Exam 3 Flashcards
(117 cards)
1
Q
What are the different types of transplants?
A
Allograft
Isograft
Autograft
Xenograft
2
Q
What is an allograft? Are IS drugs needed? match HLA/MHCS prior to transplant?
A
transplant from same species
to prevent rejection, IS drugs needed, match HLAs/MCHSs
3
Q
What is an isograft? Are IS drugs needed? match HLA/MHCS prior to transplant?
A
transplant between identical twins
no need for IS drugs
no need to match HLAs/MHCs, since they are identical
4
Q
What is an autograft? Are IS drugs needed? match HLA/MHCS prior to transplant?
A
transplant from one body part to another
no IS drugs needed
no need to match HLA/MCH
5
Q
What is a xenograft? Are IS drugs needed? match HLA/MHCS prior to transplant?
A
transplant between different species
IS drugs needed
no matching for HLA/MHS
6
Q
What is a heart murmur?
What are some causes?
A
A heart murmur is a right-sided valve disorder. It is an unusual whooshing sound heard with a stethoscope. Caused by valve problems.
Stenosis
the valve will not open all the way, making it harder for blood to pass through. A murmur will be heard when blood shoots through the narrow opening when the valve is open
Regurgitation
the valve will not close all the way, causing blood to leak backwards. A murmur will be heard when the valve should be heard.
7
Q
What effect does a heart murmur have on cardiac output?
A
valve defects can decrease CO
8
Q
What effect does hypertension have on cardiac output?
A
CO increases
9
Q
What effect does aortic valve stenosis have on cardiac output?
A
CO decreases
10
Q
What effect does mitral valve regurgitation have on cardiac output?
A
CO decreases
11
Q
What is an aneurysm?
A
the weakening of a blood vessel wall, as it increases in size, the wall gets weaker and weaker and ruptures.
12
Q
What are the different types of aneurysms?
A
Berry aneurysm
Fusiform aneurysm
Saccular aneurysm
Dissecting aneurysm
Aortic aneurysm
Aortic dissection
13
Q
What is the difference between a true aneurysm and a false aneurysm?
A
A true aneurysm is when all 3 layers of the blood vessel are weakened.
A false aneurysm is when 1 or more layers are damaged. (tear in vessel wall)
14
Q
What is a berry aneurysm? Is it a true aneurysm?
A
dilation that occurs where a blood vessel branches. It looks like a berry hanging off the vine. small, round, bulge hanging from vessel branch points.
-true aneurysm
15
Q
What is a fusiform aneurysm? is it a true aneurysm?
A
bulging of both sides of the artery wall, involves whole circumference of the vessel
-true aneurysm
16
Q
What is a saccular aneurysm? is it a true aneurysm?
A
bulge on one side of the vessel
-true aneurysm
17
Q
What is a dissecting aneurysm (aortic dissection)? is it true or false?
A
hemorrhaging (bleeding) into vessel wall with longitudinal tear
-false aneurysm
18
Q
What are the main causes of aneurysms?
A
weakening of the vessel walls which may result from congenital defects, trauma, infection, or atherosclerosis
19
Q
What is the difference between arteriosclerosis and atherosclerosis?
A
Arteriosclerosis is a general term for degenerative changes that occur with age. The arteries become narrower, and this reduces blood flow and can lead to ischemia.
Atherosclerosis is when fatty plaques (lipids, fibrin, cellular debris) build up in the walls of the arteries. The plaques often have an attached thrombus (clot). The initiating factor may be endothelial cell damage, which occurs at young age.
20
Q
What are the risk factors of atherosclerosis?
A
Non-modifiable:
age, gender, genetics, family history
Modifiable:
obesity, diet, smoking cigarettes, sedentary lifestyle, diabetes mellitus, hypertension
21
Q
What is one of the main consequences of an unstable plaque?
A
Unstable plaques have thin fibrous caps which have an increased likelihood of rupturing. Once it ruptures, a thrombus (clot) form. This may completely block the artery or may break free and become an embolus (clot that travels in blood).
