Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Health Assessment > Endocrine > Flashcards

Endocrine Flashcards

1
Q

What is the primary source of endogenous glucose production?

A

Liver

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What does a normal glucose level require?

A

a balance b/w glucose usage and endogenous production or dietary carbohydrate intake

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

How does the liver alter glucose levels/ in what ways?

A

glycogenolysis and gluconeogenesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What percentage of glucose release by the liver is metabolized by insulin-insensitive tissues?

A

70-80%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What are examples of insulin-insensitive tissues?

A

Brain, GI tract, red blood cells!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

When does the transition from exogenous usage to endogenous production of glucose occur to maintain a normal glucose level?

A

2-4 hours after eating, happens when glucose usage exceeds production (ex: doing squats to build that ass)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is fundamental for the maintenance of normal blood glucose 2-4 hours after eating?

A

diminished insulin production is fundamental! Don’t wanna completely tank

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What hormones comprise the glucose counter-regulatory system and support glucose production?

A

glucagon, epinephrine, growth hormone, and cortisol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Tell me about the role of glucagon

A

glucagon plays a primary role by stimulating glycogenolysis and gluconeogenesis, and inhibits glycolysis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is the MOST COMMON endocrine disease?

A

Diabetes Mellitus, affects 1 in 10 adults

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What does Diabetes Mellitus result from?

A

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

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is type 1a diabetes caused by?

A

T-cell-mediated autoimmune destruction of Beta cells within pancreatic islets, leading to minimal or absent circulating insulin levels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Tell me about type 1b diabetes.

A

It’s a rare disease of absolute insulin deficiency, which is not immune mediated

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Is type 2 diabetes immune mediated?

A

Nope, results from defects in insulin receptors and post-receptor intracellular signaling pathways

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Facts about type 1 DM:

A

-accounts for 5-10% of all DM
-usually diagnosed before age 40
-the exact autoimmune cause is unknown
-involves a long preclinical period (9-13 years) of b-cell antigen production that precedes the onset of symptoms
-80-90% of B cell function is lost before hyperglycemia ensues

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is hyperglycemia over several days/ weeks associated with? (S/S)

A

-fatigue, weight loss, polyuria, polydipsia, blurry vision, hypovolemia, ketoacidosis
-Dr. Mordecai’s friends realized their daughter had type 1 b/c she started peeing the bed randomly at 11 years old

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Facts about Type 2 DM:

A

-increasingly seen in younger patients and children over the past decade
-very under-diagnosed, normally present 4-7 years before diagnosed
-with disease progression, pancreatic function decreases and insulin levels become inadequate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

3 main abnormalities seen in DM Type 2:

A

-increased hepatic glucose release caused by a reduction in insulin’s inhibitory effect on the liver
-impaired insulin secretion
-insufficient glucose uptake in peripheral tissues

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What is type 2 DM characterized by?

A

insulin resistance:( in skeletal muscle, adipose and liver

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What are some causes of insulin resistance?

A

-abnormal insulin molecules
-circulating insulin antagonist
-insulin receptor defects

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What are acquired/ contributing factors to DM type 2?

A

obesity and sedentary lifestyle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

How is Diabetes diagnosed?

A

fasting blood glucose and HbA1C

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What are normal, pre-diabetic, and diabetic A1C percentages?

A

-normal: <5.7%
-pre-diabetic: 5.7-6.4%
-diabetic: >6.5%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Info on the American Diabetes Association for the Diagnosis of Diabetes chart:

A
  1. A1c >6.5%. The test should be performed in a lab using a method that is NGSP certified
  2. Fasting blood glucose >126 mg/dL (7 mmol) fasting is defined by no calorie intake for at least 8 hr
  3. 2 hour plasma glucose >200 mg/dL (11.1 mmol) during an OGTT-test should be performed using glucose load equivalent to 75 g glucose
  4. class s/s of hyperglycemia or hyperglycemic crisis, a random plasma glucose >200 mg/dL
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What are the first things you do to treat type 2 diabetes?

A

-dietary adjustments and exercise/weight loss
-decreasing body fat improves hepatic and peripheral insulin sensitivity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Tell me about Metformin.

A

-the preferred initial drug treatment!
-biguanide
-enhances glucose transport into tissues
-decreased triglycerides and LDL levels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

what do Sulfonylureas do?

A

-stimulate insulin secretion
-enhances glucose transport into tissues

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Are Sulfonylureas good long term treatment for DM?

A

Nope! d/t diabetic progressive loss of B cell function

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Side effects of Sulfonylureas:

A

hypoglycemia, weight gain, and cardiac effects :(

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

How much can lifestyle changes like weight loss and exercise drop A1c?

A

-1-2 points
-insufficient for most within first year owing to inadequate weight loss and weight gain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

How much can metformin drop A1c?

A

-1-2 points
-weight neutral
-GI side effects, contraindicated with renal insufficiency (GFR<30 mL/min)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

How much can insulin drop A1c levels?

A

-1.5-3.5 points
-no dose limit, rapidly effective, improved lipid profile
-1-4 injections daily (monitor for weight gain and hypoglycemia)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

How much can sulfonylureas drop A1c?

A

-1-2 points
-rapidly effective but can cause weight gain and hypoglycemia, especially with glibenclamide or chlorpropamide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

How much can GLP1 receptor agonists drop A1c?

A

-0.5-1.5 points
-requires injection and has frequent GI side effects

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What are the positive effects of GLP1 agonists?

A

weight loss, reduction in major adverse cardiovascular events (liraglutide, semaglutide, dulaglutide) in patients with established CVD and potentially those with high risk CVD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

How much is insulin required for type 1 and type 2 diabetes?

