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Health Assessment > Exam 4 - Endocrine > Flashcards

Exam 4 - Endocrine 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

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

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

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3
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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4
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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5
Q

What is the initial tx for DMII?

A

Lifystyle changes and Metformin

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6
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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7
Q

Insulin is necessary in ____ DMI cases & ____ DMII cases

A

all
30%

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8
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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9
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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10
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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11
Q

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

A

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12
Q

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

A

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13
Q

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

A

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14
Q

Plasma insulin levels (chart)

Memorize

A

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15
Q

What are the diagnostic features of DKA?

A

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16
Q

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

A

Diabetic Ketoacidosis
mortality 1-2%

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17
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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18
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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19
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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20
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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21
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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22
Q

What are the signs 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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23
Q

What is the treatment of Hyperglycemic Hyperosmolar Syndrome?

A

fluid resuscitation, insulin bolus + infusion, e-lytes

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24
Q

What happens when glucose load exceeds renal glucose absorption?

A

Mass solute diuresis

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25
Q

What is the microvascular complication of DM?

A

Nonocclusive microcirculatory dz w/impaired blood flow autoregulation

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26
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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27
Q

What are the signs of DM related ESRD?

A

HTN, proteinuria, peripheral edema,↓GFR

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28
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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29
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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30
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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31
Q

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

A

large sensory & motor fibers

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32
Q

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

A

Small nerve fibers

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33
Q

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

A

Recurrent infections & amputation wounds.

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34
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

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35
Q

What is the treatment of peripheral neuropathy?

A

optimal glucose control, NSAIDS, antidepressants, anticonvulsants

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36
Q

What is diabetes related retinopathy?

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

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37
Q

What is a
General
Psych
s/s of Hyperparathyroidism?

A

General: Anxious

Psych: Emotionally unstable

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38
Q

DM complications

What causes autonomic neuropathy?

A

damaged vasoconstrictor fibers, impaired baroreceptors and ineffective CV activity!

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39
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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40
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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41
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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42
Q

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

Insulinoma- 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 release w glucose
-

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43
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, phenytoin, promanalol, glucorticoids and ocreotide
-they’re at risk for hypoglycemia intraop** then hyperglycemia when tumor is removed

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44
Q

Thyroid gland is composed of 2 lobes joined by 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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45
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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46
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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47
Q

What can reduce the progression of retinopathy?

A

Glycemic control & BP control

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48
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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49
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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50
Q

What 3 glands regulate thyroid function?

A

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

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51
Q

What are top 3 pathologies for hyperthyroidism?

A

Graves disease
toxic multinodular goiter
toxic adenoma

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52
Q

What is the best test of thyroid hormone action at cellular level?

What is normal TSH level

A

TSH assay

normal TSH level is 0.4-5.0 milliunits/L

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53
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 cardiovascular responses

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54
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 enzyme?

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

A

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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55
Q

In the blood, what 3 proteins do T4 and T3 reversibly bind to?

What’s T4/T3 ratio?

A

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

10:1

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56
Q

What are HEENT s/s of Hyperthyroidism?

A
  • Flushed face
  • Fine hair
  • Exophthalmos/proptosis

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57
Q

What are
CV
GI
Skin
s/s of Hyperthyroidism?

A

CV: Palpitation

GI: Frequent BM/ Diarrhea

Skin: Warm, moist

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58
Q

What are Neurogical s/s of Hyperthyroidism?

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

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59
Q

What are Cardiac effects of Hyperthyroidism?

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

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60
Q

What is the diagnosis that confirms Graves disease?

A

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

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61
Q

What can enlarged goiter cause with Graves Disease?

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

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62
Q

What are s/s of Graves disease?

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

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63
Q

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

A

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

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64
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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65
Q

What is the 1st line treatment of Graves disease?

A

Antithyroid drug
Either Methimazole or Propylthiouracil (PTU)

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66
Q

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

A

Ablative therapy or surgery

subtotal thyroidectomy > has lower incidence of hypothyroidism than radioactive iodine therapy

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67
Q

What are complications from surgery for Graves disease?

