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Endocrine Flashcards

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1
Q

Exocrine?

Endocrine?

A

Exocrine - glandular secretion of hormones into a duct

Endocrine - glandular secretion into the bloodstream

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2
Q

Distance of action:
Endocrine
Autocrine
Paracrine

A

Endocrine - distant
Autocrine - acts on the same cell, feedback
Paracrine - adjacent cells

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3
Q

Example of:
+ synthesised or stored?
Water soluble hormones?
Fat soluble hormones?

A

Water soluble: Peptides/monoamines, stored in vesicles (think neurotransmitters)
Fat soluble: Steroid hormones, synthesised on demand

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4
Q

Peptide hormones:
Examples? (2)
Storage/synthesis?
Water solubility?

A

Insulin, Gonadotrophins
Storage (secretory granules)
Water soluble

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5
Q

Amine hormones?

Receptors? and subtypes with enzyme associated?

A

Noradrenaline, Adrenaline
Adrenoceptors
Alpha = phoshorylase C
Beta = adenylate cyclase

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6
Q

Hormone receptors:
Lipid soluble hormones act at?
Water soluble horomones act ar?

A

Lipid soluble pass through the cell membrane and bind to cytosolic/nuclear receptors

Water soluble hormones cannot pass through membrane so act at membrane receptors e.g. GPCRs, Ligand-gated ion channels, Kinase-linked receptors

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7
Q

Cholesterol derivatives and steroid hormones:

Zones of adrenal cortex and respective hormones produced

A

“salt, sugar, sex”
Zona glomerulosa - Mineralocorticoids: Aldosterone
Zona fasciculata - Glucocorticoids: Cortisol
Zona reticularis - DHEA, Androstenedione (peripherally to testosterone/oestrogen)
Adrenal medulla - Catecholamines

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8
Q 
Hormone secretion: 
Example for....
Basal secretion?
Superadded/Circadian/Diurnal rhythms? 
Controlled by inhibiting factor? 
Releasing factors?
A

Basal secretion - insulin?
Superadded/Circadian/Diurnal rhythms - Cortisol
Controlled by inhibiting factor - Prolactin constant inhibition by dopamine
Releasing factors - any of the releasing hormones GnRH (gonadotrophin releasing hormone), CRH (corticotrophin releasing hormone)

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9
Q 
*****
Posterior pituitary: 
Where are hormones secreted/stored?
Which hormones?  (2)
******
A

Oxytocin
ADH/Arginine vasopressin

Hypothalamic neurons synthesis Oxytocin and ADH

Transported down neurons (hypothalamic-hypophyseal tract) to posterior pituitary

STORED In axon terminals in posterior pituitary

Released when neurons fire into the blood

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10
Q 
****
Anterior pituitary: 
Where are hormones secreted/stored? 
Which hormones? (6 main)
*****
A 
ACTH - Adrenocorticotropic hormone
Prolactin 
LH - luteinizing hormone
FSH - Follicle stimulating hormone
GH - Growth hormone
TSH - Thyroid stimulating hormone

Neurosecretory cells produce releasing hormones which are secreted into the portal system
Anterior pituitary secretes its hormones into the blood stream

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11
Q 
Appetite: 
Obesogenic environment? 
Satiety? 
BMI = ? 
Obesity pathology associated with visceral or subcutaneous fat?
A

High carb/fat diet, less time to exercise, sedentary lifestyle
Night shift work - disruption circadian rhythm

Satiety = feeling of fullness/absence of appetite following a meal

BMI = Weight (kg) / Height x height (m)

Pathology associated with visceral fat

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12
Q

Hunger and satiety centres in hypothalamus?

