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Pathophysiology > Week 8 > Flashcards

Week 8 Flashcards

1
Q

what are the steps of atherosclerosis ?

A
  1. endotherlial cell injury
    LDL enter and become oxidized within intimal layer of arterial wall
    Foam cells from macrophages, creating fatty streak
    Inflammatory response triggers growth factors
    Smooth muscle cell proliferation and migration form tunica media to tunica intima
    Fibrous plaque formation from the growth of extracellular matrix
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2
Q

what is the #! physical stimuls taht damges endothelial cells?

A

turbulent blood flfow from hypertension - like waves crashing on a rock

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3
Q

where
does atherosclerosis most often occur

A

abdominal aorta. iliac arteries, proximal coronary

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4
Q

A deep vein thrombosis that dislodged would put someone most likely at highest risk for which of the following

A

pulmonary embolism - block in pulmonary vessels to the lungs

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5
Q

what is the clinical definition of hypertension

A

135/85 or grater

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6
Q

if the cause is unknow then it is ___ hypertesnion if it is know then it is _____ hyeptesnion

A

primary
secondary

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7
Q

what are some risk factors of hypertesnion

A

age, obesity, family history, diet, low PA, excess alcohol, smoking, stress

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8
Q

someone with a bloof pressure of 92/65 would be considered whta?

A

normal

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9
Q

what is elevted bp

A

120-129/80

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10
Q

someone wiht BP of 122/80 would be classified as ___

A

elevted

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11
Q

what is hypertension stage 1 and 2

A

stafe 1 is >130 and > 80
stage 2: >140 and >90

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12
Q

what are 4 potenital effectes of uncorolled hypetesnion

A

endothelial cell injur –> atherosclerosis
Cardiac consequences - CAD, (angina +MI) left venticular hypertophy, heart failure
PAD
organ damage - due to high pressure eaching cap network supplying organs

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13
Q

what is preload
afterload?

A

volume of blood lef in ventricles at end of diastol
afterload - reistance LV oversome to circulate blood

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14
Q

how does LV hypertophy occur in uncotrolle dhyeprtesnion

A

LV has to pump harder to overcome pressure in the arota - LV hyeprotphy

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15
Q

what is the equation for MAP

A

CO x peripheral resistacne

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16
Q

what are the three types of machnisms of BP regulation explain an example for each and how it relates to MAP equaiton

A

Neural - baroreceptors - send info to the medulla tor eg bp

Incrase/decreaes CO and resitance
(increase HR +contractility) OR constric/dilate blood vessels

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17
Q

where are baroreceptors and what do they do?

A

in arotic arch and carotid arteries - control BP by sending signals to the medulla

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18
Q

hwo does ADH refulat BP

A

incrases Blood volume nad therfor CO (by increasing SV) - reduces urin output and incrases water reabsopriton

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19
Q

3 ways to regulate BP

A

Renal/hormones, vascular + Neural

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20
Q

Nitric oxide is a vaso____

A

vasodilator

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20
Q

endothelin I. is a ____

A

vasoconstrictor

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21
Q

Explain the Renin-Angiotensin-Aldosterone pathway in response to a decrease in MAP

A

Decrase in MAP - body senses thru decrease filtration rate (kidneys)

  1. kidneys relase renin
  2. renin converts angiotensin to angiotensin I - angiotensin II (ace enzyme)

angitonesin II
- increase Vasocontriction (resitsance +BP)
- increase adolserone release - increase NA reabsoroption +water incrases BV
thirst (hypothalamus) increase BV when drink water

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22
Q

what is converted during the rening-angiotnesin -aldosteron system

A

renin - angiotensinsongen - angiotensinog I to angiotensinogne II to relase of aldosterone

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23
Q

what is the final thing of the renin-angiotensin-aldosteron sytem (not aldosteron) what are the 3 big things it does/

A

angiotensin II
1) Incrase thirs - drink water incrase. BV
2) increase aldosterone relase - NA+/H2o reabsorption increase BV and increase BP
3) Vasoconstriction - increase ressitance + BP

