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NUNP531 Applied Pathophysiology > Week 8 Endocrine > Flashcards

Week 8 Endocrine Flashcards

1
Q

There are 3 parts to the posterior pituitary gland: the
median eminence, the pituitary stalk and the pars nervosa.

Which part secretes hormones?

Which hormones does it secrete?

A

The pars nervosa secretes ADH and oxytocin.

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2
Q

What are some factors that might contribute to decreased secretion of antidiuretic hormone (ADH)?

A

ADH secretion decreases with:

-decreased plasma osmolality
-increased intervascular volume
-HTN
-alcohol ingestion
-increased estrogen, progesterone, or angiotensin II levels

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3
Q

How are intravascular volume changes monitored?

When is ADH secretion stimulated?

A

Intravascular volume changes from ADH secretion are monitored by baroreceptors in left atrium, carotid arteries, and aortic arch -> ADH secretion is stimulated by a volume loss of 7-25%

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4
Q

Where is ADH secretion regulated?

A

ADH secretion is regulated by osmoreceptors in hypothalamus, which are stimulated by increased plasma osmolality.

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5
Q

What actions stimulate oxytocin secretion?

A
  1. infant suckling; oxytocin binds to receptors in myoepithelial cells in mammary tissues, causing contraction of those cells, leading to milk expression (“let-down”)
  2. mechanical distensions of female reproductive tract at the end of labour, enhancing the effectiveness of contractions to promote delivery of placenta and post-partum clamp down of the uterus.
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6
Q

True or false:

Oxytocin has an antidiuretic effect similar to ADH.

A

True.

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7
Q

Where are the parathyroid glands located?

A

The parathyroid glands are located on the posterior aspect of the thyroid gland.

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8
Q

How many parathyroid glands are there?

A

There are usually 4 parathyroid glands but there can be between 2 and 6.

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9
Q

Which hormone is produced by the parathyroid glands?

What does this hormone do?

A

Parathyroid hormone (PTH).

PTH is responsible for regulating serum calcium levels.

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10
Q

When serum calcium is low, PTH is secreted.

What actions are stimulated to increase serum calcium?

A

PTH causes bone demineralization by stimulating osteoclast activity to release calcium

PTH stimulates the kidneys to reabsorb calcium into circulation

PTH increases absorption of calcium in the intestines

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11
Q

Calcium and ________ have a reciprocal relationship, thus PTH will also act on the kidneys to decrease __________ reabsorption. (same answer)

A

Phosphate

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12
Q

What are some possible causes for hypoparathyroidism?

A

Congenital, post-surgery or radiation, or from autoimmune disease.

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13
Q

Hypoparathyroidism leads to?

A

Hypocalcemia.

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14
Q

Hypoparathyroidism can lead to hypocalcemia.

What are the symptoms/manifestations of hypocalcemia?

A

Hypocalcemia affects nerve and muscle function causing weakness in cardiac muscle and excitability of nerves leading to muscle twitching and spasms (tetany)

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15
Q

What are some possible causes of hyperparathyroidism?

A

Adenoma, hyperplasia, secondary to renal failure

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16
Q

Hyperparathyroidism can lead to hypercalcemia.

What are the symptoms/manifestations of hypercalcemia?

A

Hypercalcemia causes forceful cardiac contractions, kidney stone risk, and osteoporosis as the high levels of PTH result in removal of calcium from the bone

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17
Q

The adrenal medulla, the inner part of an adrenal gland, controls hormones that initiate the…?

A

…the flight or fight response (Sympathetic Nervous System)

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18
Q

The adrenal medulla secretes _________, hormones that help your body respond to stress

A

Catecholamines

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19
Q

Catecholamines include adrenaline and noradrenaline, also known as…

A

Epinephrine and norepinephrine

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20
Q

Blood glucose concentration is determined by a balance between insulin and glucagon secretion by which organ?

A

Pancreas.

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21
Q

Increased blood glucose (e.g. after eating a meal) will trigger _______ in the pancreas to secret insulin.

A

B cells

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22
Q

Insulin will lower blood sugar levels by triggering tissue cells (such as fat or muscle cells) to take up glucose for energy and also by stimulating glycogen formation in the _____ (where glucose is stored as glycogen).

