Exam 4: Endocrine Part I Flashcards
(113 cards)
1
Q
A normal glucose level requires a balance btw ____ and ____ of dietary carbohydrate intake
A
glucose usage and endogenous production
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2
Q
____ is the primary source of endogenous glucose production via glycogenolysis & gluconeogenesis
A
The liver
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3
Q
70-80% of the glucose released by the liver is metabolized by insulin-insensitive tissues such as the _____, _____, and _____.
A
brain, GI tract, and red blood cells
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4
Q
____ hours after eating, when glucose usage exceeds production, a transition from exogenous usage to endogenous production occurs to maintain a normal plasma glucose level
A
2-4
During this time, diminished insulin production is fundamental for the maintenance of normal blood glucose
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5
Q
what hormones comprise the glucose counterregulatory system and support glucose production
A
glucagon, epinephrine, growth hormone, and cortisol
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6
Q
Glucagon plays a primary role by stimulating____, and inhibiting ____.
A
Stimulates: glycogenolysis &gluconeogenesis
Inhibits: glycolysis
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7
Q
Diabetes mellitus is the most common endocrine disease
and affects ____ in 10 adults
A
1
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8
Q
DM results from an inadequate supply of ____ and/or an inadequate ____.
A
- insulin
- tissue response to insulin
- This leads to increased circulating glucose levels with eventual microvascular and macrovascular complications
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9
Q
Type 1a diabetes is caused by a T-cell–mediated autoimmune destruction of ____ within pancreatic islets, leading to ____circulating insulin levels
A
- β cells
- minimal or absent
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10
Q
Type 1b diabetes is a rare disease of absolute insulin deficiency, which is not ____.
A
immune mediated
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11
Q
Type 2 diabetes is also not immune mediated and results from defects in ____ and post-receptor ____ signaling pathways
A
- insulin receptors
- intracellular
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12
Q
Type 1 DM
- Accounts for ____% of all DM cases
- Usually diagnosed before age ____
- Exact autoimmune cause of type 1a is unknown
- A long pre-clinical period (____) of B-cell antigen production precedes onset of symptoms
- At least ____% B cell function is lost before hyperglycemia ensues
A
- 5-10%
- 40 yo
- 9-13 yrs
- 80-90%
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13
Q
Hyperglycemia over several days/weeks is associated w/
A
- fatigue
- weight loss
- polyuria
- polydipsia
- blurry vision
- hypovolemia
- ketoacidosis
14
Q
Type 2 DM
- accounts for >____% DM cases
- Increasingly seen in younger pts & children over the past decade
- Very underrecognized, normally present ____ years before diagnosed
A
- > 90%
- 4-7 years
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15
Q
In initial stages of type 2 DM, insensitivity to insulin on peripheral tissues leads to
A
↑pancreatic insulin secretion
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16
Q
as DM progresses ____ function decreases and ____ levels become inadequate.
A
- pancreatic function decreases
- insulin levels become inadequate
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17
Q
3 main abnormalities seen in DM2
A
- ↑hepatic glucose release caused by a reduction in insulin’s inhibitory effect on liver
- Impaired insulin secretion
- Insufficient glucose uptake in peripheral tissues
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18
Q
DM2 is characterized by insulin resistance in?
A
skeletal muscle, adipose & liver
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19
Q
Causes of insulin resistance include:
A
- Abnormal insulin molecules
- Circulating insulin antagonists
- Insulin receptor defects
- Obesity and sedentary lifestyle are acquired and contributing factors
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20
Q
Diagnosis for Type 2 DM
A
- fasting blood glucose
- HbA1c
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21
Q
Diagnosing prediabetes or diabetes
- normal HbA1C?
- PreDM HbA1C?
- DM HbA1C?
A
- normal HbA1C: < 5.7%
- PreDM HbA1C: 5.7-6.4%
- DM HbA1C: >/= 6.5%
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22
Q
what are the 4 steps from the american DM association criteria for the diagnosis of DM?
A
- A1C >6.5%: the test should be perfomed in a laboratory using a method that is NGSP certified and standardized to the DCCT assay
- FPG?126mg/dL (7mmol/L) Fasting is definied as no caloric intake for at least 8hr
- 2-hour plasma glucose greater than/equal to 200mg/dL during an OGIT. the test should be performed as described by the WHO using a glucose load containing the equivalent of 75g dissolved in water
- In a pt with classic symptomes of hyperglycemia or hyperglycemic crisis, a random plasma glucose greater than or equal to 200mg/dL (11.1mmol/L)
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23
Q
Treatmeant for DM2
A
- dietary adjustments
- exercise/weight loss
- PO antidiabetic drugs
- insulin
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24
Q
how does exercise and weight loss treat DM2?
