Sle, Urine Catecholamines, Atenolol, Pvd, Cerebral Aneurism

Front 1

Definition of SLE

Back 1

Autoimmune disease in which organs and cells undergo damage initially mediated by tissue-binding ABs and immune complexes.

Front 2

Highest prevalence in?

Back 2

Black women

Front 3

Pathogenesis of SLE?

Back 3

1. Genes: Innate immunity, ac

2.

Front 4

Best screening test

Back 4

Antinuclear antibody

Front 5

Clinical manifestations:

Back 5

pleural effusions, butterfly rash, heart problems, lupus nephritis, arthritis, raynaud's phenomenon

Front 6

Diagnostic criteria

Back 6

have to have 4 or more of these:

Malar rash, discoid rash, photosensitivity, oral ulcers, arthritis,

Front 7

ANA staining pattern is what?

Back 7

Rim (SLE) most specific

Homogeneous (SLE very specific)

Speckled

Nuclear

Diffuse

Centromere

others indicate other disorders

Front 8

What happens when they are exposed to sunlight?

Back 8

makes any symptoms worse

Front 9

Treatment for lupus?

Back 9

No... can use corticosteroids to help control some symptoms

Front 10

which drugs can induce lupus?

Back 10

isoniazid, hydralazine, procainamide

Front 11

Why do you usually do a urine catecholamine test?

Back 11

Pheochromocytoma

Front 12

What are the main catecholamines?

Back 12

dopamine, NE, and Epi

Front 13

Which enzymes are involved in the breakdown of catecholamines?

Back 13

MAO and COMT and aldehyde dehydrogenase for NE and Epi

Front 14

Breakdown of NE and epi produces the metabolite, ___________ ______ (____) a major end product of NE and Epi metabolism

Back 14

Vanillylmandelic acid (VMA)

Front 15

Dopamine metabolized through the enzymes MAO, COMT, aldehyde dehydrogenase produces what?

Back 15

homovanillic acid (HVA)

Front 16

Epi --> ___________ --> VMA

NE--> _____________ --> VMA

both via COMT in which organs?

Back 16

Metanephrine; normetanephrine

Liver and kidney makes VMA,

ADrenal medulla, liver, and kidney make metanephrine and normetanephrine

Front 17

EPI and NE use which enzyme to become dihydroxyphenylglycol (DHPG). Then what happens to DHPG?

Back 17

Monoamine oxidase. THen COMT and aldehyde dehydrogenase transform it into VMA.

Front 18

All of these metabolites can/cannot get excreted in the urine?

Back 18

CAN

Front 19

Are the metabolites chemically active?

Back 19

nope

Front 20

Elevated urine catecholamines?

Back 20

Could mean several things, pheochromocytoma, chocolate, exercise, stress... etc

Front 21

Atenolol is used to treat what?

Back 21

Antiarrhythmic so treats arrhythmia

Front 22

Beta 1 receptors use which pathway mediator?

Back 22

Gs protein coupled receptor which increases cAMP. causing contraction, HR, Renin, Lipolysis, Saliva

Front 23

Atenolol blocks which receptor?

Back 23

Beta1 adrenergic receptor, decreasing HR, contraction

Front 24

Cholinergic system does what to decrease HR, contraction?

Back 24

inhibits Beta 1 by acting directly on the receptor

Front 25

increaesd cAMP in SA node causes more ____ permeability

Back 25

Ca++

Front 26

Atenolol blocks the sympathetic regulation of __________.

Back 26

hypoglycemia

Front 27

In PVD, what does peripheral mean?

Back 27

any medium or small vessels that are not part of the heart, aorta, or brain

Front 28

If someone has shiny skin on their lower leg with less hair than you would expect, which category of disease might they have?

Back 28

PVD

Front 29

What are the risk factors for PVD?

Back 29

smoking, diabetes (glucose glycocylates endothelial proteins), HTN, increased LDL (bigger and takes up more space)

Front 30

Definition of a cerebral aneurysm?

Back 30

weak or thin spot o a blood vessel in the brain, balloons out and fills with blood.

Front 31

Causes of cerebral aneurysm?

Back 31

Congenital, trauma or injury, HTN, infection, tumors, atherosclerosis, drug abuse (cocaine) etc.

Front 32

Chronic stress to blood vessels causes decreased _________. so if the pressure decreases your vessel won't do what?

Back 32

elasticity; bounce back.

Front 33

Myointimal hyperplasia?

Back 33

response to vascular injury. Proliferation of sm muscle cell to regain arterial elasticity... composition of vessel isn't as strong as it was before the damage occurred.

Front 34

4 diff types of cerebral aneurysm?

Back 34

Berry (circle of willis)

Fusiform (all walls are widening from atherosclerotic placque)

Dissecting aneurysm (can occur due to trauma or spontaneously, from tear within the inner and middle layer of wall)

Mycotic aneurysm (infection in wall mostly from strep)

Front 35

Risk factors?

Back 35

age, women, HTN, ETOH, drug abuse

Front 36

Complications?

Back 36

Rupture: hemorrhagic stroke, permanent nerve damage, death, subarachnoid hem (hydrocephalus), vasospasm (spasming can block off brain areas , hemorrhage, fix itself, and then do it again!)

Front 37

Which percentage of patients with ruptured aneurysm survive?

Back 37

60%

Front 38

Ejection Fraction is a measure of the ________ of the LV. equation?

Back 38

Efficiency so increased % is more efficient!

SV/EDV

Normal = 55-70%

Less than 55% depressed myocardial contractility

Front 39

Another word for EDV is ________ and refers to ________.

Back 39

preload, volume (venous pool)

Front 40

Another word for ESV is ________ and refers to _______.

Back 40

afterload, pressure (contractility)

Front 41

What increases afterload?

Back 41

dliated LV, aortic stenosis, HTN,