22
Q
What is the difference between stable plaque vs unstable plaque
A
Unstable plaque has a thin fibrous cap and has an increased likelihood of rupturing and forming a clot. A stable plaque has a thick fibrous cap and is less likely to rupture.
23
Q
What are some s/s of peripheral artery disease?
A
gradual onset
pain while walking,
claudication (cramp when walking)
calf pain, aching feeling or numbness
foot cool to touch
weak or absent pedal/femoral pulse
when blood flow is severely reduced, ischemic pain at rest, ulcerations, gangrene
24
Q
What are some causes of vasculitis? How does damage to the vascular wall
occur with vasculitis?
A
Vasculitis is inflammation, injury, and necrosis to the vessel wall. Pathogen mediated vasculitis is when a pathogen directly invades the blood vessel wall and results in an inflammatory response. Noninfectious vasculitis is non pathogen mediated immune inflammation. Some causes for vasculitis is certain medications and underlying autoimmune disease (Lupus, rheumatoid arthritis, hepatitis)
25
What are modifiable and non-modified risk factors for the development of
hypertension?
Nonmodifiable risk factors are age, family history, and race. Modifiable factors are a high salt diet, obesity, excess alcohol, insulin resistance.
26
What are some pharmacological treatment for hypertension?
mild diuretics, ACE inhibitors, beta blockers, calcium channel blockers, alpha blockers
27
What role might the renin-angiotensin system play in the development of
hypertension?
The kidneys regulate blood pressure long term. They regulate extracellular fluid volume. The renin-angiotensin system (RAS) raises bp by causing vasoconstriction and retaining sodium and water. When bp drops, kidneys release renin. Renin converts angiotensin to angiotensin I. ACE enzyme converts angiotensin I - angiotensin II. an2 causes vasoconstriction and narrows your blood vessels, adrenal glands release aldosterone, telling kidneys to hold onto salt and water. if RAS is overactive, chronic HTN can result.
28
What are some causes and risk factors for the development of primary hypertension?
90-95% of all cases for HTN. no known cause, no other disease present. Usually due to genetics, race, age, insulin resistance, diet, obesity, or alcohol.
Risk factors:
family history
race
age
high salt diet
obesity
excessive alcohol
insulin resistance
29
What are some causes and risk factors for the development of secondary hypertension?
2ndary HTN results from another disease.
Risk factors:
kidney disease (renovascular htn, acute renal failure, glomerulonephritis)
adrenal cortical disorders (hyperaldosteronism, Cushing's)
pheochromocytoma (increased epinephrine)
30
What are the s/s and detrimental effects of hypertension?
HTN (>140/>90) is often undiagnosed until complications arise.
S/S:
headache, dizziness, blurred vision, short of breath, chest pain, fatigue, nosebleed, dry cough
Detrimental effects:
Heart - left ventricular hypertrophy, angina, heart failue, MI
Brain - stroke
Kidney - chronic kidney disease
Eyes - retinopathy
Blood vessels - peripheral vascular disease
31
What are the different types of host vs. graft rejections?
Hyperacute rejection
Acute rejection
Chronic or late rejection
32
What is hyperacute rejection?
a type of tissue/organ rejection that occurs immediately as soon as blood flow has been established to the organ.
Cause: host has preexisting antibodies in their blood that immediately attack the donor tissue/organ.
33
What is acute rejection?
a type of tissue/organ rejection that occurs several weeks after transplantation when unmatched antigens cause a reaction
cause: T cells recognize donor antigens as foreign and attack
34
What is chronic/late rejection?
a type of tissue/organ rejection that occurs months to years after transplantation. Blood vessels in the graft are gradually damaged.
35
Understand the process of host vs graft disease
transplant attacks recipient typically after a bone marrow transplant or liver transplant. It occurs when there are some T-lymphocytes in the graft that attack the host.
