Exam 4 - Endocrine - organized COPY Flashcards
(216 cards)
1
Q
Liver is the primary sournce of endogenous glucose production via what 2 processes?
A
glycogenolysis & gluconeogenesis
2
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
2
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
3
4
Q
what is glucagon’s primary role?
A
stimulating glycogenolysis &gluconeogenesis, and inhibiting glycolysis
3
5
Q
what is the most common endocrine disease and how common is it?
A
Diabetes Mellitus
affects 1 in 10 adults
4
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
4
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
4
8
Q
what is type 1B DM?
A
rare disease of absolute insulin deficiency that is not immune mediated
4
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
4
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
5
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
5
12
Q
what precedes onset of symptoms in type 1 DM?
A
long pre-clinical period (9-13 yrs) of B-cell antigen production
5
13
Q
how much of b cell function is lost before hyperglycemia even shows up in type 1 DM?
A
At least 80-90%
5
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
6
15
Q
as type 2 DM progresses, what happens to pancreas and insulin levels?
A
pancreatic function decreases & insulin levels become inadequate
6
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
6
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
6
18
Q
what’s 2 tests are used for the diagnosis for DM2?
A
fasting blood glucose and HbA1c
7
19
Q
what is DM2 characterized by?
A
insulin resistance in skeletal muscle, adipose & liver
7
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!
7
21
Q
what HbA1c is considered normal?
prediabetic?
diabetic?
A
normal: <5.7%
prediabetic: 5.7-6.4%
diabetic: >/= 6.5%
8
22
Q
what is the american diabetes assoc criteria for dx of diabetes?
A
- A1c >/= 6.5
- Fasting Plasma Glucose >/= 126 mg/dL (7.0 mmol/L)* and fasting for at least 8 hrs!*
- 2-hr plasma gluc >/= 200 mg/dL during glucose tolerance test
- *in pt with classic symptoms of hyperglycemia or hyperglycemia crisis a random plasma gluc of >/= 200 mg/dL
8
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
9
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
9
25
what do sulfonylureas do?
what are some side effects?
* stimulate insulin secretion
* Enhances glucose transport into tissues
SE’s include hypoglycemia, weight gain & cardiac effects
| 9
26
why are sulfonylureas not effective long term?
d/t diabetic progressive loss of B cell function
| 9
27
What is the common s/e of metformin? Who is it contraindicated for?
GI side effects.
Contrainidicated with renal insufficiency.
| 10
28
What is the initial tx for DMII?
Lifystyle changes and Metformin
| 10
29
What are the additional therapies for DMII?
Insulin
Sulfonylurea
GLP-1 receptor agonist
Thiazolidenedione
glinide
SGLT-2 inhibitor
DPP-4 inhibitor
a- glucosidase inhibitor
Pramlintide
| 10
30
Insulin is necessary in ____ DMI cases & ____ DMII cases
all
30%
| 11
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Types of insulin
* Rapid acting (Lispro, Aspart)
* Short acting (regular)
* Basal/intermediate acting (NPH, Lente)
* Long acting (Ultralente, Glargine)
| 11
32
What is the most dangerous complication of insulin? What is it exacerbated by?
Hypoglycemia.
Exacerbated by **ETOH, metformin, sulfonylureas, ACE-I’s, MAOI’s, Non-selective BB’s**
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What does repetitive hypoglycemic episodes can lead to? What is the tx for hypoglycemia?
"**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)
| 11
34
What is the onset/peak/duration of short acting insulin (Human Regular, Lispro, Aspart)?
## Footnote
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35
What is the onset/peak/duration of intermediate insulin (Human NPH, Lente)?
## Footnote
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36
What is the onset/peak/duration of long acting insulin (ultralente, glargine)?
## Footnote
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Plasma insulin levels (chart)
| memorize
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38
What are the diagnostic features of DKA?
## Footnote
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39
What is a complication of decompensated DM? what its mortality rate?
Diabetic Ketoacidosis
mortality 1-2%
## Footnote
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40
DKA is more common in which type of DM? What can trigger DKA?
DKA more common in **DMI**, often triggered by infection/illness
## Footnote
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41
How does high glucose affect the renal function?
