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Phase 2 > Endocrine > Flashcards

Endocrine Flashcards

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?

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?

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
Q

Actions of Glucagon and other counter-regulatury hormones e.g.?
Hepatic action
Tissues
Release of?

A

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
Q

Definition of Diabetes: (3)

A

Symptoms + random plasma glucose of >11 mmol/l

Fasting plasma glucose >7mmol/l

HbA1c of 48mmol/mol

27
Q

Type 1 Diabetes Mellitus?

A

Loss of Beta cells of the pancreas due to autoimmune destruction
Due to expression of HLA antigens
chronic cell mediated immune destruction “insulitis”

28
Q

Failure to secrete insulin knock on effects?

Catabolic or anabolic state?

Glucosuria?
Ketonuria?

A

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
Q

Type 2 diabetes?

Causes?

A

Impaired insulin secretion + insulin resistance (2 defects)

  • Genetic predisposition
  • Environmental factors
30
Q

Impaired insulin action in T2D:

Only glucosuria never DKA

A

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
Q

Consequences of hypoglycaemia:
Adrenaline response in diabetes

What is neuroglyopenia?

A

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
Q

Pituitary disease:

3 key points of pituitary tumours?

A

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
Q

Cushing’s syndrome
most common cause?
ACTH independent/dependent?

A

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
Q

Cushing’s syndrome clinical features (3 main groups “FAP”)

A

Fat distribution: Central obesity + Moon face

Protein catabolism: Muscle wasting, osteoporosis and thin skin

Androgenic effects: Hirsutism + Acne

35
Q

Difference between Cushing’s disease and cushing’s syndrome?

A

Cushing’s disease is pituitary disease

Cushing’s syndrome is diagnosis of clinical symptoms (FAP)

36
Q

Investigations for cushing’s

Result of test?

A

Establish cushing’s
Identify cause:

Urinary free cortisol
Dexamethaone suppression test (cortisol levels fall)

37
Q

Acromegaly pathogenesis

2 steps two hormones

A

Overproduction of GH (e.g. tumour)

Acts on the liver to release IGF-1 (insulin-like growth factor-1)

38
Q

Comorbidities of acromegaly?

Why do some patients grow tall (gigantism)

A

Hypertension
Heart disease
Arthritis
T2D

Acromegaly before growth plates (epiphysis) fuse causes more long bone growth than normal

39
Q

Test for acromegaly?

A

Glucose tolerance test: Growth hormone is suppressed in response to glucose (due to somatostatin)
In acromegaly GH is unaffected by glucose

40
Q

Prolactinoma = Hyperprolactinaemia

Local effects and clinical features?

A

Local effects - pituitary tumour = bitemporal hemianopia, headache

Menstrual irregularity, infertility, Galactorrhoea (milk production in men and women) 
low libido (low testosterone)
41
Q

Treatment of Prolactinoma?

Which pathway would you make use of?

A

Tonic inhibition of prolactin secretion by dopamine - so use dopamine agonists (e.g. cabergoline)

42
Q

Cortisol circadian rhythm: trigger and regulation?

A

Light is the primary effector for cortisol circadian rhythm - highest on a morning with spikes at meals

43
Q

Adrenal insufficiency:
Primary?
Secondary?
Tertiary?

A 
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
Q

Adrenal crisis presentation (adrenal insufficiency)

A

Fatigue
Fever
Hypoglycemia
Hypotension and cardiovascular collapse

45
Q

Autoimmune thyroid disease
TPO associated with?
TSAb associated with?

Hypothyroidism (a.k.a?)

A

TPO - thyroid peroxidase antibodies = hashimoto’s thyroiditis = HYPOthyroidism

TSAb - thyroid stimulating antibodies IgG autoantibodies = Grave’s disease = HYPERthyroidism

Hyperthyroidism = myxoedema

46
Q

Grave’s disease:
Grave’s ophthalmopathy?
Goitre?

A

Eyelid retraction; periorbital oedema; protruding eyes
Antibodies cross react with the extraocular muscles

Goitre = diffuse or nodular enlargement of thyroid glands

47
Q

Thyroid autoimmunity risk factors (3 groups)

A 
Genetics (HLA-DR3)
Environmental factors (smoking/stress)
Endogenous factors (sex females>men)
48
Q

Hyperthyroidism 3 mechanisms of excess thyroid hormones in blood

A
  1. overproduction of thyroid hormone
  2. leakage of thyroid hormone
  3. ingestion of excess thyroid hormone
49
Q

Drugs that cause hypothyroidism? (4)

A

Iodine (required in the synthesis of thyroid hormone)
Amiodarone (iodine rich drug)
Lithium
Radiocontrast agents (reflexive hyperthyroidism)

50
Q

Clinical features of hyperthyroidism?

A 
Weight loss
Tachycardia 
Hyperphagia (increased appetite)
Anxiety
Tremor
Sweating
51
Q

Investigations of hypo/hyperthyroidism

A

Thyroid function test - assess free levels of T3/T4

Thyroid antibodies uptake scan

52
Q

Treatment of hyperthyroidism?

3 options

A

Antithyroid drugs: Thionamides e.g. Carbimazole

Radioiodine - reflexive hypothyroidism due to destruction of thyroid cells via radiation

Thyroidectomy

53
Q

Hypothyroidism
Primary?
Secondary?
Tertiary?

A

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
Q

Rare causes of hypothyroidism in children

A 
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
Q

Clinical features of hypothyroidism

A
  • Fatigue
  • Weight gain
  • Constipation
  • Cold intolerance
  • Muscle cramps
  • Dry, rough skin
  • reduced memory or cognition
56
Q

Treatment of hypothyroidism

A

Levothyroxine (L-thyroxine - T4)

Amiodarone (iodine rich drug structurally similar to T4)

57
Q

Preganancy and the thyroid: Preconception period is important for thyroid development
At what point does the feotus develop thyroid follicles?

A

Starts at 10 weeks

Phase 2 (4 decks)

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