A
Decreasing body fat improves hepatic & peripheral insulin sensitivity
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what are PO antidiabetic drugs?
* metformin
* sulfonylureas
| slide 9
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What is metformin and how does it treat DM2?
* A biguanide, preferred initial drug tx
* Enhances glucose transport into tissues
* ↓TGL & LDL levels
| slide 9
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how do sulfonylureas treat DM2?
* Stimulate insulin secretion
* Enhances glucose transport into tissues
* d/t diabetic progressive loss of B cell function, Sulfonylureas not effective long term
* SE’s include hypoglycemia, weight gain & cardiac effects
| slide 9
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What is the initial therapy and additional therapy for DM2?
| slide 10
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____ is necessary in all DM1 cases and 30% of DM2 cases
insulin
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what are the different types of insulin?
* Rapid acting (Lispro, Aspart) provide glucose-control @ mealtimes
* Short acting (regular)
* Basal/Intermediate acting (NPH, Lente)
* Long acting (Ultralente, Glargine)
| slide 11
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* what is the most dangerous complication of long acting insulin?
* what exacerbates this complication?
* Hypoglycemia is the most dangerous complication
* ETOH, metformin, sulfonylureas, ACE-I’s, MAOI’s, Non-selective BB’s
| slide 11
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* Repetitive hypoglycemic episodes lead to “____”
* Pt becomes desensitized to hypoglycemia and doesn’t show ____ sx
* ____ ensues→fatigue, confusion, h/a, seizures, coma
* Tx: ___
* hypoglycemia unawareness
* autonomic
* Neuroglycopenia
* TX: O or IV glucose (may give SQ or IM if unconscious)
| slide 11
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# Short Acting inslulin
What is onset, peak and duration of:
* Human regular
* lispro [humalog]
* aspart [novolog]
Human regular
* O: 30 min
* P: 2-4 hr
* D: 5-8 hr
lispro [humalog] & aspart [novolog]
* O: 10-15 min
* P: 1-2 hr
* D: 3-6hr
| slide 12
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# Intermediate Acting Insulin
What is onset, peak and duration of:
* human NPH
* Lente
* human NPH and Lente
* O: 1-2 Hr
* P: 6-10 Hr
* D: 10-12HR
| slide 12
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# Long acting insulin
What is onset, peak and duration of:
* ultralente
* glargine (lantus)
* ultralente
* O:4-6hr
* P 8-20hr
* D:24-48hr
* glargine (lantus)
* O: 1-2 hr
* P: n/a
* D: 24hr
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this is a complication of decompensated DM with a mortality of 1-2%. It is more common in DM1 often triggered by infection or illness.
Diabetic Ketoacidosis
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DKA: high glucose exceeds the threshold for ____ reabsorbtion which creates ____ and ____
* renal reabsorbtion
* creates osmotic diuresis and hypovolemia
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Tight metabolic coupling of ____ & ____ leads to liver overproduction of ketoacids
gluconeogenesis & ketogenesis
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DKA results in excessive glucose-counterregulatory hormones, with glucagon activating lipolysis & free fatty acids which causes
substrates for ketogenesis
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what are the diagnostic features of DKA?
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What is the treatment for DKA?
* IV volume replacement
* insulin
* correct acidosis w/ sodium bicarb
* electrolye supplement [K+, phos, mag, Na+]
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when treating DKA what is the loading dose of insulin and what is the infusion rate?
* Loading dose 0.1u/kg Regular
* low dose infusion @ 0.1u/kg/hr
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What happens if you correct glucose in DKA but dont correct sodium?
Correction of glucose w/o simultaneous correction of sodium may result in cerebral edema
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this is characterized by severe hyperglycemia, hyperosmolarity & dehydration and normally occurs in DM2 >60 y/o.
Hyperglycemic Hyperosmolar Syndrome
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Hyperglycemic Hyperosmolar Syndrome eveolve over days to weeks with persistent ____.
glucosuric diuresis
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46
When glucose load exceeds max renal glucose absorption what happens?
mass solute diuresis occurs
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47
s/s of HHS?