High glucose exceeds the threshold for renal reabsorption creating osmotic diuresis & hypovolemia.
| 13
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What causes the overproduction of ketoacids?
Tight metabolic coupling of gluconeogenesis & ketogenesis.
DKA results in excessive glucose-counterregulatory hormones, with glucagon activating lipolysis & free fatty acids→ substrates for ketogenesis.
## Footnote
13
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What is the treatment for DKA?
* 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
## Footnote
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44
What are the characteristics of hyperglycemic hyperosmolar syndrome? What is the mortality rate of HHM?
severe hyperglycemia, hyperosmolarity & dehydration
Mortality 10-20%
## Footnote
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45
What are the sings and symptoms of Hyperglycemic Hyperosmolar Syndrome?
* Polyuria
* polydipsia
* hypovolemia
* HoTN
* tachycardia
* organ hypoperfusion
- Some degree of acidosis, but not DKA
*Hyperosmolarity leads to coma.***
## Footnote
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What is the treatment of Hyperglycemic Hyperosmolar Syndrome?
fluid resuscitation, insulin bolus + infusion, e-lytes
## Footnote
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47
What happens when glucose load exceeds renal glucose absorption?
Mass solute diuresis
## Footnote
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48
What is the microvascular complication of DM?
Nonocclusive microcirculatory dz w/impaired blood flow autoregulation
## Footnote
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49
What is the neuropathic complication of DM associated w/ renal fx?
30-40% DM1, 5-10% DM2 develop **ESRD**. Kidneys develop glomerulosclerosis, arteriosclerosis, & tubulointerstitial disease
## Footnote
16
50
What are the signs of DM related ESRD?
HTN, proteinuria, peripheral edema,↓GFR
## Footnote
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51
What causes hyperkalemia in patients with ESRD?
When GFR < 15-20, kidneys no longer clear K+, Pts become hyperkalemic & acidotic
## Footnote
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52
What is the treatment for ESRD?
* 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
| 16
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What is characteristic of DM peripheral neurophathy? How does it progress?
Normally a **distal symmetric** diffuse sensorimotor polyneuropathy.
Starts in toes/feet, progresses **proximally**
## Footnote
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54
Loss of which fibers cause the reduction in light touch and proprioception?
large sensory & motor fibers
## Footnote
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55
Loss of which fibers cause the decrease in pain/temperature perception leading to neuropathic pain?
Small nerve fibers
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56
What causes the significant morbidity in someone w/ peripheral neuropathy?
Recurrent infections & amputation wounds.
## Footnote
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What is the treatment of peripheral neuropathy?
optimal glucose control, NSAIDS, antidepressants, anticonvulsants
## Footnote
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58
What is the diabetes related retinopathy?
* microvascular changes including vessel occlusion, dilation, ↑permeability, microaneurysms
* Visual impairment ranges from color loss to blindness
## Footnote
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59
What can reduce the progression of retinopathy?
Glycemic control & BP control
60
What causes autonomic neuropathy?
| Can affect any part of the ANS
Autonomic neuropathy is caused by damaged vasoconstrictor fibers, impaired baroreceptors and ineffect CV activity!
## Footnote
18
61
What are the CV and GI s/s of autonomic neuropathy?
What is the treatment?
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
| 18
62
What do you emphasize in patients with DM in the preop eval?
-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
## Footnote
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63
What are diabetics at risk for in regards to anesthesia?
-Arrhythmia risk d/t autonomic neuropathy
-risk for aspirations d/t gastroparesis
* hold PO hypoglycemic and noninsulin injectables
## Footnote
19
64
Who is at risk for insulinoma?
Dx is based on whipple triad..what are they?
| *benign insulin secreted pancreatic islet tumor!*
-occurs 2x in women than men~ 50-60 y/o
-Whipple triad:
hypoglycemia w fasting, glucose <50 w symptoms, and symptom relief w glucose
## Footnote
20
65
Insulinoma pt's have high insulin levels during 48-72 hr fast (dx). What meds should you give them preop?
diaxoide, inhibits insulin release from B cells
-verapamil, phenyoin, promanalol, glucorticoids and ocreotide
-at risk for hypoglycemia intraop** then hyperglycemia when tumor is removed
## Footnote
20
66
# 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?
-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
## Footnote
21
67
What type of cells does the thyroid gland contain?