A

needed in ALL type 1 cases and 30% of type 2 cases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

What kind of insulin do we give in the OR?

A

short-acting (regular)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

What type of insulin is NPH/Lente?

A

basal/intermediate-acting

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

What is the most dangerous complication to long-acting insulin (ultralente, glargine)

A

hypoglycemia-exacerbated by ETOH, metformin, sulfonylureas, ACE-I’s, MAOI’s, non-selective beta blockers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

What can repetitive hypoglycemic episodes lead to?

A

hypoglycemia unawareness

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

What is hypoglycemia unawareness?

A

patient becomes desensitized to hypoglycemia and doesn’t show autonomic symptoms (so patient can’t sense drop in blood sugars)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Hypoglycemia unawareness leads to neuroglycopenia. What does this include? How is it treated?

A

-fatigue, confusion, headache, seizures, coma
-treatment: po or IV glucose (may give SQ or Im if unconscious)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Here’s a pic of a graph showing that rapid insulin lasts the shortest amount of time and long acting lasts the longest:)

A

-rapid: aspart, lispro, glulisine, inhaled human insulin
-short: regular U-100
-intermediate: NPH
-long: detemir
-long: U-100 glargine
-ultra-long: glargine U-300
-ultra-long: degludec

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Lispro (Humalog) and Aspart (Novolog) onset, peak, and duration:

A

onset: 10-15 minutes
peak: 1-2 hours
duration: 3-6 hours

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Human regular insulin onset, peak, and duration:

A

onset: 30 minutes
peak: 2-4 hours
duration: 5-8 hours

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Human NPH and Lente insulin onset, peak, and duration:

A

onset: 1-2 hours
peak: 6-10 hours
duration: 10-20 hours

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

Glargine (Lantus) insulin onset, peak, and duration:

A

onset: 1-2 hours
peak: n/a
duration: 24 hours

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

Ultralente insulin onset, peak, and duration:

A

onset: 4-6 hours
peak: 8-20 hours
duration: 24-48 hours

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

What is a complication of DM?

A

DKA :( mortality is 1-2%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

Which type of DM is DKA more common with?

A

type 1-often triggered by infection/illness

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

What does the high glucose exceeding threshold for renal reabsorption that happens with DKA cause?

A

It causes osmotic diuresis and hypovolemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

What does tight metabolic coupling of gluconeogenesis and ketogenesis lead to in DKA?

A

leads to liver overproduction of ketoacidosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

What does DKA result in?

A

excessive glucose-counterregulatory hormones with glucagon activating lipless and free fatty acids-substrates for ketogenesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

Diagnostic features of DKA:

A

-serum glucose: > or equal to 300 mg/dL
-pH: < or equal to 7.3
-HCO3: < or equal to18 mEq/L
-serum osmolarity: <320 mOsm/L
-serum and urine ketone levels: moderate to high

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

DKA Treatment:

A

-IV volume replacement
-insulin: loading dose 0.1 mcg regular + low dose infusion @ 0.1 mcg/kg/hr
-correct acidosis w/ sodium bicarb
-electrolyte supplement: K+, phosphate, magnesium, and sodium
-correction of glucose w/o simultaneous correction of sodium may result in cerebral edema

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

What does HHS stand for?

A

Hyperglycemic Hyperosmolar Syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

What is HHS characterized by?

A

-severe hyperglycemia, hyperosmolarity, and dehydration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

With what type of DM does HHS normally occur and at what age?

A

-type 2 DM and over 60 years old

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

Is HHS immediate?

A

No, it evolves over days to weeks with persistent glycosuric diuresis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

What happens in HHS when glucose load exceeds max renal glucose absorption?

A

Mass solute diuresis occurs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

What are the symptoms of HHS?

A

-polyuria, polydipsia, hypovolemia, hypotension, tachycardia, and organ hypoperfusion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

What can hyperosmolarity lead to?

A

coma :(

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

With HHS and DKA, which is more likely to have acidosis?

A

DKA! HHS can have some degree of acidosis but not as much as DKA can.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

What is the treatment for HHS?

A

-fluid resuscitation, insulin bolus + infusion, electrolytes
-mortality rate is 10-20% (much higher than DKA)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

What do microvascular complications of DM refer to?

A

non-occlusive microcirculatory disease with impaired blood flow autoregulation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

What is the Diabetic Nephropathy?

A

-30-40% of DMI and 5-10% DMII develop ESRD
-Kidneys develop glomerulosclerosis, arteriosclerosis, and tubulointerstitial disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

Symptoms of Nephropathy:

A

HTN, proteinuria, peripheral edema, and decreased GFR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

What happens in reference to electrolytes when GFR drops lower than 15-20 mL/min?

A

The kidneys can no longer clear potassium and the patient becomes hyperkalemic and acidotic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

How can ACE-I’s help fight against nephropathy?

A

They slow the progression of proteinuria and the rate of GFR slowing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

What is involved in the treatment of ESSRD?

A

hemodialysis and peritoneal dialysis, and kidney transplant

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

What is something that can prevent recurrent nephropathy?

A

If you’re gonna get a kidney transplant, go ahead and get a new pancreas too-better outcomes than just kidney transplant

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

Tell me about peripheral neuropathy

A

-It’s normally a distal, symmetric diffuse sensorimotor polyneuropathy that starts in the toes/feet and progresses proximally
-involves loss of large sensory motor fibers which reduces light touch and proprioception

-also lose small nerve fibers which means decreased pain/temperature perception causing neuropathic pain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

What can peripheral neuropathy lead to?

