Lecture 2/6 Flashcards
Cardiac
1
Q
In mitral regurg, explain backflow. when does backflow start? when is it the fastest? What is happening to the volume in the L vent?
A
Backflow happens where pressure is higher in the L vent than the L atria.
Begins: beginning phase 2
Fastest in general: beginning phase 3
Fastest phase 4: beginning
Starts at beginning phase 2 –> ends at end of phase 4
Volume: decreasing during these phases bc blood going back into L atria
2
Q
In mitral regurg, when we have _________ we have backflow
A
delta P
3
Q
In mitral regurg, what effects the rate of backwars blood flow?
A
pressure in the L vent
-volume in the atria
4
Q
In mitral regurg, the less volume in the atria during systole the _______ backwards blood flow is
A
faster
5
Q
In mitral regurg, describe the EF? why?
A
artificially high
the blood being ejected from the LV is not actually reaching the systemic circulation. Instead, a portion of it is regurgitating back into the L atrium
6
Q
T/F: In mitral regurg, we can tell SV
A
F
No isometric phases
7
Q
EF =
A
SV / EDV
or
(EDV - ESV) / EDV
8
Q
What is a normal EF?
A
About 58%
70/120
9
Q
Dilated cardiomyopathy causes EF to ________. Why?
A
Decrease
Thin/stretched out walls in vent makes it harder to pump blood out
10
Q
Decreasing contractility = __________ EF and increasing contractilit = ___________ EF
A
decreased
increased
11
Q
SV =
A
EDV - ESV
12
Q
What are the 2 types of ventricle hypertropies? Describe the sacromeres in them. What causes this?
A
Eccentric LVH:
-thin wall (dilated)
-additional sacromeres in series
Causes: MI, congenital
Concentric LVH:
-thick walls (hypertrophied)
-additional sacremeres in parallel
Causes: increases afterload
13
Q
The thyroid gland is below the _______
A
Thyroid cartilage/larynx
14
Q
What is on the thyroid gland? What do they do?
A
Nodules that formed the parathyroid gland
Regulate parathyroid hormone –> controls Ca levels in the blood
15
Q
The thyroid gland is responsible for controlling many things related to _________ in the body
A
Metabolism
16
Q
The thyroid cartilage is a part of the ________ and is above the ___________. It contains the __________
A
Larynx
Thyroid gland
Adam’s apple
17
Q
Describe the presentation of an enlarged thyroid gland. What is this called?
A
Protrusion of the neck
Goiter
18
Q
Where does the right and left recurrent laryngeal nerve stem from?
A
R & L vagus nerve
19
Q
What is another name for the R & L recurrent laryngeal nerve? Why/where is it called this?
A
“recurrent laryngeal nerve”: where the vagus nerve branches off and turns
“inferior laryngeal nerve”: after the part where the vagus nerve branches off and the laryngeal nerve straightens out to go back up to attach to the thyroid cartilage
20
Q
What part of the thyroid gland comes in contact with the larynx?
A
The sides (this is why it’s called the thyroid cartilage)
21
Q
The left and right recurrent laryngeal nerves run parallel to the _______
A
Trachea
22
Q
What are the nerves that control the muscle box? What kind of muscles are in the muscle box?
A
The right and left recurrent laryngeal nerves
Small skeletal muscles
23
Q
Where does the left recurrent laryngeal nerve pass?
A
Under the aortic arch
24
Q
The thyroid is important in what system?
A
CVS
25
What things does thyroid hormone affect?
Growth
-reproduction
-fluid/mineral balance
26
Why is thyroid pathology hard to detect?
It is hard to quantify because thyroid hormone is fat soluble, and it wants to be in the oily parts of plasma/plasma protein --> hard to detect accurately in blood work
27
What is a hallmark sign of hyperthyroidism?
Increase HR at risk with no explanation/other heart pathology
28
What allows us to get thyroid hormone into the CVS?
The very vascular thyroid. It is a very vascular area allowing for rapid uptake AND CIRCULATION of hormones and fast changes to take places with the thyroid
29
What does the R recurrent laryngeal nerve pass under?