What is thyroglobulin?
parafollicular cells- which produce calcitonin
-thyroid is composed of follicles filled w/ thyroiglobulin, which is an iodinated glycoprotein and substrate for thyroid hormone synthesis
## Footnote
21
68
What innervates the rich capillary network in the thyroid gland?
What nerves are close to it?
Adrenergic and cholinergic systems innervate capillary network.
-recurrent laryngeal nerve and external motor branch of superior laryngeal nerve
## Footnote
21
69
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?
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
## Footnote
22
70
What 3 proteins to T4 and T3 reversibly bind to?
T4/T3 ratio?
thyroxine-binding globulin (80%), prealbumin (10–15%), and albumin (5–10%).
10:1
## Footnote
22
71
What does a decrease in TSH cause?
What does an increase in TSH cause?
-decreased T3 & T4 synthesis, decreased follicular cell size, and decreased vascularity
-increase in TSH yields an increase in hormone production, gland cellularity and vascularity
## Footnote
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72
What 3 glands regulate thyroid function?
hypothalamus, pituitary, and thyroid glands, in a classic feedback control system
## Footnote
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73
Thermal thyroid scans evaluate thyroid nodules as warm if they are ____ functioning, hot if they are ____ and cold if they are ____
normally, hyperfunctioning and hypofunctioning
## Footnote
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74
What is the best test of TH action?
What is normal TSH level
TSH assay
normal TSH level is 0.4-5.0 milliunits/L
## Footnote
24
75
What does the TRH stimulation test assess?
functional state of the TSH-secreting mechanism, and is used to test pituitary function
## Footnote
24
76
What are top 3 pathologies for hyperthyroidism?
Graves disease
toxic multinodular goiter
toxic adenoma
## Footnote
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77
s/s of hyperthyroidism?
T3 acts directly on what?
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
## Footnote
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78
What is a
Cardiovascular
GI
Skin
s/s of hyperthyroidism ?
CV: **Palpitation**
GI: **Frequent BM/ Diarrhea**
Skin: **Warm, moist**
## Footnote
26 table
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What are Neurogical s/s of Hyperparathyroidism?
* Wasting, weakness, fatigue of proximal limb muscles
* fine tremor of hands
* hyperactive DTR (deep tendon reflexes)
## Footnote
26 table
80
What is a
General
Psych
s/s of Hyperparathyroidism?
General: **Anxious**
Psych: **Emotionally unstable**
## Footnote
26 table
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What are Cardiac effects of Hyperparathyroidism?
* Tachycardia, arrythmias (atrial)
* Hyperdynamic
* ↑ C.O. and contractility
* Cardiomegaly
## Footnote
26 table
82
What are HEENT s/s of Hyperparathyroidism?
* Flushed face
* Fine hair
* Exophthalmos/proptosis
## Footnote
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83
What is the leading cause of hyperthyroidism, effecting 0.4% population?
Who does this typically occurs in?
**Graves disease**
Typically occurs in
**females** (7:1 in 20-40 y/o)
## Footnote
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84
Grave disease appears to be ____, caused by thyroid-stimulating ____ that bind to ____ receptors, stimulating growth, vascularity, and hypersecretion
Grave disease appears to be **autoimmune**, caused by thyroid-stimulating **antibodies** that bind to **TSH** receptors, stimulating growth, vascularity, and hypersecretion
## Footnote
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What are s/s of Graves disease?
* diffusely enlarged thyroid
* Ophthalmopathy (in 30% cases)
* enlarged goiter
## Footnote
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What can enlarged goiter cause with Graves Disease?
* dysphagia
* globus sensation
* inspiratory stridor (from tracheal compression)
## Footnote
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What is the diagnosis that confirms Graves disease?
**TSH antibodies** in the context of
**↓ TSH and ↑ T3 & T4**
## Footnote
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What is the 1st line treatment of Graves disease?
**Antithyroid drug**
Methimazole or Propylthiouracil (PTU)
## Footnote
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89
What treatment is recommended when medical treatments failed with Graves disease?
