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Mar: Sem 2 - Health Assessment > Exam 4: Endocrine Part I (bri/jia) > Flashcards

Exam 4: Endocrine Part I (bri/jia) Flashcards

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
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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
  1. A1C >6.5%: the test should be perfomed in a laboratory using a method that is NGSP certified and standardized to the DCCT assay
  2. FPG?126mg/dL (7mmol/L) Fasting is definied as no caloric intake for at least 8hr
  3. 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
  4. 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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25
Q

what are PO antidiabetic drugs?

A
  • metformin
  • sulfonylureas

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26
Q

What is metformin and how does it treat DM2?

A
  • A biguanide, preferred initial drug tx
  • Enhances glucose transport into tissues
  • ↓TGL & LDL levels

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27
Q

how do sulfonylureas treat DM2?

A
  • 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

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28
Q

What is the initial therapy and additional therapy for DM2?

A

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29
Q

____ is necessary in all DM1 cases and 30% of DM2 cases

A

insulin

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30
Q

what are the different types of insulin?

A
  • Rapid acting (Lispro, Aspart) provide glucose-control @ mealtimes
  • Short acting (regular)
  • Basal/Intermediate acting (NPH, Lente)
  • Long acting (Ultralente, Glargine)

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31
Q
  • what is the most dangerous complication of long acting insulin?
  • what exacerbates this complication?
A
  • Hypoglycemia is the most dangerous complication
  • ETOH, metformin, sulfonylureas, ACE-I’s, MAOI’s, Non-selective BB’s

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32
Q
  • Repetitive hypoglycemic episodes lead to “____”
  • Pt becomes desensitized to hypoglycemia and doesn’t show ____ sx
  • ____ ensues→fatigue, confusion, h/a, seizures, coma
  • Tx: ___
A
  • hypoglycemia unawareness
  • autonomic
  • Neuroglycopenia
  • TX: O or IV glucose (may give SQ or IM if unconscious)

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33
Q

Short Acting inslulin

What is onset, peak and duration of:
* Human regular
* lispro [humalog]
* aspart [novolog]

A

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

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34
Q

Intermediate Acting Insulin

What is onset, peak and duration of:
* human NPH
* Lente

A
  • human NPH and Lente
    • O: 1-2 Hr
    • P: 6-10 Hr
    • D: 10-12HR

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35
Q

Long acting insulin

What is onset, peak and duration of:
* ultralente
* glargine (lantus)

A
  • 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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36
Q

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.

A

Diabetic Ketoacidosis

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37
Q

DKA: high glucose exceeds the threshold for ____ reabsorbtion which creates ____ and ____

A
  • renal reabsorbtion
  • creates osmotic diuresis and hypovolemia

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38
Q

Tight metabolic coupling of ____ & ____ leads to liver overproduction of ketoacids

A

gluconeogenesis & ketogenesis

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39
Q

DKA results in excessive glucose-counterregulatory hormones, with glucagon activating lipolysis & free fatty acids which causes

A

substrates for ketogenesis

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40
Q

what are the diagnostic features of DKA?

A

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41
Q

What is the treatment for DKA?

A
  • IV volume replacement
  • insulin
  • correct acidosis w/ sodium bicarb
  • electrolye supplement [K+, phos, mag, Na+]

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42
Q

when treating DKA what is the loading dose of insulin and what is the infusion rate?

A
  • Loading dose 0.1u/kg Regular
  • low dose infusion @ 0.1u/kg/hr

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43
Q

What happens if you correct glucose in DKA but dont correct sodium?

A

Correction of glucose w/o simultaneous correction of sodium may result in cerebral edema

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44
Q

this is characterized by severe hyperglycemia, hyperosmolarity & dehydration and normally occurs in DM2 >60 y/o.

A

Hyperglycemic Hyperosmolar Syndrome

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45
Q

Hyperglycemic Hyperosmolar Syndrome eveolve over days to weeks with persistent ____.

A

glucosuric diuresis

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46
Q

When glucose load exceeds max renal glucose absorption what happens?

A

mass solute diuresis occurs

slide 15

47
Q

s/s of HHS?

A
  • polyuria
  • polydipsia
  • hypovolemia
  • HoTN
  • tachycardia
  • organ hypoperfusion

slide 15

48
Q

in HHS hyperosmolarity leads to ____.

A

coma

pts have some degree of acidosis but not DKA

slide 15

49
Q

treatment for HHS?

A
  • fluid resuscitation
  • insulin bolus + infusion
  • electrolytes

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50
Q

What has a higher mortality HHS or DKA?

A

HHS with a mortality of 10-20%

slide 15

51
Q

List the complications of DM

A
  1. Microvascular
  2. Nephropathy
  3. Peripheral neuropathy
  4. Retinopathy
  5. Autonomic neuropathy

Slide 16-18

52
Q

Microvascular is a complication of DM. What is it?

A

nonocclusive microcirculatory dz w/impaired blood flow autoregulation

Slede 16

53
Q

Nephropathy is a complication of DM.
1. Who does it commonly develop in?
2. What happens to the kidneys?