Graft vs Host disease cannot happen without the perfect storm ->
1) transplant must have functional immune cells that were not flushed out properly
2) recipient must have antigens on the cells of their body to those T-lymphocytes
3) recipient must be immunocompromised to the point where they cannot destroy transplanted T-cells
36
What are the different types of hypertensions that occur during pregnancy?
gestational htn
preeclampsia
eclampsia
chronic htn
preeclampsia superimposed on chronic htn
37
What is gestational hypertension?
hypertension that occurs at 20 weeks pregnant without proteinuria. no damage is done to liver/kidneys.
BP resolves by 12 weeks postpartum.
-increase in liver enzymes
-may progress to preeclampsia
-management may require early delivery of baby or close monitoring of bp.
-risk to develop htn later on in life
38
What is preeclampsia?
hypertension that occurs after 20 weeks pregnant with kidney damage.
-increased creatinine, increased proteinuria, increased liver enzymes, decreased platelets
-usually seen during first pregnancy, more common in women carrying multiple fetuses
-associated with kidney disease
-decreased blood flow to the placenta triggers the release of chemicals that damage the endothelium
39
HELLP syndrome
a severe pregnancy complication related to preeclampsia affecting the blood, liver, and platelets.
H: hemolysis (break down rbc)
EL: elevated liver enzymes
LP: low platelet count
40
What is eclampsia?
the development of seizures in a woman with severe preeclampsia. it is a progression of preeclampsia that leads to seizures.
-2% mortality rate
-can result in serious fetal and maternal complications
41
Chronic hypertension
htn unrelated to pregnancy.
htn present prior to pregnancy or occurs before 20 weeks' gestation or persists beyond 12 weeks postpartum.
-increased risk of developing preeclampsia
42
What is preeclampsia superimposed on chronic htn?
when a woman with pre-existing chronic htn develops preeclampsia during pregnancy. Htn before 20 weeks who develop proteinuria
-worse prognosis compared to either alone
43
What is orthostatic hypotension?
a condition where there is an abnormal drop in blood pressure when a person stands up from a sitting or lying position. When you stand, (CO) decreases, leading to a drop in blood pressure and reduced blood flow to the brain, which can cause symptoms such as dizziness, lightheadedness, or fainting (syncope).
Normally, body adapts to low bp using baroreflex by vasoconstriction, increase HR, and increasing the force of contraction. Baroreflex impaired.
44
What are some of the causes of orthostatic hypotension?
Low blood volume (dehydration)
Drug induced (diuretic decrease blood vol, beta blockers block SNS)
Aging
Bed rest
Autonomic Nervous System Dysfunction
45
Who is most susceptible to developing orthostatic hypotension?
The elderly population due to aging, decreased autonomic function, and dehydration.
46
What are varicose veins? Why do they form? who is most susceptible to
developing them.
Varicose veins are dilated superficial veins, usually in lower extremities. They form due to prolonged standing or prolonged increased pressure on abdominal veins.
People most susceptible to varicose veins are people who experience increased abdominal pressure such as obese people and during pregnancy. In addition, people who stand for prolonged periods of time are susceptible.
47
Know the difference between primary vs secondary varicose veins
primary vv can occur without an underlying condition. The main cause is weakened or damaged valves in the veins, leading to blood pooling in the veins and causing them to enlarge.
-typically, superficial veins of leg
-visible, twisted, bulging veins
secondary vv occur as a result of underlying medical condition or venous insufficiency (clots, dvt). This condition causes damage to the deep veins and leads to increased pressure in the superficial veins.
-common in people w/dvt
-occur in the deep veins and can affect both superficial and deep veins.
48
What is a hypersensitivity reaction? What are the 4 types of hypersensitivity reactions?
An abnormal immune response where the body reacts to non-harmful substances as though they are harmful and damage the body as a result.
Type I: allergic reaction
Type II: antibody mediated
Type III: immune complex hypersensitivity
Type IV: cell-mediated delayed hypersensitivity
49
What is a Type I Hypersensitivity Reaction?
