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B252 - Pathophysiology > Midterm 2 Things I do not know well! > Flashcards

Midterm 2 Things I do not know well! Flashcards

1
Q

where is the preferred metastasis of carcinomas?

A

The lymphatic tissues. but they also like the bones, liver lungs& brian or anywhere that is large is size & richly perfused

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2
Q

what are the steps of metastasis

A

1) local growth & extension (invasion) aided by enzymes
2) entrance into the lymph/blood
- most will not survive b/c turbulence & immunsystem
3) release of cytokines & mediators t decide if suitable & angiogenesis

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3
Q

Whats the dif between grading & staging

A

grading = histology approach that tells you if it is restrictive or invasive & is more subjective
Staging is a clinical approach uses TNM

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4
Q

when is the period of organogenesis

A

(15-60 days post conception) this is where most of the problems will occur because the embryo is just forming its organs

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5
Q

when are the specific critical periods

A 
CNS = 2-5 w
Heart = 3-6w 
extremities = 5-7 w 
eyes = 5-7 w
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6
Q

what is a chromosome

A

the structure the genes are arranged on. Has 100-1000 genes

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7
Q

what are homologous chromosomes

A

Make up the complementary pair, have genes for some characteristics on each location of chromosome

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8
Q

what is an allele

A

one copy of a gene is inhibited form each parent the expression of a nondom/recessive allele will be masked by the dominant allele

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9
Q

what are the 4 types of genetic abnromalities

A

1) Monogenic (only one gene on chromosome = problem)
2) Mitrochondrial gene
3) Complex trait (more than one gene + Muliple factors involved)
4) Chromososme (instead of 46 = 45,47)

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10
Q

What are the 3 types of monogenic gene disorders

A

1) Autosomal dominant
2) Autosomal recessive
3) X linked recessive

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11
Q

Explain autosomal dominant

A
  • Single allele effected on chromosome
  • 50% provability of passing onto offspring
  • Autosomal = nonsex chromosome
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12
Q

explain autosomal recessive

A
  • Need two effective alleles
  • Offsping: 25% unaffected, 50% carriers, 25% affected
  • carriers just have one defective allele so they can possibly send onto offspring.
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13
Q

what is the X linked recessive

A

sex linked abnormality
most carried on X CHROME
alterations on the X chrome has a more severe effect on the boy b/c no healthy backup gene
if its mom: 1/4 changce of female being carrier 1/2 normal female 1/4 change unaffected male. 1/4 change affected male
if its dad: all daughters are carriers & all sons are healthy

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14
Q

what do the mitochondrial gene disorders do

A

37 genes most are form the mom. Code for respiratory chain enzymes so the systems most affected are the muscle & nervous systems because they need the most ATP

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15
Q

explain complex trait gene disorders

A

A polygene is a gene whose effect is too small on the phenotype so it act with others. it need environmental factors in order to take place. its a predisposition.

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16
Q

what are the 2 types of chromosomal gene disorders

A

either numeric or structural

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17
Q

what is aneuploidy

A

when ur missing or have an extra chromosome

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18
Q

what is trisomy

A

extra chromosome pair (trisomy 21 = downsydrome)

Klinefelters sydrome

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19
Q

what is monosomy

A

missing chromosome only happens in sex chromosomes

Turners syndrome

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20
Q

what is klinefelters syndrome

A

-Male who has xxy instead of xy (1 in 500)
Clinical features: tall, lack facial hair, narrow shoulders, long arms & legs, gynocomastia (swollen breasts) wide hips, decreased pubic hair, testicular atrophy & infertile

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21
Q

what is turners syndrome

A

woman has only X (1 in 2500)
-small statue, webbed neck, broad chest with spiced nipples, no breasts, amenorrhea, estrogen & progesterone deficiency
lymphedema, coarctation of aorta & bicuspid valve, small bones, ovaries degenesis

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22
Q

what are the 7 CHROMOSOMAL Strucutral defects

A

1) INVERSION
2) TRANSLOCATION
3) DELETION
4) BALANCED TRANSLOCATION
5) ROBERTSONIAN TRANSLOCATION
6) ISOCHORMOSOMAL TRANSLOCATION
7) RING FORMATION

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23
Q

explain inversion

A

A piece has been flipped. It requires 2 breaks in a single chromome. Pericentric = around centromere. Paracentric = away from centromere

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24
Q

explain translocation

A

piece from one chromosome onto another or they trade

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25
Q

explain deletion

A

missing component leads to loss of genetic material & shortened chromosome

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26
Q

explain balanced translocation

A

both swap. Involved 2 non homologous chromosomes with the ACENTRIC (portion without centromere, swap)

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27
Q

explain robertsonan translocation

A

should have vertical separation but this time it is horizional.
Faulty centromere division, duplication of long arm and deletion of short etc.

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28
Q

explain ring formation

A

lose 2 fragments, forms from breaks in both telomeric portions of chr., deletion of eccentric fragment & fusion of the centric portions

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29
Q

explain hydrostatic pressure vs colloidal osmotic pressure

A

Hydrostatic pressure =PUSH pressure force from fluid
(Capillary filtration pressure or interstitial fluid pressure )
Colloidal osmotic pressure = PULLING force via particles
(higher in capillaries than interstitial space)

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30
Q

what is fluid

A

water & electrolytes

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31
Q

what is edema

A

fluid accumulation in the interstitial space from the inter vascular space

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32
Q

what are the 4 causes of edema

A

1) Increase capillary permeability
2) Decreased colloidal osmotic pressure
3) Increased capillary hydrostatic pressure
4) Obstruction of lymph flow

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33
Q

What causes increased capillary permeability

A

inflammation, allergic reaction, ascites, pleural effesion, tissue injury, burn, angioneurmtic malignancy

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34
Q

what can cause decrease colloidal osmotic pressure

A

only changes with renal problems, burns or decreased production of proteins by liver, starvation or malnutrition

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35
Q

what causes increased capillary hydrostaticc pressure

A

increased vascular volume( HF, KD, sodium retentions, heat stress, thiazoladone) or venous obstruction (liver disease w/ portal vein obstruct, pulmonary edema, venous thrombosis, or decreased arterial resistance)

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36
Q

what causes obstructed lymph flow

A

removal of nodes

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37
Q

what is dehydration

A

decreased fluid in the interstitial & intravascular spaces

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38
Q

what causes dehydration

A

1) Inadequate fluid intake
2) expressive GI fluid loss (vomit, diarrhea, suction, fistula)
3) Excessive renal losses (Diuretics, salt wasting, adrenal insuf.)
4) Expressive skin losses (fever, hot environ, wound)
5) Thirst spaces (burn, edema, ascites)

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39
Q

What are the manifestations of dehydration

A

1) Acute weight loss (severe = 8%+)
2) Compensatory release of antidiuretic hormone
3) Increased serum osmolarity (thirst, hematocrit, increased blood urea nitrogen)
4) Decreased vascular volume (postural hypertension, tachycardia, weak & thready pulse)
5) decreased extracellular fluid volume (sunken eyes)
6) Impaired body temp regulation (increased body temp)

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40
Q

where does third spacing occur

A

joint capsule, lungs, abdominal cavity & spinal cord

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41
Q

what is the ratio between HCO3- and H2CO3 (for normal blood ph)

A

20:1

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42
Q

what does the ratio look like for acidosis or alkalosis

A

Acidosis: 10:1
Alkalosis: 40:1

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43
Q

how to distinguish between respiratory & metabolic

A 
H2CO3 = volatile = respiratory imbalance 
Fixed acid (lactic or any else) = metabolic imbalance
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44
Q

Veins vs. arteries strucuture

A

Veins = thicker externa, less muscular media can be collapsed
arteries: very elastic, with thickest layer of tunica media

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45
Q

what effects the hemodynamic of blood flow

A

1) pressure, resistance & blood flow
2) Vessel radius
3) Cross-sectional area & velocity of flow
4) Laminar & tuburlence of flow

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46
Q

explain the layers of the heart

A

outside: Fibrous pericardium, viceral pericardium - space- parietal pericardium /epicardium, myocardium & endocardium

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47
Q

what happens @ p wave
QRS wave
T

A

P - atrias depolarize
QRS - depolarization ventricles / repel atria
T - repol ventricles

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48
Q

WHAT ARE THE MODIFIABLE & NON MODIFIABLE RISKS FOR HEART DISEASE

A

non mod: Men 45+, women 55+, family history (men or women <55) FN, african or south asian
mod: HTN, smoke, dylipidemia, diabetes, obesity, excessive alcohol, inactivity

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49
Q

what is the heart disease target organ damage

A

stroke of TIA, nephropathy, peripheral artery disease

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50
Q

what are the 3 parts of a lipid

A

cholesterol, triglycerides & phospholipids

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51
Q

which lipid is the worst?

A

LDL because it carried the most cholesterol

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52
Q

which lipid has least cholesterols

A

Chylomicrons or HDL’s

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53
Q

which lipid has most triglycerides

A

cylomicrons

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54
Q

what lipid has most protein

A

HDL

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55
Q

what is the fatty streak

A 
lesion of (macrophages, foam cells, sm. must) 
streak of yellow across vessel with no clinical manifestations
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56
Q

what is fibrous atheromatous plaque

A

Plaque = type of lesion
lipids, swelling , fibers, macrophages, foam cells, smooth muscle, scar tissue and calcification
Dystrophic calcification = accumulation of Ca2+ from cell death leads to hardening of vessel

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57
Q

briefly explain the development of atherosclerosis

A

1) Endothelial cell injury
2) Migration of inflammatory cells
3) lipid accumulation & sm. muscle proliferation
4) Plaque structure

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58
Q

what causes the endothelial cell injury

A

Smoking, increased LDL, immune mechanism, mechanical stress of HTN leads to the adhesion of monocytes & platelets

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59
Q

what haooens in the migration of inflammatory cells

A

endothelial cells express adhesion molecules which bind monocytes & other inflammatory cells - the monocytes migrate between endothelial cells to localize the intimacy & transform into macrophages

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60
Q

what happens in the lipid accumulation & smooth muscle proliferations

A

Macrophages release FR which oxidize LDLS that they then eat and become foam cells which release growth factors which contribute to migration & proliferation of smooth muscle cells & extracellular matrix

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61
Q

what does the plaque consist of

A

The Cap is : Smooth muscle & dense extracellular matrix. sm muscle produces collagen & elastin
The plaque itself has smooth muscle cells, macrophages, other leukocytes & ECM & extracellular lipids

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62
Q

which sites have the most severe atherosclerosis

A

1) Abdominal aorta & iliac arteries
2) Proximal coronary arteries
3) Throacic aorta & femoral & aortic Cartier’s
4) internal carotid arteries
5) Vertebal, basilar & middel cerebral arteries

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63
Q

what are the factors that affect MAP

A

1) Peripheral resistance (BV diameter, length, turbulence, blood viscosity)
2) CO
3) Blood volume

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64
Q

what are the 4 things that regular blood flow & BP

A

1) Neural control
2) Local/intrinic control
3) Hormonal control
4) Kidneys

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65
Q

what is neural control of BP

A

baroreceptors in the carotid & aortic arches detect less stretch or more stretch and send AP to medulla that inhibit the vasomotor or cardio accelerator enters as necessary
the sympathetic division will cause contraction of BV

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66
Q

explain local BP control

A
  • increased of Decreased CO2
    -Ph
    -NO releases smooth muscle in tunica media
    increased temp or histamine
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67
Q

What is ADH / where does it come form? what does it do?

A

Antidiuretic hormone/ vasopressin
-HYPOTHALAMIC hormone released from NEUROHYPOPHYSIS in response to dehydration (decreasd fluid increased solute) or when barareceptors detect low blood volume or when osmoreceptors detect high solutee conc.
IT TRIGGERS VASOCONSTRICITON & INCREASE H2O REABSORRB

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68
Q

what os ANP and where does it come from

A

atrial natrituetic peptide. Produced in right atrium in response to increased stretch it lowers bp & blood volume

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69
Q

what is aldosterone and where does it come from

A

released from adrenal cortex when angiotensin 2 acts on it. Acts on distal convoluted tubule to cause reabsorption of Na+ & H20 into the blood

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70
Q

what is Angiotensin 2 & what does it do

A
  • Causes vasoconstriction
  • causes release of ADH
  • causes release of aldosterone
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71
Q

explain RAAS

A

Juxtaclomerular aparatus detects low BP so in the afferent arteriole it release RENIN (an enzyme)
Renin converses angiotensinogen to angiotensin 1
Angiogentsin 1 -> angiotensin 2 by ACE
Angiotension 2 acts on adrenal cortex to release aldosterone & causes vasoconstriction & release of ADH

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72
Q

explain circadian rhythm & BP

A

Higher in the morning with gradual decline in the rest of the day (2-5am = lowest)

73
Q

what is malignant/persistent/resistant/severe HTN?

A

not cancer. DIASTOLIC greater than 120

74
Q

what is secondary HTN

A

usually because of the kidneys. (5-10% of cases)

75
Q

primary HTN

A

90% of cases.

Idiopathic we can’t find a source

76
Q

SYSTOLIC HTN

A

sup >140 but diastolic <90.
Mainly systolic b/c atherosclerosis after 50 - at rest it is ok but when pumping the occlusion makes a big difference cause can’t dilate
as we age degenerative poor compliance which decreases elasticity

77
Q

main HTN mnfts

A

1) am headache
2) dizziness
3) palpitations
4) later= organ failure

78
Q

why is the kidney so targets by HTN?

A

b/c efferent arteriole is smaller than the afferent to help maintain glomerulus pressure so an increase in pressure can cause tons of damage cause its already a high pressure area.

79
Q

what lifestyle modifications for HTN

A

1) Diet
2) 30-60 minutes of activity 4-7 times a week
3) less than 2 drinks day
4) BMI between 18.5-24.9
5) waist circumference
6) less than 2000mg/day salt
7) stop smoking
8) decrease stress

80
Q

what do diuretics do

A

urination of excess fluid - > decrease blood vol -> decrease CO
increases the permeability with increased volume of filtrate = increased urine output

81
Q

what other drugs may you need for HTN

A

1) Ace inhibitor
- prevents aldosterone & vasoconstriction
2) Calcium channel blocker
- plocks transport of calcium into cells which causes it to contract less. CA2+ usually bind to troponin and draws it out of position so myosin can bind actin
3) Angiotensin 2 receptor blockers
- Fills up active sites on adrenal gland & sm. Must. causes dilation & reduces secretion of ADH & aldosterone

82
Q

what are the 2 types of peripheral vascular disease

A

1) acute arterial occlusion

2) Atherosclerotic occlusive disease

83
Q

explain Acute arterial occlusion

A

Rapid onset -> distal tissue = ischemia
ischemia leads to infarction -> local tissue death
-not chronic
usually a thrombus or embolus

84
Q

what is infarction

A

Obstruction of blood supply to an organ or region of tissue causing local death to tissue

85
Q

what is a thrombus

A

localized or stationary clot

86
Q

what is an embolus

A

something moving in the blood that does not belong.

87
Q

what are the 7 P’s of acute arterial occlusion

A

1) pain
2) Pallor
3) Polar
4) Paralysis
5) Paresthesia
6) pistol shot
7) pulselessness

88
Q

what is the primary diagnostic for AAO

A

ultrasound doppler

89
Q

what is the treatment for AAO

A

1) Thrombotic
2) anticoagulant (blocks clotting cascade & platelet acclutination)
3) surgery (angiogram or stent)

90
Q

what is atherosclerotic occlusive disease

A

Gradual development same as atherosclerosis

91
Q

where are the most likely arteries for atherosclerotic occlusive disease

A

FEMORAL & POPLITEAL ARTERIES

92
Q

why is atherosclerotic occlusive disease more common in the elderly & the diabetic

A

B//c atherosclerosis is more common after 50 & an important complication of diabetes is vascular damage which contributes to atherosclerosis

93
Q

what is the bodies immediate compensatory response to atherosclerotic occlusive disease

A

1) STAT vasodilation (more blood flow because the distal tissue is ischemic)
2) early anaerobic mete
3) later = collateralization

94
Q

what is the major mufti of atherosclerotic occlusive disease

A

intermittent claudification

-at rest not a problem but when walking the vessels need more O2 but the cannot dilate

95
Q

what are the things to know about complications

A

1) What they are & their potential to arise
2) how to avoid via intervention
3) if it sets in you need to treat

96
Q

what are the complications of AOD

A

ulceration, gangrene, amputation & infection

97
Q

whats an aneurysm

A

weakening in a vessel wall that causes local dilation

98
Q

why do aneurysms develop

A

d/t degenerative change = loss of elasticity related to atherosclerosis or aging. This happens in certain localized areas because of pressure or bifurcation

99
Q

which vessels are most commonly effected

A

the femoral, iliac, popliteal

thoracic & abdominal aorta as well

100
Q

what are the risk factors for aneurysms

A

1) atherosclerosis -> wall dmg = wall weak
2) uncontrolled HTN
3) congenital defects

101
Q

what are the 2 characteristics that cause vessels to have aneurysms

A

huge bend

bifurcate like a fork in the road

102
Q

Explain true vs. false aneurysms

A

true - intact vessel wall that simply bulges over 50% increase in diameter
False - Compromised vessel wall (non intact) there is hemorrhaging through vessel which causes a hematoma that is surrounded by fasciae or muscle

103
Q

what is a fusiform aneurysm

A

BILATERAL (abdominal aorta)

104
Q

what is a saccular aneurysm

A

unilateral (often happens in aorta or when there is bifurcation)

105
Q

Berry aneurysms

A

occurs in the circle of willis in the brain IS A TYPE OF SACCULAR ANEURYSM

106
Q

what is a directing aneurysm

A

Vessel endothelium is compromised & the blood begins to flow in between the layers

107
Q

what are the complications of aneurysms

A

1) Rupture leading to hemorrhage
2) slower flow
3)pressure to adjacent sturcutres
4) Thrombus forms b/c pooling of blood
Distal embolization

108
Q

what is the treatment for aneurysm

A

SURGERY ONLY - repair, graft or remove

109
Q

what is the isovolumentric contraction phase

A

Left & right ventricles begin to contract but not ejection

110
Q

what is coronary artery disease

A

one or more coronary vessels undergo atherosclerotic change

111
Q

what is acute coronary artery syndrome

A

-emergency = MI or unstable angina

abrupt onset but it is decades in the making

112
Q

what is chronic ischemic heart disease

A

ongoing, no immediately life threatening. CAN BE STABLE OR VARIENT ANGINA OR MICROVASCULAR OR CARDIAC SYNDROME X ANGINA

113
Q

does ischemia ALWAYS cause pain?

A

no there is silent myocardial ischemia

114
Q

what is angina?

A

pain d/t myocardial ischemia

115
Q

what is the etiology of angina

A

atherosclerosis
vasospasm (sm. muscle contraction for no reason & involuntary locking in the constricted state NOT an occlusion)
thrombus or hemorrhage

116
Q

is angina always because of an occluded vessel?

A

NO it can be because of vasospasm or hemorrhage

117
Q

explain the patio of angina

A

atherosclerosis -> poor/no dilation -> inadequate perfusion -> ischemia -> pain

118
Q

explain stable angina

A

Fixed plaque, minimal occlusion, no pain at rest, transient & brief chest pain at exertion
Can also be triggered by cold or emotional stress

119
Q

explain variant/ vasospasm/ prinzmetals angina

A

Therorized that vasospasm causes the ischemia
occurs at rest & exertion but is most commonly between midnight & 8am
Etiology has to due with vasospasm & endothelial disfunction that allows calcium to slip past endothelial cells into the muscle and no NO production.

120
Q

explain unstable angina

A

we see platelet agglutinating… fibbing & cellular debris on endothelial cells as well. THE PLATELETS release prostaglandins when they aggregate which causes vasospasm. Thrombus begins appearing
not as brief = more prolonged & severe. Serum markers should not be present.

121
Q

what’s the treatment of angina

A

cease activity (rest no mater what type)
nitroglycerine (decreases pain, via vasodilation and decreases risk of MI)
stop smoking

122
Q

what is myocardial infarction

A

the end page of CAD with a rapid onset it is potentially fatal

123
Q

What kind of occlusion is STEMI usually

A

large artery that is fully occlude (proximal)

124
Q

what kind of occlusion is NSTEMI

A

no fully occlude in most cases could be proximal or distal

125
Q

which is most common NSTEMI or STEMI?

A

stemi

126
Q

what are the vessels most effected by MI

A

1) LEFT ANTERIOR DESCENDING ARTERY (40-50%)
2) RIGHT CORONARY ARTERY (30-40%)
3) LEFT CIRCUMFLEX ARTERY (15-20%)

127
Q

what does the left anterior descending artery profuse

A

inter ventricular septum. Left ventricle & L & R bundle branches & mitral valve

128
Q

what does the right coronary artery perfuse

A

L ventricle & R atrium & SA & AV NODES

129
Q

what does the left circumflex artery perfuse

A

L atrium & ventricle

130
Q

what is the etiology of a MI

A

mostly atherosclerosis
severe hemorrhage
or coronary artery spasm

131
Q

what is the patho of MI

A

progressive atherosclerotic change -> acute ischemia -> cardia hypoxia -> anaerobic metabolism -> metabolic acidosis -> arrhythmias -> infarct & HF

132
Q

what happens before infarction in a MI

A

1) increased respiration & anaerobic respiration

133
Q

the extent of the in fact is determined by…

A

1) vessel effected
2) degree of occlusion
3) Duration
4) What they were doing -> cardiac status (BP/rhythm)
5) Collateral vessels

134
Q

Compare transmural and subendocardial infarction

A

T R A N S M U R A L

  • is usually with STEMI = entire thickness of ventricular wall from a proxial occlusion
  • when ichemia involves the outer layer of the heart (Epicardium) the ST vector is directed outwards which leads to the elevation

S U B E N D O C A R D I A L

  • below the endocardium usually a distal occulusion
  • NSTEMI or st depression
  • only 1/2 - 1/3 inner part is infarcted
  • ST segment is directed toward interlayers so leads to a derision
135
Q

what are the MNFTS of MI

A

1) Sever chest pain the radiated to L arm, neck, jaw, fingers, back
2) Hypoxia -> tachycardia & increased workload
3) N/V -> b/c pain mediated through pain centre near vomit reflex centre AP’s emirate
4) anxiety
(additional mnfts - dyspnease, diaphoresis,dizziness, palpitations, pallor)

136
Q

why do women not have typical MI symptoms

A

they are usually suffering coronary microvascular disease where the small branches are affected

137
Q

what are the primary ECG changes in MI

A 
ST elevation or depress
T wave invasion 
no R wave 
abnormal Q 
ECG = PRIME diagnostic feature
138
Q

further diagnosis of MI

A

1) angiogram where cath goes into radial A and releases contract which shows us what arteries are occluded - can disrupt plaques
2) Labs: Tropinin I & T, Myoglobin & CKmb

139
Q

Explain the different troponin

A

I & T are specific and peak at the right time. These ones start first. levels increase when there is more death. WHILE C does not tell myocardial dmg

140
Q

explain myoglobin

A

nonspecific protein that is the hemoglobin of muscle cells released when they die

141
Q

explain CKmb

A

beings 12-24 hours & is normal within 3 days
-mb = specific to cardiac muscle
bb= in brain
mm= sk. mk.

142
Q

treatment of MI

A

1) Thromboltics
2) anticoagulants
3) antiarrthymics
4) oxygen
5) pain medication (morphine)
6) IV diuretic, vasodilator or inotrope
7) revascularization surgery angioplasty places stent or bypass for harder (1-2 weeks after)

143
Q

what is cardiomyopathy

A

disease of the cardiac muscle

144
Q

what are the 3 types of cardiomyopathy

A

1) Dilated/congested
2) Hypertrophic
3) restrictive/ amyloid

145
Q

explain hypertrophic

A

Increased cell size, thick wall with chamber unable to fill or empty properly.
Thick septum that obstructs the aorta.
Highest prevalence.
Effects the LEFT VENTRICLE the most.
Thick septum leafs to aortic valve obstruction -> blood not ejection properly -> aortic flow is impeded
1/2 genetics (autosomal dominant)
1/2 idiopathic (most have normal systolic fx and remain asymptomatic)
90% = asymptomatic while 10% will have dyspnea, syncope, angina, & palpitations
CAN CAUSE SUDDEN CARDIAC DEATH

146
Q

what is the treatment for hypertonic

A 
negative inotrop (beta blocker) 
or surgery ablation
147
Q

explain congestive/ dilated cardiomyopathy

A

Pooling of blood, loss of elasticity. Enlargement of ventricles. Thickness is unchanged. No recoil. Etiology is not clear but Alcohol, viral infections & chem drugs may play a role.
Streched wall is flacid / not elastic it remains over stretched & fills with blood.
Decreased ejection fraction (Sv/EDV x 100)

148
Q

what is the treatment for dilative /congestive cardiomyopathy

A

decrease workload via diuretics & beta blockers

149
Q

what is restrictive / amyloid cardiomyopathy

A

-Amyloid is a type of protein released when tissues are damaged. Seen in the BV of diabetes, the brain of alzheimer’s & heart
-Walls are rigid
-this is the worst/ most uncommon
-inadequate fill -> decrease CO -> HF
doesn’t perfuse aorta well so ischemia & MI can happen

150
Q

Explain the conduction pathway

A

1) sinoatrial node -> bachmanns bundle to L atria
2) internodal pathways
3) Atrioventricular node (floor r. Atrium)
4) Ap delayed (patrias contract)
5) av bundel ininterartial suptum to bundel of his to the left AP fascicles
6) right & left bundle branches
7) parking fibers i nets walls of ventricles
8) ventricles contact

151
Q

what is SA rhythm

A

70bpm

152
Q

what is arrhythmia

A

alterations in herat pattern it can be acceleration or something far worse. It is abnormal impulse propagation. change in either HR or rhythm.

153
Q

what is the etiology of arythmias

A
  • Congential defects
  • Electrolyte imbalance -> dictated by charges across membranes & the charges are dictated by ions so the electrical imbalance would dictate electrical impulse
  • some drugs (week, cocoaine, caffeine, add med) stimulants
154
Q

what is atrial flutter

A

Regular atrial & ventricular tachycardia (Atria = 300 bpm, V = 150bpm)

  • some energy dissipates as it travels to the ventricles
  • you’ll see 240-450 f waves
  • the ventricular rate remains regular
155
Q

what is atrial fibrillation

A

Grossely disorganized atrial electrical activity
IREGULAR RATE AND RHYTHM
-ventricular response is regular
-there are no distinct P waves
-NOT vasospasm
-spontaenous uncoordinated contraction (no order)
-irregular: non-functional contraction of atria (300-600bpm)
irregular ventricular rate 80-180

156
Q

explain heart block

A

abnormal or no impulse from A -> V
1st Degree - Delayed but regular conduction - Still coordinated but a bit slower (normal cycle w/ longer PR interval)
2nd degree- Intermittent l/o contraction -> some pass through & some don’t
3rd degree - No activity to ventricles - 2 uncoordinated independent paces. Worst CO

157
Q

What is ventricular fibrillation

A

V shake & quiver no relaxation or contract
NO CO
ECG shows irreg than systole
very quick fatal

158
Q

Treatment of arrhythmias

A

1) Defibrillation
2) Drugs: Class 1 = sodium ch. 2= beta block 3= potassium ch block 4= calcium channel block
3) pace maker
4) ablate the arrythmogenic tissue
5) cardioversion

159
Q

what valve is most effected in valvular disease

A

1) Mitral b/c most pressure (aortic also)

160
Q

what is the etiology of valvular disease

A

Trauma & inflammation (infection, pressure)
Ischemia of valves
degenerative changes
cognitive foramen oval never closed

161
Q

explain stenotic vs. regurgitant valve

A

Stenotic: Stiff-> narrowing -> impeded flow
Regurgitant: prolapsed leaflets -> improper closer -> regurgitation
BOTH: not enough for ventricles to pump. INCREASES work load & decreases CO
chord tendinae stretch

162
Q

treatment of valvular disease

A

Inotropes

surgery

163
Q

How does the heart help maintain cardiovascular function in hypovolemic shock

A

Increased HR & contractility

  • Medulla oblongata stimulates SNS -> increases HR (NE binds beta1)
  • NE causes increased CA2+ entry into cardiac cells from SR & ECF -> increased contractility -> increase SV
164
Q

how does the blood vessels help to maintain cardiovascular function in hypovolemic shock

A

-Vasoconstrictor in the skin & non-vital rogans via sympathetic stimulation from baroreceptors & angiotensin 2

165
Q

how does the hypothalamus maintain blood volume in hypovolemic shock

A

stimulates thefts & stimulates the neruohypohysis (posterior pituitary) to release ADH -> which causes kidneys to retain NA & H2O which decreases urine output

166
Q

how does RAAS and the liver maintain blood vol

A

liver constricts its veins & sinusoids to mobilize & blood
decreases blood flow to the kidneys causes RAAS

167
Q

what is the clinical definition of shock

A

acute failure of the circulatory system to supply the tissues & organs of body with an adequate blood supply resulting in cellular hypoxia (vitals cane normal… not a disease)

168
Q

what is the clinical definition of hypovolemic shock

A

significant decrease in blood or plasma volume such that there is inadequate filling of vascular compartment & decreased CO occurs with a loss of 20% of blood or more

169
Q

what is the etiologic of hypovolemic shock?

A 
external loss (hemorrhage, sever burns or sever dehydration vom or diarrhea) 
internal hemorrhage or 3rd space losses
170
Q

how is the stroke volume effected by hypovolemic shock?

A

as 10-25% is removed, SV fall but arterial pressure remains b/c increased peripheral pressure b/c of increased HR & VASOCON

171
Q

how is the HR effected by hypovolemic shock

A

as we lose 10-25% it increases d/t sympathetic NE

172
Q

how is the CO effected by hypovolemic shock

A

10% of blood = no effect
steady decrease after that
will be zero when you lose 35-45%

173
Q

how is BP effected by hypovolemic shockk

A

10% of blood removed without effect
10-25% can compensate by increases PR via sympathetic vasoconstriction & Increased HR
35-45% it falls to zero

174
Q

how is vessel tone effected by hypovolemic shock

A

sympathetic vasoconstriction at 10-25% by baroreceptors

175
Q

how does the the PR change by hypovolemic shock

A

increases to compensative for decreased SV causing decrease CO

176
Q

what does the sympathetic nervous system do within second of a hemorrhage

A

1) tachycardia
2) increased cardiac contractility
3) Vasoconstriction & mobilization of stored blood (350 ml in liver)
4) doesn’t effect coronary or brain until MAP <70

177
Q

what are the compensatory mechanisms to restore blood volume

A

1) absorb fluid from interstitial spaces (hydrostatic pressure decreases & h20 is drawn into vascular)
2) retention of sodium & H2O by the kidneys
3) Thirst (decreased blood volume stimulate the hypothalamic enters to stalemate thirst & ADH release)

178
Q

what are the hypovolemic manifestations

A

Beginning: Thirst & increased HR to help maintain CO
- Cool & clammy -decreased arterial pressure, decreased urine output, changes in mentation

fatal:
-metb acidosis
coagulopathy
hypothermia
circulatory failure
thready pulse & rapid rests

179
Q

what is the treatment of hypovolemic shock

A

Treat underlying cause:treat wound, O2, freq monitor, restore vascular volume via IV fluid, plasma volume expanders that stay in vascular space longer & vasoactive med if hypotension persists

B252 - Pathophysiology (21 decks)

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