A

Liver

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23
Q

Reduction of blood glucose causes a reduction in _______ secretion and brings the system back to homeostasis.

A

Insulin

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24
Q

Low blood glucose levels trigger the release of glucagon from ________of the pancreas.

A

A cells

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25
Q

Which hormone is secreted with insulin and inhibits glucagon secretion?

A

Amylin plays a role in glycemic regulation by slowing gastric emptying and promoting satiety, thereby preventing post-prandial spikes in blood glucose levels.

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26
Q

Which hormone inhibits secretion of insulin and glucagon after glucose is broken down or transferred to cell?

A

Somatostatin.

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27
Q

Define metabolic syndrome.

A

A group of disorders (central obesity, dyslipidemia, prehypertension, and an elevated blood glucose level) that together give a high risk of development type 2 diabetes and associated cardiovascular complications.

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28
Q

Which two presentations are considered the strongest predictors for the development of metabolic syndrome.

A

Elevated triglycerides and waist circumference.

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29
Q

_________ is considered a proinflammatory and prothrombotic state.

A

Metabolic syndrome.

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30
Q

What are some complications associated with metabolic syndrome?

A

-Fatty liver disease
-Cirrhosis
-Chronic kidney disease
-CV disease
-Polycystic ovarian syndrome (PCOS)
-Obstructive sleep apnea (OSA)
-Gout

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31
Q

What are some risk factors for developing metabolic syndrome?

A

*Genetic predisposition.

*Weight gain, especially central/abdominal obesity.

*Females (postmenopausal)

*Childhood obesity.

*Smoking.

*High-carbohydrate diet, especially soft drink consumption.

*Lack of exercise

*Sedentary lifestyle.

*Insulin resistance.

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32
Q

What is the treatment plan for a patient who has been diagnosed with metabolic syndrome?

A

*Identify and treat pt with hyperglycemia

*Management of hypertension, dyslipidemia and abdominal obesity

*Diet modification, exercise (minimum 30min/day), weight loss, smoking cessation

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33
Q

A term referring to impaired fasting glucose (IFG), impaired glucose tolerance (IGT) or an elevated A1C%, each of which places individuals at high risk of developing diabetes.

A

Prediabetes.

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34
Q

The combination of FPG of 6.1 - 6.9 mmol/L and an A1C of 6.0% - 6.4% is predictive of 50% progression to type 2 diabetes over a 5-year period.

True or false?

A

False. It is 100% predictive.

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35
Q

Subclinical hypothyroidism is defined biochemically as_______ T4 in the presence of an elevated TSH.

(decreased / normal / elevated?)

A

Normal

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36
Q

An autoimmune disorder where autoreactive T cells and circulating autoantibodies target and infiltrate the thyroid, resulting in gradual inflammatory destruction

A

Hashimoto’s Thyroiditis.

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37
Q

Differentiate between primary hypothyroidism and secondary hypothyroidism.

A

Primary: Caused by disease in the thyroid

Secondary: Caused by disease in the pituitary or hypothalamus.

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38
Q

True or false?

Subclinical hypothyroidism may be associated with an increased risk of cardiovascular disease.

A

True.

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39
Q

Hypothyroidism affects all body systems and symptoms can vary in relation to the magnitude of TH deficiency. Generally, hypothyroidism leads to a slowing of metabolic processes and myxedema.

What signs and symptoms could you see in terms of metabolism and neuro?

A

Metabolism: Low metabolic rate, weight gain, cold intolerance, and slightly lowered basal body temperature.

Neuro: Lethargy, fatigue, memory or mental impairment, difficulty concentrating, and slowed speech or thinking.

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40
Q

Hypothyroidism affects all body systems and symptoms can vary in relation to the magnitude of TH deficiency. Generally, hypothyroidism leads to a slowing of metabolic processes and myxedema.

What signs and symptoms could you see in terms of the physical thyroid itself and CVS?

A

Thyroid: normal, small, or increased (Goitre).

Cardio: Bradycardia, hypertension, pericardial effusion.

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41
Q

Hypothyroidism affects all body systems and symptoms can vary in relation to the magnitude of TH deficiency. Generally, hypothyroidism leads to a slowing of metabolic processes and myxedema.

What signs and symptoms could you see in terms of respiratory and GI/Reproductive systems?

A

Resp: SOB, Pleural effusion.