'allergic reactions'
-systemic or anaphylactic reactions
-local or atopic reactions (genetic)
urticaria (hives)
rhinitis (hay fever)
atopic dermatitis
bronchial asthma
-food allergies
50
What is the causative mechanism Type I Hypersensitivity Reaction?
1) you get exposed to an allergen. The allergen binds to B cells which differentiate into plasma cells. Plasma cells produce IgE antibodies.
2) Allergen bound to IgE antibody attach themselves to mast cells and become a 'sensitized mast cell'. You cannot have an allergic reaction without sensitized mast cells. No allergic reaction yet.
3) Upon subsequent exposure of same allergen, allergen will bind to IgE receptor on mast cell, causing degranulation. This will release histamine and initiate inflammatory response (vasodilation, increased capillary permeability, redness, swelling)
51
Primary early response
vasodilation
vascular damage
smooth muscle spasm
52
Secondary late response
mucosal edema
mucus secretion
leukocyte infiltration
epithelial damage
bronchospasm
53
What are examples of Type I Hypersensitivity Reactions? What are the phases?
Asthma and anaphylactic shock
Asthma [2 phases]
primary/immediate phase: mast cell degeneration, releasing histamine
resulting in vasodilation, vascular leakage, smooth muscle constriction
Secondary/late phase:
Lipid mediators and cytokines leukotrienes and prostaglandins causing tissue infiltration with eosinophils leading to tissue destruction.
Anaphylactic shock: severe hypersensitive reaction.
Due to large amounts of chemical mediators released from mast cells into general circulation quickly.
-sudden vasodilation resulting in rapid bp drop
-edema of mucosa
-bronchioles constrict, obstructing airflow
-hives, itchy, skin erythema, vomit, abdominal cramping
emergency treatment - inject epinephrine
1) cause vasoconstriction
2) increase rate/strength of heartbeat
3) relax the bronchiole smooth muscle
54
What is a Type II hypersensitivity reaction?
antibody mediated, the immune system targets and destroys cells/tissues by antibodies (IgG/IgE) binding to antigens on cell surface. Leads to cell destruction, inflammation, or dysfunction of the targeted cells or tissues.
55
What is the causative mechanism Type II Hypersensitivity Reaction?
body can mistakenly produce antibodies (IgG or IgM) against antigens that are found on the surface of RBC, WBC, or tissues. The antibodies bind to the antigens on the surface of these cells. Once the antibody is bound to the antigen, it activates a group of proteins in your blood called the complement system. The complement system is like a “cleanup crew” that helps destroy the cells that are marked by antibodies.
56
What are examples of Type II hypersensitivity reactions?
Blood transfusion reactions
Drug reactions (heparin induced thrombocytopenia)
On tissues
Goodpasture syndrome (antibodies attack basement membrane in lungs and kidneys), Graves disease, myasthenia gravis
57
What are 3 types of type II hypersensitivity reactions?
1) Complement and antibody mediated cell destruction
-blood incompatibility - know blood typing
-drug reactions - hemolytic anemia from penicillin
2) Complement and antibody mediated inflammation
-Antibodies deposited on extracellular tissue, tissue damage results from inflammation
-reject organ graft
3)Antibody mediated cellular activation or destruction
-produce antibodies that attach to receptor cells in the thyroid gland and release large amounts of T3/T4
-Graves' disease antibodies bind to the receptor on the thyroid gland, overactivation hyperparathyroidism
-Myasthenia Gravis - binds to Ach receptor destroying the receptor
58
What is a Type III hypersensitivity reaction? Mechanism? S/S? Examples?
Antigen antibody complex being deposited into the wall of the blood vessel, causing inflammation of vessel wall and damage.
-free floating antigen + antibody
[Systemic]
autoimmune vasculitis, glomerulonephritis, serum sickness
-urticaria(hives), patchy/generalized rash, extensive edema, fever
59
What is a Type IV hypersensitivity reaction? Mechanism? S/S? Examples?
cell mediated- sensitized T-cells attack antigen. *NO B CELLS*
Direct cell mediated cytotoxicity:
Cytotoxic T cells directly attack and kill cells that contain an antigen.