R subclavian artery
30
Where are the motor neurons housed that control the voice box skeletal muscles?
The branch of the vagus nerve
31
Which recurrent laryngeal nerve is more inferior?
Left
32
What happens if you damage the L or R recurrent laryngeal nerves?
damage 1: raspy voice
damage/cut both: lose ability to speak
33
What are the primary hormones that the thyroid gland releases? Which is the majority? What are their names? what are their percentages?
T3:
-Triiodothyronine
7%
**T4:**
-Thyroxine
93%
34
What does T3 mean?
T = tyrosine amino acid
3 = the amount of iodides attached
35
Describe T1
Monoiodotyrosine
-1 benzine ring
-1 iodide
36
Describe T2
Diiodotyrosine
-1 benzine
-2 iodides
37
Describe T3
Triiodothyronine
-Enzyme combination of T1 & T2
-2 benzine rings
-3 iodides
-7% secreted
38
Describe T4
Thyroxine
-Enzyme combination of T2 & T2
-2 benzine rings
-4 iodides
-93% secreted
39
How much iodine does the body require to maintain enough thyroid hormone? Where do we mostly get this from?
50 mg per year
table salt (not other types of salt: the kind with the lady in the umbrella only. no sea salt)
40
What happens if you dont get enough iodine in your body?
decreased levels of thyroid hormone --> goiters
41
What is the main controller of the thyroid gland? Where is it produced?
TSH (thyroid stimulating hormone)
Anterior pituitary gland
42
What is another name for the anterior pituitary gland?
adenohypophysis
43
Where is TSH produced?
adenohypophysis
44
What does increasing TSH do?
Stimulates thyroid gland to release T3 & T4 into the bloodstream (increases T3/T4 levels)
45
The hypothalamus releases _________ which helps regulates the release of __________
TRH (thyrotropin releasing hormone)
TSH (thyroid stimulating hormone)
46
What does the hypothalamus monitor? What does it do in response to these things?
Body conditions:
Temperature
-blood levels
-infection
Adjust the release of TRH --> release of TSH affected
47
What happens in your body when your temperature is too low?
hypothalamus releases TRH --> TRH binds to receptors on pituitary gland --> anterior pituitary gland releases TSH --> TSH binds to receptors on thyroid gland --> thyroid gland release T4 & T3
48
T3 & T4 are ______soluble. What does this mean & require?
lipid
They cannot travel freely within the bloodstream
They require carrier proteins
49
What are the carrier protiens for T4 & T4? Which one is the main one?
**TBG: Thyroxine binding globulin (main)**
Thyroxine binding prealbumin
Albumin
**These 3 carry both T3 & T4**
50
Where are thyroid carried proteins produced at? What pathologies can affect this? What can this cause?
Liver
Liver failure --> decrease in carrier proteins --> decrease in thyroid hormone circulation
51
What happens once T3 & T4 get inside on a cell?
Lipid soluble = cross membrane freely
inside cell --> bind to proteins & transported to nucleus --> influene gene expression --> helps regulate body changes like increasing body temp/improving resistance to stress
52
Thyroid hormone is allowed through the nucleus via ________
Nuclear pores
53
How does our body gain access to genetic codes?
Via thyroid hormones
54
Which thyroid hormone is the primary hormone responsible for going into the nucleus and gaining access to our genes?
T3
**But T4 also does but to a lesser extent**
55
Where are thyroid hormone receptors at?
Inside the nucleus of cells
56
What happens when thyroid hormones react with their receptors?
genes turn on --> increases cell processes --> new proteins/growth --> increases metabolic demand --> increases glucose consumption --> increases O2 consumption --> increase HR & RR/depth
57
T/F: BP normally goes up when thyroid hormone interacts with their receptor. Why?
F
Normally just heart rate. This is due to decrease SVR.
58
Does hyperthyroidism cause low or high blood glucose? why?
High
Increased Gluconeogenesis & Glycogenolysis
-Thyroid hormones stimulate the liver to break down glycogen and produce more glucose.
59
Why is thyroid hormone important in growth and development?