A
  • hypothyroidism
  • hemorrhage with tracheal compression
  • RLN (recurrent laryngeal nerve) damage
  • damage to parathyroid glands

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68
Q

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

A

high concentrations of iodine (this inhibits TH release)

The effect is short lived

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69
Q

Pre-op considerations for Graves disease are:

____ ____should be established pre op

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

A

Thyroid levels should be established pre op

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

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70
Q

What drugs are usually necessary in emergent cases of Graves disease?

A
  • IV Beta-Blockers
  • Glucocorticoids
  • PTU

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71
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

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72
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

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73
Q

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

A

Malignant Hyperthermia

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74
Q

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

A

Thyroid hormone

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75
Q

When do Thyroid storm most often occurs?

A

postoperatively in untreated or inadequately treated hyperthyroid pts

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76
Q

What are the treatments for Thyroid storm?

A
  • rapid alleviation of thyrotoxicosis
  • supportive care

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77
Q

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

A

Myxedema

a slow, progressive course

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78
Q

What are the lab results of primary Hypothyroidism?

A

↓ T3 & T4 production with adequate TSH

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79
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)

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80
Q

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

A

Hashimoto thyroiditis

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81
Q

What other syndrome commonly occurs with Hypothyroidism?

A

SIADH

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82
Q

What are the general and psych symptoms of Hypothyroidism?

A

General symptoms:
-fatigue
-listlessness
-weight gain

Psych:
apathy

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83
Q

What are the HEENT symptoms of Hypothyroidism?

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

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84
Q

What are the neurologic symptoms of Hypothyroidism?

A
  • slow speech
  • slowing of motor function
  • prolonged relaxation phase of DTR

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85
Q

What are the GI symptoms of Hypothyroidism?

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

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86
Q

What are the skin symptoms of Hypothyroidism?

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

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87
Q

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

A

Diabetes Mellitus

affects 1 in 10 adults

s4

88
Q

What are the respiratory symptoms of Hypothyroidism?

A
  • fluid overload
  • pleural effusions
  • dyspnea

S31

89
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

S31 and S32 table

90
Q

Myxedema Coma is triggered by what type of pathologies?

A
  • infection
  • trauma
  • cold
  • CNS depressants

Slide 35

91
Q

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

Slide 35

A

Mxyedema
Coma

35

92
Q

what is glucagon’s primary role?

A

stimulating glycogenolysis &gluconeogenesis, and inhibiting glycolysis

s3

93
Q

what precedes onset of symptoms in type 1 DM?

A

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

s5

94
Q

Hypothermia is a ____feature that determine impaired thermoregulation

A

cardinal

Slide 35

95
Q

Myxedema Coma occurs most commly in what population of patients

A

elderly women with a long history hypothyroidism?

Slide 35

96
Q

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

A

> 50%

Slide 35

97
Q

What leads to diabetes mellitus?
and what does DM lead to w/ glucose?

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

s4

98
Q

What are treatments plan for Myxedema Coma

long list

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

Slide 35

99
Q

True or false: Mechanical ventilation is not frequently required

A

false, mechanical ventilation is frequently required

Slide 35

100
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

s4

101
Q

what is type 1B DM?

A

rare disease of absolute insulin deficiency that is not immune mediated

s4

102
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

s6

103
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

s4

104
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

s5

105
Q

What are the 3 vitial signs that improve within 24 hours of given electrolyte ?

A
  • Heart Rate
  • BP
  • Temp

Slide 35

106
Q

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

A

Goiter & Thyroid Tumors

Slide 36

107
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

Slide 36

108
Q

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

A

Euthyroid

Slide 36

109
Q

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

A

L-thyroxine

Slide 36

110
Q

When is surgery indicated for a Goiter and thyroid Tumors?