A

-ulcers b/c mechanical and traumatic injury goes unnoticed:(
(this is why always wears boots lol)
-significant morbidity results from recurrent infections and amputation wounds

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

What is the treatment for peripheral neuropathy?

A

-Optimal glucose control
-NSAIDS
-Antidepressants
-Anticonvulsants

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

What is diabetic retinopathy?

A

It’s caused by microvascular changes including vessel occlusion, dilation, increased permeability, and micro aneurysms
-visual impairment ranges from color loss to blindness
-glycemic control and BP control reduces the progression

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

What is autonomic Neuropathy?

A

It can affect any part of ANS and is caused by damaged vasoconstrictor fibers, impaired baroreceptors, and ineffective cardiovascular activity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

What are the CV symptoms of autonomic neuropathy?

A

abnormal HR control and vascular dynamics, resting tachycardia, loss of HR variability, progresses to orthostatic hypotension and dysrhythmias

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

What are the GI symptoms of autonomic neuropathy?

A

-decreased gastric secretions and motility, eventually causing gastroparesis
-N/V, early satiety, bloating, and epigastric pain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

What is the treatment for autonomic neuropathy?

A

glucose control, small meals, and prokinetics

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

What to include in preop eval for DM patients:

A

-emphasize CV, renal, neuro, and MDK systems and remember that silent ischemia is possible with autonomic neuropathy
-consider stress test in pts w/ multiple cardiac risk factors and poor exercise tolerance
-pay close attention to hydration status, avoid nephrotoxins, and preserve renal blood flow

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

What does autonomic neuropathy predispose patient to?

A

peri-operative dysrhythmia and hypotension

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

What does gastroparesis increase your risk for?

A

Aspiration, REGARDLESS of NPO status

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

What meds should you hold when it comes to DM patients?

A

Hold p.o. hypoglycemic and non-insulin injectable drugs should be held the morning of surgery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

What is Insulinoma?

A

It’s a rare, benign insulin-secreting pancreatic islet tumor that occurs 2x more in females than males, normally b/w 50-60 years old

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

What is Whipple’s triad, which is used to diagnose Insulinoma?

A
  1. Hypoglycemia with fasting
  2. Glucose <50 with symptoms
  3. Symptoms relief with glucose

diagnosis based on inappropriately high insulin level during 48-72 hour fast

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
86
Q

What to do for Insulinoma patients preop:

A

-Diazoxide which inhibits insulin release from B cells
-Other treatment: verapamil, phenytoin, propranolol, glucocorticoids, and octreotide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
87
Q

True or false: surgery is curative for Inulinoma?

A

TRUE!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
88
Q

What is important to consider intra-op for patients with Insulinoma?

A

Hypoglycemia can occur intra-op followed by hyperglycemia once the tumor is removed. Tight glycemic control is paramount!
Per Dr. Mordecai, the pt will probably be on an insulin get post-op

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
89
Q

How much does the thyroid gland weigh and what are the two lobes joined together by?

A

20 grams, 2 lobes are joined together by an isthmus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
90
Q

What is the thyroid gland affixed to?Just

A

the anterior and lateral trachea, with upper border just below the cricoid cartilage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
91
Q

Where are the parathyroid glands located?

A

On the posterior aspects of each thyroid lobe

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
92
Q

What is the rich capillary network that permeates the thyroid gland innervated by?

A

The adrenergic and cholinergic nervous systems

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
93
Q

What nerves are in close proximity to the thyroid?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
94
Q

The thyroid is composed of follicles. What are they filled with?

A

Thyroglobulin, an iodinated glycoprotein and substrate for thyroid hormone synthesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
95
Q

What are the specific cells in the thyroid that produce calcitonin?

A

Parafollicular cells!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
96
Q

What does production of normal quantities of thyroid hormone depend on?

A

The availability of exogenous iodine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
97
Q

What is the primary source of iodine?

A

Our diet!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
98
Q

What is iodine reduced to in the GI tract?

A

Iodide-after reduction it is rapidly absorbed into the blood and then transported into thyroid follicular cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
99
Q

What is the binding of iodide to thyroglobulin catalyzed by? What does this yield?

A

an iodinate enzyme and yields inactive monoiodotyrosine and diiodotyrosine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
100
Q

What percentage of monoiodotyrosine and diiodotyrosine undergoes coupling with thyroid peroxidase? What does this form?

A

25%, forms active triiodothyronine (T3) and Thyroxine (T4)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
101
Q

True or false: the thyroid has a large store of hormones and has a low turnover rate?

A

True!

This allows protection against depletion if hormone synthesis is impaired.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
102
Q

What is the T4/T3 ratio?

A

10:1 (so more T4 than T3)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
103
Q

T4 and T3 reversibly bound to these three major proteins:

A

TBG or thyroxine-binding globulin (80%), pre albumin (10-15%) and albumin (5-10%)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
104
Q

What metabolic processes does thyroid hormone stimulate?

A

Virtually all of them!

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
105
Q

What are the controllers of regulation of thyroid function?

A

Hypothalamus, pituitary gland, and thyroid glands-in a classic feedback control system

So thyroid has an auto regulatory mechanism that maintains consistent hormone stores!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
106
Q

What hormone does the hypothalamus secrete and where does it go?

A

It secretes thyrotropin-releasing hormone (TRH) which makes a lil trip down to the pituitary “stalk” lol.

107
Q

TRH binding to pituitary gland promotes the release of what hormone?

A

Thyrotropin-stimulating hormone (TSH) is released from the ANTERIOR pituitary

108
Q

What does TSH do?

A

It binds to receptors on the thyroid cell membrane and enhances the synthesis and secretion of T3 and T4.