The nervous system requires a healthy amount of thyroid hormone for proper maturation.
Absence of thyroid hormone can manifest in personality, cognitive or memory issues
60
Hyperthyroidism causes your blood cholesterol & triglyceride levels to _______. Why?
Drop
Cholesterol is being consumed at the cellular level fast faster than normal to build things dt increase metabolic rate
61
How long does it take for a thyroid hormone to start working in the body?
Enormous amount: 6 - 8 hrs
small amount: 10 days for peak
62
Thyroid hormone problems are typically a ________ term problem, but what is another situation that can happen?
long
thyroid-storm (very quick & high levels of T3/T4) which can be triggered by surgery, stress, and iodine exposure.
63
What is the feedback mechanism for endocrine tumors?
Hypothalamus
64
Describe the pathology for a pituitary tumor. How would your labs look?
increases TSH --> increase thyroid hormone --> HYPOTHALAMUS senses this --> decreases/stops TRH
TSH: increase
T3/T4: increase
TRH: decrease
65
Describe the pathology for a thyroid gland tumor. How would your labs look?
Increase T3/T4 --> increase metabolic rate --> HYPOTHALAMUS senses this --> decrease TRH --> decrease TSH
TSH: decrease
T3/T4: increase
TRH: decrease
66
Describe the pathology for a hypothalamus tumor. How would your labs look?
increase TRH --> increase TSH --> increase T3/T4
Everything is elevated in labs
**Hypothalamus is the area for adjustments/feedback and its messed up so theres nobody coming to help :(**
67
What has to happen for T4 to have normal amount of activity at the nucleus membrane?
Before entering the nuclues, one of the iodides must be pulled off.
68
What enzyme is required for T4 at the nucleus? What does it do?
Iodinase
Pulls a iodide off T4 --> T3
69
_____ is the predominant form that binds with the thyroid receptor in the nucleus
T3
70
T/F: T4 & T3 can both get into the cell and the nucleus
T
But T4 gets a iodide pulled off of it and converts to T3 mostly. T3 mostly interacts with the receptor in the nucleus.
71
Hyperthyroidism from tumors will cause increased _______ dt increased metabolic rate and nutrient demand.
hunger
72
What is Graves disease? What are hallmark SE?
Autoimmune disorder
-body produces antibodies that interact/activate TSH receptors on pituitary gland --> increased thyroid hormone
SE: Goiter
Exophthalmus (protuding eyes)
73
What is Tx for Graves disease?
Plasmaphersis to remove some of the antibodies
74
_________ is where the eyes are protruding from their normal state. What is this common in? What am I worried about with this?
Exophthalmus
Graves disease
The health of the cornea dt not being able to close eyes properly
75
What is Hashimoto thyroiditis?
Body produces antibodies that attack thyroid gland
-1st irritation --> destroys thyroid gland --> hypothyroidism
76
Who is Hashimoto thyroiditis most common in?
Asians
77
Describe the pathology in lack of iodine
Body doesnt have iodide to attach to tyrosine --> decrease T3/T4 --> HYPOTHALAMUS senses --> increase TRH --> increase TSH --> none of that matter tho bc still no iodine to attach to tyrosine --> Goiter :(
78
Describe the pathology in excess of iodine
massive amount of iodine in a short amount of time --> cellular system confused --> DECREASES thyroid hormone production
79
Thyroid hormone production decreases with excessive iodine intake due to __________ reactions
redox
80
What can high iodine intake be use to Tx?
Acute hyperthyroid issues
81
What are the best treatments for thyroid cancer? What are the risks?
Radioactive iodine (Isotope I-131)
Removal: very vascular area so removal can be bloody and high risk
82
What is the Isotope used for thyroid cancer
Radioactive isotope I-131
83
What is the only organ that needs iodine?
Thyroid gland
84
What are the effects of hypothyroidism on younger and older people?
younger: severe developmental problems
older: less cholesterol and fatty acid use --> unused cholesterol, and triglycerides buildup --> thickens blood vessel walls --> atherosclerosis
85
What is the treatment for hypothyroidism? What are the issues we have with this?
Synthetic thyroid hormone
Noncompliant dt insomnia, increase HR, palpitations, anxiety, restlessness
86
Cardiogenic shock is what type of problem? What can cause this?
Heart pump --> unable to push out CO needed (contractility problem)
MI
87
Cardiogenic shock can be secondary to ___________
decreased venous return
88
What can cause decrease venous return? What does this lead to?
Hemorrhage
-Embolism in big vein
This all can lead to decrease venous return -->circulatory problem --> cardiogenic shock
89
What type of shock do we induce with most anesthetics? Why does this happen? How can we fix it?
Neurogenic shock
Anesthetic drugs will take some of the CNS/SNS/PNS offline --> decrease sympathetic stimulation (heart/systemic)
Replace synthetic catecholamines
90
The higher the spinal block, the ______ of the SNS is effect. What does this mean?
More
Higher spinal block --> more SNS offline --> increase risk of neurogenic shock/loss of CVS functioning
91
Analphylactic shock causes _______ tone in your blood vessels
decreased
**causes blood vessels to have NO TONE**
92
What is anaphylactic shock driven by?
histamine released from mast cells from the immune system coming in contact with an allergen
93
What is the most common shock? What are its causes?
Hypovolemic shock
Causes: massive blood loss, dehydration
94
What drug can remove part of the SNS system? How does this affect blood loss?
ACE inhibitors
-ANESTHETICS
Removal of part of your SNS will not allow your body to clamp down on your arteries and shunt blood where needed temporarily (Increasing SVR/decreasing CO) with blood loss
-Therefore smaller amounts of blood loss may have bigger effects on arterial BP & CO
95
With a normal SNS, what happens to arterial BP and CO with a 10% blood loss? 20%?
10% - Art BP & CO will be about normal
20% - Art BP will be about normal
-CO will be LOW (as a function of trying to maintain art. BP)
96
T/F: With an MI, blood loss is the same as a healthy person
F
97
What is the max blood loss thats survivable in a healthy person without help?
20%
1 liter
98
What is non-progressive shock?
Blood loss that results in MAP decrease of <49%
Does not result in death
99
What is progressive shock?
Blood loss that results in MAP decrease of >49%
Results in death
100
What are the feedback mechanisms for nonprogressive/progressive shock to compensate?
-increased catecholamines by SNS --> increase tone/HR
-RAS by kidneys --> conserve volume
-compartment fluid shifts into the CVS
-Spleen stores Hgb/RBC
- Pulmonary circuit has hundreds of cc's of blood it can shift
- GI system has lots of blood to shunt
101
Why do you die during progressive shock?
LOW BP/CO --> decrease coronary artery perfusion
-everything not perfused enough --> loss of autonomic NS
102
___% of blood loss is not survivable at all
50
103
____% of blood loss is survivable, but you need to get to a hospital immediately
30 - 40
104
In HF, why does our Psf keep increasing?
To try to get to a normal CO of 5 L/min
105
What happens in HF if the body cant compensate to get to 5L/min?
Psf will continue to increase --> HF will get worse --> CO will decrease --> death
106
What are medications that can help supplement in severe HF to get to 5L/min? How does this help the heart?
Cardiac glycoside = Digoxin
Phosphodiesterase inhibitors = Milrinone
This allows the heart to get to 5L/min for CO --> decreases work of heart --> allows heart to heal
107
Why does CO decrease after a certain point with compensatory measures from the kidney with HF?
Kidneys retaining fluid to increase pressure --> fluid being pumped back into the heart --> heart eventually gets very stretched out from increased filling pressure/excess fluid --> decreased contractility --> decreased CO --> BP still low --> kidneys are still trying to retain more fluid --> vicious cycle (positive feedback)
108
Why do we give diuretics why HF? How does this effect BP?
Prevent kidneys from reaching its "unattainable" BP goal --> Prevent overfilling of the heart
This means that we live at a lower BP than normal
109
T/F: BP is a good indicator of CO
F
It is absolutely not reliable for CO!!!!!!!!
110
Why do we have to correlate BP to CO?
CO monitoring is invasive and expensive.