-viral infections (cytotoxic T) kill infected cells to eliminate the virus.
Delayed-Type Hypersensitivity
-takes a couple days for inflammation & adverse effects
-IT helper cells & macrophages are involved in the inflammation and tissue damage. The body responds to soluble proteins from the antigen by recruiting these immune cells to the site of exposure.
-TB TEST
-allergic contact dermatitis
-poison ivy
-transplant rejection
-rheumatoid arthritis
-IBD
-type I diabetes
60
What is Deep Vein Thrombosis (DVT)? Why is it dangerous?
Blood clot that occurs in deeper veins, typically in the legs (femoral, popliteal, posterior tibial, and peroneal veins)
-dangerous because clot can break off and lead to pulmonary embolism
61
What is the etiology/cause of DVT?
factors that slow blood flow, increase blood clotting, or injure the vessel wall.
1.Stasis of blood
-bed rest
-immobility
-congestive heart failure - reduced heart function leads to poor blood circulation, making blood pool
2. Increased blood coagulation
-dehydration
-pregnancy
-genetic factors
3. Vessel Wall Injury
-indwelling catheters
-surgery
-trauma
-infection
62
S/S of DVT
inflammation
-pain
-swelling
-deep muscle tenderness
-elevated wbc count
-fever
63
How do you treat DVT? What are preventative measures?
The first line of treatment is to dissolve the clot with tPA/ thrombolytic agent. After clot is dissolved you can put the patient on preventative measures like anticoagulants (blood thinners) and pneumatic compression devices.
64
What is Acute Coronary Syndrome?
A spectrum of conditions that ranging from
unstable angina
non-ST wave elevation MI,
ST elevation Mi
These conditions occur due to sudden, reduced blood flow to the heart, leading to ischemia. This blocks the heart and heart tissue dies.
-blockage can be sudden and complete or incomplete. It can come and go
65
S/S of Acute Coronary Syndrome
chest pain
short of breath
nausea/vomiting
diaphoresis
fatigue/dizziness
ECG changes
-ST segment elevated
-Serum cardiac markers like troponin - indicate heart muscle damage
66
What is the difference between a stable plaque and unstable plaque?
Stable plaque:
atherosclerotic plaques have a thick fibrous cap, which help protect the cap from rupturing.
-Less likely to cause sudden blockages
-plaque narrows a coronary artery, it causes stable angina, chest pain happens during physical exertion or stress and is relieved by rest.
Unstable plaque:
atherosclerotic plaques have a thin fibrous cap, more prone to rupturing.
-if unstable plaque ruptures, its content get exposed to the blood stream, triggering a blood clot (thrombus) that can block flow to the heart, leading to unstable angina or MI.
67
What is chronic stable angina?
-caused by a fixed coronary obstruction due to stable plaques in the coronary arteries.
-results from an imbalance between blood flow and metabolic demand.
-when the hearts demand increases, like physical exertion or emotional stress, it leads to chest pain/discomfort.
-relieved by nitroglycerin (NOT USED FOR MI)
68
Silent Myocardial ischemia
You have myocardial ischemia - reduced blood flow to the heart, but without any pain or s/s.
69
Variant/Vasospastic angina
pain when the coronary arteries spasm, causing angina.
-occur at rest or w/minimal activity
70
Unstable angina
unpredictable, occurs usually by resting,
-It results from reduced blood flow to the heart due to narrowed coronary arteries caused by fatty buildups (plaques). When these unstable plaques rupture, they form blood clots that further block blood flow, leading to intense, prolonged chest pain.
lead to (MI) if not treated
71
How can you diagnose angina?
