Module 2 Flashcards
(133 cards)
1
Q
What does a HA1C test for?
A
The average blood glucose values of the previous 2-3 months
2
Q
What is indicated by an elevated HA1C? What are normal levels?
A
The greater amount of hemoglobin is glycated.
Normal /= 6.5%
3
Q
What is the endocrine function of the pancreas?
A
consists of several million clusters (islets) of cells. Islets of Langerhans produce glucagon, insulin and somatostatin.
4
Q
What do Langerhans alpha cells secrete?
A
glucagon
5
Q
What do Langerhans Beta cells secrete?
A
Insulin
6
Q
What do Langerhans delta cells secrete?
A
Pancreatic Somatastatin (not the same as hypothalamic somatastatin)
7
Q
What effect does glucagon have on insulin?
A
Glucagon is an antagonist for insulin
8
Q
What does glucagon function to do?
A
Prevents hypoglycemia by:
increasing blood glucose levels
Mobilizes fuel (catabolic)
Opposite (antagonist) action of insulin by “making glucose,” and “making ketones”—-catabolic effect of mobilizing fuel storage
9
Q
What are the target tissues for glucagon?
A
Liver
Fat tissue
Muscle
10
Q
How does Glucagon effect the liver?
A
Stimulates glycogenolysis, and glucogenesis
11
Q
How does glucagon effect the fat tissue?
A
Stimulates lypolysis (catabolic breakdown of fatty acids)
Ketogenic effect as FFA are metabolized in liver
Ketones are used as fuel by CNS
12
Q
How does glucagon effect the Muscle?
A
Proteolysis-breakdown for amino acid release. AA can be used as fuel but it is not very efficient
13
Q
What is the reasoning behind why glucagon functions in response to hypoglycemia?
A
In response to hypoglycemia: Glucagon tries to make “fuel” so it will increase blood levels of
Glucose
Free fatty acids and assoc. ketones
and Amino acids
14
Q
What is the precursor for glucose and ketone formation?
A
Free fatty acid (FFA) oxidation in the liver
15
Q
What stimulates glucagon secretion?
A
Hypoglycemia (Major factor), exercise, stress, fasting
16
Q
What factors inhibit glucagon secretion?
A
Hyperglycemia (negative feedback), Amylin
17
Q
When is Amylin secreted?
A
during feeding, co-secreted with insulin
18
Q
What does Amylin function to do?
A
Inhibits plasma glucose by slowing glucose entering blood via GI tract and liver:
Suppress glucagon
Increase satiety/decrease appetite
Inhibit GI mobility/emptying
19
Q
What does insulin function to do?
A
Prevents hyperglycemia by: Promoting metabolic “feul” storage.
Decreases blood glucose levels-increases uptake
Decreases AA concentration and FFA/ketones
Decreases serum potassium levels-promotes uptake
20
Q
Why is injection of insulin used in cases of excessive potassium? (hyperkalemia)
A
Insulin decreases serum potassium levels by promoting uptake of potassium into the cells
21
Q
T/F the brain and CNS also require insulin for glucose uptake?
A
F the brain and RBC do not require insulin for glucose uptake
22
Q
What are the 3 target tissues of insulin?
A
- Liver
- Muscle
- Adipose tissue
23
Q
What effect does Insulin have on the liver?
A
Increased: Glucose uptake, formation of glycogen, lipid/protein synthesis.
Decreased: Ketogenesis, glycogenolysis
24
Q
What effect does insulin have on muscle?
A
Increased: glucose uptake, formation of glycogen, amino acid uptake, protein synthesis
Decreased: glycogenolysis
25
What effect does insulin have on adipose tissue?
Increased: Glucose uptake, glucose to form glycerol phosphate, fat storage
Decreased: lypolysis
26
What factors stimulate insulin secretion from the pancreas?
Hyperglycemia
Increased serum AA, and FFA
GI/digestive hormones
Parasympathetic sim of pancreatic beta cells
27
What factors inhibit insulin secretion from the pancreas?
