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Health Assessment Exam 4 > Exam 4 - Endocrine - organized COPY > Flashcards

Exam 4 - Endocrine - organized COPY Flashcards

1
Q

Liver is the primary sournce of endogenous glucose production via what 2 processes?

A

glycogenolysis & gluconeogenesis

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2
Q

70-80% of glucose released by liver is metabolized by?

A

insulin-insensitive tissues such as the brain, GI tract, and red blood cells

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3
Q

what are the Hyperglycemia-producing hormones and why are they important?

A
  • glucagon, epinephrine, growth hormone, and cortisol
  • comprise the glucose counterregulatory system and support glucose production

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4
Q

what is glucagon’s primary role?

A

stimulating glycogenolysis &gluconeogenesis, and inhibiting glycolysis

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5
Q

what is the most common endocrine disease and how common is it?

A

Diabetes Mellitus
affects 1 in 10 adults

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6
Q

What causes DM?
and what does DM lead to?

A

an inadequate supply of insulin and/or an inadequate tissue response to insulin

  • DM leads to increased circulating glucose levels with eventual microvascular and macrovascular complications

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7
Q

what is type 1A DM caused by?

A

T-cell–mediated autoimmune destruction of β cells within pancreatic islets resulting in minimal or absentcirculating levels of insulin

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8
Q

what is type 1B DM?

A

rare disease of absolute insulin deficiency that is not immune mediated

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9
Q

what is type 2 DM? is it immune mediated?

A

DM type 2 is not immune mediated
and results from defects in insulin receptors and post-receptor intracellular signaling pathways

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10
Q

what are the key facts for type 1 DM regarding etiology?
is type 1 cause known?

A
  • Accounts for 5-10% of all DM cases
  • Usually diagnosed before age 40

Exact autoimmune cause of type 1a is unknown

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11
Q

what s/s hyperglycemia over several days/weeks associated with in type 1 DM?

A

fatigue, weight loss, polyuria, polydipsia, blurry vision, hypovolemia, ketoacidosis
- she mentioned POLYURIA loudly lol

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12
Q

what precedes onset of symptoms in type 1 DM?

A

long pre-clinical period (9-13 yrs) of B-cell antigen production

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13
Q

how much of b cell function is lost before hyperglycemia even shows up in type 1 DM?

A

At least 80-90%

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14
Q

what happens in the initial stages of type 2 DM regarding insulin?

A

insensitivity to insulin on peripheral tissues leads to ↑pancreatic insulin secretion

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15
Q

as type 2 DM progresses, what happens to pancreas and insulin levels?

A

pancreatic function decreases & insulin levels become inadequate

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16
Q

what are the 3 main abnormalities 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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17
Q

What are some facts regarding etiology of Type 2 DM?

A
  • Accounts for >90% DM cases
  • Increasingly seen in younger pts & children over the past decade
  • Very underrecognized, normally present 4-7 years before diagnosed

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18
Q

what’s 2 tests are used for the diagnosis for DM2?

A

fasting blood glucose and HbA1c

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19
Q

what is DM2 characterized by?

A

insulin resistance in skeletal muscle, adipose & liver

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20
Q

what are the 3 causes of insulin resistance?
what may also contribute regarding lifestlye?

A
  • Abnormal insulin molecules
  • Circulating insulin antagonists
  • Insulin receptor defects

OBESITY AND SEDENTARY LIFESTYLE also contribute!

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21
Q

what HbA1c is considered normal?
prediabetic?
diabetic?

A

normal: <5.7%
prediabetic: 5.7-6.4%
diabetic: >/= 6.5%

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22
Q

what is the american diabetes assoc criteria for dx of diabetes?

A
  1. A1c >/= 6.5
  2. Fasting Plasma Glucose >/= 126 mg/dL (7.0 mmol/L)* and fasting for at least 8 hrs!*
  3. 2-hr plasma gluc >/= 200 mg/dL during glucose tolerance test
  4. *in pt with classic symptoms of hyperglycemia or hyperglycemia crisis a random plasma gluc of >/= 200 mg/dL

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23
Q

what is the DM2 treatment? (3 things)

A
  • Dietary adjustments
  • Exercise/weight loss
  • PO antidiabetic drugs - metformin (preferred initial med tx) and/or sulfonylureas

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24
Q

what drug class is metformin? and how does it help DM2?

A

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

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25
Q

what do sulfonylureas do?
what are some side effects?

A
  • stimulate insulin secretion
  • Enhances glucose transport into tissues

SE’s include hypoglycemia, weight gain & cardiac effects

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26
Q

why are sulfonylureas not effective long term?

A

d/t diabetic progressive loss of B cell function

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27
Q

What is the common s/e of metformin? Who is it contraindicated for?

A

GI side effects.
Contrainidicated with renal insufficiency.

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28
Q

What is the initial tx for DMII?

A

Lifystyle changes and Metformin

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29
Q

What are the additional therapies for DMII?

A

Insulin
Sulfonylurea
GLP-1 receptor agonist
Thiazolidenedione
glinide
SGLT-2 inhibitor
DPP-4 inhibitor
a- glucosidase inhibitor
Pramlintide

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30
Q

Insulin is necessary in ____ DMI cases & ____ DMII cases

A

all
30%

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31
Q

Types of insulin

A
  • Rapid acting (Lispro, Aspart)
  • Short acting (regular)
  • Basal/intermediate acting (NPH, Lente)
  • Long acting (Ultralente, Glargine)

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32
Q

What is the most dangerous complication of insulin? What is it exacerbated by?