* polyuria
* polydipsia
* hypovolemia
* HoTN
* tachycardia
* organ hypoperfusion
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48
in HHS hyperosmolarity leads to ____.
coma
*pts have some degree of acidosis but not DKA*
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treatment for HHS?
* fluid resuscitation
* insulin bolus + infusion
* electrolytes
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50
What has a higher mortality HHS or DKA?
HHS with a mortality of 10-20%
| slide 15
51
List the complications of DM
1. Microvascular
2. Nephropathy
3. Peripheral neuropathy
4. Retinopathy
5. Autonomic neuropathy
| Slide 16-18
52
Microvascular is a complication of DM. What is it?
nonocclusive microcirculatory dz w/impaired blood flow autoregulation
| Slede 16
53
Nephropathy is a complication of DM.
1. Who does it commonly develop in?
2. What happens to the kidneys?
* 30-40% DM1, 5-10% DM2 develop ESRD.
* Kidneys develop glomerulosclerosis, arteriosclerosis, & tubulointerstitial disease
| Slide 16
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1. What are the s/sx of Nephropathy
2. What happens when When GFR < 15-20?
* Sx: HTN, proteinuria, peripheral edema,↓GFR
* When GFR < 15-20, kidneys no longer clear K+, Pts become hyperkalemic & acidotic
| Slide 16
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What is the tx Nephropathy?
* ACE-I’s slow progression of proteinuria and the rate of GFR slowing
* ESRD tx: HD, PD, kidney transplant
* Combined kidney-pancreas transplant may prevent recurrent nephropathy
| Slide 16
56
1. What is peripheral Neuropathy?
2. How does it start?
1. Normally a distal symmetric diffuse sensorimotor polyneuropathy
2. Starts in toes/feet, progresses proximally
| Slide 17
57
Peripheral Neuropathy results in a loss of?
How do ulcers develope?
* Loss of large sensory & motor fibers, reducing light touch & proprioception
* Loss of small nerve fibers decrease pain/temp perception, causing neuropathic pain
* Ulcers develop from unnoticed mechanical & traumatic injury
| Slide 17
58
1. In Peripheral Neuropathy, what does morbidity result from?
2. What is the treatment of Peripheral Neuropathy
* Significant morbidity results from recurrent infections & amputation wounds
* Tx: optimal glucose control, NSAIDS, antidepressants, anticonvulsants
| slikde 17
59
1. What is Retinopathy caused by?
2. What is the treatment?
1. Caused by microvascular changes including vessel occlusion, dilation, ↑permeability, microaneurysms.
2. Visual impairment ranges from color loss to blindness
3. Tx: Glycemic control & BP control reduces the progression
| Slide 17
60
1. What is Autonomic Neuropathy?
2. What is it caused by?
3. Tx?
1. Can affect any part of the ANS
2. Caused by damaged vasoconstrictor fibers, impaired baroreceptors, ineffective cardiovascular activity
3. Tx: glucose control, small meals, prokinetics
| Slide 18
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What are the cardiax sx of Autonomic Neuropathy
* abnormal HR control & vascular dynamics
* resting tachycardia
* loss of HR variability
* progresses to ortho-HoTN & dysrhythmias
| Slide 18
62
What are the GI sx of Autonomic Neuropathy
* ↓gastric secretions & motility
* eventually causing gastroparesis
* N/V, early satiety, bloating, epigastric pain
| Slide 18
63
For DM, what does preop evaluation consist of?
o Emphasize on cardiovascular, renal, neurologic, and musculoskeletal systems
o Silent ischemia is possible w/autonomic neuropathy
o Consider stress test in pts w/multiple cardiac risk factors and poor exercise tolerance
o Meticulous attention to hydration status, avoid nephrotoxins, and preserve RBF
o Autonomic neuropathy predisposes pt's to peri-op dysrhythmia and HoTN
o Gastroparesis may ↑aspiration rx, regardless of NPO status
o PO hypoglycemic and noninsulin injectable drugs should be held
| Slide 19
64
What is insulinoma? Who does it occur in/what age?
* Rare, benign insulin-secreting pancreatic islet tumor
* Occurs 2x more in women than men, normally in 50s-60s
| Slide 20
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How is insulinoma diagnosed?
* Dx based on Whipple triad.
* Dx b/o inappropriately high insulin level during 48-72h fast
| Slide 20
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What is the Whipple triad?
* Hypoglycemia w/fasting
* Glucose <50 w/sx
* Sx relief w/glucose
| Slide 20
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Preoperatively, what medications do you give for insulinoma?