Hypoglycemia
Negative feedback loop (increased insulin levels)
Sympathetic sim of pancreatic beta cells
Prostaglandins (PGE2)
28
t/f the body can down or up regulate insulin receptors?
T. excessive insluin levls will decrease the number of insulin receptors
29
What is the explanation behind Type 2 / obesity diabetes
Down regulation /impairment of receptors of insulin results in insulin resistance (decread sensitivity) progresses.
30
What effect does obesity/sedentary exposure to elevated insulin levels have on the body?
Body becomes very inefficient at glucose metabolism
31
What effect does exercise: promotion of glucagon/inhibitory action on insulin have on the body?
The body becomes very efficient at glucose metabolism
32
DM type 1 is referred to as ___________ or _____ ______ diabetes.
Juveline-onset or insulin dependent
33
DM type 2 is referred to as ______ _______ or ____________ diabetes
Adult onset diabetes or non-insulin dependent d
34
What are the three poly's of diabetes?
polyuria
polydipsia
polyphagia (tissue cells can't get enough fuel despite elevated levels of plasma glucose-insulin is in charge of metabolic fuel storage, so if there is no way to hold on to the fuel stores the body doesn't feel full)
35
DM1 cause?
destruction of beta cells islet of Langerhans (evidence suggests autoimmune do)
36
What are the results of decreased insulin associated with DM1?
Hyperglycemia
Hyperlipidemia
Increased ketone bodies/ketoacidosis
Catabolic effect on muscle mass
37
What are the values and consequences and s/s of Hyperglycemia with DM1?
Cells unable to take up glucose from the blood.
Lab values: >180-200 mg/dl
s/s: polyuria, polydipsia
38
Around what blood glucose level does glucose start dumping into the urine?
200 mg/dl
39
What are the consequences of Hyperlipidemia due to decreased insulin in DM1?
Lack of insulin is inhibitory to fat storage
Promotes atherosclerotic changes in BV
Cells unable to uptake FFA
Increased FFA in blood leads to lipid deposits in blood vessels-atherosclerosis
40
What are the consequences of Increased ketone bodies/ketoacidosis?
Ketones form from inquired FFA metabolism in liver
The result of increased ketones is metabolic acidosis
this will increase raise H+ concentration and can result if severe in coma, death
41
What are the consequences s/s of the catabolic affect of muscle mass due to decreased insulin in DM1?
attempt to mobilize AA for "fuel"
| s/s: muscle wasting, wt loss, weakness/fatigue
42
Signs and sx of insulin shock
shaky, bradycardia, sweating, dizzy, anxious, hungry, blurry vision, weakness, fatigue, headache, irritability,
43
Tx for insulin schock?
Oral or IV administration of simple sugar
| Glucagon injection
44
What is the major cause for DM2?
obesity-occurs primarily in adults
45
What is the cycle of obesity and DM2?
Genetics and environmental changes cause inefficient blood glucose clearance--->inefficient clearance of glucose from blood stream and results in MORE insulin being secreted------>this increases the resistance (by down regulating the insulin receptors) and decreases insulin sensitivity------->inefficient blood glucose clearance.......
46
What can improve insulin sensitivity in a pt with DM2?
Diet changes and exercise can improve insulin sensitivity.
47
What are the parameters for fasting plasma glucose?
Fasting plasma glucose:
Fasting > 8 hours
normal < 100mg/dl
diabetes > 126mg/dl
48
What are the parameters for Oral glucose tolerance test?
Measure blood glucose before and 2 hours after administration of glucose.
Normal 200
49
What are the parameters for A1C?
Normal 6.5%
50
What is included in a thyroid function lab panel?
TSH-assess thyroid function
FT4: form that cana bind to target tissue (hypothyroid determ.)
FT3: Form that can bind to target tissue (most potent) (hyperthyroid determ.)
51
What are the hormones of the thyroid gland?
T3 (thyroxine), T4 (triiodothyronine), calcitonin
52
Where does synthesis and secretion of thyroid hormones occur?
In follicle cells of thyroid.
53
Where does storage of thyroid hormones occur after synthesis in the follicle cells of thyroid?
Storage in the colloid (follicle cavities)
54
pathway for synthesis of thyroid hormone?
1. TGB precursor in follicle cell
2. tyrosine is synthesized into TGB precursor
3. TSH sensitive ion pump transports iodide into follicular cell (and traps 25% of iodide "iodide trapping")
4. iodide that is trapped then bind to tyrosine/TGB molecule "organification"
5. T3 and T4 formed via coupling reaction of iodide-tyrosine molecules
6. TGB containing T3 and T4 are stored in colloid
55
What occurs after T3/T4 secreted from thyroid?
1. TSH stimulates endocytosis of T3/T4 back into follicle cell
2. Enzymes separate T3/T4 from TGB
3. T3/T4 diffuses into bloodstream
56
T/F T3 is found in much greater quantities than T4?
F. T4 = 90% and T3 = 10%
57
How does most T3 and T4 circulate in the bloodstream?
Bound to carrier proteins
58
What carrier proteins bind to T3 and T4?
TBG, Albumin, Transthyretin
59
What percent of T3 and T4 is found free thus active in blood?
0.03% of both
| They are fat soluble so can enter cell and bind to thyroid receptor, Measurements can indicate hyper/hypothyroid
60
Why is the biological activity of T3 so much greater than T4?
T3 has 100X the affinity for receptor than T4 therefore T3 is much more potent (weakly bound at carrier protein level and strongly bound to receptor of target tissue)
61
What is the fate of most of T4?
Conversion to T3 or rT3 and exists the cell. A very small percentage can bind and exert biological effect.
62
What is rT3? and what is its action on the cell?
Inactive T3 (or converted T4), blocks binding at the T2 site. Too much rT3 will act as an antagonistt by blocking available T3.
63
What is the primary site of T3 T4 conversion?
Liver
64
Why is the biological activity of T4 so much less than T3?
T4 is strongly bound to the carrier protein and the target cell of the effector organ has a weaker affinity for T4.
65
what is the purpose in the body of converting T4 to T3?
Serves as a circulating "reserve pool" of thyroid hormone to maintain free/active T3 levels
66
What is the final fate of both T3 and rT3
Conversion to T2 a completely inactive form of thyroid hormone
67
What stimulates thyroid hormone release?
```
Metabolic demand
TSH directly controls release of T3/T4
pregnancy
gonadal and adrenocortical steroids
extreme cold/temp environment
catecholamines (epinephrine/NE)-stress
```
68
What inhibits thyroid hormone release?
Serum levels of T3/T4 inhibit release of TSH from anterior pituitary (negative feedback)
GHIH (somatastatin)
Dopamine (prolacting inhibiting hormone)
69
What are thyroid hormones most critical in?
Growth/development, esp. CNS.
| Rate of metabolism
70
Target tissues of Thyroid Hormone?
All cells except brain, gonads, and spleen
71
What are the effects of an increase BMR?
Increase O2 consumption, heat production and increased demand for fuel
72
Liver produces glucose for fuel via?
Glycogenolysis
| Glucogenesis
73
Define glycogenolysis
Breakdown of glycogen stores to glucose
74
Define the action of glycogenesis
Breakdown of AA-from muscle
| Breakdown of glycerol and FFA from adipose tissue (lipolysis)
75
What effect does thyroid hormone have on the heart?
Ionotropic and chronotropic effects by increasing sensitivity to sympathetics. increases HR and SV
76
What effect does thyroid hormone have on Blood vessels?
Decrease total peripheral resistance to accommodate increase CO.
77
What effect does Thyroid hormone have on Brainstem relative to the CV system?
Ventilation center in the brain stimulates increased respiratory rate to supply increased O2
78
What effect does thyroid hormone have on the CNS?
Fetal/infant development critical!!! if limited T3/T4 cognitive impairment/CNS development.
Increases sympathetic activity
Overall systemic overdrive!
79
What effect does thyroid hormone have on Adipose tissue?
Increase lipolysis-mobilizes FFA for metabolic fuel. Catabolic to provide fuel for increased BMR.
80
What effect does thyroid hormone have on Muscle?
