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Patho I - Exam #2: Endocrine > Module 2 > Flashcards

Module 2 Flashcards

1
Q

What is an A1C test?

A
  • reflects the average blood glucose values of previous 2-3 mo
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2
Q

How does an A1C work?

A
  • measures the % of Hb “coated” with glucose
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3
Q

What are A1C levels?

A
  • normal < 5.7%

- diabetes < or = 6.5%

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4
Q

Where does the pancreas secrete into?

A
  • duodenum
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5
Q

T/F: The pancreas has endocrine but not exocrine function.

A
  • False, both endocrine and exocrine
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6
Q

What area of the pancreas is relevant to its endocrine function?

A
  • Islets of Langerhans
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7
Q

What are the three cell types of the Islets of Langerhas?

A
  • alpha
  • beta
  • delta
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8
Q

What do alpha cells of the Islets of Langerhans secrete?

A
  • glucagon
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9
Q

What do beta cells of the Islets of Langerhans secrete?

A
  • insulin

co-secretion of amylin

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10
Q

What do delta cells of the Islets of Langerhans secrete?

A
  • somatostatin (technically not the same as the hypothalamic somatostatin but still think inhibitor)
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11
Q

What is the function of glucagon?

A
  • prevents hypoglycemia/mobilizes “metabolic fuels”
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12
Q

How does glucagon achieve its function?

A
  • increases blood glucose levels by mobilizing glucose and FFA
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13
Q

What is the relationship of glucagon and insulin?

A
  • opposite

- glucagon is antagonist to insulin

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14
Q

T/F: Glucagon is a catabolic hormone.

A
  • True
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15
Q

What is the target tissue of glucagon?

A
  • liver
  • fat
  • muscle
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16
Q

What does glucagon do in the liver?

A
  • glycogenolysis (breakdown of glycogen to glucose)

- glucogenesis (glucose formation)

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17
Q

What does glucagon do in the fat?

A
  • stimulates lipolysis
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18
Q

What does glucagon do in the muscle?

A
  • proteolysis
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19
Q

What is proteolysis?

A
  • breakdown for a.a. release but not efficient
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20
Q

In response to _______, glucagon is trying to make “____”

A
  • hypoglycemia

- fuel

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21
Q

What does glucagon increase blood levels of in response to hypoglycemia?

A
  • glucose
  • FFA & ketones
  • a.a.
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22
Q

What is the precursor for glucose and ketone formation?

A
  • FFA oxidation in the liver
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23
Q

What are used as fuel by the CNS, heart, and body?

A
  • ketones
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24
Q

What does excess ketones (and glucose) blood levels lead to?

A
  • acidosis (ketoacidosis)
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25
Q

What factors stimulate glucagon secretion from pancreas?

A
  • hypoglycemia (major)
  • exercise
  • stress
  • fasting
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26
Q

What factors inhibit glucagon secretion from pancreas?

A
  • hyperglycemia

- amylin

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27
Q

When is amylin secreted?

A
  • with insulin during feeding
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28
Q

What is the function of amylin?

A
  • suppress glucagon which leads to increased satiety/decreased appetite and inhibits GI mobility
  • inhibits plasma glucose (tells glucose to stay in pancreas)
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29
Q

What is the function of insulin?

A
  • prevents hyperglycemia

- promotes “metabolic fuel” storage

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30
Q

How does insulin make its functions?

A
  • decreases blood glucose levels by increasing uptake into cells
  • decreases blood levels of [a.a.] and FFA/ketones
  • decreases serum K+ levels by promoting uptake into cells
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31
Q

What two parts of the body DO NOT require insulin for glucose uptake?

A
  • brain

- RBC

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32
Q

Why are insulin and glucose administered for hyperkalemia?

A
  • decreases serum K+ levels by promoting uptake into cells
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33
Q

What is the target tissues of insulin?

A
  • liver
  • muscle
  • adipose tissue
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34
Q

What does insulin increase in the liver?

A
  • glucose uptake
  • form glycogen
  • lipid/protein synthesis
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35
Q

What does insulin decrease in the liver?