* Diazoxide, which inhibits insulin release from B cells
* Other tx: verapamil, phenytoin, propranolol, glucorticoids, octreotide
* Surgery is curative
| Slide 20
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What are intraop considerations for insulinoma?
* Hypoglycemia can occur intra-op, followed by hyperglycemia once tumor removed.
* Tight glycemic control is paramount
| Slide 20
69
* Thyroid gland weighs ____ and is composed of ____ lobes joined by an ____
1. 20g
2. two
3. isthmus
| Slide 21
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* The gland is affixed to the ________, with upper border just below the _____ ______.
1. anterior & lateral trachea
2. cricoid cartilage
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____ ______ located on posterior aspect of each lobe
Parathyroid glands
| Slide 21
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* A rich capillary network permeates the gland, which is innervated by the _____ and ______ nervous systems
* adrenergic
* cholinergic
| Slide 21
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The ______ nerve and ______nerve are in close proximity to the thyroid
1. recurrent laryngeal
2. external motor branch of superior laryngeal
| Slide 21
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* The thyroid is composed of follicles that are filled with ______ which is a ________, & _______for thyroid hormone synthesis
1. thyroglobulin
2. an iodinated glycoprotein
3. substrate
| Slide 21
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* The thyroid gland also contains ______ cells, which produce _____
1. parafollicular C
2. calcitonin
| Slide 21
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The production of normal quantities of thyroid hormones d/o availability of?
exogenous iodine
| Slide 22
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* _____ is the primary source of iodine. Iodine is reduced to ____ in the GI tract, rapidly absorbed into the blood, then transported into ________cells
1. Diet
2. iodide
3. thyroid follicular
| Slide 22
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The binding of iodide to _____ is catalyzed by an _____ enzyme and yields inactive _____ & _____
1. thyroglobulin
2. iodinase
3. monoiodotyrosine and diiodotyrosine
| Slide 22
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_____% monoiodotyrosine & diiodotyrosine undergo coupling w/thyroid peroxidase to form active _____ & ______.
1. ̴25
2. triiodothyronine (T3) and thyroxine (T4)
| Slide 22
80
The thyroid contains a large store of hormones and has a low turnover rate. What does this allow for
allowing protection against depletion if hormone synthesis is impaired
| Slide 22
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The T4/T3 ratio is ____. Upon entering the blood, T4 and T3 reversibly bind to what three major proteins?
1. 10:1
2. thyroxine-binding globulin (80%)
3. prealbumin (10–15%)
4. albumin (5–10%).
| Slide 22
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Thyroid hormones stimulate virtually all metabolic processes. How?
They influence growth and maturation of tissues, enhance tissue function, and stimulate protein synthesis and carbohydrate and fat metabolism
| Slide 22
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What is the regulation of thyroid function is controlled by?
Regulation of thyroid function is controlled by the hypothalamus, pituitary, and thyroid glands, in a classic feedback control system
| Slide 23
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Thyrotropin-releasing hormone (TRH) is secreted from?
The hypothalamus, traverses the pituitary stalk, and promotes release of thyrotropin-stimulating hormone (TSH) from the anterior pituitary
| Slide 23
85
What happens when TSH binds to receptors on the thyroid cell membrane?
It enhances the synthesis and secretion of T3 & T4
| Slide 23
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A decrease in TSH causes a decrease in?
* T3 & T4 synthesis
* decreased follicular cell size
* decreased vascularity
| Slide 23
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An increase in TSH yields an increase in?
* hormone production
* gland cellularity
* vascularity
| Slide 23
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TSH secretion is also influenced by?
* plasma levels of T3 & T4 via a negative feedback loop
| Slide 23
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The thyroid has an autoregulatory mechanism that maintains
consistent hormone stores
| Slide 23
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_____ is best test of thyroid hormone action at the cellular level
* TSH assay
| Slide 24
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What are the normal TSH levels?
0.4-5.0 milliunits/L
| Slide 24
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Small changes in thyroid function cause
significant changes in TSH secretion
| Slide 24
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What does the TRH stimulation test assess?
The functional state of the TSH-secreting mechanism, and is used to test pituitary function
| Slide 24
94
List all the thyroid testing available as discussed in class
* TSH assay
* serum anti-microsomal antibodies
* antithyroglobulin antibodies,
* thyroid-stimulating immunoglobulins.
* Thermal thyroid scans evaluate thyroid nodules as “warm” (normally functioning), “hot” (hyperfunctioning), or “cold” (hypofunctioning)
| Slide 24
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* US is _____% accurate in determining whether a lesion is?