-influenced by plasma levels of T3 and T4 via negative feedback loop

109
Q

What does a decrease in TSH cause?

A

It causes decreased T3 and T4 levels which leads to a decreased follicular size and decreased vascularity of the thyroid gland

110
Q

What does an increase in TSH cause?

A

It causes an increase in hormone production, gland cellularity and vascularity

111
Q

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

A

TSH ASSAY ;)

112
Q

What can small changes in thyroid function cause? What is a normal TSH level?

A

Small changes can cause significant changes in TSH secretion! Normal values for TSH are 0.4-0.5 milliunits/L

113
Q

What does the TRH stimulation test assess?

A

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

114
Q

What are other tests listed that can assess thyroid function?

A

serum anti-microsomal antibodies, antithyroglobulin antibodies, and thyroid-stimulation immunoglobulins

115
Q

What do thermal thyroid scans evaluate thyroid nodules as?

A

-Warm (normal function)
-hot (hyper-functioning)
-cold (hypo-functioning)

116
Q

How accurate is ultrasound in determining whether a lesion is cystic, solid, or mixed?

A

90-95% accurate!

117
Q

What is hyper-thyroidism?

A

hyper-functioning thyroid gland with excessive secretion active hormones

118
Q

What are the 3 major pathologies causing hyperthyroidism?

A

-graves disease
-toxic multi-nodular goiter
-toxic adenoma

119
Q

What are examples of symptoms that are related to having a hyper metabolic state?

A

-sweating
-heat intolerance
-fatigue
-inability to sleep

120
Q

True or false: osteoporosis and weight loss can accompany hyperthyroidism

A

TRUE

121
Q

Is it T3 or T4 that acts directly on the myocardium and peripheral vasculature to cause a CV response?

A

T3

122
Q

List of S/S associated with hyperthyroidism:
(everything in overdrive)

A

anxious, flushed face, fine hair, exophthalmos/proptosis, palpitations, wasting, weakness, fatigue of proximal limb muscles, fine tremor of hands, hyperactive deep tendon reflexes, frequent BM’s/Diarrhea, emotionally unstable, warm/ moist skin

CV: tachycardia, arrhythmias, hyper dynamic, increased CO and contractility, cardiomegaly

123
Q

Tell me about Grave’s Disease

A

-the leading cause of hyperthyroidism affecting 0.4% of the population
-typically occurs in females (7:1) b/2 20-40 yrs old
-autoimmune, caused by thyroid-stimulating antibodies that bind to TSH receptors to stimulate growth, vascularity, and hypersecretion
-Ophthalmopathy occurs in 30% of cases

124
Q

Is the thyroid bigger or smaller with graves disease?

A

Usually diffusely enlarged-graves can arise from a long-standing goiter

125
Q

How is Grave’s Diagnosis confirmed? How may people present?

A

-Confirmed with TSH antibodies in the context of low TSH and high T3 and T4

-present with extreme enlargement causing dysphagia, globes sensation, and inspiratory stridor from TRACHEAL COMPRESSION**

126
Q

What is the number 1 treatment for thyroid disease?

A

Antithyroid drugs! Either Methimazole or Propylthiouracil (PTU)

127
Q

Why don’t we just bolus everyone with Grave’s Disease with high concentrations of Iodine? Will that not fix the problem?

A

-High concentrations of iodine will cause immediate inhibition of the release of thyroid hormone, but the effect is short-lived and therefore reserved for pre-op and thyroid storm

-not just for day-to-day life

128
Q

How do beta blockers help treat grave’s disease?

A

-They don’t affect the underlying abnormality but they do help treat the symptoms!

-Propranolol impairs the peripheral conversion of T4 to T3

129
Q

What is recommended for graves disease treatment when medication therapy has failed?

A

Ablative therapy or surgery

130
Q

What is a subtotal thyroidectomy associated with?

A

lower incidence of hypothyroidism than radioactive iodine therapy

131
Q

What are potential complications of surgery for treating hyperthyroidism?

A

hypothyroidism, hemorrhage with tracheal compression, recurrent laryngeal nerve damage, and damage to or inadvertent removal of the parathyroid glands

132
Q

Anesthesia Pre-op things to consider for hyperthyroidism:

A

-thyroid levels should be established pre-op
-elective cases may need to wait 6-8 weeks for antithyroid drugs to take effect

-In emergent cases, IV BB’s, Glucocorticoids and PTU are usually needed

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

133
Q

What is thyroid storm?

A

It’s a life-threatening exacerbation of hyperthyroidism precipitated by trauma, infection, medical illness, or surgery

134
Q

What can thyroid storm present very similarly to?

A

Malignant Hyperthermia! Can be very hard to differentiate b/w the 2

135
Q

Do thyroid levels always go sky high in the case of thyroid storm?

A

No, sometimes they can look like pretty normal hyperthyroidism and may just rise a little during storm

136
Q

When does thyroid storm most often occur?

A

Post-op in untreated or inadequately treated hyperthyroidism patients after emergency surgery

137
Q

What treatment is involved with thyroid storm?

A

rapid alleviation of thyrotoxicosis and supportive care-mortality rate is 20%

138
Q

What’s the other name for hypothyroidism?

A

-Myxedema-effects 0.5-0.8% of adults

139
Q

How prevalent is sublingual hypothyroidism?

A

-20% of women >60 years old have subclinical hypothyroid which is associated with increased risk for CAD if TSH >10 milliunits/L

-thyroid replacement for subclinical disease remains controversial

140
Q

What does primary hypothyroidism result in?

A

It takes up 95% of cases and results in decreased T3 and T4 production despite adequate TSH

141
Q

What’s the first most common cause of hypothyroidism?