A

Hypoglycemia.
Exacerbated by ETOH, metformin, sulfonylureas, ACE-I’s, MAOI’s, Non-selective BB’s

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33
Q

What does repetitive hypoglycemic episodes can lead to? What is the tx for hypoglycemia?

A

“Hypoglycemia unawareness”
Pt becomes desensitized to hypoglycemia and doesn’t show autonomic sx.
Neuroglycopenia ensues→fatigue, confusion, h/a, seizures, coma.

Tx: PO or IV glucose (may give SQ or IM if unconscious)

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34
Q

What is the onset/peak/duration of short acting insulin (Human Regular, Lispro, Aspart)?

A

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35
Q

What is the onset/peak/duration of intermediate insulin (Human NPH, Lente)?

A

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36
Q

What is the onset/peak/duration of long acting insulin (ultralente, glargine)?

A

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37
Q

Plasma insulin levels (chart)

memorize

A

12

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38
Q

What are the diagnostic features of DKA?

A

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39
Q

What is a complication of decompensated DM? what its mortality rate?

A

Diabetic Ketoacidosis
mortality 1-2%

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40
Q

DKA is more common in which type of DM? What can trigger DKA?

A

DKA more common in DMI, often triggered by infection/illness

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41
Q

How does high glucose affect the renal function?

A

High glucose exceeds the threshold for renal reabsorption creating osmotic diuresis & hypovolemia.

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42
Q

What causes the overproduction of ketoacids?

A

Tight metabolic coupling of gluconeogenesis & ketogenesis.
DKA results in excessive glucose-counterregulatory hormones, with glucagon activating lipolysis & free fatty acids→ substrates for ketogenesis.

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43
Q

What is the treatment for DKA?

A
  • IV volume replacement
  • Insulin: Loading dose 0.1u/kg Regular + low dose infusion @ 0.1u/kg/hr
  • Correct acidosis: sodium bicarb
  • Electrolyte supplement: k+, phos, mag, sodium
    *Correction of glucose w/o simultaneous correction of sodium may result in cerebral edema

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44
Q

What are the characteristics of hyperglycemic hyperosmolar syndrome? What is the mortality rate of HHM?

A

severe hyperglycemia, hyperosmolarity & dehydration

Mortality 10-20%

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45
Q

What are the sings and symptoms of Hyperglycemic Hyperosmolar Syndrome?

A
  • Polyuria
  • polydipsia
  • hypovolemia
  • HoTN
  • tachycardia
  • organ hypoperfusion
  • Some degree of acidosis, but not DKA
    Hyperosmolarity leads to coma.**

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46
Q

What is the treatment of Hyperglycemic Hyperosmolar Syndrome?

A

fluid resuscitation, insulin bolus + infusion, e-lytes

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47
Q

What happens when glucose load exceeds renal glucose absorption?

A

Mass solute diuresis

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48
Q

What is the microvascular complication of DM?

A

Nonocclusive microcirculatory dz w/impaired blood flow autoregulation

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49
Q

What is the neuropathic complication of DM associated w/ renal fx?

A

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

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50
Q

What are the signs of DM related ESRD?

A

HTN, proteinuria, peripheral edema,↓GFR

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51
Q

What causes hyperkalemia in patients with ESRD?

A

When GFR < 15-20, kidneys no longer clear K+, Pts become hyperkalemic & acidotic

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52
Q

What is the treatment for ESRD?

A
  • ESRD tx: HD, PD, kidney transplant
  • ACE-I’s slow progression of proteinuria and the rate of GFR slowing

Combined kidney-pancreas transplant may prevent recurrent nephropathy

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53
Q

What is characteristic of DM peripheral neurophathy? How does it progress?

A

Normally a distal symmetric diffuse sensorimotor polyneuropathy.
Starts in toes/feet, progresses proximally

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54
Q

Loss of which fibers cause the reduction in light touch and proprioception?

A

large sensory & motor fibers

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55
Q

Loss of which fibers cause the decrease in pain/temperature perception leading to neuropathic pain?

A

Small nerve fibers

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56
Q

What causes the significant morbidity in someone w/ peripheral neuropathy?

A

Recurrent infections & amputation wounds.

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57
Q

What is the treatment of peripheral neuropathy?

A

optimal glucose control, NSAIDS, antidepressants, anticonvulsants

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58
Q

What is the diabetes related retinopathy?

A
  • microvascular changes including vessel occlusion, dilation, ↑permeability, microaneurysms
  • Visual impairment ranges from color loss to blindness

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59
Q

What can reduce the progression of retinopathy?

A

Glycemic control & BP control

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60
Q

What causes autonomic neuropathy?

Can affect any part of the ANS

A

Autonomic neuropathy is caused by damaged vasoconstrictor fibers, impaired baroreceptors and ineffect CV activity!

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61
Q

What are the CV and GI s/s of autonomic neuropathy?
What is the treatment?

A

CV: abnormal HR control (variability), vascular dynamics, resting tachycardia, orthostatic hypotension and dysrhythmias
GI: N/V, bloating, impaired secretions & mobility–> gastroparesis
Tx: glucose control, small meals, prokinetics

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62
Q

What do you emphasize in patients with DM in the preop eval?

A

-emphasize CV, renal, neurologic, & muscoskeletal systems
-silent ischemia is possible!
-meticulus attention to hydration, preserve RBF!
-Consider stress test if multiple cardiac risk factors and poor exercise tolerance

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63
Q

What are diabetics at risk for in regards to anesthesia?

A

-Arrhythmia risk d/t autonomic neuropathy
-risk for aspirations d/t gastroparesis
* hold PO hypoglycemic and noninsulin injectables

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64
Q

Who is at risk for insulinoma?
Dx is based on whipple triad..what are they?

benign insulin secreted pancreatic islet tumor!

A

-occurs 2x in women than men~ 50-60 y/o
-Whipple triad:
hypoglycemia w fasting, glucose <50 w symptoms, and symptom relief w glucose

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65
Q

Insulinoma pt’s have high insulin levels during 48-72 hr fast (dx). What meds should you give them preop?

A

diaxoide, inhibits insulin release from B cells
-verapamil, phenyoin, promanalol, glucorticoids and ocreotide
-at risk for hypoglycemia intraop** then hyperglycemia when tumor is removed

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66
Q

Thyroid gland is composed of 2 lobes joined y an isthmus.

Where is the thyroid gland located?

What is located on the posterior aspect of each lobe?

A

-The gland is affixed to the anterior & lateral trachea, with upper border just below the cricoid cartilage

-parathyroid gland located on posterior aspect of each lobe

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67
Q

What type of cells does the thyroid gland contain?

What is thyroglobulin?

A

parafollicular cells- which produce calcitonin

-thyroid is composed of follicles filled w/ thyroiglobulin, which is an iodinated glycoprotein and substrate for thyroid hormone synthesis

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68
Q

What innervates the rich capillary network in the thyroid gland?

What nerves are close to it?

A

Adrenergic and cholinergic systems innervate capillary network.

-recurrent laryngeal nerve and external motor branch of superior laryngeal nerve

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69
Q

We eat iodide, it is reduced in the GI tract and absorbed, then transported to follicular cells. Iodide then binds to thyroglobulin with the help of what?

After that, how do we form active T3, T4?

A

The binding of iodide to thyroglobulin is catalyzed by an **iodinase enzyme ** and yields inactive monoiodotyrosine and diiodotyrosine.

Then, T1 and T2 undergo coupling w/ **thyroid peroxidase **to form T3 and T4

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70
Q

What 3 proteins to T4 and T3 reversibly bind to?

T4/T3 ratio?

A

thyroxine-binding globulin (80%), prealbumin (10–15%), and albumin (5–10%).

10:1

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71
Q

What does a decrease in TSH cause?

What does an increase in TSH cause?

A

-decreased T3 & T4 synthesis, decreased follicular cell size, and decreased vascularity

-increase in TSH yields an increase in hormone production, gland cellularity and vascularity

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72
Q

What 3 glands regulate thyroid function?

A

hypothalamus, pituitary, and thyroid glands, in a classic feedback control system

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73
Q

Thermal thyroid scans evaluate thyroid nodules as warm if they are ____ functioning, hot if they are ____ and cold if they are ____

A

normally, hyperfunctioning and hypofunctioning

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74
Q

What is the best test of TH action?

What is normal TSH level

A

TSH assay

normal TSH level is 0.4-5.0 milliunits/L

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75
Q

What does the TRH stimulation test assess?

A

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

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76
Q

What are top 3 pathologies for hyperthyroidism?

A

Graves disease
toxic multinodular goiter
toxic adenoma

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77
Q

s/s of hyperthyroidism?

T3 acts directly on what?

A

hypermetabolic state: sweating, heat intolerance & fatigue w/inability to sleep, osteoporosis and weight loss

T3 acts directly on the myocardium and peripheral vasculature to cause cardiovascularresponses

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78
Q

What is a
Cardiovascular
GI
Skin
s/s of hyperthyroidism ?

A

CV: Palpitation

GI: Frequent BM/ Diarrhea

Skin: Warm, moist

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79
Q

What are Neurogical s/s of Hyperparathyroidism?

A
  • Wasting, weakness, fatigue of proximal limb muscles
  • fine tremor of hands
  • hyperactive DTR (deep tendon reflexes)

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80
Q

What is a
General
Psych
s/s of Hyperparathyroidism?

A

General: Anxious

Psych: Emotionally unstable

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81
Q

What are Cardiac effects of Hyperparathyroidism?

A
  • Tachycardia, arrythmias (atrial)
  • Hyperdynamic
  • ↑ C.O. and contractility
  • Cardiomegaly

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82
Q

What are HEENT s/s of Hyperparathyroidism?

A
  • Flushed face
  • Fine hair
  • Exophthalmos/proptosis

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83
Q

What is the leading cause of hyperthyroidism, effecting 0.4% population?
Who does this typically occurs in?

A

Graves disease

Typically occurs in
females (7:1 in 20-40 y/o)

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84
Q

Grave disease appears to be ____, caused by thyroid-stimulating ____ that bind to ____ receptors, stimulating growth, vascularity, and hypersecretion

A

Grave disease appears to be autoimmune, caused by thyroid-stimulating antibodies that bind to TSH receptors, stimulating growth, vascularity, and hypersecretion

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85
Q

What are s/s of Graves disease?

A
  • diffusely enlarged thyroid
  • Ophthalmopathy (in 30% cases)
  • enlarged goiter

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86
Q

What can enlarged goiter cause with Graves Disease?

A
  • dysphagia
  • globus sensation
  • inspiratory stridor (from tracheal compression)

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87
Q

What is the diagnosis that confirms Graves disease?

A

TSH antibodies in the context of
↓ TSH and ↑ T3 & T4

27

88
Q

What is the 1st line treatment of Graves disease?

A

Antithyroid drug
Methimazole or Propylthiouracil (PTU)

28

89
Q

What treatment is recommended when medical treatments failed with Graves disease?

A

Ablative therapy or surgery

subtotal thyroidectomy > radioactive iodine therapy with lower incidence of hypopthyroidism

28

90
Q

What are complications of surgery of Graves disease?

A
  • hypothyroidism
  • hemorrhage with tracheal compression
  • RLN (recurrent laryngeal nerve) damage
  • damage to or inadvertent removal of the parathyroid glands

28

91
Q

What treatment for Graves disease is reserved for pre-op or thyroid storm and why?

A

high concentrations of iodine (inhibit release of thyroid hormones)

its effect is short lived

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92
Q

What medication doesn’t affect the underlying abnormality, but may relieve sx of Graves disease?

A

Beta Blockers

Propranolol impairs the peripheral conversion of T4 to T3

28

93
Q

Pre-op considerations for Graves disease are:

____ ____should be established preoperatively

Elective cases may need to wait ____ weeks for antithyroid drugs to take effect

Evaluate upper airway for evidence of tracheal ____ or ____ caused by a goiter

A

Thyroid levelsshould be established preoperatively

Elective cases may need to wait 6-8 weeks for antithyroid drugs to take effect

Evaluate upper airway for evidence of tracheal compression or deviation caused by a goiter

29

94
Q

What are usually necessary in emergent cases of Graves disease?

A
  • IV Beta-Blockers
  • Glucocorticoids
  • PTU

29

95
Q

Why do you need to evaluate upper airway of pt with Graves Disease pre-operatively?

A

for evidence of tracheal compression or deviation caused by a goiter

29

96
Q

What is a life-threatening exacerbation of hyperthyroidism precipitated by trauma, infection, medical illness, or surgery?

What is the mortality rate?

A

Thyroid Storm

20% mortality rate

30

97
Q

What kind of condition presents very similar to Thyroid storm and differentiation between the two can be extremely difficult?

A

Malignant Hyperthermia

30

98
Q

____ levels in thyroid storm may not be much higher than basic hyperthyroidism

A

Thyroid hormone

30

99
Q

When do Thyroid storm most often occurs?

A

postoperatively in untreated or inadequately treated hyperthyroid pts

30

100
Q

What are the treatments for Thyroid storm?

A
  • rapid alleviation of thyrotoxicosis
  • supportive care

30

101
Q

What is another name for Hypothyroidism?
What is the course of this disease in adults?

A

Myxedema

a slow, progressive course

31

102
Q

What are the lab results of primary Hypothyroidism?

A

↓ T3 & T4 production with adequate TSH

31

103
Q

What is the 1st common cause of Hypothyrodism?

What is the 2nd common cause?

A

1st common cause: ablation of the gland
(by radioactive iodine or sx)

2nd common cause: idiopathic and probably autoimmune
(antibodies blocking TSH receptors)

31

104
Q

What is an *autoimmune disorder *characterized by goitrous enlargement and hypothyroidism that usually affects middle-aged women?

A

Hashimoto thyroiditis

31

105
Q

Hypoparathyroidism ::

  • Present when PTH is_________ or peripheral tissues are_________ to its effects
  • Absence or deficient PTH is almost always__________, reflecting inadvertent removal of parathyroid glands, as during _____
  • Pseudohypoparathyroidism is a________ disorder where PTH is adequate, but the ________ are unable to respond to it
A

deficient … resistant

iatrogenic … thyroidectomy

congenital … kidneys

31

106
Q

What other syndrome commonly occurs with Hypothyroidism?

A

SIADH

31

107
Q

What are the general and psych symptoms of Hypothyroidism?

A

General symptoms:
-fatigue
-listlessness
-weight gain

Psych:
apathy

31 & 32 Chart

108
Q

What are the HEENT symptoms of Hypothyroidism?

A
  • dry brittle hair
  • large tongue
  • deep hoarse voice
  • periorbital edema

31 & 32 Chart

109
Q

What are the GI symptoms of Hypothyroidism?

A
  • constipation
  • slow GI function
  • adynamic ileus may occur

31 & 32 chart

110
Q

What are the respiratory symptoms of Hypothyroidism?

A
  • fluid overload
  • pleural effusions
  • dyspnea

31

111
Q

What are the skin symptoms of Hypothyroidism?

A
  • pale
  • cool
  • dry
  • thickened
  • non-pitting peripheral edema
  • cold intolerance

31 & 32 chart

112
Q

What are the cardiac effects of Hypothyroidism?

A
  • ↓ C.O.
  • Baroreceptor function impaired
  • Hypothyroid cardiomyopathy
  • Pericardial effusions

on EKG:
* Flattened or inverted T waves
* low-amplitude P waves & QRS complexes
* Sinus bradycardia
* Ventricular dysrhtymias

31 & 32 table

113
Q

True or false: Mechanical ventilation is not frequently required

A

false, mechanical ventilation is frequently required

35

114
Q

Hypothermia is a ____feature that determine impaired thermoregulation

A

cardinal

35

115
Q

What are treatments plan for Myxedema Coma

long list

A
  • IV L-thyroxine or levotriiodothyronine
  • IV - hydration with glucose- saline solutions
  • Tempature regulation
  • Correction of electrolytes implance
  • Stabliization of cardiac and pulmonary system

35

116
Q

What are the 3 vitial signs that improve within 24 hours of given electrolyte (myxedema coma)

A
  • Heart Rate
  • BP
  • Temp

35

117
Q

Myxedema Coma occurs most commly in what population of patients

A

elderly women with a long history hypothyroidism?

35

118
Q

What is a rare form of hypothyroidism characterized by delirium, hypoventilation, hypothermia, bradycardia, HoTN, and severe dilutional hyponatremia?

A

Mxyedema
Coma

35

119
Q

Myxedema Coma is triggered by what type of pathologies?

A
  • infection
  • trauma
  • cold
  • CNS depressants

35

120
Q

Myexdema Coma is a medical emergency, What is the mortality percentage?

A

50%

35

121
Q

Swelling of thyroid gland determine by hypertrophy & hyperplasia of follicular epithelium can be define as a……

A

Goiter & Thyroid Tumors

36

122
Q

What are the causes of Goiter & Thyroid Tumors?

A
  • lack of iodine
  • ingestion of goitrogen (cassava,phenylbutazone, lithium)
  • defect in the hormonal biosynthetic pathway

36

123
Q

Goiter and Thyroid Tumors are assoicated with what type of compenstated state?

A

Euthyroid

36

124
Q

Goiter and Thyriod Tumors are treated with what type of medication in most cases?

A

L-thyroxine

36

125
Q

When is surgery indicated for a Goiter and thyroid Tumors?

A
  • medical therapy is ineffective
  • compromises of air way
  • cosmetically unacceptable

36

126
Q

What pathology during pre-op history would be predictive of possible airway obstruction during general anesthesia?

A

dyspnea in upright or supine postition

37

127
Q

What imaging testing is used to examine and assess the extent of the tumor?

A

CT

37

128
Q

Which pulmoary funtion test is used to demonstrate the site and degree of obstruction?

The test is given with the patient in what 2 positions?

A
  • FLow - volume loop
  • upright and supine postition

37

129
Q

Limitations in the_____ limb of the loop indicate ____-thoracic obstruction

Delayed flow in the______ limb indicates an ____-thoracic obstruction

A
  • Inspiratory, extra-thoracic obstructions
  • expiratory, intra-thoracic obstructions

37

130
Q

Echo in an upright and/or supine position to indicate the degree of ?

A

cardiac compression

37

131
Q

What is the morbidity percentage regarding thyroid surgery?

A

13%

38

132
Q

Right laryngeal nerve injury can be____ or bilateral and temporary or ____.

A
  • unilateral
  • permanent

38

133
Q

What can happen to the patients airway if they expereince unilateral trauma to the thryoid?

How long does it take the thyroid to return to normal?

A
  • hoarseness but no airway obstruction
  • function return in 3-6 months

38

134
Q

What causes permanent hoarsness for a patient after thyriod surgery?

A

Ligation or transection of the nerve

38

135
Q

How does bilateral traurma effect the patient after surgery?

A
  • cause airway obstructin
  • difficulty coughing
  • may warrant tracheostomy

38

136
Q

Hypoparathyriodism due to thyriod surgery is caused by?

A

inadvertent parathyroid damage

38

137
Q

What is a sign and / or symptom of hypoparathyroidism that takes place 24-48 hours postoperativiely?

A

hypocalcemia

38

138
Q

What type of thyroid surgery complication can lead to tracheal compression?

A

Hemoatoma

A trach-set should be kept at bedside during immediate postop period

38

139
Q

What are the structures found within the adrenal gland?

A
  • cortex
  • medulla

39

140
Q

What steroids and / or hormones are synthesizes in the cortex?

A
  • glucocorticoids
  • mineralocorticoids (aldosterone)
  • androgens

39

141
Q

Hypothalamus sends ____ to the anterior pituitary, which stimulates ____ release from the anterior pituitary

A
  • corticotropin-releasing hormone (CRH)
  • corticotropin (ACTH)

39

142
Q

Corticotropin is release from the anterior pituitary to stimulate the adrenal cortex to produce, ____.

A

Cortisol

39

143
Q

Cortisol facilitate conversion of ___ to ___ .

This takes place in what part of the adrenal gland?

A
  • norepinephrine to epinphrine
  • adrenal medulla

39

144
Q

How does cortisol effects glucose in the body?

A
  • induces hyperglycemia
  • reflectinggluconeogenesis
  • inhibition of glucose uptake by cells

39

145
Q

What hormones casuses sodium retention and potassium excretion?

A

cortisol
aldosterone

39

146
Q

What is a pheochromocytoma?

A

a catecholamine-secreting tumor that arise from chromaffin cells of the sympathoadrenal system

40

147
Q

Uncontrolled catecholamine release can lead to what disease process?

A
  • malignant HTN
  • CVA
  • MI

40

148
Q

____% are an isolated finding
____% inherited (familial)

A

90%
10%

40

149
Q

____% occur in the adrenal medulla,
____% in organ of Zuckerkandle,
____% neck/thorax

A

80%
18%
2%

40

150
Q

Malignant Pheochromocytoma spread to through what body system’s

A

venous system
lymph systems

40

151
Q

What is the ratio of NE:EPI that is secrete by adrenal medulla with at patient that has Pheochromocytoma?

A

NE:EPI , 85:15
​
inverse of normal adrenal secretion

40

152
Q

Some pheochromocytoma secrete higher levels of ____and, more rarely, ____

A

epi
dopamine

40

153
Q

How long can a pheochromocytoma attack last?

A

between 1min and several hours

maybe occasional to frequent

41

154
Q

How does the pheochromocytoma attacks occur?

A
  • spontaneously
  • triggered by injury, stress, or meds

41

155
Q

What are the signs and symptoms of pheochromocytoma?

A
  • pallor
  • sweating
  • palpitations
  • orthostatic hypotension
  • cornary vasoconstriction
  • cardiomyopathy
  • CHF
  • EKG changes

41

156
Q

What are some tests that are utilize to diagnose pheochromocytoma?

A
  • 24h urine collection for. Etanephrines and catecholamines
  • CT & MRI
  • I-metaiodobenzylguanidine (MIBG) scintigraphy localize the tumor

41

157
Q

A 24 hour urine collection test for a pateint that has pheochromocytoma will be postive what to substances?

A

metanephrines catecholamines

41

158
Q

What are some pre -op consideration to take into acconut for with patients who have a pheochromocytoma?

A
  • α blocker to lower BP
  • decrease intravascular volume
  • allow sensitization of adrenergic receptors
  • decrease myocardial dysfunction

42

159
Q

What is the most frequently used preop Alpha blocker for phepchromocytoma?

A

Phenoxybenzamine

a noncompetitive α1 antagonist with some α2-blocking properties

42

160
Q

What other medication can be use to treat pheochromocytoma?

A

Prazosin
doxazosin

pure α1 blockers, shorter acting w/ less tachycardia

42

161
Q

True or false: Tachycardia after an α blockade should be treated with a BB.

A

True

42

162
Q

True or false: Give a selective BB before α blocker b/c blocking vasodilatory β2 receptors results in unopposed α agonism, leading to vasoconstriction and hypertensive crises

A

False: Never give nonselective BB before α blocker b/c blocking vasodilatory β2 receptors results in unopposed α agonism, leading to vasoconstriction and hypertensive crises

42

163
Q

What other class of blood pressure medication is use to control HTN for patients with pheochromocytoma?

A

CCBs

42

164
Q

ACTH- Independent Cushing: _____ cortisol production by abnormal _________ tissue that is not regulated by ____ and ACTH.

A
  • excessive
  • adrenocortical
  • CRH

44

165
Q

Acute Ectropic ACTH syndrome is a form of ACTH -_______ Cushing that is the most often associated with _______ __________ __________ carcinoma.

A
  • dependent
  • Small Cell Lung

44

166
Q

In ACTH- Independent Cushing:
CRH and ACTH levels are _
or tumors are the most common cause of ACTH-independent Curshing Syndrome.

A
  • suppressed
  • Benign or Malignant Adrenocortical

44

167
Q

Diagnosis of Hypercortisolism (Cushing Syndome is done with ___ hour urine ______.

A
  • 24 hour urine cortisol

45

168
Q

Distinguishing Cushings ACTH Dependent from ACTH Independent involves measuring ________ ACTH and ________________ assays.

A
  • plasma
  • immunoradiometric

45

169
Q

A high-doses dexamethasone suppression test distringuishes _______ from ______ ACTH Syndrome.

A
  • Cushing’s
  • Ectopic

45

170
Q

In Hypercortisolism (Cushing Syndrome) Imaging is useful for determining tumor ______________, but isn’t helpfu if gauging _________ function.

A
  • location
  • adrenal

45

171
Q

Treatment of choice for Hypercortisolism (Cushing Syndrome):
* transsphrenoidal _______________ if ________ is resectable.
* Alternatively, 85-90% resection of the _______ pituitary.

A
  • microadrenomectomy
  • microadenoma
  • anterior pituitary

46

172
Q

Hypercortisolism (Cushing Syndrome): Surgical adrenolectomy is the treatmetn for adrenal __________ or ___________.

A
  • adenoma
  • carcinoma

46

173
Q

Pituitary ________ and bilateral total ___________ are necessary for some patients with Cushings.

A
  • irradation
  • adrenalectomy

46

174
Q

Pre-Op Considerations for Cushing Syndome:
* evaluate/treat ____,
* ______ balance
* blood glucose
* Consider ____________ in position

A
  • BP
  • Electrolye
  • Osteoporosis

46

175
Q

Name the (8) Classic Signs of Cushings Syndome:
* Fat Pad: _____ ______
* ______ face
* Extra _____ and body hair
* Thin skin– _______
* ______ arms and legs
* ______ Cheeks
* _________ hair
* Stretch ______

A
  • Buffalo Hump
  • Moon Face
  • Face
  • bruising
  • thin
  • red
  • marks

48

176
Q

Hyperaldosteronims (Conn Syndrome) is the secretion of __ from a functional that acts __ of a physiologic stimulus.

A
  • excessive
  • tumor
  • independently

48

177
Q

Hyperaldosteronims (Conns Syndrome)
Occurs more in what gender?
* Occasionally associated with ______________, _________________ or acromegaly.

A
  • women>men
  • Pheochromocytoma
  • hyperparathyroidism

48

178
Q

Secondary Hyperaldosteronism: presents when serum _______ is increased, stimulating the release of _____________.

A
  • renin
  • aldosterone

48

179
Q

Symptoms of Hyperaldosteronism (Conns Syndrome):
* _______
* _________kalemia
* hypokalemia _______ ________-

A
  • HTN
  • Hypokalemia
  • Hypokalemia metabolic alkalosis

48

180
Q

Hyperaldosteronism (Conn Syndrome) is diagnosised with Spontaneous _______ in presense of systemic ______.

A
  • hypokalemia
  • HTN

49

181
Q

In Primary Hyper-Aldosteronism, plasma _____ activity is ______.

A
  • renin
  • supressed

49

182
Q

In Seconday Hyper-Aldosteronism the plasma ______ activity is ______.

A
  • renin
  • high

49

183
Q

Long-term ingestion of _____ can cause a syndrome that mimics the features of ______________________. Which include HTN, __________ and suppression of ______.

A
  • licorice
  • hyperaldosteronism
    Hypokalemia
  • RAAS

49

184
Q

Hyperaldosteronism (Conn Syndrome): treatment
* Competetive aldosterone antagonist (________)
* _____ replacement
* antihypertensives
* diuretics
* ________ removal
* possible _______________

A
  • Spironolactone
  • Potassium
  • tumor
  • adrenalectomy

49

185
Q

Hypoaldosteronism is ________ in the absence of ________ insufficiency.

A
  • hyperkalemia
  • renal

50

186
Q

Hypoaldosteronism:
* Hyperkalemia may be enhanced by ________.
* _________ metabolic acidosis is common.

A
  • hyperglycemia
  • Hypercholemic

50

187
Q

Hypoaldosteronism patients may experience ____ _____ d/t hyperkalemia, ________ HoTN, and ___________

A
  • heart block
  • orthostatic
  • hyponatremia

50

188
Q

Hypoaldosteronims lack of aldosterone may be caused by ________ deficiency of aldosterone synthetase or hypoeninemia d/t defects in the ________ apparatus or _______ inhibitors.

A
  • congential
  • juxtaglomerular
  • ACE

50

189
Q

Hyporeninemic Hypoaldosteronism typically occus in pts > ____ years old with Chronic ________ failure or _______ _______.

A
  • 45 years
  • Renal
  • Diabetes Mellitus

50

190
Q

__________ - induced ________ deficiency is a reversible cause of Hyporeninemic Hypoaldosteronism.

A
  • Imadomethacin
  • prostaglandin

50

191
Q

Treatment of Hypoaldosteronism includes liberal _____ intake and daily administration of ____________.

A
  • Sodium
  • fludrocortisone

50

192
Q

Name the (2) types of Adrenal Insufficency

A
  • Primary
  • Seconday

51

193
Q

Primary Adrenal Insufficency is one as ______ disease

A

Addisons

51

194
Q

Primary Arenal Insufficency (Addison dz) is when adrenal glands unable to produce enough ________, ___________ and adrogen hormones.

A
  • glucocorticoid
  • mineralcorticoid

51

195
Q

_________ ___________ is the most common cause of autoimmune adrenal destruction.

A
  • Primary Adrenal Insufficiency (Addison)

51

196
Q

In Primary Adrenal Insufficiency (Addison) >____% of the gland must be involved before signs appear.

A

90%

51

197
Q

Secondary Adrenal Insufficiency: ______________ -pituitary dz or suppression leading to _______ in the production of CRH or ACTH.

A
  • hypothalmic
  • failure

51

198
Q

Seconday Adrenal Insufficency is a deficiency of ________, while Primary (Addison) Adrenal Insufficency is a deficency in glucocorticoid, mineralocorticoid and _________ hormones.

A
  • glucocorticoid
  • adrenal

51

199
Q

Seconday Adrenal Insufficency is caused is _______, such as with the use of synthetic glucocorticoids, _________ surgery or ___________.

A
  • pituitary surgery
  • radiation

51

200
Q

Seconday Adrenal Insufficency patients lack _________ and may demonstrate only mild ________ abnormalities.

A
  • hyperpigmentation
  • electrolyte

51

201
Q

Adrenal Insufficiency diagnosis is baseline cortisol <____ ug/dL and remains <____ after ACTH stimulation

A
  • <20
  • <20

52

202
Q

Adrenal Insufficeny postive test demonstrates a ______ response to _______ and indicates an _________ of the adrenal.

A
  • poor
  • ACTH
  • impairment

52

203
Q

Absolute Adrenal Insufficency is characterized by a ______ baseline cortisol and a ______ ACTH stimulation test.

A
  • low
  • postitive

52

204
Q

Relative Adrenal Insufficency is indicated by a ______ baseline cortisol and a _______ ACTH test.

A
  • high
  • positive

52

205
Q

The treatment of Adrenal Insufficiency is _________.

A

Steroids.

52

206
Q

Parathyroid dysfx ::

  • The ___ parathyroid glands are behind upper & lower poles of the thyroid gland + produce _______, which is released into the circulation by a _________ feedback that depends on plasma _______ level
  • __________ stimulates the release of PTH
    o ___________ suppresses hormonal synthesis and release
  • PTH maintains normal plasma calcium level by promoting the movement of calcium across ________, __________, and ________.
A

4 … parathyroid hormone (PTH) … negative … calcium

Hypocalcemia

hypercalcemia

GI tract, renal tubules, and bone

53

207
Q

Hyperparathryoidism ::

  • Present when secretion of PTH is ________
  • Serum calcium concentrations may be _______, ______, or ______
  • Hyperparathyroidism is classified as _____, ______, or _______
A

increased
increased, decreased, or unchanged
primary, secondary, or ectopic

54

208
Q

Hypoparathyroidism ::

  • Dx: hypocalcemia < ____ and iCa < ____ along w/↓ PTH & ↑_______
  • Sx: d/o _______
    o thyroidectomy hypocalcemia may cause ________ ______ reflecting irritability of intrinsic_________ musculature
    o Chronic hypocalcemia is assoc w/ fatigue, cramps, ______ ______, lethargy, _______, SQ ______, thickening of the _____, neurologic deficits

_______ is most common cause of chronic hypocalcemia

  • 2 treatments?
A

4.5 … 2.0 … phosphate

speed of onset

inspiratory stridor … laryngeal

prolonged QT , cataracts … calcifications … skull

Chronic renal failure

calcium replacement + vitamin D

54

209
Q

Secondary Hyperparathyroidism ::
__________ response of the parathyroid glands to counteract a separate disease process producing _________ s/a CRF
o adaptive, it seldom produces ____________
o Tx ?? (2)

A

compensatory … hypocalcemia

hypercalcemia

treat underlying cause
phosphate binder - renal pts to normalize serum phos

55

210
Q

Pituitary gland is located in the ______ ______ + consists of Anterior + Posterior

The ANTERIOR pituitary secretes 6 hormones under control of the ________.
** name them
Over production of these hormones often assocaited with hyper secretion of _____ (cushing’s) by anterior pituitary _________-

______ and ________ are made in hypothalamus + stored in POSTERIOR pituitary
To release these 2 hormones , stimulate the __________ in the hypothalamus that sense plasma osmolarity.

A

Sella Turcica

Hypothalamus
GH, ACTH, TSH, FSH, LH, Prolactin
ACTH … adenomas

vasopressing (ADH) + oxytocin
osmoreceptors

57

211
Q

ACROMEGALY ::

is d/t excessive secretion of ____ _______ + most common cause is ________ in ANT pituitary gland
**Treatment? (2)

*Serum insulin-like growth factor 1 is ________
*What test measures plasma growth hormone ?
*Overgrowth of soft tissue makes pt susceptible to … ?
*Overgrowth of surrounding cartilagenous structures can cause ? (3)
*______ ________ is common d/t nerve trapping by connective tissues

A

growth hormone … adenoma
Tx = transphenoidal surgical excision of adenoma .. OR .. LA somatostatin analogue (if can’t operate)

*elevated
*Oral glucose tolerance test – elevated GH above 1 after 2 hrs of ingesting 75g glucose
*Upper airway obstruction
*hoarseness … abnormal movement of vocal cords .. RLN paralysis
*Peripheral Neuropathy

58

212
Q

ACROMEGALY ANESTHESIA IMPLICATIONS ::
*difficult mask ventilation d/t _
*enlarged and predisposes to upper airway obstructions + interferes with _ visualizations during DL.
*increased distance bw lips + vocal cords d/t _
*Glottic opening may be narrowed d/t _
*May require smaller , video larygoscopy , or _ induction

A

*distorted facial anatomy
*tongue + epiglottis … vocal cord
*mandible overgrowth
*vocal cord enlargement
* ETT … awake fiberoptic

58

213
Q

DIABETES INSIPIDUS ::

reflects absence of _________
*caused by destruction of _______ _________ (neurogenic)
*caused by failure of _______ ________ to respond to ADH (nephrogenic)
* the two types are differentiate based on responses to _________
»» this causes urine concentration in _______ type

A

*vasopressin
*posterior pituitary
*renal tubules
*desmopressin
*neurogenic

60

214
Q

DIABETES INSIPIDUS ::

Symptoms?
Initial treatment?
Neurogenic treatment?
Nephrogenic treatment?
Anesthesia?

A

*polydipsia , increased serum osmo , dilute urine
*IV electrolytes
*DDAVP
*low-salt , low-protein , diuretics , NSAIDs
*monitor UOP + lytes

60

215
Q

DIABETES INSIPIDUS ::

Treatment ? (4)
Hyponatremia treated with ____ _____ raising it less than within 24 hrs?

A

*fluid rest. , salt tablets ,, loop diuretics ,, vasopressin antagonists
*hypertonic saline @ <8 mEq/L within 24 hrs

60

216
Q

SYNDROME OF INAPPROPRIATE ADH ::

occurs in diverse pathologies like …? (4)
elevated ADH most likely to occur following ______ ________
Sx - increased urine _____ and _______ … in presence of _______ and decreased serum _________
Decrease in sodium can result in ______ ______ and _____

A

*intracranial tumors, hypothyroidism, porphyria, lung carcinoma
*major surgeries
*sodium and osmolarity … hyponatremia … osmolarity
*cerebral edema + seizures

61

Health Assessment Exam 4 (7 decks)

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