Pt history
ECG
Exercise Stress Test
Nuclear Imaging
CT scan
Cardiac catheterization
72
How can you treat angina?
direct treatment towards symptom relief
lifestyle changes
drugs
-nitrates (nitroglycerin)
-beta blockers
-calcium channel blockers
73
What is MI? main cause of death?
when you have complete obstruction to a coronary vessel -> infarction ( heart attack)
-affected area of heart muscle becomes necrotic
-dead myocardial tissue gets replaced by fibrous tissue
-cardiac arrhythmias main cause of death
74
What is the difference between ST-segment elevation MI and non-ST elevation MI?
complete obstruction to a coronary vessel -> ST Wave Elevation MI
partial obstruction of a coronary vessel resulting in cardiac death -> Non-ST wave elevation MI
75
Acute MI
-s/s vary for men and women
-chest pain that radiated to left arm/neck
(severe, crushing, constrictive, or like heartburn)
SNS response
-GI distress, nausea, vomit
-tachycardia and vasoconstriction (pallor)
-anxiety, restlessness, feeling impending doom
Hypotension and shock
-dizzy,
-weakness in arms + legs
76
What is a cardiomyopathy? What are the different types of cardiac myopathy?
Disorders of the heart muscle/myocardial function
1. Genetic: hypertrophic and arrhythmogenic right ventricular
2. Dilated and restrictive
3. Acquired: myocarditis, peripartum
77
What is Hypertrophic Cardiomyopathy?
A genetic condition where heart cells have a defect in contractile proteins and they do not have enough actin & myosin, heart cells work harder and hypertrophy.
-cells too weak to function properly
-To compensate for the weakness in individual cells, the heart muscle cells hypertrophy to do the same amount of work as normal cells.
-The enlarged cells need more O2, but are less efficient at pumping blood, person is prone to heart failure and may suffer sudden death during exertion
-MOST COMMON CAUSE OF CARDIAC DEATH IN ATHLETES
-enlarged septum
78
What is dilated cardiomyopathy?
Progressive cardiac dilation where the heart becomes enlarged 2-3x normal size. All 4 chambers of the heart are affected and the walls become thinned, impairing the hearts' ability to pump blood efficiently. It's easy for blood to enter but not leave.
-s/s related to heart failure
dyspnea, orthopnea, exercise intolerance
Treatment:
relieving symptoms of heart failure
-beta blockers, diuretics, ACE inhibitors, heart transplant
79
Restrictive Cardiomyopathy
The heart muscle becomes stiff, preventing the heart from filling properly.
-Restricted cardiac filling
symptoms
-dyspnea
-PND
-orthopnea
-peripheral edema
80
Paripartum Cardiomyopathy
A type of dilated cardiomyopathy that occurs in the last month of pregnancy or within 5 months of delivering.
-half of women recover with no loss of cardiac function, half recover with loss of cardiac function
-if mother gets it after 1 child, high risk of developing it with all children
81
In what type of patient do you see ST wave elevation, ST wave depression?
ST Wave Elevation - MI
ST Wave Depression - Ischemia
82
What does non-ST wave elevation MI and ST wave elevation MI have in common?
Cause: Both are caused by a blockage in a coronary artery, leading to reduced blood flow to the heart.
Symptoms: Both include chest pain, shortness of breath, nausea, dizziness, and fatigue.
Cardiac Enzyme Elevation: Both cause an increase in cardiac enzymes (like troponin) because of damage to the heart muscle.
Risk Factors: Both are linked to high blood pressure, diabetes, smoking, and high cholesterol.
Complications: Both can lead to serious problems like heart failure, arrhythmias, or even death if not treated quickly.
83
Understand the difference between right and left sided heart failure.
one side of the heart falls first
LEFT:
systemic htn
aortic stenosis
left ventricular infarction (main cause of heart failure)
RIGHT:
pulmonary htn
pulmonary valve stenosis
pulmonary disease
84
Forward Effect Left/Right Heart Failure
Decreased CO
SAME IN LEFT AND RIGHT
-blood backs up into lungs because the left side of the body can't pump it effectively into the body.
-lungs fill with blood, causing an increase in pulmonary pressure, resulting in pulmonary edema.