Promotes muscle protein growht/development synergistically w/ other growth hormones. Excess will promote catabolic met of muscle to provide fuel for increased BMR.
81
What effect does thyroid hormone have on bone?
Promote growth and development synergistically with GH/IGF-1. Stimulates osteoclast/osteoblast activity.
82
What effect does thyroid hormone have on GI?
Maintains secretions
83
What can happen with hyperthyroidism (Grave's Dz)
Thyroid-enlargement (goiter)
CV-Palpitations, HTN, Increased pulse pressure, tachycardia, increased CO
Pulm-elevated resp rate
CNS-hyperactivity, tremor, nervousness, increased sympathetic activity
Integumentary: Warm, moist skin (heat prod assoc. w/ BMR), thin hair
Excess sweating: elevated BMR, therm regulation, heat intolerance
Wt loss-muscle mass waste, proc weakness, fat loss
Eyes-exopthalmos
GI-increased motility-increased BM's
84
What is indicated by increased TSI, Increased T3/T4, Decreased TSH, Decreased TRH
Primary hyperthyroidism, Grave's DZ. (TSHdown, T3/4UP)
85
What is indicated by Normal TSI, Increased T3/T4 (mostly T3), Increased TSH, and decreased TRH?
Secondary hyperthyroidism (TSH and T3/T4 match increasing)
86
What is thyroid storm?
Rare life threatening, hyperthyroidism.
87
What is indicated by Decrease in T3/T4 (mostly T4), and increase in TSH
Primary hypothyroidism (myxedema-adult onset) (TSHup, T3/4DOWN)
88
What are the s/s of adult onset myxedema?
bilat. ptosis, puffy face, hands, feet, enlarged tongue, decreased BMR, cool dry skin, cold intolerance, decreased DTR's, Slow GI, fatigue, lethargy, slow cognitive fx.
89
What does congenital hypothyroidism/cretinism result in?
stunted growth, neuro/cognitive defect, infantile appearance
90
What is indicated by a decrease of both TSH and T3/T4?
Secondary hypothyroidism (deficient pituitary function)
91
What is the major player in Calcium homeostasis/balance?
PTH
92
What is the function of calcium?
```
in summary: most physiological processes are dependent on calcium:
formation of bone and teeth
membrane permeability
release of neurotrans.
muscle contractions
```
93
What percent of calcium is stored in mineralized form in the bone? Where is the remainder?
99% is in bone
| 1% is in a "pool" available for immediate exchange into blood stream (extracellular fluid)
94
What is the breakdown of the 1-2% ECF circulating calcium?
50%-free
45%-protein bound (albumin)
5%-phosphate/citrate bound
-so a tiny amount is really in the cell---most is free or bound to other molecules
95
T/F there is more calcium in the ICF (intracellular fluid) then in the Extracellular fluid
F there is a 1,000xs less in ICF than ECF
96
What is the role of calcium in ICF?
cell function: intracellular signaling, enzyme secretion, muscle contraction
97
What are the lab values for calcium levels?
Normal: 8-10mg/dl
Hypercalcemia: >10.5 mg/dl
Severe (crisis): 14-16mg/dl
98
What is the difference between the terms calcium homeostasis and calcium balance
Calcium homeostasis=moment to moment (osteoclast stimulation)
Calcium Balance = lifetime (bone density over life)
99
What three systems maintain calcium exchange?
GI tract, Kidneys, Bone
100
What is the function of the GI tract in Calcium exchange?
Absorption
101
What is the highest absorption possible for Calcium at one time?
500mg
102
What is the difference between calcium carbonate and calcium citrate?
Carbonate is cheaper and best absorbed with food
| Citrate is expensive, slight advantage of absorption (w/wout food)
103
What is the function of the kidney in calcium exchange?
1. Most calcium in glomerular fitrate is reabsorbed- 90% in PCT, and 8-9% late DCT collecting
2. Site of conversion of inactive vitamin D to active (calcitriol)
104
What is the function of Bone in calcium exchange?
1. Storage of calcium
| 2. Stimulation to increase calcium resorption
105
What are the primary regulatory hormones of ECF calcium?
