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tACCP > Endo Physiology > Flashcards

Endo Physiology Flashcards

1
Q

What is the main function of the endocrine system?

A

Regulate homeostasis, growth, metabolism, and reproduction.

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2
Q

What is the difference between autocrine, paracrine, and juxtacrine signalling?

A
  • Autocrine: Acts on the same cell.
  • Paracrine: Acts on neighboring cells.
  • Juxtacrine: Requires direct cell-to-cell contact.
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3
Q

What are the main chemical classes of hormones?

A
  • Amino acids (e.g., adrenaline).
  • Peptides/proteins (e.g., insulin).
  • Steroids (e.g., cortisol).
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4
Q

How do lipid-soluble hormones exert their effects?

A

Bind intracellular receptors, affecting DNA transcription.

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5
Q

What are the primary mechanisms controlling hormone secretion?

A

Nervous system signals, other hormones, and metabolite levels.

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6
Q

Which hormones regulate metabolic fuel use?

A

Insulin, glucagon, cortisol, adrenaline, and growth hormone.

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7
Q

What happens during the anabolic state?

A
  • Increased insulin.
  • Glucose and FFAs taken up.
  • Activation of anabolic enzymes.
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8
Q

What happens during the catabolic state?

A
  • Increased glucagon.
  • Release of glucose and FFAs.
  • Activation of catabolic enzymes.
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9
Q

What are the consequences of insulin failure?

A

Hyperglycemia, ketoacidosis, coma, and death.

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10
Q

What are the consequences of excess insulin?

A

Hypoglycemia, coma, and death.

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11
Q

Where is insulin secreted?

A

Pancreatic β-cells.

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12
Q

What stimulates insulin release?

A

Increased plasma glucose, parasympathetic activity, and secretin.

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13
Q

Where is glucagon secreted?

A

Pancreatic α-cells.

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14
Q

What are glucagon’s effects?

A

Opposes insulin by promoting gluconeogenesis and glycogenolysis.

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15
Q

How does glucagon ensure basal insulin levels?

A

Stimulates insulin release.

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16
Q

What percentage of the UK population is diabetic?

A

~4-5%.

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17
Q

What are the two main types of diabetes?

A

Type 1 (autoimmune) and Type 2 (insulin resistance).

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18
Q

What percentage of diabetes cases are Type 2?

A

~90%.

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19
Q

What is the main pathophysiology of Type 1 DM?

A

Autoimmune destruction of β-cells.

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20
Q

What is the significance of GAD antibodies in Type 1 DM?

A

Marker of autoimmune β-cell destruction.

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21
Q

What are the plasma glucose thresholds for diabetes diagnosis?

A
  • Random: >11.1 mmol/L.
  • Fasting: >7.0 mmol/L.
  • OGTT: >11.1 mmol/L (2 hours post-test).
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22
Q

What does HbA1c measure?

A

Glycated hemoglobin, reflecting long-term glucose control.

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23
Q

What is the diagnostic HbA1c threshold?

A

48 mmol/mol (6.5%).

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24
Q

What is the role of C-peptide in DM diagnosis?

A

Differentiates Type 1 (low) from Type 2 (normal/high).

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25
Q

What are the three hallmark features of DKA?

A

Hyperglycemia, ketosis, and acidosis.

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26
Q

What causes DKA?

A

Insulin deficiency and uncontrolled catabolic state.

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27
Q

What are common triggers for DKA?

A

Infection, missed insulin doses, stress, and drug/alcohol use.

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28
Q

What are the key symptoms of DKA?

A

Polyuria, polydipsia, weight loss, and abdominal pain.

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29
Q

What are Kussmaul respirations?

A

Deep, labored breathing due to acidosis.

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30
Q

What metabolic abnormalities are seen in DKA?

A
  • Hyperkalemia (plasma).
  • Total body potassium deficit.
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31
Q

What is the anion gap in DKA?

A

Elevated (>12).

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32
Q

What is the primary goal of DKA treatment?

A

Correct dehydration, acidosis, and electrolyte imbalance.

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33
Q

What distinguishes HHS from DKA?

A

Extreme hyperglycemia without significant ketosis.

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34
Q

What is the plasma glucose level in HHS?

A

30 mmol/L.

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35
Q

What is the typical osmolality in HHS?

A

320 mOsm/kg.

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36
Q

What complications are associated with HHS?

A

Stroke, MI, DVT, cerebral edema.

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37
Q

What is the primary treatment for HHS?

A

Gradual normalization of osmolality, fluids, and glucose.

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38
Q

What are the two divisions of the pituitary gland?

A
  • Anterior (adenohypophysis).
  • Posterior (neurohypophysis).
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39
Q

How is the anterior pituitary controlled?

A

Via hypothalamic releasing and inhibiting hormones.

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40
Q

What hormones are stored in the posterior pituitary?

A

Oxytocin and vasopressin (ADH).

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41
Q

What hormones are secreted by the thyroid?

A

T3, T4, and calcitonin.

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42
Q

What is the primary action of thyroid hormones?

A

Increase metabolic rate via Na-K ATPase production.

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43
Q
A
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43
Q

Which thyroid hormone is more potent?

A

T3 (10x more than T4).

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44
Q

What percentage of T4 is bound in the blood?

A

~99.98%.

45
Q

What is the main transport protein for T4?

A

Thyroid-binding globulin (TBG).

46
Q

What is sick euthyroid syndrome?

A

Low T3 levels with normal/low TSH in critical illness.

47
Q

What causes thyrotoxic storm?

A

Poorly controlled hyperthyroidism with a precipitating event.

48
Q

What are the features of myxedema coma?

A

Decreased consciousness, hypothermia, and cardiovascular collapse.

49
Q

What is the primary treatment for thyrotoxic storm?

A

Carbimazole, propranolol, and iodine (post-blocking).

50
Q

What is the primary treatment for myxedema coma?

A

Gradual thyroid hormone replacement and supportive care.

51
Q

What are the three zones of the adrenal cortex?

A
  • Zona glomerulosa: Aldosterone.
  • Zona fasciculata: Cortisol.
  • Zona reticularis: Androgens.
52
Q

What hormones are secreted by the adrenal medulla?

A

Adrenaline and noradrenaline.

53
Q

What triggers cortisol release?

A

ACTH from the anterior pituitary.

54
Q

What is the diurnal pattern of cortisol release?

A

Peak in the morning, trough at night.

55
Q

What are the primary causes of adrenal insufficiency?

A

Autoimmune Addison’s, infections (TB, sepsis), malignancy.

56
Q

What are secondary causes of adrenal insufficiency?

A

Pituitary or hypothalamic dysfunction (e.g., Sheehan’s syndrome).

57
Q

What electrolyte abnormalities are seen in adrenal insufficiency?

A

Hyperkalemia, hyponatremia, and metabolic acidosis.

58
Q

What is the definitive test for adrenal insufficiency?

A

Short Synacthen Test.

59
Q

What is the emergency treatment for adrenal crisis?

A

Hydrocortisone 100 mg QDS.

60
Q

What distinguishes endocrine signaling from nervous signaling?

A

Endocrine signaling is slower, uses hormones in the bloodstream, and has widespread effects.

61
Q

What are the key features of peptide hormones?

A
  • Water-soluble.
  • Act on cell-surface receptors.
  • Quick onset but short duration.
62
Q

What are the key features of steroid hormones?

A
  • Lipid-soluble.
  • Act on intracellular receptors.
  • Slow onset but long-lasting effects.
63
Q

What role do G-protein-coupled receptors play in hormone signaling?

A

Activate intracellular signaling cascades (e.g., cAMP, IP3 pathways).

64
Q

How does negative feedback maintain hormonal balance?

A

A rise in hormone levels inhibits its further release.

65
Q

What secondary messenger system does glucagon primarily use?

A

cAMP signaling pathway.

66
Q

How does insulin affect glycogen synthesis?

A

Activates glycogen synthase in liver and muscle cells.

67
Q

What effect does insulin have on fat metabolism?

A

Promotes triglyceride formation and inhibits lipolysis.

68
Q

How does glucagon affect protein metabolism?

A

Stimulates amino acid mobilization for gluconeogenesis.

69
Q

What is the “basal state” in glucose regulation?

A

Resting condition where glucagon maintains blood glucose levels.

70
Q

What is the role of genetics in Type 1 DM?

A

HLA-DR3 and HLA-DR4 are genetic markers associated with increased risk.

71
Q

Why is Type 2 DM often associated with obesity?

A

Increased fat mass promotes insulin resistance through inflammatory cytokines.

72
Q

What is MODY (Maturity-Onset Diabetes of the Young)?

A

A monogenic form of diabetes caused by a single gene mutation.

73
Q

What is the significance of ketones in diabetes?

A

Indicate a shift to fat metabolism due to glucose unavailability.

74
Q

What are the vascular complications of DM?

A
  • Microvascular: Retinopathy, nephropathy, neuropathy.
  • Macrovascular: Stroke, MI, peripheral artery disease.
75
Q

What is euglycemic DKA?