85
S/S of Forward Effect
- decreased CO
- decreased blood supply to tissues
- fatigue
- weakness
- cold intolerance
- dizziness
86
Compensatory Mechanism of forward effect
tachycardia
pallor - shunt blood away from skin
daytime oliguria - no urine in day
87
Back Up effect LEFT SIDE heart failure
pulmonary congestion due to increased pressure
-dyspnea and orthopnea
-coughing w/ frothy sputum
-paroxysmal nocturnal dyspnea
-rails/crackles
-harder to inhale
- cyanosis, signs of hypoxia
88
What is paroxysmal nocturnal dyspnea and in what patients would you expect to see this ?
Severe nighttime shortness of breath
-pt with acute pulmonary edema
-wake up gasping for air
-cough up frothy, blood stained sputum
89
Back up effect RIGHT SIDED heart failure
Right heart can pump blood to lungs, backs up in venous system. Venous system fills w/blood.
fluid accumulation in neck veins and lower extremities causing edema.
-edema in feet/legs
-enlarged liver and spleen w/ impaired function
-Ascites
-distended neck veins
-lungs do not oxygenate enough blood
90
What are some causes of right sided and left sided heart failure and how is heart failure diagnosed?
Causes:
1) infarction or valve defect
2) htn
3) lung disease
4) combination of factors
Heart failure is diagnosed by increased BNP levels.
91
What is shock? Compensatory mechanism?
Failure of the circulatory system to supply peripheral tissues and organs with an adequate blood supply. Hypoperfusion of tissue/organs.
-SNS activates - try to increase BP
-Renin angiotensin system activates
-AII
-ADH
-Aldosterone
92
Decompensated shock
Various organs in the body are failing
93
What are the different types of shock?
Hypovolemic shock
Cardiogenic shock
Obstructive shock
Distributive
94
Hypovolemic shock, compensatory mechanism activated?
lack of blood supply, bleeding out.
Loss of whole blood and plasma
vasoconstriction
increase HR
kidney retain salt and water
release ADH
renin angiotensin activated
95
Cardiogenic shock
Heart fails to pump blood adequately
Decreased CO - Decreased BP
-SNS activates
-vasoconstriction - increased resistance to blood flow
-increased workload on the heart worsens heart failure
96
Distributive shock
Blood vessels dilate, not enough blood to fill circulatory system
blood flow decreases
less blood returned to heart; less blood circulated to body
caused by
decreased SNS activity
- brain/spine injury, anesthetics, insulin shock, emotion
Vasodilator substances in blood
-Type 1 Hypersensitivity (anaphylactic shock)
-inflammatory response to infection (sepsis)
Vessel damage from severe hypovolemia
97
Anaphylactic shock
-type of distributive shock
- massive amounts of histamine released from mast cells resulting in vasodilation and bronchoconstriction
98
Sepsis
due to systemic infection, has a high mortality rate
inflammatory mediators released into circulation, cause systemic signs of inflammation
-distributive shock, vasodilation occurs and blood pools in vessels, blood is unable to get distributed to the heart to get pumped out.
99
Obstructive shock
inability of heart to fill
-cardiac tamponade
100
What is the difference between cardiac effusion and cardiac tamponade?
Cardiac effusion is when fluid SLOWLY builds up in the pericardial sac w/few to no symptoms
Cardiac tamponade is when fluid RAPIDLY accumulates in the pericardial sac and compresses the heart.
101
Simple Ventricular Septal Defect
A hole in septum between the 2 ventricles
LV > RV
When LV contracts, some blood goes through the ventricular septal defect from LV to RV, some blood goes out to the body. All blood entering circulation is fully oxygenated, so it is ACYANOTIC condition.
102
Tetralogy of Fellot
4 cardiac abnormalities
1) Ventricular Septal Defect
2) Pulmonary stenosis
3) Right ventricular hypertrophy
4) overriding aorta
Now the RV > LV
Blood flows from RV to LV into aorta
Blood did not go to the lungs so the blood going to systemic circulation is deoxygenated, CYANOTIC condition
103
What are cardiac enzymes and how are they used?