Ablative therapy or surgery
**subtotal thyroidectomy** > radioactive iodine therapy with lower incidence of hypopthyroidism
## Footnote
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90
What are complications of surgery of Graves disease?
* hypothyroidism
* hemorrhage with tracheal compression
* RLN (recurrent laryngeal nerve) damage
* damage to or inadvertent removal of the parathyroid glands
## Footnote
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91
What treatment for Graves disease is reserved for pre-op or thyroid storm and why?
high concentrations of iodine (inhibit release of thyroid hormones)
its effect is short lived
## Footnote
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92
What medication doesn’t affect the underlying abnormality, but may relieve sx of Graves disease?
Beta Blockers
Propranolol impairs the peripheral conversion of T4 to T3
## Footnote
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93
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
**Thyroid levels** should 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
## Footnote
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94
What are usually necessary in emergent cases of Graves disease?
* IV Beta-Blockers
* Glucocorticoids
* PTU
## Footnote
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95
Why do you need to evaluate upper airway of pt with Graves Disease pre-operatively?
for evidence of **tracheal compression or deviation** caused by a goiter
## Footnote
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96
What is a life-threatening exacerbation of hyperthyroidism precipitated by trauma, infection, medical illness, or surgery?
What is the mortality rate?
Thyroid Storm
20% mortality rate
## Footnote
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97
What kind of condition presents very similar to Thyroid storm and differentiation between the two can be extremely difficult?
Malignant Hyperthermia
## Footnote
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98
____ levels in thyroid storm may not be much higher than basic hyperthyroidism
Thyroid hormone
## Footnote
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99
When do Thyroid storm most often occurs?
**postoperatively** in *untreated or inadequately treated* hyperthyroid pts
## Footnote
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100
What are the treatments for Thyroid storm?
* rapid alleviation of thyrotoxicosis
* supportive care
## Footnote
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101
What is another name for Hypothyroidism?
What is the course of this disease in adults?
Myxedema
a slow, progressive course
## Footnote
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102
What are the lab results of primary Hypothyroidism?
↓ T3 & T4 production with adequate TSH
## Footnote
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103
What is the 1st common cause of Hypothyrodism?
What is the 2nd common cause?
1st common cause: **ablation of the gland**
(by radioactive iodine or sx)
2nd common cause: **idiopathic and probably autoimmune**
(antibodies blocking TSH receptors)
## Footnote
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104
What is an *autoimmune disorder *characterized by goitrous enlargement and hypothyroidism that usually affects middle-aged women?
Hashimoto thyroiditis
## Footnote
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105
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
deficient ... resistant
iatrogenic ... thyroidectomy
congenital ... kidneys
## Footnote
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106
What other syndrome commonly occurs with Hypothyroidism?
SIADH
## Footnote
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107
What are the general and psych symptoms of Hypothyroidism?
General symptoms:
-fatigue
-listlessness
-weight gain
Psych:
apathy
## Footnote
31 & 32 Chart
108
What are the HEENT symptoms of Hypothyroidism?
* dry brittle hair
* large tongue
* deep hoarse voice
* periorbital edema
## Footnote
31 & 32 Chart
109
What are the GI symptoms of Hypothyroidism?
* constipation
* slow GI function
* adynamic ileus may occur
## Footnote
31 & 32 chart
110
What are the respiratory symptoms of Hypothyroidism?
* fluid overload
* pleural effusions
* dyspnea
## Footnote
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111
What are the skin symptoms of Hypothyroidism?
* pale
* cool
* dry
* thickened
* non-pitting peripheral edema
* cold intolerance
## Footnote
31 & 32 chart
112
What are the cardiac effects of Hypothyroidism?
* ↓ 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
## Footnote
31 & 32 table
113
True or false: Mechanical ventilation is not frequently required
false, mechanical ventilation is frequently required
## Footnote
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114
Hypothermia is a ____feature that determine impaired thermoregulation
cardinal
## Footnote
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115
What are treatments plan for Myxedema Coma
| long list
* IV L-thyroxine or levotriiodothyronine
* IV - hydration with glucose- saline solutions
* Tempature regulation
* Correction of electrolytes implance
* Stabliization of cardiac and pulmonary system
## Footnote
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116
What are the 3 vitial signs that improve within 24 hours of given electrolyte (myxedema coma)
* Heart Rate
* BP
* Temp
## Footnote
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117
Myxedema Coma occurs most commly in what population of patients
elderly women with a long history hypothyroidism?