A
  • ketogenesis

- glycogenolysis

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36
Q

What does insulin increase in the muscle?

A
  • glucose uptake
  • form glycogen
  • a.a. uptake
  • protein synthesis
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37
Q

What does insulin decrease in the muscle?

A
  • glycogenolysis
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38
Q

What does insulin increase in the adipose?

A
  • glucose uptake
  • glucose to form glycerol phosphate
  • fat storage
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39
Q

What does insulin decrease in the adipose?

A
  • lipolysis
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40
Q

What factors stimulate insulin release from the pancreas?

A
  • hyperglycemia (major)
  • increased serum FFA & a.a. levels
  • GI/digestive hormones
  • parasympathetic stimulation of beta cells
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41
Q

What factors inhibit insulin release from the pancreas?

A
  • hypoglycemia
  • neg feedback loop
  • sympathetic stimulation of beta cells
  • prostaglandins (PGE2)
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42
Q

Describe obesity and its relationship with insulin regulation/Type II diabetes

A
  • increased insulin will down-regulate receptors
  • fewer receptors lead to glucose remaining elevated despite sufficient insulin
  • elevated glucose down-regulates receptors
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43
Q

What is the result of type II diabetes?

A
  • insulin resistance (decreased sensitivity)
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44
Q

What are the two types of diabetes mellitus?

A
  • type I

- type II

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45
Q

What are the three “poly’s” of diabetes?

A
  • polyuria (excessive urine production)
  • polydipsia (excessive thirst)
  • polyphagia (increased appetite)
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46
Q

What is DM type I?

A
  • insulin insufficiency d/t destruction of beta cells

- ? autoimmune

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47
Q

T/F: DM type I is not associated with obesity.

A
  • True
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48
Q

What is the result of DM type I?

A
  • hyperglycemia
  • hyperlipidemia
  • increased ketone bodies/ketoacidosis
  • catabolic affect on muscle mass
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49
Q

What is a risk of hyperlipidemia?

A
  • atherosclerosis from lipid deposits in blood vessels
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50
Q

What does metabolic acidosis lead to?

A
  • increase [H+] ==> coma & death
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51
Q

What is insulin shock?

A
  • reaction to hypoglycemia
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52
Q

What are causes of insulin shock?

A
  • excessive insulin admin
  • increased physical activity
  • poor glucose monitoring
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53
Q

What is the treatment for insulin shock?

A
  • bring glucose levels back up via oral or IV simple sugar or glucagon injection
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54
Q

What can improve DM type II?

A
  • diet changes

- exercise

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55
Q

What is OGTT?

A
  • oral glucose tolerance test
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56
Q

What are the values for a fasting plasma glucose test?

A
  • normal < 140mg/dL

- diabetes > or = 200mg/dL

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57
Q

What are the values for OGTT?

A
  • normal < 100 mg/dL

- diabetes > or = 140mg/dL

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58
Q

What is seen on a thyroid function lab panel?

A
  • TSH
  • T4
  • T3
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59
Q

What are the hormones of the thyroid gland?

A
  • T4 (thyroxine)
  • T3 (tri-iodothyronine)
  • calcitonin
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60
Q

Where are T3 & T4 synthesized?

A
  • follicle cells
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61
Q

Where are T3 & T4 stored?

A
  • follicle cavities (colloid)
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62
Q

Are T3 & T4 hydrophilic or lipophilic?

A
  • lipophilic
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63
Q

Describe the synthesis of T3 & T4

A

FOLLICLE CELL

  • tyrosine synthesized into TGB precursor
  • iodine pumped into cell
  • TGB binds iodine
  • TGB/I complex (aka T3/T4 with TGB) pumped into FOLLICLE CAVITY for storage
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64
Q

How is iodine pumped into the follicle cell?

A
  • TSH sensitive iodine pump

- captures 25% dietary iodine

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65
Q

Describe the secretion of T3 & T4

A
  • TRH released from hypothalamus
  • TRH stimulates ant. pit to release TSH
  • TSH stimulates transport of T3/T4 back into follicle cell
  • enzymes separate T3/T4 from TGB
  • T3 & T4 diffuse into bloodstream
66
Q

What is the percentage of T3 & T4 secreted into blood stream?