A

ablation of the thyroid gland by radioactive iodine or surgery

142
Q

What’s the second most common cause of hypothyroidism?

A

Idiopathic and probably autoimmune with antibodies blocking TSH receptors

143
Q

What is Hashimoto’s Thyroiditis?

A

an autoimmune disorder characterized by goitrous enlargement and hypothyroidism, usually affects middle-aged women

144
Q

Is hypothyroidism an acute illness?

A

No, it’s slow and progressive (in adults specifically)

145
Q

What are some symptoms of Hashimoto’s/ hypothyroidism?

A

cold intolerance, weight gain, nonpitting edema, fatigue, listlessness, dry brittle hair, deep hoarse voice, periorbital edema, slow speech, prolonged relaxation of DTRs, constipation, apathy, pale/cool skin

146
Q

CV side effects of hypothyroidism:

A

decreased CO, baroreceptor function impaired, flattened or inverted T waves, low-amplitude P waves and QRS complexes, sinus bradycardia, ventricular dysrhythmias

147
Q

What diagnoses is also common to have with Hashimoto’s?

A

SIADH, fluid overload, pleural effusion and dyspnea

148
Q

Is GI function fast or slow with hypothyroidism?

A

SLOW… adynamic ileum may occur:(
adynamic= loss of strength or function

149
Q

What is criteria for diagnosis of secondary hypothyroidism?

A

Reduced levels of T3, T4, and TSH

150
Q

What test can differentiate primary from secondary hypothyroidism and how does it work?

A

TRH stimulation test can confirm if the pituitary is the cause by measuring pituitary responsiveness to IV TRH

-In primary: TRH further elevates TSH
-With pituitary dysfunction, there is no response to TRH

151
Q

What is euthyroid sick syndrome?

A

abnormal thyroid functions tests in critically ill patients

152
Q

What are the typical lab values for pt with euthyroid sick syndrome?

A

-Low T3 and T4 with normal TSH level
-Likely a response to stress and it can be induced by surgery

153
Q

What is the treatment for hypothyroidism?

A

L-thyroxine is DOC

154
Q

What are pre-op implications for hypothyroidism?

A

-assess for airway compromise d/t swelling, edematous vocal cords, and goitrous enlargement
-expect slower gastric emptying and aspiration risk
-CV system may be hypodynamic
-Resp. function may be compromised
-MORE PRONE TO HYPOTHERMIA
-possible electrolyte imblances

155
Q

What should be done in the case of elective surgery for a pt with hypothyroidism?

A

thyroid medication/treatment should be initiated at least 10 days prior

156
Q

What should be given in the case of emergent surgery for thyroid patients?

A

IV thyroid replacement along with steroids ASAP

157
Q

What is Myxedema Coma?

A

A rare, severe form of hypothyroidism characterized by delirium, hypoventilation, hypothermia, bradycardia, hypotension, and severe dilution Hyponatremia

158
Q

Who most common gets diagnosed with Myxedema Coma?

A

most commonly in elderly women with a long history of hypothyroidism-often triggered by infection, trauma, cold, and CNS depressants

159
Q

Is Myxedema Coma a medical emergency?

A

YES! mortality rate is literally >50%. More than half of the people diagnosed, die:(((

160
Q

What is the treatment for myxedema coma?

A

-IV L-thyroxine or L-triiodothyronine
-Also, Iv hydration with glucose-saline solutions, temp regulation, correction of e-lyte imbalances, and stabilization of cardiac and pulmonary systems are needed

161
Q

Is mechanical ventilation frequently required with treating myxedema coma?

A

Yes

162
Q

How long after treating myxedema coma does it take HR, BP, and temp to improve?

A

24 hours

163
Q

What’s a goiter and what are the typical causes?

A

-Swelling of thyroid gland due to hypertrophy and hyperplasia of follicular epithelium

-caused by lack of iodine, ingestion of goitrogen (cassava, phenylbutazone, lithium) or a defect in the hormonal biosynthetic pathway

164
Q

Are goiters most often associated with a hypo, hyper, of euthyroid state?

A

A compensated euthyroid state

165
Q

What are most goiters treated with?

A

L-thyroxine

166
Q

When is surgery indicated for goiters?

A

Only if medical therapy is ineffective and goiter is compromising the airway or is cosmetically unacceptable

167
Q

What are indications of possible airway obstruction during general anesthesia?

A

pre-op history of dyspnea in upright or supine position

168
Q

What test can be done to assess the extent of the thyroid tumor?

A

CT scan

169
Q

What PFT can be done to demonstrate the site and degree of obstruction? (for thyroid goiter causing airway obstruction)

A

Flow volume loops in the upright and supine positions

170
Q

Limitations in the inspiratory limb of flow volume loops mean what?

A

indicate extra-thoracic obstruction

171
Q

Limitations/delayed flow in the expiratory limb of flow volume loop indicates what?

A

an intrathoracic obstruction

172
Q

What test can indicate degree of cardiac compression related to goiter complications?

A

Echocardiogram in the upright and supine positions

173
Q

What is the probability of morbidity post-thyroid surgery? What is a big complication we worry about?

A

13%, Recurrent Laryngeal Nerve Injury (can unilateral, bilateral, temporary or permanent)

174
Q

What would be the effect on the patient if RLN injury was unilateral?

A

If trauma is unilateral, pt experiences hoarseness but NO airway obstruction

function usually returns in 3-6 months

175
Q

What would cause permanent hoarseness post-thyroid surgery?

A

Ligation or transection of the nerve:(

176
Q

What would bilateral RLN injury cause?

