Exam 3 part 1 Flashcards
Allograft
(homograft): same species
Isograft
identical twins
Autograft
one part of body to another
Xenograft
between different species
immunosuppressive drugs and
matching HLA/MHC’s are needed prior to performing which transplants
xenograft and allograft
What is the protocol
to minimize rejection
closely matched HLA/MHCs (7-10 matched) and immunosuppressive drugs if needed
Graft vs host disease
t lymphs in graft attack the host “the perfect storm” - 3 traits must occur at the same time for this to happen
Graft vs host disease perfect storm
- Transplant must have a functional cellular immune component
- Recipient tissue must have antigens foreign to the donor T-lymphocytes
- Recipient immune system must be compromised to the point where it cant destroy the transplanted T cells
heart murmur
Swooshing extra heart sound heard during stenosis (valve not opening all the way so blood shoots through narrow opening)
and regurgitation (valve doesn’t close all the way, will hear murmur of blood leaking back through valve)
cause of heart murmur
stenosis and regurgitation, prolapsed mitral valve.
What effect does a heart murmur, hypertension, aortic valve stenosis, mitral valve
regurgitation have on cardiac output?
decreased CO
True aneurysm
bound by a complete vessel wall, the blood is within the vascular compartment
False aneurysm
local injury to the vessel wall causing a tear in the vessel wall -extravascular hematoma (hematoma bound by extravascular CT)
Berry aneurysm
dilation that occurs where a blood vessel branches
fusiform aneurysm
involves entire circumference of vessel - gradual/progressive dilation of the vessel
saccular aneurysm
extends over part of the circumference of the vessel
dissecting aneurysm
hemorrhaging into vessel wall
Aortic aneurysm
abdominal aortic aneurysm, thoracic aneurysm
aortic dissection
bleeding into vessel wall with longitude tear
- Hypertension
- Marfan syndrome
main cause of aneurysms
Weakening of arterial walls from:
Congenital defects
Trauma
Infection
Atherosclerosis
atherosclerosis
has atheromas which are plaques having lipids, cells, fibrin and cellular debris; they often have an attached thrombus. The initiating factor may be endothelial cell damage (occurs at young age)
arteriosclerosis
general term for degenerative changes that occur with age - narrowing of small arteries and arterioles - ischemia
non modifiable risk factors of Atherosclerosis
Age
Gender
Genetics/family history
modifiable risk factors of atherosclerosis
- Obesity or diet
(Increase lipids/LDL) - Cigarette smoking
(Increase LDL/decreases HDL) - Sedentary life style
- Diabetes mellitus
- Hypertension
main consequences of an unstable plaque
Can rupture - clot forms
- Can block artery completely
- May break free and become embolus
difference between a stable vs unstable plaque
Unstable plaque - thin fibrous cap, stable plaque - thick fibrous cap
s/s of peripheral artery disease (PAD)
- Gradual onset
- Pain while walking claudication or intermittent claudication
– Calf pain
– Vague aching felling or numbness (blockage of at least 70% of the vessel) - Foot cool to the touch
- Weak or absent pedal pulse or femoral pulse
**When blood flow is severely reduced - Ischemic pain at rest
- Ulcerations
- gangrene
causes of vasculitis
Inflammation, injury and necrosis to the blood vessel wall
how does damage to the vascular wall occur with vasculitis
Can occur anywhere in the body
- Direct invasion of pathogen into the vascular wall and immune mediated inflammation
- Non-infectious vasculitis - non-pathogen mediated immune inflammation, medications 7-21 days (antibiotics, thiazide diuretics, NSAID, Warfarin or other diseases (Lupus, rheumatoid arthritis, hepatitis)
– Vessel obstruction and ischemia
primary HTN
90-95% of cases, no other disease is present
modifiable risk factors primary HTN
High salt diet
Obesity
Excessive alcohol consumption
Insulin resistance
non modifiable risk factors primary HTN
Family history
Race
Age
secondary HTN risk factors
results from another disorder
- Kidney disease (ie:renovascular hypertension, acute renal failure, glomerulonephritis)
- Adrenal cortical disorders (hyperaldosteronism, Cushing disease)
- Pheochromocytoma (increased epin/norepin)
HTN treatments
life style changes
reduce body weight
Exercise
Low salt diet
pharmacological treatments if lifestyle treatments fail: HTN
mild diuretics, ACE inhibitors, beta blockers, calcium channel blockers, alpha blockers
renin-angiotensin system’s role in the development of
hypertension
Activation of this system aims to increase BP. overactivation leads to hypertension - this system increases synthesis of
angiotensin II, which vasoconstricts the blood vessels, and increases release of aldosterone, which causes kidneys to retain sodium and water, and ADH, which also causes fluid retention. These all increase blood pressure.
s/s and detrimental effects of hypertension
Heart
- Left ventricular hypertrophy
- Angina
- Heart failure
- MI
Brain
- stroke
Kidney chronic - kidney disease
Eyes - retinopathy
Blood vessels - peripheral vascular disease
Host vs graft rejection types
recipient’s immune system attacks the transplant
- hyperacute rejection
- acute rejection
- chronic or late rejection
hyperacute rejection
occurs immediately after transplantation when blood flow is reestablished. Due to preexisting antibodies in the host. The blood vessels are effected and consequently blood flow to the transplanted organ is compromised
acute rejection
occurs several weeks after transplantation when unmatched antigens cause a reaction Generation of T cells, antibodies against the graft
chronic or late rejection
occurs several months after transplantation. Blood vessels in the graft are gradually damaged
graft vs host disease process
occurs when there are some T-lymphocytes in the graft that attack the host (host is immunologically compromised) commonly from bone marrow transplant, liver transplant
Preeclampsia–eclampsia
- Eclampsia is the development of seizures in a woman with severe preeclampsia It has a 2% mortality rate
- Hypertension after 20 weeks, proteinuria, elevated serum creatinine and liver enzymes, decreased platelets
- Usually seen during first pregnancy
- Seen in multiple fetuses
- Kidney disease
- Decreased blood flow to placenta causes release of toxic chemicals that damage the endothelium.
- Delivery of the baby is curative - HTN often goes away
Chronic HTN
- Hypertension unrelated to pregnancy
- Hypertension present prior to pregnancy or occurs before 20 weeks gestation or persists beyond 12 weeks postpartum
Increased risk of developing preeclampsia
Preeclampsia superimposed on chronic hypertension
- Hypertension before 20 weeks who develop proteinuria
- Worse prognosis compared to either alone
orthostatic hypotension
Abnormal drop in BP upon standing
- Fall in CO → fall in BP → fall in blood flow to brain
- Dizziness, syncope or both
- low blood volume - baroreflex doesn’t work as efficiently (decreased thirst reflex in the elderly causes them to have lower blood volumes - increased risk of orthostatic hypotension and falls)
- Autonomic dysfunction - problem with autonomic nervous system baroreflex can’t react quickly enough
orthostatic hypotension causes
- Low blood volume - dehydration
- Drug induced
- Aging
- Bed rest
- Autonomic nervous system problems
varicose veins
Dilated veins, usually in lower extremity. valves in veins weaken and cause backflow and pooling of blood, making them superficial
cause of varicose veins
- Prolonged standing
- Prolonged increased pressure on abdominal veins
- Obesity and pregnancy cause high risk
primary varicose veins
weakness in vein walls that is often hereditary
secondary varicose veins
develop as a results of another condition, like DVT or pregnancy
