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M2 Endocrine > physiology + pathology > Flashcards

physiology + pathology Flashcards

1
Q

function of endocrine glands

A

endocrine glands secrete chemical substances (hormones) which travel through the bloodstream to effect changes in distant cells or organs

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2
Q

types of hormones

A

peptides and proteins (bind to cell surface receptors), amino acid derivatives, steroid derivatives (diffuse through plasma membrane and bind to intracellular receptors)

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3
Q

hypothalamic hormones

A

• thyrotropin releasing hormone
• gonadotropin releasing hormone
• corticotropin releasing hormone
• growth hormone releasing hormone
• growth hormone inhibitory hormone
• prolactin inhibiting hormone

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4
Q

growth hormone actions

A

promotes linear growth of skeleton in childhood, promotes growth of body tissues and intermediary metabolism, inhibits actions of insulin on carbs and lipids, increased protein synthesis and decreased catabolism of proteins and amino acids

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5
Q

regulation of growth hormone secretion

A

hypothalamic control: GH releasing hormone stimulates production of GH by somatotrophs –> GH stimulates secretion of IGF-1 by liver, somatostatin inhibits production of GH

thyroid and sex hormone stimulation of GH

negative feedback: IGF-1 inhibits GH and GnRH and stimulates somatostatin

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6
Q

factors affecting GH secretion

A

diurnal variation, age, body weight, stress, exercise, blood glucose, amino acids

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7
Q

tests for GH

A

exercise GH stimulation test, glucose tolerance test, IGF-1 blood conc test

NOTE: random blood glucose test for GH is not indicative because GH secretion is episodic

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8
Q

GH deficiency syndromes

A
  1. dwarfism: all physical parts of body develop in the appropriate proportions but rate of development decreased
  2. panhypothyroidism: tumour compressing pituitary gland –> ant pit cells destroyed –> hypothyroidism, decreased production of glucocorticoids by adrenal glands, suppressed secretion of GH
  3. Kallmann syndrome: congenital hypogonadotropic hypogonadism
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9
Q

GH excess syndromes

A
  1. gigantism: excess GH before adolescence (and fusion of growth plates) leading to height increase and excessive growth of long bones, usually caused by pit gland tumour
  2. acromegaly: excess GH after adolescence, bones become thicker and soft tissues continue to grow –> lower jaw protrusion, forward slant of forehead, large nose feet hands, enlargement of soft tissue organs
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10
Q

antidiuretic hormone (ADH) actions

A

collecting ducts of renal tubules becomes permeable to water due to fusion of aquaporins into the collecting duct membrane, causing water to be reabsorbed into the blood –> urine is concentrated and in small volume

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11
Q

regulation of ADH secretion

A
  1. real decrease in ECF volume
  2. baroreceptors detecting change in ECF volume

low ECF volume causes ADH to be released from the posterior pituitary

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12
Q

causes of polydipsia (thirst) and polyuria (high urine output)

A
  1. diabetes mellitus causing osmotic diuresis
  2. diabetes insipidus causing ADH deficiency (central) or ADH resistance (nephrogenic)
  3. psychiatric cause (primary polydipsia)
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13
Q

T3 and T4 actions

A
  1. brain development in fetal and postfetal life
  2. growth (GH production)
  3. regulation of growth metabolism: increases basal metabolic rate, has thermogenic actions
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14
Q

tests for thyroid hormones

A

free T4 levels

NOT T3: can come from thyroid gland or other tissues, most serum T3 comes from the peripheral conversion of T4 to T3

NOT total T4: only free T4 is physiologically active and bound T4 doesn’t contribute to hyperthyroidism

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15
Q

hypothyroidism causes

A

primary hypothyroidism: disease affecting thyroid gland, T4 is low but TSH is high (eg Hashimoto Thyroiditis, dietary iodine deficiency)

secondary hypothyroidism: disease affecting pituitary gland, T4 is low and TSH is low/normal

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16
Q

symptoms of hypothyroidism

A

cretinism (in childhood cases), slow thinking, cold intolerance, slow HR, sluggishness, (may have a goiter)

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17
Q

hyperthyroidism causes

A

primary hyperthyroidism: disease affecting thyroid gland, T4 is high, TSH is low (eg Grave’s disease, subacute thyroiditis)

secondary hyperthyroidism: disease affecting pituitary gland, T4 is low, TSH is high/normal (eg TSH producing tumour in pituitary gland)

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18
Q

pathophysiology of Grave’s disease

A

• autoimmune condition where thyroid stimulating immunoglobulins stimulate thyroid gland to be overactive
• GRAVES SPECIFIC: exothalmos, proptosis, upper eyelid retraction, dryness and irritation of eyes

