Functional lack of ADH as animal is over hydrated so no ADH released.
46
Q
A

BVETMED2 (10 decks)

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