A

Lateral hypothalamus = hunger “FATeral hypothalamus”

Ventromedial nucleus = satiety centre

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13
Q 
Main two satiety hormones? 
Act where? and action on: 
- NPY/AgRP neuron?
- POMC neuron?
Results?
A

Leptin + Insulin
Act on the arcuate nucleus of the hypothalamus
- Stimulate POMC neuron
- Inhibit NPY/AgRP neuron
results in feeling of satiety and reduces food intake

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14
Q 
Satiety or hunger stimulating?
Peptide YY? 
CCK? 
Ghrelin? 
NPY/AgRP? 
POMC/Melanocortin receptors?
Leptin? where secreted from?
A

Peptide YY - Satiety: structural antagonistic analogue of NPY (hunger peptide)
CCK - satiety: released by duodenum following meal
Ghrelin - Hunger activates AgRP
NPY/AgRP: Hunger stimulating
POMC/Melanocortin receptors: Satiety pathway within arcuate nucleus

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15
Q

POMC deficiency?

Leptin insensitivity or deficient

A

POMC deficiency = ginger, adrenal insufficiency (no cortisol) and obese
Leptin insensitivity or deficient = obese

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16
Q

Satiety and hunger:

Malonyl CoA?
decreased Malonyl CoA?
increased Malonyl CoA?

A

Malonyl CoA is a central mediator of energy metabolism
Increased = decreased appetite
Decreased = increased appetite

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17
Q

Effects of parathyroid hormone? (3 sites)

PTH released in response to decrease or increase in serum calcium?

A

PTH released in response to decreased serum calcium = Increased Calcium!!
Kidneys:
Increased Calcium reabsorption
Increased hydroxylation/activation of Vit D

Bone:
Increased bone resorption

Gut:
INDIRECT EFFECT of increased calcium absorption due to activated vitamin D

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18
Q

PTH changes can be inappropriate and cause calcium imbalance
Features of Hypocalcemia?

A 
"SPASMODIC"
Spasms (trousseau's sign - blood pressure cuff = hand spasm)
Paresthesia
Anxiety
Seizures
Muscle tone increase
Orientation confusion
Dermatitis
Impetigo 
Chvostek's sign - mouth twitch if facial nerve tapped
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19
Q

Causes of hypocalcemia? (4)

Appropriate PTH response

A

Vit D deficiency - PTH up =appropriate
Hypoparathyroidism e.g. Di George syndrome - PTH down = inappropriate
Pseudohypoparathyroidism e.g. albright osteodystrophy (short fat round faces) - PTH up = appropriate
Pseudopseudohypoparathyroidsm

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20
Q

PTH changes can be inappropriate and cause calcium imbalance
Features of Hypercalcemia?

A

“Bones, stones, abdominal groans and psychiatric moans” -
Painful bones
Kidney stones
GI symptoms: nausea, vomiting, constipation
Nervous system effects: lethargy, fatigue

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21
Q

Causes of Hypercalcaemia? (3)

A

Malignancy - PTH lowers appropriate response
Primary hyperparathyroidism - PTH increases = inappropriate
Secondary hyperparathyroidism -PTH increases = inappropriate

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22
Q 
Regulation of carbohydrate metabolism 
Fasting state? 
Glucose source? 
Insulin independent tissues?
Insulin levels? 
Muscle fuel?
A 
All glucose comes from the kidney - 
Glycogenolysis 
Gluconeogenesis
Glucose delivered to Brain and Erythrocytes (insulin independent tissues) 
Insulin levels low 
Lipolysis Muscles use FFAs as fuel
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23
Q

Regulation of carbohydrate metabolism

Fed state?

Study These Flashcards
A

Glucose serum levels rise =
Insulin secretion + Glucagon inhibition
Glucose replenishes glycogen stores in liver and muscle

24
Q

Actions of Insulin:
Hepatic actions?
Tissues?
Suppresses?