Troponin I elevates in blood within 3-4 hours after injury and remains elevated for 10-14 days. They will get serial blood samples. The higher the cardiac enzyme, the worse the cardiac damage/ prognosis. Elevated troponin = MI
104
What is BNP? How is it used?
BNP is used in chronic volume overload situations. It is a marker for heart failure.
BNP diagnoses heart failure, severity of heart failure, and efficacy of treatments
105
Why do people suffering from heart failure suffer from hypervolemia?
Decreased Cardiac Output:
In heart failure, the heart is unable to pump blood efficiently, leading to decreased cardiac output As a result, organs and tissues receive less blood, including the kidneys.
106
Inotropic Cardiac Meds
deal with the force of ventricular contraction
+ inotropic = greater foc
- inotropic = weaker foc
107
Chronotropic Cardiac Meds
deal with HR
+ chronotropic = increase HR
- chronotropic = decrease HR
108
Dromotropic Cardiac Meds
deal with conduction velocity- how fast the aps are moving through the cardiac conduction system
+dromotropic = greater conduction velocity
-dromotropic = weaker conduction velocity
109
What virus causes AIDS? How is it transmitted?
Human immunodeficiency virus,
transmitted by body fluids
-sexual contact
-breast milk
-blood to blood contact (contaminated needles, transfusions, during pregnancy/birth)
110
What are the different phases of HIV infection?
1) Primary infection phase
-general malaise
-signs of systemic infection (flu like symptoms)
-seroconversion (IS responds and antibodies against HIV appear 1-6mon)
2) Latency phase (abt 10-20 years)
-virus replicates
-T helper cell count falls (normally 500-1500)
3)Overt AIDS phases
T- helper cell count less than 200cells/mm3
111
AIDS-Associated Illnesses
Opportunistic infections
-Respiratory (pneumocytosis, pneumonia, pulmonary TB,
-GI: esophageal candidiasis, CMV, Herpes simples, esophagitis,
-NS
-Malignancies
-KAPOSI SARCOMA
-non-hodgkins lymphoma
Wasting syndrome:
involuntary weight loss of > 10% of starting weight, diarrhea, chronic weakness and fever
Metabolic disorders:
insulin resistance, diabetes, lipodystrophy (abnormal fat loss or accumulation), hyperlipidemia
112
What's the difference between being HIV+ and suffering from acquired immunodeficiency syndrome?
If T- Helper cells fall below 200 cells/mm3, you have moved from being HIV+ to having AIDS.
113
Primary Immunodeficiency
Primary immunodeficiency is genetic.
B cell deficiency
T cell deficiency (thymic aplasia)
Severe Combined Immunodeficiency Disorder (SCID): deficient in B and T cell due to non functional T-helper cells
Wiskott-Aldrich syndrome: not enough antibodies produced, have B cells, not enough antibodies
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Secondary/ Acquired Immunodeficiency
Acquired- consequence of another event
-malnutrition
-immunosuppressant drugs
-AIDS
-kidney disease
-Hodgkin lymphoma
-chemotherapy
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What are some treatments for a patient suffering from an MI, from angina?
-rest, o2 therapy, analgesics
-anticoagulants
-thrombolytic agents
-low dose aspirin (ASA)
-coronary bypass surgery
-percutaneous coronary intervention
first dissolve clot w/thrombolytic agent, then warfarin, heparin, antiplatelets, low dose ASA
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Understand how aging is associated w the development of hypotension?
aging, autonomic function, dehydration, reduced baroreceptor activity,
Many older adults take medications such as diuretics, beta-blockers, or calcium channel blockers for other health conditions, which can lower blood pressure
chronic conditions
decreased fluid volume
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What compensatory mechanism occurs in the heart in patients suffering from
hypertension or aortic valve stenosis that helps to maintain cardiac output?
In hypertension or aortic valve stenosis, the heart thickens its muscle (hypertrophy) to pump more blood and overcome increased pressure. This helps maintain blood flow. However, over time, the heart becomes less efficient, needing more oxygen, which can lead to heart failure.