A
  • 90% T4
  • 10% T3
    (T4 significantly more than T3)
67
Q

How does T3/T4 circulate in the bloodstream and why?

A
  • bound to carrier proteins

- fat soluble

68
Q

How much of circulating T3/T4 is free?

69
Q

How is free T3 & T4 excreted?

70
Q

What can a free T3/T4 do that a protein bound T3/T4 cannot do?

A
  • enter cell

- protein bound must dissociate

71
Q

____ has 1000x the affinity for receptor than ____, therefore ____ is much more potent.

72
Q

Free (active) T4 has a ____ affinity for the receptor while free (actvite) T3 has a ____ affinity.

A
  • weak

- strong

73
Q

What are the two pathways for T4 once it enters the cell?

A
  • bind to receptor in cell nucleus

- convert to T3 of rT3 in cytoplasm/membrane

74
Q

What is the primary site of T4 to T3 conversion?

75
Q

How is T2 produced?

A
  • rT3 and any T3 not utilized
76
Q

What is the stimuli for thyroid hormone release?

A
  • metabolic demand
  • TSH
  • pregnancy (growth)
  • gonadal and adrenocortical steroids (growth)
  • extreme cold temp (stress/energy production)
  • catecholamines (stress)
77
Q

What inhibits thyroid hormone release?

A
  • negative feedback from elevated TSH
  • GHIH (somatostatin) (inhibits growth)
  • DA (PIH) (inhibits growth)
78
Q

What are the big picture functions of thyroid hormones?

A
  • growth & development (critical for CNS development)
  • control metabolism rate
    THEREFORE: regulate/influence every organ of the body
79
Q

What is affected in metabolism by thyroid hormones?

A
  • increases BMR and O2 of the body
  • increases BMR in all tissues except brain, spleen, testes
  • temperature regulation of increased heat from increased BMR
80
Q

What is affected in growth & development by thyroid hormones?

A
  • stimulates GH release

- CNS maturation is dependent

81
Q

What could a clinical sign be of decreased thyroid function on the CNS?

A
  • cognitive impairments
82
Q

What is the target tissue of thyroid hormone?

A
  • all cells except brain, gonads, and spleen
83
Q

What is the general action of thyroid hormone?

A
  • increased cellular respiration

- elevated BMR –> increased demand for fuel –> glycogenolysis & gluconeogenesis ==> increased liver glucose production

84
Q

What do thyroid hormones cause in the heart?

A
  • increased CO & CO via increased sensitivity to sympathetic system/E
85
Q

What do thyroid hormones cause in the vasculature?

A
  • vasodilation
86
Q

What do thyroid hormones cause in the pulmonary?

A
  • increased resp. rate via stimulation of ventilation center in brainstem
87
Q

What do thyroid hormones cause in the CNS?

A

STIMULATES:

  • myelin/axonal growth and development
  • sympathetic activity
88
Q

What do thyroid hormones cause in the adipose?

A
  • increased lipolysis (mobilize FFA for metabolic fuel)
89
Q

What do thyroid hormones cause in the muscle?

A
  • promote muscle protein growth/development synergistically with other growth hormones
90
Q

What will excessive levels of thyroid hormones cause in the muscle?

A
  • promote catabolic metabolism to provide fuel for increased BMR
91
Q

What do thyroid hormones cause in the bone?

A
  • promote bone growth/development synergisticaly with IGF-1/growth hormones
92
Q

What do thyroid hormones cause in the liver?

A
  • promote TG and cholesterol metabolism

- regulate LDL homeostasis

93
Q

What do thyroid hormones cause in the GI?

A
  • maintain GI secretions
94
Q

What do thyroid hormones cause in the pit. gland?

A
  • inhibits TSH
  • stimulates release of GH
  • stimulates synthesis of pit hormones
95
Q

What are the clinical symptoms of hyperthyroidism?