GI/Repro: Constipation, heavy or irregular menstrual periods.

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42
Q

Hypothyroidism affects all body systems and symptoms can vary in relation to the magnitude of TH deficiency. Generally, hypothyroidism leads to a slowing of metabolic processes and myxedema.

What signs and symptoms could you see in terms of skin and GI/Reproductive systems?

A

Skin: Dry and flaky skin. Course and brittle hair with possible loss.

MSK: Delayed deep tendon reflexes, muscle aches, and paresthesia to hands and feet.

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43
Q

What are some presentations of myxedema?

A

Myxedema: Characteristic sign of severe or longstanding hypothyroidism. Usually seen in the eyes, hands, feet, and supraclavicular fossa. The tongue and laryngeal and pharyngeal mucous membranes can also thicken, producing thick, slurred speech and hoarseness.

Myxedema coma: Severe hypothyroidism. Mortality 30-50%. Usually occurs in undiagnosed or untreated hypothyroid patients, and can be precipitated by an acute event.

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44
Q

Pretibial myxedema is a presentation unique to which disease?

A

Graves disease.

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45
Q

↑TSH and normal fT4

Subclinical hypothyroidism or primary hypothyroidism?

A

Subclinical hypothyroidism.

In primary hypotension you will also see decreased fT4.

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46
Q

Which lab test may help determine if Hashimoto’s thyroiditis is the cause of hypothyroidism?

A

Anti-TPO (antithyroid antibody).

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47
Q

Treatment of hypothyroidism can be initiated and monitored by the family practitioner. Which patient conditions would you want to refer for?

A

A referral to endocrinology for certain patient situations which include, but is not limited to, hypothyroidism and:

pregnancy

goiter

thyroid nodules

pituitary dysfunction

cardiac disease

medications causing hypothyroidism (thyroid.ca)

48
Q

What is the pineal gland? What hormone does it secrete?

A

Located near centre of brain & comprised of photoreceptive cells that secrete melatonin

49
Q

What inhibits and stimulates melatonin secretion?

A

Light and dark

50
Q

What is melatonin synthesized from?

A

Tryrptophan (converted to serotonin, then melatonin)

51
Q

Functions of melatonin?

A

circadian rhythm, reproductive system incl. secretion of GRH and onset of puberty, immune regulation, may affect aging process, increases NO release from blood vessels, removes toxic free radicals & decreses insulin secretion

52
Q

Pancreas has both endocrine and exocrine functions. What does it produce in each?

A

endocrine = produces hormones
exocrine = produces digestive enzymes

53
Q

What part of the pancreas secretes hormones?

A

Islets of Langerhans

54
Q

Alpha cells in the pancreas islet of langerhans secrete what hormone?

A

Glucagon

55
Q

Beta cells in the pancreas islet of langerhans secrete what 2 hormones?

A

Insulin and amylin

56
Q

What 2 hormones are secreted from the delta cells of the pancreas (in Islets of Langerhans)

A

Gastrin & somatostatin

57
Q

F (or PP) cells – secrete what hormone in pancreas? (PP cells are in Islet of Langerhans)

A

pancreatic polypeptide

58
Q

Fx of insulin

A

*Promotes glucose uptake primarily in the liver, muscle & adipose tissue

*Decreases blood glucose levels

*Stimulate protein & fat synthesis

59
Q

T/F Insulin is regulated by chemical control only (not hormonal or neural)

A

FALSE. All of them.
*Secretion regulated by chemical, hormonal, and neural control

60
Q

What triggers release of insulin from the beta cells?

A

Released when beta cells stimulated by parasympathetic NS, usually before eating meal

Secretion can also be stimulated by increased blood glucose levels, increased amino acids (leucine, arginine, and lysine), and increased GI hormones (gastrin, glucagon, cholecystokinin, and secretin)

61
Q

What does Amylin do? When is it secreted?

A

Co-secreted with insulin by beta cells in response to nutrient stimuli

*Regulates blood glucose concentration by delaying gastric emptying and suppressing glucagon secretion after meals

  • Satiety effect

*Antihyperglycemic effect overall

62
Q

Where is glucagon made?

A

Alpha cells of pancreas + cells lining GI tract

63
Q

Where does glucagon act?

A

Mostly liver
Also muscle & fat tissue

64
Q

Function of glucagon?