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19
Q

pathophysiology of subacute thyroiditis

A

• viral infection affecting thyroid gland, causing inflammation
• dying thyroid cells leak out preformed thyroid hormones into circulation
• disease subsides after a few weeks or months

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20
Q

symptoms of hyperthyroidism

A

heat intolerance, weight loss, increased HR, heart palpitations, fatigue and insomnia, hands tremor, nervousness, increased sweating, thyroid gland hyperplasia

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21
Q

pathophysiology of pheochromocytoma

A

tumour of adrenal medulla producing adrenaline and/or norepinephrine, resulting in increased BP, HF, pulmonary edema, stroke, sudden death

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22
Q

aldosterone actions

A

increases Na+ reabsorption in collecting ducts, increases ECF volume, enhances K+ secretion in collecting ducts

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23
Q

regulation of aldosterone secretion

A

RAAS regulation: angiotensinogen –> angiotensin I by renin –> angiotensin II by ACE, angiotensin II stimulates aldosterone release

[K+] in blood: acts directly on aldosterone producing cells when [K+] is high (above 3.5-5mmol/L) to produce more aldosterone

adrenocorticotropic hormone (ACTH): released from anterior pituitary to stimulate aldosterone production

24
Q

symptoms of aldosterone excess

A

hypokalemia (muscle weakness and paralysis), hypertension (increase in ECF volume), mild metabolic alkalosis

NOTE aldosterone escape: increase in ECF volume can lead to renal perfusion pressure increase and excretion of Na+ and H2O (pressure natriuresis and diuresis)

25
Q

symptoms of aldosterone deficiency

A

hyperkalemia, cardiac toxicity, severe ECF dehydration and low blood volume, natriuresis and diuresis

26
Q

actions of cortisol

A

survival during stress, intermediary metabolism, vascular reactivity of catecholamines (adrenaline and norepinephrine)

pharmacological effects: anti-inflammatory effects, suppression of immune system

27
Q

regulation of cortisol secretion

A

corticotropin releasing hormone (CRH): released by hypothalamus, carried to ant pit to induce ACTH secretion, ACTH stimulates cortisol secretion in the adrenal cortex

physical, mental or emotional stress: enhances ACTH –> cortisol secretion

negative feedback from cortisol: decreases formation of CRH and ACTH (but stress can override this inhibition)

28
Q

tests for cortisol

A
  1. plasma/urine cortisol (measure over 24h due to circadian variation)
  2. dexamethasone suppression test: can suppress CRH and ACTH to distinguish between pituitary gland disorder (will still have high ACTH) and primary adrenal disorder (low ACTH)
  3. ACTH levels in blood: low ACTH indicates adrenal gland overproduction (negative feedback to ant pit), normal/high ACTH indicates ant pit overproduction
  4. ACTH injection for adrenal insufficiency: measure cortisol response - if low, adrenal gland failure
29
Q

pathophysiology of Cushing’s syndrome

A

excess amounts of cortisol caused by: ACTH producing pituitary tumour, abnormal hypothalamus, ectopic ACTH syndrome, adrenal cortex adenoma, iatrogenic corticosteroid medication

leading to: buffalo torsal, truncal obesity, moon face and red cheeks, hypertension, increased blood glucose concentration, decreased tissue proteins, muscle weakness, suppressed immune system, osteoporosis

30
Q

types of adrenal failure

A

primary: Addison’s disease (failure of adrenal cortices to produce adrenocortical hormones)

secondary: due to ACTH deficiency (aldosterone levels remain normal)

31
Q

concentration of calcium in the body

A

50%: ionised/free, diffusible through capillary membrane
41%: combined with plasma proteins, non-diffusible through capillary membrane
9%: complexed with anions of plasma and interstitial fluids, non ionised, diffusible through capillary membrane

more calcium is bound to proteins in alkaline pH

32
Q

composition of bone

A

hydroxyapatite, osteoid, osteoblasts, osteocytes, osteoclasts, chondrocytes

33
Q

process of vit D formation

A

7 - dehydrocholesterol –> (UV rays) vitamin D3 –> (liver) 25-hydroxycholecalciferol –> (kidneys) 1,25-dihydroxycholecalciferol aka active form of vit D

vit D can also be obtained from the diet (eg fatty fish)

34
Q

regulation of vit D formation in the kidneys

A

positive feedback by parathyroid hormone, negative feedback by increased concentrations of phosphate (PO4-)

35
Q

vitamin D actions

A

promotes PTH effect on bone resorption, increases kidney calcium and phosphate reabsorption, increases GIT calcium and phosphate absorption for bone mineralisation