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

Slide 36

111
Q

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

A

dyspnea in upright or supine postition

Slide 37

112
Q

what is 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

s5

113
Q

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

A

At least 80-90%

s5

114
Q

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

A

CT

Slide 37

115
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

Slide 37

116
Q

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

A

pancreatic function decreases & insulin levels become inadequate

s6

117
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

s6

118
Q

____ in the inspiratory limb of the loop indicate ____-thoracic obstruction

____ flow in the expiratory limb indicates an ____-thoracic obstruction

A
  • Limitations, extra-thoracic obstructions
  • Delayed, intra-thoracic obstructions

Slide 37

119
Q

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

A

fasting blood glucose and HbA1c

s7

120
Q

what is DM2 characterized by?

A

insulin resistance in skeletal muscle, adipose & liver

s7

121
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!

s7

122
Q

What type of imaging test can be adminstered to a patient who has a goiter or thyroid tumor in an upright and/or supine position to indicate the degree of cardiac compression ?

A

Echocardiogram

Slide 37

123
Q

what HbA1c is considered normal?
prediabetic?
diabetic?

A

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

s8

124
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

s8

125
Q

What is the morbidity percentage regarding thyroid surgery?

A

13%

Slide 38

126
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

s9

127
Q

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

A
  • unilateral
  • permanent

38

128
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

s9

129
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

s9

130
Q

why are sulfonylureas not effective long term?

A
  • d/t diabetic progressive loss of B cell function

s9

131
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
  • ___________ 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

132
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

133
Q

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

A
  • excessive
  • adrenocortical
  • CRH

44

134
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

135
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

136
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

137
Q

Symptoms of Hypercortisolism (Cushing Syndrome) are:
* Sudden weight ____.
* ↑_______ fat (______ face)
* Ecchymoses
* HTN
* ______________ intolerance
* muscle __________
* depression
* insomnia

A
  • weight gain
  • facial
  • Moon
  • intolereance
  • wasting

45

138
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

56

139
Q

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

A
  • 24 hour urine cortisol

45

140
Q

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

A
  • plasma
  • immunoradiometric

45

141
Q

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

A
  • Cushing’s
  • Ectopic

45

142
Q

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

A
  • location
  • adrenal

45

143
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

144
Q

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

A
  • adenoma
  • carcinoma

46

145
Q

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

A
  • irradation
  • adrenalectomy

46

146
Q

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

A
  • BP
  • Electrolye
  • Osteoporosis

46

147
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

47

148
Q

Hyperaldosteronims (Conn Syndrome) is the _______ secretion of _________ from a functional ______ that acts __________ of a physiologic stimulus.

A
  • excessive
  • tumor
  • independently

48

149
Q

Hyperaldosteronims (Conns Syndrome)
* _____ > ______
* Occasionally associated with ______________, _________________ or acromegaly.

A
  • women>men
  • Pheochromocytoma
  • hyperparathyroidism

48

150
Q

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

A
  • renin
  • aldosterone

48

151
Q

What does the TRH stumulation test assess?

A

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

24

152
Q

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

A
  • HTN
  • Hypokalemia
  • Hypokalemia metabolic alkalosis

48

153
Q

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

A
  • hypokalemia
  • HTN

49

154
Q

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

A
  • renin
  • supressed

49

155
Q

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

A
  • renin
  • high

49

156
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

157
Q

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

A
  • Spironolactone
  • Potassium
  • tumor
  • adrenalectomy

49

158
Q

Hypoaldosteronism is ________ in the absence of ________ insufficiency.

A
  • hyperkalemia
  • renal

50

159
Q

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

A
  • hyperglycemia
  • Hypercholemic

50

160
Q

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

A
  • heart block
  • orthostatic
  • hyponatremia

50

161
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

162
Q

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

A
  • 45 years
  • Renal
  • Diabetes Mellitus

50

163
Q

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

A
  • Imadomethacin
  • prostaglandin

50

164
Q

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

A
  • Sodium
  • fludrocortisone

50

165
Q

Name the (2) types of Adrenal Insufficency

A
  • Primary
  • Seconday

51

166
Q

Primary Adrenal Insufficency is known as ______ disease

A

Addisons

51

167
Q

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

A
  • glucocorticoid
  • mineralcorticoid

51

168
Q

What is the most common cause of autoimmune adrenal destruction.

A
  • Primary Adrenal Insufficiency (Addison)

51

169
Q

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

A

90%

51

170
Q

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

A
  • hypothalmic
  • failure

51

171
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

172
Q

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

A

*iatrogenic
* pituitary surgery
* radiation

51

173
Q

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

A
  • hyperpigmentation
  • electrolyte

51

174
Q

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

A
  • <20
  • <20

52

175
Q

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

A
  • poor
  • ACTH
  • impairment
176
Q

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

A
  • low
  • postitive

52

177
Q

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

A
  • high
  • positive
178
Q

The treatment of Adrenal Insufficiency is _________.

A

Steroids.

52

179
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

180
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

181
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

182
Q

SIADH ::

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

A

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

60

183
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

Slide 38

184
Q

What causes permanent hoarsness for a patient after thyriod surgery?

A

Ligation or transection of the nerve

Slide 38

185
Q

How does bilateral traurma effect the patient after surgery?

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

Slide 38

186
Q

Hypoparathyriodism due to thyriod surgery is caused by?

A

inadvertent parathyroid damage

Slide 38

187
Q

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

A

hypocalcemia

Slide 38

188
Q

What complication from thyroid surgery can lead to tracheal compression?

A

Hemoatoma

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

Slide 38

189
Q

What are the structures found within the adrenal gland?

A
  • cortex
  • medulla

slide 39

190
Q

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

A
  • glucocorticoids
  • mineralocorticoids (aldosterone)
  • androgens

Slide 39

191
Q

Pertaining to Adrenal Gland function ::
Hypothalamus sends ____ to the anterior pituitary, which stimulates ____ release from the anterior pituitary

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

Slide 39

192
Q

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

A

Cortisol

Slide 39

193
Q

Cortisol facilitate conversion of ___ to ___ .

This takes place in what part of the adrenal gland?

A
  • norepinephrine to epinphrine
  • adrenal medulla

Slide 39

194
Q

How does cortisol effects glucose in the body?

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

39

195
Q

What hormones casuses sodium retention and potassium excretion?

A

cortisol
aldosterone

Slide 39

196
Q

What is a pheochromocytoma?

A

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

40

197
Q

Uncontrolled catecholamine release can lead to what disease process?

A
  • malignant HTN
  • CVA
  • MI

slide 40

198
Q

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

A

90%
10%

Slide 40

199
Q

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

A

80%
18%
2%

Slide 40

200
Q

Malignant Pheochromocytoma spread to through what body system’s

A

venous system
lymph systems

Slide 40

201
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

Slide 40

202
Q

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

A

epi
dopamine

Slide 40

203
Q

How long can a pheochromocytoma attack last?

A

between 1min and several hours

maybe occasional to frequent

41

204
Q

How does the pheochromocytoma attacks occur?

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

Slide 41

205
Q

What are the signs and symptoms of pheochromocytoma?

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

Slide 41

206
Q

What are some tests that are utilize to diagnose pheochromocytoma?

A
  • 24h urine collection
  • CT & MRI
  • I-metaiodobenzylguanidine (MIBG) scintigraphy
    localize the tumor

Slide 41

207
Q

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

A

metanephrines catecholamines

Slide 41

208
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

Slide 42

209
Q

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

A

Phenoxybenzamine

a noncompetitive α1 antagonist with some α2-blocking properties

Slide 42

210
Q

What other medication can be use to treat pheochromocytoma?

A

Prazosin
doxazosin

pure α1 blockers, shorter acting w/ less tachycardia

Slide 42

211
Q

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

A

True

Slide 42

212
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

Slide 42

213
Q

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

A

CCBs

Slide 42

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 ::

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

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 (11 decks)

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