Study These Flashcards
A 
-	Suppresses hepatic glucose output
o	Decreased glycogenolysis
o	Decreased gluconeogenesis
-	Increases glucose uptake in insulin dependent tissues (Fat and muscle - GLUT4)
-	Suppresses
o	Lipolysis 
o	Muscle breakdown
25
Actions of Glucagon and other counter-regulatury hormones e.g.? Hepatic action Tissues Release of?
Counterregulatory hormones e.g. adrenaline, cortisol and GH Stimulates glycogenolysis, gluconeogenesis Reduces peripheral uptake of glucose Stimulates release of GLUCONEOGENIC PRECURSORS - glycerol and AAs = lipolysis + muscle glycogenolysis
26
Definition of Diabetes: (3)
Symptoms + random plasma glucose of >11 mmol/l Fasting plasma glucose >7mmol/l HbA1c of 48mmol/mol
27
Type 1 Diabetes Mellitus?
Loss of Beta cells of the pancreas due to autoimmune destruction Due to expression of HLA antigens chronic cell mediated immune destruction "insulitis"
28
Failure to secrete insulin knock on effects? Catabolic or anabolic state? Glucosuria? Ketonuria?
No inhibition of Glucagon secretion from alpha cells pancreas Continual glycogenolysis Unrestrained lipolysis and muscle breakdown (for gluconeogensis) Catabolic state Increased cortisol and adrenaline Ketogenesis (continual lipolysis and metabolism of FFAs) --> Diabetic Ketoacidosis (medical emergency)
29
Type 2 diabetes? | Causes?
Impaired insulin secretion + insulin resistance (2 defects) - Genetic predisposition - Environmental factors
30
Impaired insulin action in T2D: Only glucosuria never DKA
Less glucose enters peripheral tissues - No suppression of lipolysis and high circulating FFAs - High glucose output after a meal Even low levels of insulin prevent muscle catabolism and ketogenesis
31
Consequences of hypoglycaemia: Adrenaline response in diabetes What is neuroglyopenia?
Autonomic, Neuroglycopenic and Non-specific symptoms most people Glucagon (released 3.5mmol/L) and Adrenaline (released 3.8mmol/l) are defences Glucagon is lost in T1D/T2D Glucagon is not produced by Alpha-cells due to the disruption caused by defective Beta-cells “Low plasma glucose causing impaired brain function neuroglycopenia ≤ 3 mmol/l”
32
Pituitary disease: | 3 key points of pituitary tumours?
1) pressure on local structures e.g. optic nerves leading to bitemporal hemianopia 2) pressure on the pituitary = lack of function = hypopituitarism 3) Functioning tumours: cell type that becomes oncogenic produces more hormone: - GH producing cell = acromegaly - ACTH = cushing's - prolactin = prolactinoma
33
Cushing's syndrome most common cause? ACTH independent/dependent?
chronic, excessive and inappropriate elevated plasma glucocorticoids (cortisol) Exogneous corticoid steroids - most common Pituitary and ectopic tumours = ACTH dependent i.e. release ACTH "ectopic tumour - metastasis ACTH producing" Adrenal tumour = Direct cortisol release; independent of ACTH
34
Cushing's syndrome clinical features (3 main groups "FAP")
Fat distribution: Central obesity + Moon face Protein catabolism: Muscle wasting, osteoporosis and thin skin Androgenic effects: Hirsutism + Acne
35
Difference between Cushing's disease and cushing's syndrome?
Cushing's disease is pituitary disease Cushing's syndrome is diagnosis of clinical symptoms (FAP)
36
Investigations for cushing's | Result of test?
Establish cushing's Identify cause: Urinary free cortisol Dexamethaone suppression test (cortisol levels fall)
37
Acromegaly pathogenesis | 2 steps two hormones
Overproduction of GH (e.g. tumour) | Acts on the liver to release IGF-1 (insulin-like growth factor-1)
38
Comorbidities of acromegaly? | Why do some patients grow tall (gigantism)
Hypertension Heart disease Arthritis T2D Acromegaly before growth plates (epiphysis) fuse causes more long bone growth than normal