A

*Increases blood glucose concentration in the liver by stimulating glycogenolysis

*Causes gluconeogenesis in muscle

*Causes Lipolysis in adipose tissue
(Glucagon is the ANTAGONIST to insulin)

65
Q

What inhibits and increases glucagon secretion?

A

*Inhibited by high glucose levels

*Stimulated by low glucose levels, sympathetic stimulation, and amino acids

66
Q

What does pancreatic somatostatin do? (Different than hypothalamic somatostatin!)

A
  • Released into bloodstream in response to food intake

*Regulates alpha & beta cell within the islets = inhibits secretion of insulin, glucagon & pancreatic polypeptide

*Essential to carbohydrate, fat, protein metabolism

67
Q

Function of gastrin?

A

*Targets stomach, stimulates secretion of gastric acid

68
Q

Where is ghrelin made?

A

Stomach
*Brain, small intestine & pancreas release small amounts of Ghrelin

69
Q

What does Ghrelin do?

A

Hunger hormone
*Stimulates GH secretion, controls appetite, plays a role in obesity & regulation of insulin sensitivity

70
Q

Fx of pancreatic polypeptide?

A

*Response to hypoglycemia and protein-rich meals

*Inhibits gallbladder contraction & exocrine pancreas secretion

*Frequently increased with Diabetes Mellitus & pancreatic tumors

71
Q

Where is pituitary located

A

In sella tucica of the sphenoid bone

72
Q

Describe the anterior pituitary

A
  • Accounts for 75% of pituitary
  • Connects to hypothalamus through stalk and hypophyseal blood vessels
  • Pars distalis (source of ant pit hormones)
    Pars tuberalis (layer of cells on stalk)
    Pars intermedia (between the others)
  • 2 main cell types: Chromophobes: non secretory
    Chromophils: secretory
73
Q

What are the two main cell types of the anterior pituitary? which one of these is secretory?

A

Chromophobes: non secretory
Chromophils: secretory

74
Q

Difference between tropic and somatotropic hormones

A

Tropic hormones (affect physiologic function of specific target organs
Somatotropic hormones (diverse effects on body tissues)

75
Q

List all the hormones released by the anterior pituitary

A

FSH, LH, TSH, MSH, GH, Prolactin

76
Q

Where is the thyroid located

A

in the neck, just below larynx, normally not palpable

77
Q

Describe the structure of the thyroid

A

-contains two lobes that lay on either side of the trachea, joined by a small band of tissue called the isthmus

-consists of follicles that contain follicular cells surrounding a viscous substance called colloid

-contain C-cells that secrete polypeptides

78
Q

What cells of the thyroid synthesize and secrete thyroid hormone

A

Follicular cells

79
Q

Other than thyroid hormones T3 and T4, what other hormone does the thyroid secrete? What cells secrete this?

A

Calcitonin

80
Q

What does calcitonin do

A

lowers serum calcium by inhibiting bone-reabsorbing osteoclasts

81
Q

How much TH is stored in thyroid

A

Approx 2 mo worth

82
Q

Describe the effects of TH

A

Significant effect on growth, maturation, and function of cells/tissue throughout the body

-essential for normal growth and neurological development in fetus/infant

-affects metabolic, neurological, cardiovascular, respiratory functions in all ages

-required for the metabolism and function of blood cells

-required for normal muscle functioning

-required for integrity of skin, nails, hair

-affects cell metabolismà increases heat production and oxygen consumption

83
Q

Describe the feedback loops that occurs if TH is low.

A

Low thyroid hormone levels sensed by hypothalamus, which releases TRH (thyroid releasing hormone) which stimulates the anterior pituitary to released TSH (thyroid stimulating hormone). This stimulates the thyroid to release TH (T3 and T4). Once released into circulation, TH are transported by thyroxine binding prealbumin, albumin, or lipoproteins. Only the unbound form is active. In tissues, T4 converts to T3, which acts on the target cell.

84
Q

Primary vs. secondary thyroid disorders

A

Primary thyroid disorders: alteration of TH levels with secondary feedback effects on TSH
Secondary (central) thyroid disorders- due to pituitary of hypothalamic alterations (disordered pituitary gland TSH production

85
Q

Describe the adrenal cortext

A

he Adrenal cortex is the outer aspect of the adrenal glands. The adrenal glands are paired organs behind the peritoneum and close to the upper pole of each kidney. The adrenal cortex is divided into three zones

86
Q

3 zones of adrenal cortex?