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24
what are the two pathophysiological bases of priamry hypertension
increase blood volume (due to defect in NA+ handling) - incrase NA+ due to ecess intake or reabsorbotion increase peripheral vascular resistance - endothelial cell dysfunction (vasocontstiiton) activation of RAAS incrased activation of SNs - increase CO and PR
25
what three things are involved in the pathophysiology of hypertension in terms of an increase in peripheral resistance
1) endothelial cell dysfucntion/vasoconstirciton increase RAAS incrase SNS
26
explain 2 drugs that could treat hyeprtesnion? how>
ACE inihbitot- inhibits angiotensin I to angiotensin II - inhibit effects of angiotensin II like ( Vasocnotriction, thrist, aldosterone release) beta blcker - inhibit SNS activity anti-renin - prevents renin to anioteninsin 1
27
what are some common treatemnets for hypertension?
Pharmaceuticals - ACe inhibitor, diuretics Lifestyle - limit smoking, alc, stress, increase PA Diet - DASH, reduce NA+ ,reduc cafeine
28
what is an example of a vasodilator andhow does it help with hypertesnion?
ACE - prevents angiotensin --> angiotenisn II, prevents vasoconstriction
29
How do diuretics help with blood pressure?
dcrease blood volume - decrease CO
30
how do cardioinhibitoru druigs?
inhbit contractility (inortropY), HR (chronotropy) + lower CO
31
how does exrcise help hypertension
moderate intesnity- leads to post-exrcise hypotension - decrases BP likely due to vasoilation
32
how does acute hypotension occur - what is it also knwon as
inadequtae tissue perfusion - tisue ischemia/hypxoa --? cellular damage also known as shock
33
what are 3 signs/symptoms of shock (acute hypotension)
tachycardia, decrased urine output, dizziness, faint,altered mental status
34
Cold shock is due to? what si the compensation?
cold shock is due to a decrease in CO compensation is vasoconsticiton, increase R, increased MAP - blood flow redirecte dto ital otgans
35
what are the 2 types of cold shock and hoe does each lead to hypotension?
hypovolemic - decrease Blood Volume --> decrase venous return + CO - hemmoragic or non (diarrhea/vomitting) cardiogenic - problem wiht Heart function/pumping ability --> decrease CO - Heart failure, MI, valve
36
what are the 2 rypes of cold shock and 2 types of warm shock ?
2 types of cold - hypovolemic _+ cardiogenic warm - septic + anaphylactic
37
what is the diffenrece between cold and warm shock in therms of MPA equation ?
cold affects CO Warm affects ressitance
38
what are the 2 types of warm shock and how do they lead to BP decrease (MAP equaiton)
q) anaphylactic shock - mast cell relase histamine +bradykini --> vasodilation, edema + bronchocnstiction - decrease CO b) septic shock - infection in blood - macrophage activation - cytokines - vasodilation
39
how is anaphylactic shock traeted?
epeniephine -->incrase CO, smooth muscle ralxation + vasocontriciton
40
how is septic shock trated? what type of shock is this?
septic shock is due to ifection - macophage + cytokines lead to vasodilation treatement is IV and antibiotics
41
what is neurogenic shock? what part of MAP equation does it affect?
affectc R and CO Autonomic balacne tips towards PNS --> vasodiation, bradycardia - can be from SC injury, brain injury, vasovagal reflex - ovveractivation of vaug nerve - pain, emotion, fear blood w
42
what is teh vasovagal reeflex and what s it an example of?
an example of neurogenic shock where the PNS is overactived due to overacivation of the vagus nerve - cna happen from emotion, fear pain - fianitnig from sight blood ro pain
43
what is orthostatic hypotension? what can cause it sings + symptoms
sudden drop in BP from standing up from lying/sitting postion cause - imapried baraorecpetor feflex funcion, hypovolemia, blood pooling - meds (diuretics, vasodilators, antihyupertesnives) signs and symptoms dizzines, fainting, blurred vision, pallor, nausea
44
what are some tratement options for orthostatic hypotension?
leg resistance exercise, sleep a little urpguhit (activated baroreceptors) water intake increase, salt intake, compression stocking s
45
what is normal sinus rhytm determined bty and what do cardiac arrythmias lead to?
detemrneined by action ptoenial frequency of SA node - impaired CO from arrythmias (rate or path of conduction)
46
what are 2 abnormalites in rate of heart and hwat is each defined as?
sinus tachycardia >100 at reat sinus bradycardia ( slower <60bpm) at rest automaticoty
47
sinus tachycardia or bradycharia are due to issues in _____
automaticity - SA node autmaticll sts pace of heart with input of NS
48
How is SA node AP frequncey increased. What sytem involved?
SNS - epniephrin +NE released onto SA node _ bind to bet-adrenergenic rectpors
49
the SA node is modulate dbased on phase _____ slope being increased or decrease
phase 4
50
the SNS leads to ___ of SA node and phase ___ slope
increase SA node and icncrease phasde. 4 slope
51
when SA node frequency firin is increase ___ and __ ar releases when it is decreased ____ is released
NE and epinephrine ACH relased
52
what are some casues of increased autmaticity?
hypovolemia hyueprcapnia (high blood CO2) or hypxia (low blood O2) pain/anciet icnrease metabolic actiivty of pacemaker cells NE or EPinep
53
high blood co2 and low o2 is assocaited with _____ automaticity?
icnrease
54
hypovolemia is assocaited with ____ automaticity
incrase
55
what are some common causes of decrased autmaticity?
decrease metabolic activity of pacemaker cells, electrolyte imbalance, heart damage or disease hear damge/disease
56
name 2 types of arrhythmias due to electrical conduction - briefly describe each. give a specific example for each
triggered activity - an irritable area in the heart triggers spontaneous AP firing outside of the normal system - premature ventricular contractions re-entry circuits - abnormal conduction pathway forms - block in pathy or additional path forms - paroxysmal supraventricular tachcardia
57
what are premature ventricular contractions and what is an example of.
a common arrhythmia where triggered activity occurs because an electrical signal initiated by Purkinje instead of the SA node + ventricles contract prematurely - brief pause before normal rythms
58
what is Paroxysmal Supraventricular Tachycardia. It leds to venticular ____cardua
- an arrhythmia due to electrical conduction issues - a new pathway begins somewhere in the atria - new signal travel down vntricle --> ventricular tachycardia begins and ends suddenly
59
what is fibrilliation arryhtmia mean and what are the 2 types and waht is worse?
electrical activtiy is independent of the SA node --> leads to chaotic contractions atrial fibrillation + ventricular ventircular is worse
60
what is worse atrial or entricular fibrillation and why?
atrial fibrillation - hert stil fucnnctions a s a pump ventricular fibrillation - hear no lunger functions as effective pump - collapse (electrical shock needed to reset NSR)
61
what are some sumptoms of atrial fibrillation?
plpitations, chest discomfort, shotness of rbeath, dizziness
62
what are 3 types of treatment for arrythmias - summarize each
1. drugs - rate and rhyt, control beta-blioker (block SNS effect) Na+, K+, ca+ channel blockers ablation therapy - destroy sepcific region of heart tissue that is causing the issue pacemaker implanattion - pacemaker - regualtes rhythm thru elctriculsal pulses ICD - implantable cardio defibrillator - senses topped heart and gives strong electrical shock to restart

Pathophysiology (11 decks)

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