## Footnote
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118
What is a rare form of hypothyroidism characterized by delirium, hypoventilation, hypothermia, bradycardia, HoTN, and severe dilutional hyponatremia?
Mxyedema
Coma
## Footnote
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119
Myxedema Coma is triggered by what type of pathologies?
* infection
* trauma
* cold
* CNS depressants
## Footnote
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120
Myexdema Coma is a medical emergency, What is the mortality percentage?
50%
## Footnote
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121
Swelling of thyroid gland determine by hypertrophy & hyperplasia of follicular epithelium can be define as a......
Goiter & Thyroid Tumors
## Footnote
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122
What are the causes of Goiter & Thyroid Tumors?
* lack of iodine
* ingestion of goitrogen (cassava,phenylbutazone, lithium)
* defect in the hormonal biosynthetic pathway
## Footnote
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123
Goiter and Thyroid Tumors are assoicated with what type of compenstated state?
Euthyroid
## Footnote
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124
Goiter and Thyriod Tumors are treated with what type of medication in most cases?
L-thyroxine
## Footnote
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125
When is surgery indicated for a Goiter and thyroid Tumors?
* medical therapy is ineffective
* compromises of air way
* cosmetically unacceptable
## Footnote
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What pathology during pre-op history would be predictive of possible airway obstruction during general anesthesia?
dyspnea in upright or supine postition
## Footnote
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127
What imaging testing is used to examine and assess the extent of the tumor?
CT
## Footnote
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128
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?
* FLow - volume loop
* upright and supine postition
## Footnote
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129
Limitations in the_____ limb of the loop indicate ____-thoracic obstruction
Delayed flow in the______ limb indicates an ____-thoracic obstruction
* Inspiratory, extra-thoracic obstructions
* expiratory, intra-thoracic obstructions
## Footnote
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130
Echo in an upright and/or supine position to indicate the degree of ?
cardiac compression
## Footnote
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131
What is the morbidity percentage regarding thyroid surgery?
13%
## Footnote
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132
Right laryngeal nerve injury can be____ or bilateral and temporary or ____.
* unilateral
* permanent
## Footnote
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133
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?
* hoarseness but no airway obstruction
* function return in 3-6 months
## Footnote
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134
What causes permanent hoarsness for a patient after thyriod surgery?
Ligation or transection of the nerve
## Footnote
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135
How does bilateral traurma effect the patient after surgery?
* cause airway obstructin
* difficulty coughing
* may warrant tracheostomy
## Footnote
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136
Hypoparathyriodism due to thyriod surgery is caused by?
inadvertent parathyroid damage
## Footnote
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137
What is a sign and / or symptom of hypoparathyroidism that takes place 24-48 hours postoperativiely?
hypocalcemia
## Footnote
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138
What type of thyroid surgery complication can lead to tracheal compression?
Hemoatoma
*A trach-set should be kept at bedside during immediate postop period*
## Footnote
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139
What are the structures found within the adrenal gland?
* cortex
* medulla
## Footnote
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140
What steroids and / or hormones are synthesizes in the cortex?
* glucocorticoids
* mineralocorticoids (aldosterone)
* androgens
## Footnote
39
141
Hypothalamus sends ____ to the anterior pituitary, which stimulates ____ release from the anterior pituitary
* corticotropin-releasing hormone (CRH)
* corticotropin (ACTH)
## Footnote
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142
Corticotropin is release from the anterior pituitary to stimulate the adrenal cortex to produce, ____.
Cortisol
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143
Cortisol facilitate conversion of ___ to ___ .
This takes place in what part of the adrenal gland?
* norepinephrine to epinphrine
* adrenal medulla
## Footnote
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144
How does cortisol effects glucose in the body?