A

more serious than unilateral, may cause airway obstruction and difficulty coughing and may warrant a tracheostomy:(

177
Q

What can result from inadvertent parathyroid damage during thyroid surgery? What symptoms would you see and when?

A

-hypoparathyroidism

-symptoms of hypocalcemia occur in the first 24-48 hours post-op

178
Q

What would a hematoma from thyroid surgery cause? What should always be kept at bedside?

A

-tracheal compression

-a trash-set should be kept at bedside during immediate post-op period

179
Q

What two things does each adrenal gland consist of?

A

A cortex and a medulla

180
Q

What does the cortex of the adrenal gland do?

A

It synthesizes glucocorticoids mineralocorticoids (like aldosterone), and androgens

181
Q

How does the hypothalamus work on the anterior pituitary?

A

It sends corticotropin-releasing hormone (CRH) to the anterior pituitary-which stimulates corticotropin (ACTH) release from the anterior pituitary

182
Q

What does ACTH release stimulate the adrenal cortex to produce?

A

Cortisol

183
Q

What does cortisol production cause?

A

-It facilitates the conversion of Norepinephrine to Epinephrine in the adrenal medulla

-Cortisol also indices hyperglycemia, reflecting gluconeogenesis and inhibition of glucose uptake by cells

184
Q

So, what specifically do Cortisol and Aldosterone do when they work together?

A

They cause sodium retention and Potassium excretion

185
Q

What is a pheochromocytoma and what are some serious complications of them?

A

-A catecholamine-secreting tumor that arises from chromatin cells of the sympathoadrenal system

-Uncontrolled catecholamine release can result in malignant HTN, CVA, and MI

186
Q

Is the precise cause of Pheochromocytoma known?

A

No, the cause is unknown :/

187
Q

Pheochromocytoma list of percentages:

A

-90% are isolated findings, 10% are inherited
-80% occur in the adrenal medulla, 18% in the organ of Zuckerkandle, and 2% in the neck/ thorax

188
Q

What systems do malignant Pheo’s spread through?

A

The venous and lymph systems

189
Q

What is the typically NE:EPI secretion ratio for Pheo’s?

A

NE:EPI ratio is 85:15

-note that this is the inverse of normal adrenal secretion

(some secrete higher levels of EPI and more rarely, dopamine)

190
Q

How long are Pheo-attacks usually?

A

-Attacks range from occasional to frequent and may last b/w 1 minute to several hours

-attacks can occur spontaneously or triggered by injury, stress, or meds

191
Q

What are the symptoms of Pheochromocytoma?

A

-headache, pallor, sweating, palpitations, orthostatic hypotension (due to down-regulation of adrenergic receptors and the desensitization of baroreceptors I believe)

-cardiomyopathy, coronary vasoconstriction, CHF, & EKG changes may occur

192
Q

How do you diagnose Pheo’s? What imaging is helpful?

A

-24 hour urine collection for metanephrines and catecholamines

-CT and MRI, MIBG (I-metaiodobenzylguanidine) scintigraphy can help localize the tumor

193
Q

What to do pre-op for pheo’s?

A

-Give an alpha blocker to lower blood pressure
-decrease intravascular volume
-allow sensitization of adrenergic receptors
-decrease myocardial dysfunction

194
Q

What is the MOST common alpha-blocker to give to pheochromocytoma patients and why?

A

-Phenoxybenzanine is the most frequently used pre-op drug! It’s a non-competitive alpha1 antagonist with some alpha2 blocking properties

-can also use Prazosin and Doxazosin which are pure alpha 1 blockers-shorter acting with less tachycardia

195
Q

If treatment for pheochromocytoma cause tachycardia, what can we give to counteract that?

A

Beta Blockers! But NEVER give a nonselective BB before an alpha-blocker b/c blocking vasodilatory B2 receptors results in unopposed alpha agonism, leading to vasoconstriction and hypertensive crisis**

196
Q

Why would we also give calcium channel blockers to control HTN with Pheo’s?

A

Calcium triggers catecholamine release from the tumor, and excess calcium entry into myocardial cells contributes to a catecholamine-mediated cardiomyopathy

So basically CCB’s can prevent cardiomyopathy with pheo’s!

197
Q

What are the two possible forms of Hypercortisolism?

A

It’s either ACTH dependent or ACTH independent

198
Q

ACTH-dependent Cushing’s:

A

-high plasma ACTH stimulates the adrenal cortex to produce excessive cortisol

-acute ectopic ACTH syndrome is a form of ACTH-dependent Cushing’s that is most often associated with small cell lung carcinoma

199
Q

ACTH-independent Cushing’s:

A

excessive cortisol production by abnormal adrenocortical tissue that is not regulated by CRH and ACTH-these levels are actually suppressed instead of elevated

-benign or malignant adrenal cortical tumors are the MOST common cause of this kind of cushing’s

200
Q

What are symptoms of Cushing Syndrome?

A

sudden weight gain, usually central with increased facial fat (moon face), ecchymoses, HTN, glucose intolerance, muscle wasting, depression, insomnia

201
Q

What test do you do to diagnose Cushing’s? What does the differentiating b/w the ACTH-dependent or ACTH-independent type depend on?

A

-24-hour urine cortisol test

-requires reliable measurements of plasma ACTH using immunoradiometric assays

202
Q

What test distinguishes Cushing’s from the ectopic ACTH syndrome?

A

The high-side dexamethasone suppression test does!

203
Q

Can imaging be used to gauge adrenal function with Cushing’s?

A

No, imaging is helpful for determining tumor location but that is it

204
Q

What are treatment options for Cushing Syndrome?