PTH (parathyroid hormone)
Calcitonin
Calcitriol (active form of Vitamin D)
106
What are the secondary regulatory hormones of ECF calcium?
GH
Thyroid hormoes
Adrenal/gonadal steroid hormones
107
What is the location of synthesis and role of PTH?
Synthesized in Parathyroid glands, and increases plasma (ECF) calcium levels
108
What are the target tissues for parathyroid hormone?
Bone
| Kidney
109
What does PTH do to target tissue : Bone
Stimulates osteoclastic activity which promotes calcium resorption from bone
Increase of plasma (ECF) within 1-2 hours
Also promotes phosphate release from bone
110
What does PTH do to target tissue : Kidney
stimulates reabsorb calcium
stimulates conversion of inactive Vit D to active
Excrete posphate and bicarb
111
What might hyperparathyroidism result in (considering its role in the body)
Hypercalcemia, hypophosphatemia, metabolic acidosis (getting rid of too much bicarb), and hypercalciuria (dumping too much ca into urine)
112
What stimulates the release of PTH?
Small decreases of plasma (ECF) calcium
113
What inhibits the release of PTH?
Elevated ECF Plasma calcium and elevated active vitamin D (negative feedback)
114
What environmental exposure is necessary for Vitamin D formation?
Sunlight
115
What is the function of calcitriol?
```
Increased plasma (ECF) Calcium levels
also elevates phosphate levels in blood
Immune system function
```
116
What are the target tissues for calcitriol?
Intestine
Bone
Kidney
117
What is the role of Calcitriol at the target tissue : Intestine
Most important role in ECF calcium regulation
also stims phosphate absorption in small intestine
Stimulates calcium absorption in small intestine
118
What is the role of Calcitriol at the target tissue : Bone
Works synergistically with PTH
stimulates osteoclastic activity
also promotes phosphate release from bone
119
What is the role of Calcitriol at the target tissue : Kidney
Opposite of PTH (which excretes phosphate)-stimulates phosphate resorption in kidneys
PTH excretion of phosphate is much stronger than vitamin D resorption
120
What factor stimulates release of calcitriol?
Elevated PTH levels
121
What factor inhibits release of calcitriol?
Decreased PTH levels
122
Where is calcitonin secreted from? And what happens when you remove the thyroid gland?
the parafollicular cells of the thyroid gland. You can remove the thyroid and that will limit calcitonin but that won't have a huge impact on the body's ca levels
123
What is the primary function of calcitonin?
Decrease plasma ECF levels (opposite of PTH)
124
What are the target tissues and effects of calcitonin on bone and kidney?
Bone: Calcitonin inhibits calcium resorption by inhibiting osteoclasts
Kidney: Stimulates calcium (and phosphate) excretion in renal tubules
125
What stimulates calcitonin release?
Large increases of plasma (ECF) calcium
126
What inhibits calcitonin release?
Decreased levels of plasma (ECF) calcium
127
What is most common cause of hyperparathyroidism?
Neoplasms secreting PTH
128
Why will lab results of hypercalcemia be present with hyperparathyroidism?
Increased resorption of calcium from bone
Decreased renal excretion of calcium
increased intestinal absorption of calcium
129
Why will lab results of hypercalciuria be present with hyperparathyroidism?
Excessive hypercalcemia
| Kidney filtration overloaded...excess ca spill into urine
130
Why will lab results of hypophosphatemia be present with hyperparathyroidism
Low phosphate levels in blood due to increased phosphate excretion in kidneys
net effect of elevated PTH is decreased phosphate levels.
131
S/S of hyperparathyroidism:
```
Kidney stones
muscle weakness
polyuria, nocturia, polydipsia
confusion, drowsy, coma
nausea, vomit, constipation
potential decrease in bone density (with hyperparathyroidism not hypo)
```
132
s/s of hypoparathyroidism?
Neuromuscular excitability
muscle spasms, tetany
cardiac dysfunction
133
Lab symptoms of hypoparathyroidism?
hypocalcemia: increased excitability of tissue
nerve irritability
Hyperphosphatemia