A

zona glomerulosa, zona fasiculata, zona reticularis

87
Q

What does each zone of the adrenal cortext secrete

A

Zona Glomerulosa

The outer layer. Primarily produces the mineralocorticoid aldosterone.

Zona Fasciculata (largest portion)

Middle layer. Secretes glucocorticoids: cortisol, cortisone and corticosterone.

Zona Reticularis

Inner layer. Secretes aldosterone, androgens/estrogens and glucocorticoids

88
Q

What effects do glucocorticoids have on the body

A

Glucocorticoids directly affect carbohydrate metabolism. They cause an increase in glucose concentration through gluconeogenesis in the liver and decreasing the use of glucose

Glucocorticoids also inhibit immune and inflammatory responses, suppress growth and promote protein breakdown `

89
Q

What are the effects of mineralcorticoids on the body

A

Mineralocorticoids directly affect ion transport by renal tubular cells

Aldosterone’s primary role is renal reabsorption of sodium and secretions of potassium and hydrogen

90
Q

Name the 3 mechanisms of regulation of the anterior pituitary

A

Anterior Pituitary

Regulated by

Secretion of hypothalamic peptide hormones or releasing factors

Feedback effects of the hormones secreted by target glands

Direct effects of other mediating neurotransmitters

91
Q

What regulates the release of ADH and oxytocin from the posterior pituiitarty?

A

Release of ADH and Oxytocin - regulated by:

Cholinergic and adrenergic neurotransmitters

Glutamate (to stimulate release)

GABA (to inhibit release)

92
Q

Describe ADH regulation

A

ADH regulation:

Primarily regulated by the osmoreceptors of the hypothalamus

When osmolarity increases the rate of ADH secretion increases to encourage water reabsorption in the kidneys

Increased secretion when baroreceptors sense changes in intravascular volume

A volume loss of 7 – 25% will stimulate increased secretion of ADH

Increases are also affected by stress, trauma, pain, exercise, nausea, nicotine, exposure to heat, and medications like morphine

Decreases are affected by decreased plasma osmolality, increased intravascular volume, HTN, alcohol, increase in estrogen, progesterone or angiotensin II levels

93
Q

Describe insulin and its general effects

A

Hormone- water soluble peptide
Secreted in pulsatile way in response to parasymp stimulation of beta cells, increased blood levels glucose/ AA, and GI hormones
ANABOLIC (building)
Net effects: stimulate protein and fat synthesis, reduce blood glucose levels

94
Q

Insulin action on liver

A

-increased glucose uptake

-increased glycogenesis, glycolysis, and gluconeogenesis (glycogen formation, breakdown of glucose to make pyruvate and ATP, formation of glucose from non carb substrates like amino acids)

-decreased glycogenolysis, ketogenesis, and urea cycle activity (decreases glycogen breakdown, decreases formation of ketone bodies)

95
Q

Insulin action on muscle?

A

-increased glucose uptake

-increased glycogenesis, glycolysis, amino acid uptake, and protein synthesis

-decreased glycogenolysis, proteolysis

96
Q

Insulin action on adipose?

A

-increased glucose uptake

-increased glucose use, glycolysis, fat esterification, fat storage

-decreased lipolysis

97
Q

Summarize glucose effects on liver, muscle, and adipose

A

Anabolic effect- builds stuff! (i.e., glycogen, protein, fat synthesis) and decreases blood glucose levels.

98
Q

What is type 2 diabetes

A

Type 2 Diabetes:

When the pancreas does not produce enough insulin or when the body does not effectively use the insulin that is produced.

May range from predominant insulin resistance with relative insulin deficiency to a predominant secretory defect with insulin resistance.

99
Q

What are the diagnostic criteria for T2DM

A

Fasting plasma glucose (FPG) - baseline fasting sugar, fasting of 8hrs, greater than or equal to 7.0mmol/L OR

FPG correlates most closely with 2-hour plasma glucose (2hPG) greater than or equal to 11.0mmol/L with a 75g oral glucose tolerance test (OGTT) OR

HbA1C greater than or equal to 6.5% (in adults). Not to use for suspected type 1 diabetes OR

Random plasma glucose: at any time of the day and is greater than or equal to 11.1 mmol/L.