A

-treatment of choice is transsphenoidal micro-adenectomy if micro adenoma is resectable

-Alternatively, pts may undergo 85-90% resection of the anterior pituitary

-Pituitary irradiation and bilateral total adrenalectomy are needed in some patients

205
Q

What is the specific treatment for adrenal adenoma or carcinoma causing Cushing’s?

A

Surgical Adrenalectomy

206
Q

Anesthesia considerations for Cushing’s:

A

-Evaluate and treat BP pre-op as well as electrolyte imbalances and blood sugar

-Consider osteoporosis in positioning

207
Q

What’s another name for Hyperaldosteronism?

A

Conn Syndrome

208
Q

Tell me about Primary Hyperaldosteronism

A

-excess secretion aldosterone from a functional tumor (aldosteronoma) that acts independently of a physiologic stimulus
-women>men
-associated with pheochromocytoma, hyperparathyroidism, or acromegaly
-in primary, plasma renin activity is suppressed

209
Q

Tell me about Secondary Hyperaldosteronism:

A

presents when serum renin is increased, stimulating the release of Aldosterone
-In secondary, plasma renin activity is high**

210
Q

What are symptoms of Hyperaldosteronism?

A

-HTN, hypokalemia, and hypokalemic metabolic acidosis
-Can be nonspecific or asymptomatic as well
-spontaneous hypokalemia in presence of systemic HTN is highly suggestive of Hyperaldosteronism though! (think how increased aldo=decreased K+)

211
Q

What is a random-ass thing you can do to cause a syndrome that mimics the features of Hyperaldosteronism?

A

Long-term ingestion of Licorice lol
-can cause HTN, hypokalemia, and suppression of RAAS (so looks like primary type)

212
Q

What is the treatment for Hyperaldosteronism?

A

competitive aldosterone antagonist like Spironolactone, K+ replacement, antihypertensive drugs, diuretics, tumor removal, and possible adrenalectomy

213
Q

Now tell me about Hypoaldosteronism:

A

Hyperkalemia in the absence of renal insufficiency suggests Hypoaldosteronism

Hyperkalemia may be enhances by hyperglycemia

214
Q

What type of metabolic acidosis is common with Hypoaldosteronism?

A

Hyperchloremic metabolic acidosis is common

215
Q

Symptoms of Hypoaldosteronism:

A

orthostatic hypotension, hyponatremia, and pts can experience heart block d/t hyperkalemia

216
Q

What may be the cause of Hypoaldosteronism?

A

Lack of ALDO may be cause by a congenital deficiency of aldosterone synthetase or hyporeninemia due to defects in the JGA or ACE inhibitors

-hyporeninemic hypoaldosteronism typ. occurs in pts >45 with chronic renal failure or DM

217
Q

What is a possible reversible cause of Hypoaldosteronism?

A

Indomethacin-induced prostaglandin deficiency

218
Q

What is possible treatment for Hypoaldosteronism?

A

~liberal~ sodium intake and daily admin of Fludrocortisone

219
Q

What is the primary type of Adrenal Insufficiency?

A

Primary= Addison’s Disease

-adrenal glands are unable to produce enough glucocorticoid, mineralocorticoid, and androgen hormones
-most common cause= autoimmune adrenal destruction
->90% of the glands must be involved before signs appear

220
Q

Tell me about Secondary Adrenal Insufficiency

A

-hypothalamic-pituitary disease or suppression leading to failure in the production of CRH or ACTH
-ONLY glucocorticoid deficiency
-In most cases, the cause is iatrogenic like with the use of synthetic glucocorticoids, pituitary surgery, or radiation
-These patients lack hyperpigmentation and may demonstrate only mild electrolyte abnormalities

221
Q

How do we diagnose Adrenal Insufficiency?

A

-Baseline cortisol <20 mcg/dL and remains <20 AFTER ACTH stimulation

-A positive test demonstrates a poor response to ACTH and indicates an impairment of the adrenal cortex

222
Q

Absolute versus Relative Adrenal Insufficiency:

A

-Absolute AI is characterized by a low baseline cortisol and a positive ACTH stimulation test

-Relative AI is indicated when the baseline cortisol level is higher but the ACTH stimulation test is positive

223
Q

What do we use to treat Adrenal Insufficiency?

A

Steroids

224
Q

How many parathyroid glands to we have, where are they located and what do they produce?

A

4, located behind the upper and lower poles of the thyroid gland

Produce Parathyroid Hormone (PTH) which is released into the circulation by negative feedback that depends on plasma calcium level

225
Q

How do calcium levels affect PTH?

A

-Hypocalcemia stimulates the release of PTH, whereas hypercalcemia suppresses hormonal synthesis and release

-PTH maintains normal plasma calcium levels by promoting the movement of calcium across GI tract, renal tubules, and the bone

226
Q

What is hyperparathyroidism?

A

-elevated PTH levels
-can be primary, secondary, or ectopic

227
Q

Are serum calcium concentrations increased or decreased or the unchanged with hyperparathyroidism?

A

They can be any of them! low, high, or unchanged

228
Q

What is primary hyperparathyroidism caused by?

A

-benign parathyroid adenoma (90%)
-carcinoma (<5%)
-parathyroid hyperplasia

229
Q

How is hyperparathyroidism diagnosed and treated?

A

-Dx: plasma calcium and 24-hour urinary calcium
-Tx: surgical removal of abnormal portions of the gland

230
Q

What is secondary hyperparathyroidism?