A
  • goiter
  • palpitations, HTN, increased pulse pressure, tachycardia, increased CO
  • elevated RR
  • hyperactive, fine tremor, increased “nervousness”, increased sympathetic activity
  • warm, moist skin (d/t elevated heat production from elevated BMR), excessive sweating, thin/fine hair
  • wt loss: muscle wasting, proximal weakness, fat loss
  • exophthalmos
  • increased motility and BMs
96
Q

What are two forms of symptoms that can produce exophthalmos associated with hyperthyroidism?

A
  • sympathetic hyperactivity leading to wide open eyes

- infiltrative changes (i.e. Graves dz)

97
Q

What are the forms of hyperthyroidism?

A
  • primary

- secondary

98
Q

What are the types of primary hyperthyroidism?

A
  • endogenous
  • iatrogenic
  • “thyroid storm”
99
Q

What is endogenous hyperthyroidism?

A
  • excessive TSI (thyroid-stimulating immunoglobulins) bind to TSH receptors and stimulate T3/T4
  • increased T3/T4 functions normally to negatively feedback and inhibit TSH
100
Q

What will the labs look like for endogenous hyperthyroidism?

A
  • elevated: TSI & T3/T4 (mostly T3)

- decreased: TSH & TRH

101
Q

What is an example of endogenous hyperthyroidism?

102
Q

What is iatrogenic hyperthyroidism?

A
  • excessive use of synthetic thyroixine
103
Q

What is “Thyroid Storm”?

A
  • rare but life threatening form of hyperthyroidism
104
Q

What is secondary hyperthyroidism?

A
  • continued secretion of TSH regardless of neg. feedback loop
105
Q

What are the types of hypothyroidism?

A
  • adult onset (primary)

- congenital (secondary)

106
Q

What is the most common cause of hypothyroidism?

A
  • Hashimoto’s thyroiditis (autoimmune)
107
Q

What is hypothyroidism?

A
  • malfunctioning thyroid which does not secrete T3/T4 in response to elevated TSH
108
Q

What will the labs look like for primary/adult onset hypothyroidism?

A
  • elevated TSH

- decreased T3/T4 (mostly T4)

109
Q

What happens to T4 when T3 and T4 are both low?

A
  • converted to T3 as the body demands
110
Q

What will the labs look like for secondary/congenital hypothyroidism?

A
  • decreased TSH
  • decreased T3/T4
    “all are low”
111
Q

Define goiter

A
  • enlarged thyroid gland
112
Q

What causes a goiter?

A
  • elevated TSH attempting to stimulate the thyroid
113
Q

T/F: A goiter always predicts abnormal thyroid function.

114
Q

What is Grave’s disease?

A
  • hyperthyroidism

- enlargement d/t immunoglobulins (TSI) stimulating thyroid gland to produce T3/T4

115
Q

What is Hashimoto’s disease?

A
  • hypothyroidism

- enlargement d/t elevated TSH trying to stimulate thyroid gland to produce T3/T4

116
Q

What is an iodine deficiency?

A
  • low dietary iodine inhibits sufficient production of T3/T4

- low T3/T4 negatively feeds back to increase TSH

117
Q

What are most physiological processes dependent on?

118
Q

Describe the ratio of calcium in the body

A
  • 98-99% stored in bone via mineralized form

- 1-2% “free” in ECF

119
Q

T/F: There is more calcium in the ICF than the ECF.

A
  • false, thousands of times less
120
Q

______ exchange of Ca2+ occurs constantly b/t _____, ______, ______, and the _____.

A
  • large
  • GI
  • bone
  • kidney
  • cells
121
Q

What are normal serum Ca2+ values?

122
Q

What are hypercalcemia serum values?

A
  • > 10.5mg/dL
123
Q

What does PTH do in relation to Ca2+?

A
  • stimulate osteoclasts within minutes to increase serum Ca2+ levels within 1-2hrs
124
Q

Who requires a positive calcium balance?

A
  • growing children
125
Q

What 3 organs maintain calcium exchange?

A
  • GI tract
  • kidney
  • bone
126
Q

Where is dietary/supplementary Ca2+ absorbed?

127
Q

What are the two forms of supplementary Ca2+?