36
Q

regulation of parathyroid hormone

A

decrease in ECF [Ca2+] detected by calcium sensing receptors on parathyroid gland cells –> PTH secretion –> increase in ECF [Ca2+] –> PTH secretion suppressed

37
Q

parathyroid hormone actions

A

activation of existing osteocytes to promote calcium and phosphate absorption, proliferation of osteoclasts and increased osteoclastic reabsorption of bone, decreased phosphate reabsorption in PCT, increased calcium reabsorption in DCT and activation of vitamin D

38
Q

regulation of calcitonin secretion

A

secreted by C/parafollicular cells in thyroid gland as stimulated by high [Ca2+]

39
Q

action of calcitonin

A

decreases resorption of bone (opposes PTH and vit D actions), decreases calcium resorption in kidney

40
Q

fibroblast growth factor 23 regulation

A

secretion stimulated by high [PO42-], formed by osteoblasts and osteocytes

41
Q

fibroblast growth factor 23 action

A

decreases PCT and gut phosphate reabsorption, decreases concentration of active vit D

42
Q

pathophysiology of hypocalcemia

A
  1. hypoparathyroidism leading to PTH deficiency
  2. vitamin D deficiency

increased excitability of nervous system leading to tetany and musculopathies, neuropathies, cardiopathies, poor dentition, nail and hair issues

43
Q

pathophysiology of hypercalcemia

A
  1. hyperparathyroidism leading to overproduction of PTH
  2. vitamin D intoxication
  3. malignancy: certain lung cancers can secrete PTH
44
Q

vitamin D deficiency syndromes

A
  1. rickets: lack of vitamin D in children causing bone to be undermineralised, low phosphate levels and extreme osteoclastic resorption of bone
  2. osteomalacia: usually steatorrhea in adults leading to vitamin D deficiency
45
Q

pathophysiology of osteoporosis

A

resorption of bones > formation of bones, osteoblastic activity decreased and/or osteoclastic activity increased

causes: postmenopausal decrease in estrogen, inactivity and lack of physical stress on bones, lack of vitamin C, malnutrition, old age, Cushing’s syndrome

46
Q

actions of insulin

A

increase glucose uptake, glycogen synthesis, fat synthesis, protein synthesis, glycolysis

47
Q

actions of glucagon

A

glycogenolysis, lipolysis, gluconeogenesis, ketogenesis

48
Q

hormones regulating the fasted state

A

epinephrine (glycogenolysis, lipolysis, gluconeogenesis), cortisol (lipolysis, proteolysis, gluconeogenesis, ketogenesis), growth hormone (lipolysis)

49
Q

types of diabetes mellitus

A

type 1: absolute insulin deficiency causing disordered metabolism, autoimmune disease usually presenting in youth

type 2: relative insulin deficiency with insulin resistance causing disordered metabolism, multifactorial causes including genetics

50
Q

normal blood glucose levels

A

random: 4-7.8mmol/L
fasting: 4-6mmol/L
post-prandial: 4-7.7mmol/L

51
Q

indicators of metabolic syndrome

A
  1. waist circumference: ≥90cm (men), ≥80cm (women)
  2. high triglyceride ≥1.7mmol/L
  3. high fasting glucose ≥6.1mmol/L
  4. high blood pressure ≥130/85 mmHg
  5. low HDL cholesterol ≤1.0mmol/L (men) or ≤1.3mmol/L (women)
52
Q

effects of metabolic syndrome

A

adipose tissue dysfunction
persistent low-grade inflammation (M2 macrophages become M1 macrophages)
insulin resistance
physical indicators: apple body shape and high amounts of abdominal fat

53
Q

diagnosis of diabetes mellitus

A
  1. fasting blood glucose ≥7.0
  2. oral glucose tolerance test ≥11.1
  3. HbA1C > 6.9%
54
Q

effects of diabetes mellitus

A

high plasma glucose, accumulation of ketone bodies (type 1, ketoacidosis), retinopathy, nephropathy and nephrotic syndrome, vascular damage, neuropathy, osmotic diuresis

55
Q

diagnosis of hypoglycemia (Whipple’s triad)

A
  1. low blood sugar
    level 1: 3.0-3.9mM
    level 2: 2.2-2.9mM
    level 3: <2.2mM
  2. symptoms of hypoglycemia
  3. relief of symptoms upon eating
56
Q

symptoms of hypoglycemia

A

cold sweats, palpitations, shakiness, headache

severe: weakness, blurred vision, slurred speech, confusion and abnormal behaviour, seizures

57
Q

causes of hypoglycemia

A
  1. insulin excess
  2. medications
  3. insulinomas

M2 Endocrine (3 decks)

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