A
  • 30-40% DM1, 5-10% DM2 develop ESRD.
  • Kidneys develop glomerulosclerosis, arteriosclerosis, & tubulointerstitial disease

Slide 16

54
Q
  1. What are the s/sx of Nephropathy
  2. What happens when When GFR < 15-20?
A
  • Sx: HTN, proteinuria, peripheral edema,↓GFR
  • When GFR < 15-20, kidneys no longer clear K+, Pts become hyperkalemic & acidotic

Slide 16

55
Q

What is the tx Nephropathy?

A
  • 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
Q
  1. What is peripheral Neuropathy?
  2. How does it start?
A
  1. Normally a distal symmetric diffuse sensorimotor polyneuropathy
  2. Starts in toes/feet, progresses proximally

Slide 17

57
Q

Peripheral Neuropathy results in a loss of?
How do ulcers develope?

A
  • 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
Q
  1. In Peripheral Neuropathy, what does morbidity result from?
  2. What is the treatment of Peripheral Neuropathy
A
  • Significant morbidity results from recurrent infections & amputation wounds
  • Tx: optimal glucose control, NSAIDS, antidepressants, anticonvulsants

slikde 17

59
Q
  1. What is Retinopathy caused by?
  2. What is the treatment?
A
  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
Q
  1. What is Autonomic Neuropathy?
  2. What is it caused by?
  3. Tx?
A
  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

61
Q

What are the cardiax sx of Autonomic Neuropathy

A
  • abnormal HR control & vascular dynamics
  • resting tachycardia
  • loss of HR variability
  • progressesto ortho-HoTN & dysrhythmias

Slide 18

62
Q

What are the GI sx of Autonomic Neuropathy

A
  • ↓gastric secretions & motility
  • eventually causing gastroparesis
  • N/V, early satiety, bloating, epigastric pain

Slide 18

63
Q

For DM, what does preop evaluation consist of?

A

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
Q

What is insulinoma? Who does it occur in/what age?

A
  • Rare, benign insulin-secreting pancreatic islet tumor
  • Occurs 2x more in women than men, normally in 50s-60s

Slide 20

65
Q

How is insulinoma diagnosed?

A
  • Dx based on Whipple triad.
  • Dx b/o inappropriately high insulin level during 48-72h fast

Slide 20

66
Q

What is the Whipple triad?

A
  • Hypoglycemia w/fasting
  • Glucose <50 w/sx
  • Sx relief w/glucose

Slide 20

67
Q

Preoperatively, what medications do you give for insulinoma?

A
  • Diazoxide, which inhibits insulin release from B cells
  • Other tx: verapamil, phenytoin, propranolol, glucorticoids, octreotide
  • Surgery is curative

Slide 20

68
Q

What are intraop considerations for insulinoma?

A
  • Hypoglycemia can occur intra-op, followed by hyperglycemia once tumor removed.
  • Tight glycemic control is paramount

Slide 20

69
Q
  • Thyroid gland weighs ____ and is composed of ____ lobes joined by an ____
A
  1. 20g
  2. two
  3. isthmus

Slide 21

70
Q
  • The gland is affixed to the ________, with upper border just below the _____ ______.
A
  1. anterior & lateral trachea
  2. cricoid cartilage

Slide 21

71
Q

____ ______ located on posterior aspect of each lobe

A

Parathyroid glands

Slide 21

72
Q
  • A rich capillary network permeates the gland, which is innervated by the _____ and ______ nervous systems
A
  • adrenergic
  • cholinergic

Slide 21

73
Q

The ______ nerve and ______nerve are in close proximity to the thyroid

A
  1. recurrent laryngeal
  2. external motor branch of superior laryngeal

Slide 21

74
Q
  • The thyroid is composed of follicles that are filled with ______ which is a ________, & _______for thyroid hormone synthesis
A
  1. thyroglobulin
  2. an iodinated glycoprotein
  3. substrate

Slide 21

75
Q
  • The thyroid gland also contains ______ cells, which produce _____
A
  1. parafollicular C
  2. calcitonin

Slide 21

76
Q

The production of normal quantities of thyroid hormones d/o availability of?

A

exogenous iodine

Slide 22

77
Q
  • _____ is the primary source of iodine. Iodine is reduced to ____ in the GI tract, rapidly absorbed into the blood, then transported into ________cells
A
  1. Diet
  2. iodide
  3. thyroid follicular

Slide 22

78
Q

The binding of iodide to _____ is catalyzed by an _____ enzyme and yields inactive _____ & _____

A
  1. thyroglobulin
  2. iodinase
  3. monoiodotyrosine and diiodotyrosine

Slide 22

79
Q

_____% monoiodotyrosine & diiodotyrosine undergo coupling w/thyroid peroxidase to form active _____ & ______.

A
  1. ̴25
  2. triiodothyronine (T3) and thyroxine (T4)

Slide 22

80
Q

The thyroid contains a large store of hormones and has a low turnover rate. What does this allow for

A

allowing protection against depletion if hormone synthesis is impaired

Slide 22

81
Q

The T4/T3 ratio is ____. Upon entering the blood, T4 and T3 reversibly bind to what three major proteins?

A
  1. 10:1
  2. thyroxine-binding globulin (80%)
  3. prealbumin (10–15%)
  4. albumin (5–10%).

Slide 22

82
Q

Thyroid hormones stimulate virtually all metabolic processes. How?

A

They influence growth and maturation of tissues, enhance tissue function, and stimulate protein synthesis and carbohydrate and fat metabolism

Slide 22

83
Q

What is the regulation of thyroid function is controlled by?

A

Regulation of thyroid function is controlled by the hypothalamus, pituitary, and thyroid glands, in a classic feedback control system

Slide 23

84
Q

Thyrotropin-releasing hormone (TRH) is secreted from?

A

The hypothalamus, traverses the pituitary stalk, and promotes release of thyrotropin-stimulating hormone (TSH) from the anterior pituitary

Slide 23

85
Q

What happens when TSH binds to receptors on the thyroid cell membrane?

A

It enhances the synthesis and secretion of T3 & T4

Slide 23

86
Q

A decrease in TSH causes a decrease in?

A
  • T3 & T4 synthesis
  • decreased follicular cell size
  • decreased vascularity

Slide 23

87
Q

An increase in TSH yields an increase in?

A
  • hormone production
  • gland cellularity
  • vascularity

Slide 23

88
Q

TSH secretion is also influenced by?

A
  • plasma levels of T3 & T4 via a negative feedback loop

Slide 23

89
Q

The thyroid has an autoregulatory mechanism that maintains

A

consistent hormone stores

Slide 23

90
Q

_____ is best test of thyroid hormone action at the cellular level

A
  • TSH assay

Slide 24

91
Q

What are the normal TSH levels?

A

0.4-5.0 milliunits/L

Slide 24

92
Q

Small changes in thyroid function cause

A

significant changes in TSH secretion

Slide 24

93
Q

What does the TRH stimulation test assess?

A

The functional state of the TSH-secreting mechanism, and is used to test pituitary function

Slide 24

94
Q

List all the thyroid testing available as discussed in class

A
  • 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

95
Q
  • US is _____% accurate in determining whether a lesion is?
A
  • 90-95 %
  • cystic, solid, or mixed

Slide 24

96
Q

What is hyperthyroidism?

A

Hyperfunctioning thyroid gland w/ excessive secretion of active hormones

Slide 25

97
Q

The majority of cases for hyperthyroidism are caused by 1 of 3 pathologies

A
  1. Graves disease
  2. Toxic multinodular goiter
  3. Toxic adenoma

Slide 25

98
Q

What are the sx of hyperthyroidism?

A
  • Sx are r/t the hypermetabolic state
  • Sweating
  • heat intolerance
  • fatigue w/inability to sleep
  • Osteoporosis & weight loss may occur
  • cardiovascular responses

Slide 25

99
Q

What causes the CV response for hyperthyroid?

A

T3 acts directly on the myocardium and peripheral vasculature to cause cardiovascular responses

Slide 25

100
Q

List the s/sx for hyperthyroid:

A
  • 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
Q

List the cardiac effects of hyperthyroidism

A
  • Tachycardia, arrhythmias [atrial]
  • Hyperdynamic
  • Increase CO and contractility.
  • Cardiomegaly

Slide 26

102
Q

This is the leading cause of hyperthyroidism, effecting ____% population.

A
  • Graves disease
  • 0.4 %

Slide 27

103
Q

What is graves disease/caused by? Common in?

A
  • 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

104
Q

How is a diagnosis of graves disease made

A
  • confirmed w/TSH antibodies in the context of low TSH + high T3 & T4

Slide 27

105
Q

Graves disease may present with?

A
  • extreme enlargement causing dysphagia, globus sensation, and inspiratory stridor from tracheal compression

Slide 27

106
Q

What is the medical treatment for graves disease? How does this work

A
  • 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

107
Q

What is the surgical treatment for graves disease

A
  • 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

108
Q

What are some complications that can occur from surgery for graves disease?

A
  • hypothyroidism, hemorrhage with tracheal compression, RLN damage, and damage to or inadvertent removal of the parathyroid glands

Slide 28

109
Q

What are the preop considerations for graves disease

A
  • 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

110
Q

Graves disease s/sx include?

A
  • Exophthalmos, goiter, sweating, arrhythmias/tachycardia, N/D, oligomenorrhea, muscle weakness, tremors

Slide 29

111
Q

Define thyroid storm. Its presenting sx are similar to?

A
  • 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

112
Q

When does thyroid storm most often occur?

A
  • Thyroid storm most often occurs postoperatively in untreated or inadequately treated hyperthyroid pts after emergency surgery

Slide 30

113
Q

What is the tx for thyroid storm? Mortality rate?

A
  • Tx includes rapid alleviation of thyrotoxicosis and supportive care
  • The mortality rate is 20%

Slide 30

Mar: Sem 2 - Health Assessment (32 decks)

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