39
Test for acromegaly?
Glucose tolerance test: Growth hormone is suppressed in response to glucose (due to somatostatin) In acromegaly GH is unaffected by glucose
40
Prolactinoma = Hyperprolactinaemia | Local effects and clinical features?
Local effects - pituitary tumour = bitemporal hemianopia, headache ``` Menstrual irregularity, infertility, Galactorrhoea (milk production in men and women) low libido (low testosterone) ```
41
Treatment of Prolactinoma? | Which pathway would you make use of?
Tonic inhibition of prolactin secretion by dopamine - so use dopamine agonists (e.g. cabergoline)
42
Cortisol circadian rhythm: trigger and regulation?
Light is the primary effector for cortisol circadian rhythm - highest on a morning with spikes at meals
43
Adrenal insufficiency: Primary? Secondary? Tertiary?
``` Primary = Addison's disease (autoimmune destruction of the adrenal glands so no cortisol) or CAH (congenital adrenal hyperplasia) Secondary = hypopituitarism Tertiary = exogenous glucocorticoid suppression of the HPA axis ```
44
Adrenal crisis presentation (adrenal insufficiency)
Fatigue Fever Hypoglycemia Hypotension and cardiovascular collapse
45
Autoimmune thyroid disease TPO associated with? TSAb associated with? Hypothyroidism (a.k.a?)
TPO - thyroid peroxidase antibodies = hashimoto's thyroiditis = HYPOthyroidism TSAb - thyroid stimulating antibodies IgG autoantibodies = Grave's disease = HYPERthyroidism Hyperthyroidism = myxoedema
46
Grave's disease: Grave's ophthalmopathy? Goitre?
Eyelid retraction; periorbital oedema; protruding eyes Antibodies cross react with the extraocular muscles Goitre = diffuse or nodular enlargement of thyroid glands
47
Thyroid autoimmunity risk factors (3 groups)
``` Genetics (HLA-DR3) Environmental factors (smoking/stress) Endogenous factors (sex females>men) ```
48
Hyperthyroidism 3 mechanisms of excess thyroid hormones in blood
1. overproduction of thyroid hormone 2. leakage of thyroid hormone 3. ingestion of excess thyroid hormone
49
Drugs that cause hypothyroidism? (4)
Iodine (required in the synthesis of thyroid hormone) Amiodarone (iodine rich drug) Lithium Radiocontrast agents (reflexive hyperthyroidism)
50
Clinical features of hyperthyroidism?
``` Weight loss Tachycardia Hyperphagia (increased appetite) Anxiety Tremor Sweating ```
51
Investigations of hypo/hyperthyroidism
Thyroid function test - assess free levels of T3/T4 Thyroid antibodies uptake scan
52
Treatment of hyperthyroidism? | 3 options
Antithyroid drugs: Thionamides e.g. Carbimazole Radioiodine - reflexive hypothyroidism due to destruction of thyroid cells via radiation Thyroidectomy
53
Hypothyroidism Primary? Secondary? Tertiary?
Primary = Hashimoto's thyroiditis, or primary atrophic hypothyroidism Drugs: Iodine, lithium, antithyroid drugs e.g. carbimazole Secondary = pituitary dysfunction (no TSH) Tertiary = hypothalamic dysfunction (no TRH)
54
Rare causes of hypothyroidism in children
``` Thyroid agenesis (thyroid gland doesn’t develop) Thyroid ectopia (displacement or misplacement of organ) Thyroid dyshormonogenesis (thyroid hormone synthesis defect) ``` Thyroid hormone resistance TSH deficiency
55
Clinical features of hypothyroidism
- Fatigue - Weight gain - Constipation - Cold intolerance - Muscle cramps - Dry, rough skin - reduced memory or cognition
56
Treatment of hypothyroidism
Levothyroxine (L-thyroxine - T4) | Amiodarone (iodine rich drug structurally similar to T4)
57
Preganancy and the thyroid: Preconception period is important for thyroid development At what point does the feotus develop thyroid follicles?
Starts at 10 weeks

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