* induces hyperglycemia
* reflecting gluconeogenesis
* inhibition of glucose uptake by cells
## Footnote
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145
What hormones casuses sodium retention and potassium excretion?
cortisol
aldosterone
## Footnote
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146
What is a pheochromocytoma?
a catecholamine-secreting tumor that arise from chromaffin cells of the sympathoadrenal system
## Footnote
40
147
Uncontrolled catecholamine release can lead to what disease process?
* malignant HTN
* CVA
* MI
## Footnote
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148
____% are an isolated finding
____% inherited (familial)
90%
10%
## Footnote
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149
____% occur in the adrenal medulla,
____% in organ of Zuckerkandle,
____% neck/thorax
80%
18%
2%
## Footnote
40
150
Malignant Pheochromocytoma spread to through what body system's
venous system
lymph systems
## Footnote
40
151
What is the ratio of NE:EPI that is secrete by adrenal medulla with at patient that has Pheochromocytoma?
NE:EPI , 85:15
*inverse of normal adrenal secretion*
## Footnote
40
152
Some pheochromocytoma secrete higher levels of ____and, more rarely, ____
epi
dopamine
## Footnote
40
153
How long can a pheochromocytoma attack last?
between 1min and several hours
*maybe occasional to frequent*
## Footnote
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154
How does the pheochromocytoma attacks occur?
* spontaneously
* triggered by injury, stress, or meds
## Footnote
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155
What are the signs and symptoms of pheochromocytoma?
* pallor
* sweating
* palpitations
* orthostatic hypotension
* cornary vasoconstriction
* cardiomyopathy
* CHF
* EKG changes
## Footnote
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156
What are some tests that are utilize to diagnose pheochromocytoma?
* 24h urine collection for. Etanephrines and catecholamines
* CT & MRI
* I-metaiodobenzylguanidine (MIBG) scintigraphy *localize the tumor*
## Footnote
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157
A 24 hour urine collection test for a pateint that has pheochromocytoma will be postive what to substances?
metanephrines catecholamines
## Footnote
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158
What are some pre -op consideration to take into acconut for with patients who have a pheochromocytoma?
* α blocker to lower BP
* decrease intravascular volume
* allow sensitization of adrenergic receptors
* decrease myocardial dysfunction
## Footnote
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159
What is the most frequently used preop Alpha blocker for phepchromocytoma?
Phenoxybenzamine
*a noncompetitive α1 antagonist with some α2-blocking properties*
## Footnote
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160
What other medication can be use to treat pheochromocytoma?
Prazosin
doxazosin
*pure α1 blockers, shorter acting w/ less tachycardia*
## Footnote
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161
True or false: Tachycardia after an α blockade should be treated with a BB.
True
## Footnote
42
162
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
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
## Footnote
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163
What other class of blood pressure medication is use to control HTN for patients with pheochromocytoma?
CCBs
## Footnote
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164
ACTH- Independent Cushing: _____ cortisol production by abnormal _________ tissue that is not regulated by ____ and ACTH.
* excessive
* adrenocortical
* CRH
## Footnote
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165
Acute Ectropic ACTH syndrome is a form of ACTH -_______ Cushing that is the most often associated with _______ __________ __________ carcinoma.
* dependent
* Small Cell Lung
## Footnote
44
166
In ACTH- Independent Cushing:
CRH and ACTH levels are _
or tumors are the most common cause of ACTH-independent Curshing Syndrome.
* suppressed
* Benign or Malignant Adrenocortical
## Footnote
44
167
Diagnosis of Hypercortisolism (Cushing Syndome is done with ___ hour urine ______.
* 24 hour urine cortisol
## Footnote
45
168
Distinguishing Cushings ACTH Dependent from ACTH Independent involves measuring ________ ACTH and ________________ assays.
* plasma
* immunoradiometric
## Footnote
45
169
A high-doses dexamethasone suppression test distringuishes _______ from ______ ACTH Syndrome.
* Cushing's
* Ectopic
## Footnote
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170
In Hypercortisolism (Cushing Syndrome) Imaging is useful for determining tumor ______________, but isn't helpfu if gauging _________ function.
* location
* adrenal
## Footnote
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171
Treatment of choice for Hypercortisolism (Cushing Syndrome):
* transsphrenoidal _______________ if ________ is resectable.
* Alternatively, 85-90% resection of the _______ pituitary.
* microadrenomectomy
* microadenoma
* anterior pituitary
## Footnote
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172
Hypercortisolism (Cushing Syndrome): Surgical adrenolectomy is the treatmetn for adrenal __________ or ___________.
* adenoma
* carcinoma
## Footnote
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173
Pituitary ________ and bilateral total ___________ are necessary for some patients with Cushings.
* irradation
* adrenalectomy
## Footnote
46
174
Pre-Op Considerations for Cushing Syndome:
* evaluate/treat ____,
* ______ balance
* blood glucose
* Consider ____________ in position
* BP
* Electrolye
* Osteoporosis
## Footnote
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175
Name the (8) Classic Signs of Cushings Syndome:
* Fat Pad: _____ ______
* ______ face
* Extra _____ and body hair
* Thin skin-- _______
* ______ arms and legs
* ______ Cheeks
* _________ hair
* Stretch ______
* Buffalo Hump
* Moon Face
* Face
* bruising
* thin
* red
* marks
## Footnote
48
176
Hyperaldosteronims (Conn Syndrome) is the secretion of __ from a functional that acts __ of a physiologic stimulus.
* excessive
* tumor
* independently
## Footnote
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177
Hyperaldosteronims (Conns Syndrome)
Occurs more in what gender?
* Occasionally associated with ______________, _________________ or acromegaly.
* women>men
* Pheochromocytoma
* hyperparathyroidism
| 48
178
Secondary Hyperaldosteronism: presents when serum _______ is increased, stimulating the release of _____________.
* renin
* aldosterone
## Footnote
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179
Symptoms of Hyperaldosteronism (Conns Syndrome):
* _______
* _________kalemia
* hypokalemia _______ ________-
* HTN
* Hypokalemia
* Hypokalemia metabolic alkalosis
## Footnote
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180
Hyperaldosteronism (Conn Syndrome) is diagnosised with Spontaneous _______ in presense of systemic ______.
* hypokalemia
* HTN
## Footnote
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181
In Primary Hyper-Aldosteronism, plasma _____ activity is ______.
* renin
* supressed
## Footnote
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182
In Seconday Hyper-Aldosteronism the plasma ______ activity is ______.
* renin
* high
## Footnote
49
183
Long-term ingestion of _____ can cause a syndrome that mimics the features of ______________________. Which include HTN, __________ and suppression of ______.
* licorice
* hyperaldosteronism
Hypokalemia
* RAAS
## Footnote
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184
Hyperaldosteronism (Conn Syndrome): treatment
* Competetive aldosterone antagonist (________)
* _____ replacement
* antihypertensives
* diuretics
* ________ removal
* possible _______________
* Spironolactone
* Potassium
* tumor
* adrenalectomy
## Footnote
49
185
Hypoaldosteronism is ________ in the absence of ________ insufficiency.
* hyperkalemia
* renal
## Footnote
50
186
Hypoaldosteronism:
* Hyperkalemia may be enhanced by ________.
* _________ metabolic acidosis is common.
* hyperglycemia
* Hypercholemic
## Footnote
50
187
Hypoaldosteronism patients may experience ____ _____ d/t hyperkalemia, ________ HoTN, and ___________
* heart block
* orthostatic
* hyponatremia
## Footnote
50
188
Hypoaldosteronims lack of aldosterone may be caused by ________ deficiency of aldosterone synthetase or hypoeninemia d/t defects in the ________ apparatus or _______ inhibitors.
* congential
* juxtaglomerular
* ACE
## Footnote
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189
Hyporeninemic Hypoaldosteronism typically occus in pts > ____ years old with Chronic ________ failure or _______ _______.
* 45 years
* Renal
* Diabetes Mellitus
## Footnote
50
190
__________ - induced ________ deficiency is a reversible cause of Hyporeninemic Hypoaldosteronism.
* Imadomethacin
* prostaglandin
## Footnote
50
191
Treatment of Hypoaldosteronism includes liberal _____ intake and daily administration of ____________.
* Sodium
* fludrocortisone
## Footnote
50
192
Name the (2) types of Adrenal Insufficency
* Primary
* Seconday
## Footnote
51
193
Primary Adrenal Insufficency is one as ______ disease
Addisons
## Footnote
51
194
Primary Arenal Insufficency (Addison dz) is when adrenal glands unable to produce enough ________, ___________ and adrogen hormones.