A

DKA with normal glucose levels, often seen in SGLT2 inhibitor use.

76
Q

What distinguishes HHS from DKA?

A

HHS has higher glucose levels, no significant ketosis, and more severe dehydration.

77
Q

What is the role of sodium correction in DKA?

A

Accounts for pseudo-hyponatremia caused by hyperglycemia.

78
Q

Why is cerebral edema a complication of DKA treatment?

A

Rapid fluid shifts during treatment disrupt osmotic balance in the brain.

79
Q

What is the role of potassium in DKA management?

A

Replace potassium to prevent hypokalemia as insulin therapy lowers serum K+.

80
Q

What are tropic hormones?

A

Hormones that regulate the secretion of other hormones (e.g., TSH, ACTH).

81
Q

What is the role of the hypothalamic-pituitary portal system?

A

Transports releasing and inhibiting hormones directly to the anterior pituitary.

82
Q

What is Sheehan’s syndrome?

A

Postpartum pituitary necrosis due to ischemia from severe blood loss.

83
Q

Which hypothalamic hormone inhibits prolactin secretion?

A

Dopamine.

84
Q

What is the feedback loop for cortisol release?

A

Hypothalamus → CRH → Anterior pituitary → ACTH → Adrenal cortex → Cortisol.

85
Q

How is iodine used in thyroid hormone synthesis?

A

Iodine is incorporated into tyrosine residues to form T3 and T4.

86
Q

What is the Wolff-Chaikoff effect?

A

Excess iodine temporarily inhibits thyroid hormone synthesis.

87
Q

How does thyroid hormone influence cardiovascular function?

A

Increases heart rate and cardiac output by enhancing β-adrenergic sensitivity

88
Q

What is the most sensitive test for thyroid dysfunction?

A

TSH levels.

89
Q

What is the role of reverse T3 (rT3)?

A

An inactive form of T3 that competes for receptor binding.

90
Q

What is a toxic multinodular goiter?

A

Thyroid nodules that autonomously secrete thyroid hormones, leading to hyperthyroidism.

91
Q

What is a common cause of hypothyroidism worldwide?

A

Iodine deficiency.

92
Q

What is the pathophysiology of Graves’ disease?

A

Autoantibodies stimulate TSH receptors, causing excessive thyroid hormone production.

93
Q

How does subacute thyroiditis present?

A

Painful, tender thyroid with transient hyperthyroidism followed by hypothyroidism.

94
Q

What is the typical TFT pattern in sick euthyroid syndrome?

A

Low T3, normal/low TSH, and normal/low T4.

95
Q

How does cortisol affect blood glucose?

A

Increases gluconeogenesis and decreases glucose uptake in tissues.

96
Q

What is the primary action of aldosterone?

A

Increases Na+ reabsorption and K+ excretion in the kidney.

97
Q

What are the three stages of the stress response?

A
  • Alarm: Catecholamine release.
  • Resistance: Cortisol release.
  • Exhaustion: Prolonged stress leading to system failure.
98
Q

What is the role of DHEA?

A

A precursor to sex steroids, with minor androgenic effects.

99
Q

What is Cushing’s syndrome?

A

Chronic excess cortisol due to endogenous or exogenous causes.

100
Q

How does Addison’s disease present?

A

Fatigue, weight loss, hyperpigmentation, hypotension, and salt craving.

101
Q

What is the hallmark electrolyte abnormality in Addison’s?

A

Hyponatremia and hyperkalemia.

102
Q

What is adrenal crisis?

A

Life-threatening exacerbation of adrenal insufficiency with refractory hypotension.

103
Q

What causes secondary adrenal insufficiency?

A

Pituitary or hypothalamic dysfunction reducing ACTH production.

104
Q

What is the treatment for chronic adrenal insufficiency?

A

Hydrocortisone and, if necessary, fludrocortisone for aldosterone replacement.

105
Q

What is pheochromocytoma?

A

A catecholamine-secreting tumor of the adrenal medulla.

106
Q

What are the clinical features of pheochromocytoma?

A

Episodic headache, sweating, tachycardia, and hypertension.

107
Q

How is hyperaldosteronism diagnosed?

A

Elevated aldosterone-to-renin ratio.

108
Q

What is the function of growth hormone?

A

Stimulates growth and metabolism via IGF-1 from the liver.

109
Q

What is the role of somatostatin?

A

Inhibits the release of growth hormone, TSH, insulin, and glucagon.

110
Q
A

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