* 90-95 %
* cystic, solid, or mixed
| Slide 24
96
What is hyperthyroidism?
Hyperfunctioning thyroid gland w/ excessive secretion of active hormones
| Slide 25
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The majority of cases for hyperthyroidism are caused by 1 of 3 pathologies
1. Graves disease
2. Toxic multinodular goiter
3. Toxic adenoma
| Slide 25
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What are the sx of hyperthyroidism?
* Sx are r/t the hypermetabolic state
* Sweating
* heat intolerance
* fatigue w/inability to sleep
* Osteoporosis & weight loss may occur
* cardiovascular responses
| Slide 25
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What causes the CV response for hyperthyroid?
T3 acts directly on the myocardium and peripheral vasculature to cause cardiovascular responses
| Slide 25
100
List the s/sx for hyperthyroid:
* **General s/sx**: anxious
* **HEENT**: flushed face, fine hair, exophthalmos/proptosis
* **CV**: palpitation
* **Neuro**: wasting, weakness, fatigue of proximal limbs, fine tremor of hands, hyperactive DTR.
* **GI**: frequent bowel movement/diarrhea
* **Psych**: emotionally unstable
* **Skin**: warm, moist
| Slide 26
101
List the cardiac effects of hyperthyroidism
* Tachycardia, arrhythmias [atrial]
* Hyperdynamic
* Increase CO and contractility.
* Cardiomegaly
| Slide 26
102
This is the leading cause of hyperthyroidism, effecting ____% population.
* Graves disease
* 0.4 %
| Slide 27
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What is graves disease/caused by? Common in?
* Appears to be autoimmune, caused by thyroid-stimulating antibodies that bind to TSH receptors, stimulating growth, vascularity, and hypersecretion
* Typically occurs in females (7:1), 20-40 y/o
* The thyroid is usually diffusely enlarged. Ophthalmopathy occurs in 30% cases
* Usually arises from a long-standing goiter
| Slide 27
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How is a diagnosis of graves disease made
* confirmed w/TSH antibodies in the context of low TSH + high T3 & T4
| Slide 27
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Graves disease may present with?
* extreme enlargement causing dysphagia, globus sensation, and inspiratory stridor from tracheal compression
| Slide 27
106
What is the medical treatment for graves disease? How does this work
* 1st line is antithyroid drug, either methimazole or propylthiouracil (PTU)
* High concentrations of iodine immediately inhibit release of thyroid hormones, but the effect is short lived, therefore its usually reserved for pre-op or thyroid stor
* β-blockers don’t affect the underlying abnormality, but may relieve sx. Propranolol impairs the peripheral conversion of T4 to T3
| Slide 28
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What is the surgical treatment for graves disease
* Ablative therapy or surgery is recommended when medical tx has failed
* Surgery (subtotal thyroidectomy) is effective and is associated with a lower incidence of hypothyroidism than radioactive iodine therapy
| Slide 28
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What are some complications that can occur from surgery for graves disease?
* hypothyroidism, hemorrhage with tracheal compression, RLN damage, and damage to or inadvertent removal of the parathyroid glands
| Slide 28
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What are the preop considerations for graves disease
* Thyroid levels should be established preoperatively
* Elective cases may need to wait 6-8 weeks for antithyroid drugs to take effect
* In emergent cases, IV BBs, glucocorticoids, and PTU usually necessary
* Evaluate upper airway for evidence of tracheal compression or deviation caused by a goiter
| Slide 29
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Graves disease s/sx include?
* Exophthalmos, goiter, sweating, arrhythmias/tachycardia, N/D, oligomenorrhea, muscle weakness, tremors
| Slide 29
111
Define thyroid storm. Its presenting sx are similar to?
* Life-threatening exacerbation of hyperthyroidism precipitated by trauma, infection, medical illness, or surgery.
* Thyroid storm and malignant hyperthermia can present very similar, therefore differentiation between the two may be extremely difficult
* Thyroid hormone levels in thyroid storm may not be much higher than basic hyperthyroidism
| Slide 30
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When does thyroid storm most often occur?
* Thyroid storm most often occurs postoperatively in untreated or inadequately treated hyperthyroid pts after emergency surgery
| Slide 30
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What is the tx for thyroid storm? Mortality rate?
* Tx includes rapid alleviation of thyrotoxicosis and supportive care
* The mortality rate is 20%
| Slide 30