* glucocorticoid
* mineralcorticoid
## Footnote
51
195
_________ ___________ is the most common cause of autoimmune adrenal destruction.
* Primary Adrenal Insufficiency (Addison)
## Footnote
51
196
In Primary Adrenal Insufficiency (Addison) >____% of the gland must be involved before signs appear.
90%
| 51
197
Secondary Adrenal Insufficiency: ______________ -pituitary dz or suppression leading to _______ in the production of CRH or ACTH.
* hypothalmic
* failure
## Footnote
51
198
Seconday Adrenal Insufficency is a deficiency of ________, while Primary (Addison) Adrenal Insufficency is a deficency in glucocorticoid, mineralocorticoid and _________ hormones.
* glucocorticoid
* adrenal
## Footnote
51
199
Seconday Adrenal Insufficency is caused is _______, such as with the use of synthetic glucocorticoids, _________ surgery or ___________.
* pituitary surgery
* radiation
## Footnote
51
200
Seconday Adrenal Insufficency patients lack _________ and may demonstrate only mild ________ abnormalities.
* hyperpigmentation
* electrolyte
## Footnote
51
201
Adrenal Insufficiency diagnosis is baseline cortisol <____ ug/dL and remains <____ after ACTH stimulation
* <20
* <20
## Footnote
52
202
Adrenal Insufficeny postive test demonstrates a ______ response to _______ and indicates an _________ of the adrenal.
* poor
* ACTH
* impairment
## Footnote
52
203
Absolute Adrenal Insufficency is characterized by a ______ baseline cortisol and a ______ ACTH stimulation test.
* low
* postitive
## Footnote
52
204
Relative Adrenal Insufficency is indicated by a ______ baseline cortisol and a _______ ACTH test.
* high
* positive
## Footnote
52
205
The treatment of Adrenal Insufficiency is _________.
Steroids.
## Footnote
52
206
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 ________.
4 ... parathyroid hormone (PTH) ... negative ... calcium
Hypocalcemia
hypercalcemia
GI tract, renal tubules, and bone
## Footnote
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207
Hyperparathryoidism ::
* Present when secretion of PTH is ________
* Serum calcium concentrations may be _______, ______, or ______
* Hyperparathyroidism is classified as _____, ______, or _______
increased
increased, decreased, or unchanged
primary, secondary, or ectopic
## Footnote
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208
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?
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
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)
compensatory ... hypocalcemia
hypercalcemia
treat underlying cause
phosphate binder - renal pts to normalize serum phos
## Footnote
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210
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.
Sella Turcica
Hypothalamus
GH, ACTH, TSH, FSH, LH, Prolactin
ACTH ... adenomas
vasopressing (ADH) + oxytocin
osmoreceptors
## Footnote
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211
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
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
## Footnote
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212
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
*distorted facial anatomy
*tongue + epiglottis ... vocal cord
*mandible overgrowth
*vocal cord enlargement
* ETT ... awake fiberoptic
## Footnote
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213
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
*vasopressin
*posterior pituitary
*renal tubules
*desmopressin
*neurogenic
## Footnote
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214
DIABETES INSIPIDUS ::
Symptoms?
Initial treatment?
Neurogenic treatment?
Nephrogenic treatment?
Anesthesia?
*polydipsia , increased serum osmo , dilute urine
*IV electrolytes
*DDAVP
*low-salt , low-protein , diuretics , NSAIDs
*monitor UOP + lytes
## Footnote
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215
DIABETES INSIPIDUS ::
Treatment ? (4)
Hyponatremia treated with ____ _____ raising it less than within 24 hrs?
*fluid rest. , salt tablets ,, loop diuretics ,, vasopressin antagonists
*hypertonic saline @ <8 mEq/L within 24 hrs
## Footnote
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216
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 _____
*intracranial tumors, hypothyroidism, porphyria, lung carcinoma
*major surgeries
*sodium and osmolarity ... hyponatremia ... osmolarity
*cerebral edema + seizures
## Footnote
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