A
  • calcium carbonate

- calcium citrate

128
Q

How is Ca2+ best dosed?

A
  • multiple, small doses
129
Q

What is the function of the kidneys in regards to Ca2+?

A
  • reabsorb Ca2+ from glomerular filtrate

- convert inactive Vit D to calcitriol

130
Q

What is the function of the bones in regards to Ca2+?

A
  • storage

- increase Ca2+ resorption to increase ECF Ca2+ (osteoclastic activity)

131
Q

What are the primary hormones that regulate ECF Ca2+?

A
  • PTH
  • calcitonin
  • calcitriol (active form of Vit D)
132
Q

What are the secondary “influencing” hormones that regulate ECF Ca2+?

A
  • GH
  • thyroid
  • adrenal/gonadal steroids
133
Q

Where is PTH synthesized and released from?

A
  • parathyroid gland
134
Q

What is the function of PTH?

A
  • increase plasma Ca2+ levels
135
Q

What are the target tissues of PTH?

A
  • bone

- kidney

136
Q

What is the activity of PTH in the bone?

A
  • stimulates osteoclastic activity (resorbs Ca2+ from the bone)
  • promotes phosphate release
137
Q

What is the activity of PTH in the kidney?

A
  • converts inactive vit D to active calcitriol
  • stimulates Ca2+ resorption in kidney tubules
  • stimulates phosphate excretion in kidney
138
Q

What stimulates PTH release?

A
  • small decreases of plasma Ca2+
139
Q

What inhibits PTH release?

A
  • elevated plasma Ca2+

- elevated calcitriol (neg. feedback)

140
Q

What does prolonged PTH stimulation cause the kidneys to produce?

A
  • more calcitriol
141
Q

What is calcitriol?

A
  • active form of Vit D
142
Q

What is the function of calcitriol?

A
  • increases plasma Ca2+ & phosphate levels

- other roles in immune and reproduction

143
Q

What is the target tissue of calcitriol?

A
  • intestine
  • bone
  • kidney
144
Q

What does calcitriol do in the intestine?

A
  • stimulates Ca2+ & phosphate absorption in sm. intestine
145
Q

What does calcitriol do in the bone?

A
  • stimulates osteoclastic activity (resorbs Ca2+ from the bone)
  • promotes phosphate release
146
Q

What does calcitriol do in the kidney?

A
  • stimulates Ca2+ resorption in kidney tubules

- stimulates phosphate resorption in kidney

147
Q

Which hormone stimulates phosphate resorption in kidney? excretion?

A
  • calcitriol

- PTH

148
Q

Which two hormones work synergistically?

A
  • calcitriol

- PTH

149
Q

What stimulates calcitriol release?

A
  • elevated PTH
150
Q

What inhibits calcitriol release?

A
  • decreased PTH
151
Q

What is calcitriol’s most important role?

A
  • plasma Ca2+ regulation via intestines
152
Q

PTH excretion of phosphate is much ______ than calcitriol resorption of phosphate.

153
Q

What is the “other” hormone of the thyroid gland and of Ca2+ homeostasis/balance?

A
  • calcitonin
154
Q

Where is calcitonin produced/secreted from?

A
  • parafollicular cells of the thyroid gland
155
Q

What is the function of calcitonin?

A
  • decrease plasma Ca2+ level

- promotes reabsorption of Ca2+ back into the bone

156
Q

Calcitonin has a minor role in maintaining plasma Ca2+ levels when compared to what?

A
  • PTH

- calcitriol

157
Q

What are the target tissues of calcitonin?

A
  • bone

- kidney

158
Q

What does calcitonin do in the bone?

A
  • inhibits Ca2+ resorption by inhibiting osteoclasts
159
Q

What does calcitonin do in the kidney?

A
  • stimulates Ca2+ and phosphate excretion in renal tubules
160
Q

What stimulates calcitonin release?

A
  • large increases in plasma Ca2+
161
Q

What inhibits calcitonin release?

A
  • decreased levels of plasma Ca2+

Patho I - Exam #2: Endocrine (4 decks)

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