100
Q

What is primary hypothyroidism

A

Deficient production of Thyroid Hormone by the thyroid gland

101
Q

What are the diagnostic criteria for primary hypothyroidism?

A

High serum TSH
Low serum T4

102
Q

What is considered the coordinating system of the endocrine system?

A

The hypothalamus

103
Q

How are steroid hormones excreted?

A

steroid hormones are excreted either directly by the kidneys or metabolized by the liver which inactivates them and makes them more water soluble for renal excretion

104
Q

How are peptide hormones excreted?

A

peptide hormones (e.g. hypothalamic hormones) are catabolized by circulating enzymes and eliminated via urine or feces

105
Q

Where is hypothalamus located? What structure connects it to the pituitary?

A

Located at base of the brain, connected to pituitary gland by pituitary stalk

106
Q

How does the hypothalamus talk to the anterior pituitary vs the posterior pit?

A

Connected to anterior pituitary by hypophysial portal blood vessels –> communicates via BLOOD SUPPLY to induce release of hormones

Connects to posterior pituitary via a nerve tract –> communicates via NERVE SIGNALS to induce release of hormones

107
Q

T/F The posterior pituitary makes its own hormones.

A

Posterior does NOT make its own hormones (just stores & releases ADH & oxytocin)

108
Q

What is the deal with neurosecretory cells in the hypothalamus?

A

Has neurosecretory cells that are similar to other neurons but can synthesize & secrete the hypothalamic-releasing hormones that regulate release of hormones from the anterior pituitary

These neurosecretory cells also synthesize ADH & oxytocin

Hypothalamic hormones have special circulation so that they reach their target cells in the pituitary in high concentrations

These hormones are small peptides that are generally active only at the relatively high concentrations achieved in the pituitary portal blood system

109
Q

Overall fx of the hypothalamus in hormone regulation…

A

Consolidates signals from upper cortical inputs, autonomic function, environmental cues such as light and temperature and peripheral endocrine feedback

Delivers precise signals to the pituitary gland

110
Q

What is considered the “master gland”

A

Pituitary

111
Q

Describe the structures that a hormonal signal passes through from the hypothalamus to the pituitary gland

A

Pituitary stalk connects median eminence to the pituitary gland

Hormones released from hypothalamus are released into median eminence and then move down pituitary stalk to pituitary gland.

112
Q

What is prediabetes?

A

This is a classification used for individuals with higher than normal glucose that do not yet meet diabetes diagnostic criteria

While people with prediabetes do not have increased risk for microvascular disease as seen in diabetes, they are at risk for the development of diabetes and CVD (cardiovascular disease).

People with prediabetes, particularly in the context of the metabolic syndrome, would benefit from CV risk factor modification.

113
Q

Diagnostic criteria for prediabetes?

A

Impaired fasting glucose: Fasting plasma glucose of 6.1-6.9 mmol/L

Impaired glucose tolerance: 2-hour plasma glucose in 75g oral glucose tolerance test of 7.8-11.0mml/L

A1C of 6.0%-6.4%

114
Q

What is subclinical hypothyroidism? What do you see on lab results (T4 and TSH)?

A
  • Normal serum T4 concentration + elevated serum TSH concentration.
  • Some pt’s may have vague nonspecific symptoms suggestive of hypothyroidism
  • Normally this disorder is diagnosed on the basis of lab test results
115
Q

Causes of subclinic hypothyroidism?

A

Causes are the same as those of overt (aka Primary) hypothyroidism.

Most pt’s have chronic autoimmune (Hashimoto’s) thyroiditis w/high serum concentrations of antithyroid peroxidase (anti-TPO) antibodies.

Other major causes: prior ablative or antithyroid drug therapy for hyperthyroidism caused by Graves’ disease; prior partial thyroidectomy; external radiation therapy in pt’s w/Hodgkin Lymphoma, leukemia, or brain tumours; inadequate T4 replacement therapy for overt hypothyroidism; drugs impairing thyroid function

116
Q

What is the diagnostic criteria for subclinic hypothyroidism

A

Usually just labs. Elevated TSH, normal T4

NUNP531 Applied Pathophysiology (24 decks)

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