A

compensatory response of the parathyroid glands to counteract a separate disease process producing hypocalcemia (often with chronic renal failure)

-rarely produces hypercalcemia b/c it is “adaptive”

-Tx: control underlying disease, normalize phosphate levels in pts with renal disease by administering a phosphate binder

231
Q

Symptoms of hyperparathyroidism:

A

sedation, N/V, decreased strength and decreased sensation, polyuria, renal stones, PUD, cardiac disturbances

232
Q

What is hypothyroidism?

A

-present when PTH is deficient or peripheral tissues are resistant to its effects

-absence/ deficient PTH is almost always iatrogenic-from removal of parathyroid glands or thyroidectomy

233
Q

What is pseudo-hypothyroidism?

A

A congenital disorder where PTH is adequate but the kidneys are unable to respond to it

234
Q

How is hypothyroidism diagnosed and what do symptoms depend on?

A

-Dx: hypocalcemia <4.5 mEq/L and iCa <2 mg/dL with decreased PTH and increased phosphate

-Sx: depend on speed of onset

235
Q

What may acute hypocalcemia due to accidental removal of parathyroid during thyroidectomy cause?

A

Inspiratory stridor reflecting irritability of the laryngeal musculature

236
Q

What symptoms are chronic hypocalcemia associated with?

A

fatigue, cramps, prolonged QT interval, lethargy, cataracts, SQ calcifications, thickening of the skull, near deficits

237
Q

What is the MOST common cause of chronic hypocalcemia?

A

Chronic Renal Failure

238
Q

How do you treat hypothyroidism?

A

Calcium replacement and vitamin D-to help absorb the Calcium

239
Q

Where is the pituitary gland located?

A

located in the sella turica at the base of the brain, consists of the anterior pituitary and the posterior pituitary

240
Q

What 6 hormones does the anterior pituitary secrete under the control of the hypothalamus?

A

Growth Hormone, ACTH, TSH, FSH, LH, Prolactin

241
Q

Where are Vasopressin and Oxytocin synthesized and then where are they transported and stored?

A

-Synthesized in the hypothalamus
-transported and stored in the posterior pituitary

242
Q

What stimulates the release of Vasopressin and Oxytocin from the posterior pituitary?

A

The stimulus for release arises from osmoreceptors in the hypothalamus that sense plasma osmolarity

243
Q

What is the overproduction of the anterior pituitary hormones often associated with?

A

Often associated with hyper secretion of ACTH (Cushing Syndrome) by an anterior pituitary adenoma

244
Q

What is acromegaly?

A

It’s caused by excessive secretion of growth hormone in adults, most often by an adenoma in the anterior pituitary gland

245
Q

Which specific growth factor is elevated in acromegaly?

A

Serum insulin-like growth factor (IGF-1) is elevated w/ acromegaly

246
Q

What test can be done to assess for Acromegaly?

A

an oral glucose test-done by measuring plasma growth hormone which remains above 1 ng/mL 2 hours after ingestion of 75g glucose

247
Q

What does the overgrowth of tissues make patients susceptible of?

A

upper airway obstruction

248
Q

What may result from overgrowth of the surrounding cartilaginous structure with Acromegaly?

A

Hoarseness and abnormal movement of vocal cords or recurrent laryngeal nerve paralysis

249
Q

Why is peripheral neuropathy common with acromegaly?

A

It is common due to the nerve-trapping by connective tissues from the excessive growth

250
Q

How do you treat acromegaly?

A

-Transsphenoidal surgical excision of pituitary adenoma

-If surgery is not feasible, treatment is a long-acting somatostatin analogue

251
Q

What are some anesthesia implications for acromegaly when it comes to the upper airway?

A

-The distorted facial anatomy can interfere with the placement of a face mask
-Tongue and epiglottis can be enlarged and cause obstruction and also interferes with visualization of vocal cords
-increased distance b/w lips and vocal cords d/t mandible overgrowth
-glottic opening may be narrowed d/t vocal cord enlargement
-pt may require a smaller ETT, video laryngoscopy or awake fiberoptic intubation

252
Q

What is diabetes insidious?

A

DI reflects the absence of vasopressin (ADH) caused by the destruction of the posterior pituitary (neurogenic DI) or failure of renal tubules to respond to ADH (nephrogenic DI)

253
Q

How are nephrogenic and neurogenic DI differentiated?

A

-differentiated based on the response to desmopressin
-desmopressin causes urine-concentration in neurogenic but not nephrogenic DI

254
Q

Symptoms of DI:

A

polydipsia and high output of poorly concentrated urine despite increased serum osmolarity

255
Q

What is the initial treatment for DI?

A

-IV electrolytes to offset polyuria

256
Q

What is neurogenic DI treatment?

A

DDAVP (desmopressin)

257
Q

What is nephrogenic DI treatment?

A

low salt, low protein, diuretics, and NSAIDs

258
Q

Anesthesia considerations for DI:

A

monitor UOP and serum electrolyte concentrations

259
Q

What can SIADH (syndrome of inappropriate ADH) occur in the presence of?

A

diverse pathologies like…
-intracranial tumors
-hypothyroidism
-porphyria
-lung carcinoma

260
Q

What levels are often elevated in patient following major surgeries?

A

elevated ADH levels

261
Q

What is highly suggestive of SIADH?

A

Inappropriately increased urinary sodium and osmolarity in the presence of hyponatremia and decreased serum osmolarity are highly suggestive of SIADH

262
Q

What can abrupt decreased in serum sodium concentration result in?

A

cerebral edema and seizures :(

263
Q

What is the treatment for SIADH?

A

fluid restriction, salt tablets, loop diuretics and ADH antagonists like Demeclocycline

264
Q

What is the treatment for hyponatremia often accompanying SIADH?

A

treat with hypertonic saline @ <8 mEq over 24-48 hours

Health Assessment (8 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions