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PATHO > Final✅ > Flashcards

Final✅ Flashcards

1
Q

Abscess

A

a swollen area within body tissue, containing an accumulation of pus.

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2
Q

Adhesion

A

Adhesions are bands of scar-like tissue that form between two surfaces inside the body and cause them to stick together
Common in the GI tissue

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3
Q

Angiogenesis

A

Blood vessel formation

Found in malignant tumors

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4
Q

Atherosclerosis

A

a disease of the arteries characterized by the deposition of plaques of fatty material on their inner walls.
Increase r soak of heart attack

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5
Q

Bradykinin

A

Part of inflammatory causes vasodialation and cause pain

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6
Q

C-reactive protein

A

Sign of systemic inflammation …
Normal risk 1-3
Les than 1 is low idk
Greater than 3 high

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7
Q

Calor

A

Sign of inflammation.

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8
Q

CBC

A 
# OF BLOOD CELLS, HEMOGLOBIN, CREATIN
HELO ASSES OFOR ANEMIA/ AKA Blood count   Complete blood count
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9
Q

Cellular response.

A

Cellular immediate response.. all part of inflammatory and healing process and part of that is chemotaxis, let cells know to go to site

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10
Q

Cicatricaton

A

Cell formation; scar formation during healing ex: keloids

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11
Q

Collagen

A

The building block of our healing rocks; used to make connective tissue

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12
Q

Complement

A

PArt of the humoral immediate response ……….

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13
Q

Cytokines

A

Causes fever.. all part of inflammatory process. Think of inflammation

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14
Q

Dolor - pain

A

One of the signs of inflammation

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15
Q

Emigrate

A

Healing cells move through capillary walls

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16
Q

ESR

A

A blood test that … systemic marker of inflammation ..

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17
Q

First intention

A

Aka primary healing; preferred type of healing;; nice clean Lin or cut

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18
Q

HDL

A

Good cholesterol; the higher the better over 69

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19
Q

Hernia

A

When vein s buldging

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20
Q

Histamine

A

Causes inflammation and inflammation

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21
Q

Homocysteine

A

Another markers of the stystemic inflammation. If this is high means inflammation

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22
Q

Inflammation

A

Part of the body natural immune response.

Know the signs of inflammation

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23
Q

Interferons

A

Proteins link the inflammation response/ Interferons are proteins that are part of your natural defenses. They tell your immune system that germs or cancer cells are in your body. And they trigger killer immune cells to fight those invaders. Interferons got their name because they “interfere” with viruses and keep them from multiplying

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24
Q

Keloid

A

Excess granuloma; excessive scar. Pruilish color

Common site is on ear

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25
Q

LDL

A

Bad cholesterol

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26
Q

Leukocytois

A

Increase of WBC.. infection

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27
Q

Compliance

A

The “stretch ability” of the myocardial walls. / ability of the heart to stretch; gives space for the heart to fill.

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28
Q

Elasticity

A

The ability of the myocardial wall to return to its original shape “SnapBack”; l think of a rubber band

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29
Q

Contractility

A

The force of the contraction generated by the myocardium. We need good contractility to be able to push the blood forward.

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30
Q

Pre-load

A

The maximum degree of stretch of the myocardial muscle fibers, just prior to contraction. /The amount of the heart can stretch and fill. We want an optimal amount of preload so we can have enough blood to distribute throughout the body when the heart contracts. If we dont have enough preload, wont have enough to pump out. If we have too much preload, we are going to stretch that heart past maximum and when it’ll be hard for the heart to snap. Back

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31
Q

What influences the preload?

A

Fluid volume/body position: When we have adequate fluid.. it will have good cardia output; if its low, we are not able to fill the heart. Too much volum, gonna over fill the hear and the heart cant contract efficiently. body position influence. When we stand up gravity of fluids goes to feet. Position will help..
• Ischemia: are talking about those coronary arteries that feed the heart blood… if those arteries have blockages in them and reverts adequate amount of blood to get to the heart muscle, the heart muscle cant conract efficiently..
• Hypertrophy: The thicker the heart muscle, the worst it works, give it less room to have adequate preload
• Pericardial restriction:
When the heart cant expand because something is causing not to expand; ex: inflammation of the heart tissue (pericarditis) makes it hard for the heart to expand and contract , and pericardial effusion to fusion (fluid btwn tissues) heart cant expand and contract.

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32
Q

After load

A

the resistance of the system, i.e. the amount of resistance that the heart has to overcome to pump the blood/ the higher the after load, the harder heart has to work to pump the blood out.

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33
Q

Wall stress

A

the amount of strength and stretch required of the heart to pump /We want adequate stretching and contraction to push the blood forward.

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34
Q

Mean arterial pressure (MAP)

A

the optimum pressure for assuring
continuous oxygen and nutrient supply to the body cells/ ….systolic# - diastolic#/ 3 + diastolic
That number means (if its a good MAP) that the heart has adequate pressure to allow the tissue to get adequate oxygenation and nutrients.
Normal btwn 90-05

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35
Q

Stroke volume

A

the amount of blood ejected by the ventricles (both ventricles*) with each contraction

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36
Q

Cardiac output

A

the volume of blood ejected by the left ventricle per minute. CO= SVRxHR
AKa Blood pressure (systemic vascular resistance) X Heart rate
If one of these goes down CO goes down

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37
Q

Sterling’s law

A

We need the heart to adequately stretch enough, but not too much.. to be able to snap back and contract efficiently. If we underdo, over do the contraction/ stretch we ar not going to have adequate heart function.

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38
Q

What influences our Heart?

A

The central nervous system: Sympathetic nervous system, parasympathetic system, baroreceptors, chemoreceptors.

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39
Q

Sympathetic Nervous System

A

Also known as fight or flight response; releases epinephrine and norepinephrine. When these are released, increase HR, BP and CO

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40
Q

Parasympathetic System

A

vagus nerve may decrease heart rate/ calms down; activated by vagus nerves, tells the body to lower HR, BP sometimes its a bad thing, person can pass out if HR too low

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41
Q

Chemoreceptors

A

sense changes in O2, CO2, and pH and respond
to changing heart rate and respiratory rate
/ senses changes in our oxygen, co2 and ph levels. Ex: Our body says “oxygen is too low, we need to do something!”

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42
Q

Blood vessel and volume effects

A
  • Our blood vessels help to keep the TPR (total peripheral resistance) in check / help regulate it.
  • our blood pressure and volume is regulated by hormone. Ex: epinephrine,norepinephrine, renin-angiotensin-aldosterone system, ADH
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43
Q

Total Peripheral Resistance

A

Aka blood pressure (TPR and BP are used interchangeably)
the amount of obstruction to blood flow produced by the system./
As our blood vessels are working, we want them to expand and contract as needed. If blood vessels get too thick and cant contract and relax, thats when we see abnormalities.
As we get older, the lumen gets smaller.
TPR is determined by:
-Valvular flexibility or stiffness
• Vascular resistance: impedance of arteries (health and
constriction of artery walls)
• Volume of blood

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44
Q

Vascular resistance

A

AKA Blood Pressure

the pressure of the system is inversely proportional to the diameter of the lumen, given a constant volume
• Constricted narrow arteries have a higher pressure, dilated arteries
have a lower pressure.
Meaning, the tighter the arteries, the higher the blood pressure, the bigger the arteries, the lower the pressure
-* our autonomic nervous system is going to help control that:
-Baroreceptors: ( “blood pressure to high.. let’s dilate” or “blood pressure too low, lets constrict”.
- localized myotonic response: locally the little blood vessels are able to react as well.. think about being outside and your hands are freezing because the capillary constrict.

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45
Q

Baroreceptors

A

Part of the autonomic nervous system…. a receptor sensitive to changes in pressure. /respond to increased stretch of the aorta causing vasodilation, and decreased stretch by vasoconstriction

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46
Q

Localize myogenic response

A

Part of the autonomic nervous system…local blood vessels dilate or constrict in response to increases or decreases in blood flow- Autoregulation
/ the myogenic response is the reflex response of the afferent arterioles to changes in blood pressure

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47
Q

Hormonal regulation

A

Blood pressure and volume is regulated by hormone;

-Catecholamine’s: epinephrine and norepinephrine increase
vasoconstriction

  • Renin-Angiotensin-aldosterone System when we activate it, its going to increase blood pressure. Hold on to sodium and water
  • ADH when its release, going to hold on to sodium and water which increases blood volume and bp
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48
Q

Hypertension

A

When the BP to high, we want to inhibit the Reno-angiotensin-alderstone system and ADH (anti diuretic hormone) because they hold on to more fluid; we dont want that id BP is high.
Definition: the consistent elevation of systemic elevation of arterial blood pressure above 120/80/ when bp is higher than 120/80.
Normal BP is less than 120/80
Pre-HTN: 120-139/80-89 Stage I: 140-159/90-99 Stage II: >160/100

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49
Q

Primary HTN

A

Most people who get HTN gets it for idiopathic reasons.. we dont know why. Unknown causes 90% we only know the risk factors

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50
Q

Secondary HTN

A

Is caused either by your kidneys…./ caused by another disease. Reversible if disease controlled

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51
Q

Hypertension Risk Factors

A 
Modifiable:
• Obesity 
• Smoking 
• Excess ETOH 
• High NA+ intake 
• low K+ , Ca+, Mg+ intake • Glucose intolerance
Non-modifiable :
• Family History 
• Increased age 
• African American 
• Males< 50, female >50

Modifiable: lose weight and reduce BP, smoking (take a puff every time, cause constriction of the arteries and increase bp; activates sympathetic system), ETOH (kidneys release more renin, causes vasoconstriction; blood pressure goes up), high sodium intake (salt alswy follow water,, hold on to more fluids, higher fluid volume), Glucose intolerance (increase insulin resistance, the more inflammation, the heigher the pressure, inside the blood vessels get damage evertme it goes high),

Non-modifiable: famil history, increased age( as we get older, blood vessels get tighter , blood presser goes u), african American (tends to develop in life earlier ), males earlier. In life.

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52
Q

Etiologies of HTN

A

• Age related thickening and stiffening of the arterial walls • Atherosclerosis related thickening and stiffening of the walls • Chronic over-activity of the sympathetic nervous system, leading to
loss of relaxation responsiveness overtime • Over activity of the Renin-Angiotensin-Aldosterone system (excessive alcohol intake)• Salt-Water retention by the kidneys • Hormonal inhibition of the sodium-potassium pump • Arteries damaged by insulin resistance (REMBER THE MORE INSULIN IS RELASED, THE MORE DAMAGE TO THE ARTERIES)

  • is reffed to as the “silent killer”; no signs and symptoms.
    -late symptoms: frontal headache in the A.M, dizziness, nose
    bleeds, confusion
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53
Q

HTN complications

A

Complications in the CV (cardiovascular) like atherosclerosis because every time to blood pressure goes up, damages the endothelial cells and increases plaque formation(which allows patlets to stick together) in the blood vessels and cause turbulent blood flow

  • kidneys: decreased blood flow because the pressure is so high to get blood to the kidneys and causes the glomeruli to damage; which leads to chronic kidney disease
  • hypertensive encephalopathy: this when someone has hTN for a long time and brain starts to swell, and mimics like a stroke.
  • Retinal vascular sclerosis: is when we have HTN for long periods of time and damages the vessels in eyes. And causes glaucoma. If look in a persons eye the vessels are very skinny
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54
Q

Atherosclerosis

A

damage to endothelial cells increases plaque formation, narrowing or rupture can lead to: heart attack/strokes, angina, MI (myocardial infraction/ heart attack), TIA (transient ischemic attack/mini stroke ), CVA (cerebral vascular accident/ stroke), Aortic Aneurysm , PVD (peripheral vascular disease)

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55
Q

Isolated systolic hypertension

A

Have high systolic but low diastolic.
Systolic: >140
Diastolic: <90

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56
Q

Malignant HTN

A

When someone has a rapid increase in HTN
May lead to papilledema (eye swelling), CVA, encephalopathy (brain disease), CHF (heart failure), uremia (blood in urine)
Could lead to kidney failure.

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57
Q

Orthostatic hypotension

A

Drop in blood pressure from supine to upright position with
drop in SBP at least 20 mmHg or diastolic 10 mmHg within 3
minutes of standing

Causes:
Dehydrated ; less fluid in body, give patients diuretic and get rid f too much water, hypertensive meds lower BP. , stiffed vessel when old, bed rest for long period of time and sympathetic is not activated.. , autonomic: meaning sympathetic system is not reacting the right way…/reduced blood volume, drug-induced, aging,
bedrest, autonomic nervous system dysfunction
• Tilt table test to diagnose (strap to table and flip you around to see if BP drops)
• Treatment- alleviate the cause (dehydrate them by giving fluids, meds to increase BP)

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58
Q

Varicose veins

A

Dilated or tortuous veins that typically lead to venous insufficiency / veins that are dialated.. have a lot of pressure on the veins and the valves become insufficient ; long periods of standing causes this.. nurse experience this WEAR COMRESSION SOCKS.. so the blood. Doesn’t pool
• Etiology- long periods of standing, increased intraabdominal
pressure (pregnancy), the prolonged pressure causes valves to become incompetent

S&S: distended veins, aching in lower extremities, edema
• treatment-: support hose, sclerotherapy, surgery (helps remove bulging veins)

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59
Q

Venous insufficiency

A

Chronic venous disease of the lower extremity
• Caused by incompetent valves
• Edema, venous stasis dermatitis, ulcers

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60
Q

Venous thrombosis (thrombophlebitis)

A

AKA DVT… DVT: thrombosis or clot in veins. It can be anywhere besides legs
Typically we are referring to the legs when talking about DVT. / blood clot in the deep veins
- can lead to PE (pulmonary embolism) which is blood clot in leg that travels to the lungs*

S/S: pain, swelling fever, general malaise(discomfort), elevated D-dimmer >500 (a blood test; when d-dimer is elevated, usually mean. That they MAY have a clot.)

The homans sign dorsiflexion: when someone flexes their foot, and there is pain in calf, usually signifies that they have a DVT.. dont do this anymore.

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61
Q

Risk factor for Venous thrombosis (DVT

A

venous stasis- aka bedrest
• hypercoagulable states- ex: birth control (someone on birth control, at risk for DVT), Leiden Factor V (genetic disorder that causes the blood to clot more), Cancer , pregnancy (theres a lot of blood and bleeding during delivery, increase risk for DVT),
childbirth (4 weeks after)
• Vessel wall injury- (clotting cascade happens but can lead to DVT) orthopedic surgery (INTRODUCING A FOREING DEVICE IN BODY CAN lead to DVT) , surgery, venous catheters, massive
trauma or infections

62
Q

Treatment for DVT

A 
Treatments are anticoagulants*
• Heparin
• Lovenox
Oral:
• Pradaxa
• Eliquis
• Xarelto
• Savaysa
63
Q

Hyperlipidemia

A

High fats in blood/ Elevation of the lipid profiles and lipoproteins in the blood
Primary: its genetic; may excercise and still have high cholesterol. Small portion of the population
Secondary: results from disease process and their diet ex: diabetes (when their blood sugar is high, their lipids also increase), thyroid disorders (slow down the metabolism of lipids), renal disease, ETOH, obesity, diet and medications

Exogenous lipoproteins and endogenous causes hyperlipidemia

Treatment: low fat sodium and cholesterol, *exercise, high good fat; statins medications help lower cholesterol

64
Q

Exogenous lipoproteins

A

Are the ones we ingest ex: fatty foods such as cheeses, fried food,

65
Q

Endogenous

A

The fats that are produced by the liver

66
Q

LDL

A

Bad cholesterol; this what we want low as possible
Optimal LDL is <100 mg/dl
For anyone who has diabetes or CAD we would want their LDL levels to be less than 70

67
Q

HDL

A

Are the good cholesterol.
Helps removes bad cholesterol from the body. The goal is o have high HDL and low LDL
We want HDL greater than 60 mg/dl (>60)
Low HDL is <40
We increase HDL by exercising. Eating good fats.

68
Q

Triglycerides

A

Want it to be less than 150 mg/dl

People who have diabetes or drink high amounts of alcohol, tends to have elevated triglycerides

69
Q

Atherosclerosis

A

Artery thickens because of accumulation of fatty materials, plaque
formation in main arteries • Leading cause of CAD, stroke, PAD (peripheral artery disease

Coronary arteries that lay on top of th heart…. It feeds the heart’s muscles.. this is how the heart’s muscle gets its oxygen if it develops plaque/blockages, this can lead to CAD, stroke, PAD when they’re is bloackeges

70
Q

Risk factors for atherosclerosis

A 
Non-Modifiable:
 • Increasing age 
• Gender • Family history
Modifiable:
 • Smoking 
• Obesity 
• HTN 
• HLD- especially LDL 
• DM

Males have a higher chance than females of developing atherosclerosis.
Every time you smoke increases a thrombis formation and ….
Obesity: lipids levels are high

HTN: lumens are smaller and the pressure is higher.. destroyers the arteries and leads to atherosclerosis
DM: Curvey arteries increase the risk

71
Q

Pathogenesis (development) of the disease process

A

We are born with nice smooth open arteries; about age 10-14, we develop FATTY STREAKS that form in arteries.. over times years and years the fatty streaks become a bit bigger and start to have plaque formation (atherosclerosis) these plaques become calcified (very stiff) increases chance of heart attack/stroke because giving these platelets places to hang out(FIBROUS ATHEROMA) The plaques can break off and make the the lumen of arteries uneven; platelets hang out; lead to heart attack and stroke (complicated atherosclerosis)

72
Q

Fatty streaks

A

thin yellow lines in major arteries- cholesterol and

macrophages- starts 10-14 years old

73
Q

Fibrous atheroma

A

develop from fatty streaks, clinical atherosclerosis,
accumulation of intra and extracellular lipids, smooth muscle
proliferation, scar tissue and calcification

74
Q

Complicated atherosclerosis

A

fibrous plaque breaks open, producing

hemorrhage, ulceration and scar tissue deposits

75
Q

Clinical manifestations of atherosclerosis

A
  • Usually no symptoms until significant lesion/narrowing
  • Depends on Vessel involved
  • Heart attack, stroke, TIA, angina
76
Q

Angina

A

is a type of chest pain caused by reduced blood flow to the heart.

77
Q

transient ischemic attack (TIA)

A

is a temporary period of symptoms similar to those of a stroke. A TIA usually lasts only a few minutes and doesn’t cause permanent damage. Often called a ministroke

78
Q

Acute Coronary Syndrome (ACS)

A

Is one of the things we worry about when someone has arteriosclerosis; Its someone who has potential symptoms of MI/heart attack;
It include all types of ischemic heart attack: unstable angina, non-ST-elevation myocardial infarction (NSTEMI), STEMI

S/S: chest pain, pressure, crushing, left arm, neck
and jaw pain

Diagnosis: ekg, symptoms, history and *biomarkers(elevated troponin)
• Treatment: oxygen, ASA (going to give them aspirin; they are going to chew it so it can get to the body quicker; and stop the platelets from getting together), nitrates (dialates the arteries), antiplatelet (ASA, clopidogrel), AC,
BB(beta blockers), ACE inhibitors, PCI (putting a stent in), CABG (coronary artery bypass graphing)
• Concerns: death, arrhythmia’s, shock, heart failure, pericarditis

79
Q

NSTEMI

A

is caused by a block in a minor artery or a partial obstruction in a major artery.

80
Q

STEMI

A

STEMI occurs when a ruptured plaque blocks a major artery completely.

81
Q

Biomarkers

A

A blood test; when there is damage to the heart tissue, it release troponin, and when the troponin is elevated, a long with other symptoms, the person is most likely having MI/heart attack.
-elevated 3 hours after onset of MI….Can stay elevated for 7-10 days,

Unstable angina-persistent and progressive course, occurs at rest,
lasts more than 20 mins

  • NSTEMI: no ST changes, but biomarkers are elevated
  • STEMI: ST elevated and elevated biomarkers.
82
Q

Chronic Stable Angina

A

We know what is going to cause it. Ex: excerise

Chronic paroxysmal chest pain/pressure associate with cardiac
ischemia from ASHD ( Atherosclerotic heart disease).

Pt experiences symptoms when excess demand on the heart- cold
exposure, physical exertion, stress, relieved typically with rest of
nitroglycerin
Changing in intensity, duration or exacerbation, or at rest should be
evaluated
• Treatment- BB, CA+ blockers, Ranexa, Nitroglycerin

83
Q

Variant angina

A

Aka vasospastic angina;
When the arteries SPASM; and cause acute coronary syndrome. The spasm occuldes the blood long enough and hopefully the spasm can release before it cause significantly heart damage.
Occurs at rest; it can lead to sudden death due to arrhythmias.

84
Q

What is the difference between chronic stable angina and unstable angina?

A

Stable angina is when you get angina symptoms during moderate physical activity or when you are pushing yourself physically. These symptoms go away with rest and/or medication. Unstable angina is when you get angina symptoms while doing very little or resting.

85
Q

Myocardial and valvular disorders

A

The most common valves (aortic and mitral) have issues.
When you have valvular disorders, you can have ENDOCARDITIS
Infective endocarditis

86
Q

Ineffective Endocarditis

A

Means that there is an infection on the valve. The problem is this: that bacteria starts to destroy the valve; if not healed quick enough, may lead to insufficiency of the valve (regurgitation/ the valves doesnt close all the way) then theres black flow of the heart;now the blood has to pump harder and harder because nothing is there to prevent the backflow.
-another thing we need to worry about with endocarditis, the bacteria on the valve may cause the immune response to clean it and cause inflammation, which leads to blood clots. The blood clots are sitting on the valve; blood clot can travel to the brain and cause a stroke.
This can happen on any valve but aortic valve and mitral valves are common.

Can happen in IV drug abusers ( they are introducing dirty needle into bloodstream and land right in the heart), tooth abscess ( strep;)

Systemic infection- fever, rigors, murmur, sob and can cause emboli
• Diagnosis: blood culture, echo, TEE (put a camera down a tube and send it down the esophagus and do a echo gram through the esophagus), IV abx (antibiotic), valve replacement

87
Q

Rheumatic Heart disease

A

Is another way to cause damage to the valve
it happens because of a not well treated of a hemolytic strep.
Rheumatic heart: patients valves became stenotic or regurgitated

/an immune-mediated, multi system inflammatory
disease, occurs a few weeks after Group a beta- hemolytic strep
pharyngitis in children and young adults

Destroys the valves
• Uncommon in developed countries (USA)
• Caused due to chronic under treated infection

88
Q

Stenosis

A

The valve doesn’t open fully.

89
Q

Regurgitation

A

A backflow of blood caused by failure of the valve to close tightly.

90
Q

Mitral stenosis

A

incomplete opening of the valve, most commonly
result of rheumatic fever, congenital defect or calcification in elderly
The heart s working harder to get the blood flow through the stiff valves.
S/s: depend on severity of the valve: increased left atrial
pressures, sob, decreased exercise tolerance, orthopnea,
palpitations, chest pain and fatigue, atrial tachycardia

91
Q

Mitral insufficiency/regurgitation

A

“leaky valve”- due to RH (rheumatic fever), ruptured chordae from MI, endocarditis
S/s: • SOB, edema, fatigue, exercise intolerance

92
Q

Aortic Valve disorders

A

AORTA IS THE LARGEST VESSLE IN THE BODY… if body not getting blood flow of the aorta.. gonna pass out. The aorta feeds the coranory arteries.. and if that doesnt happen can be fatal.
Aortic valve stenosis
Aortic valve insufficiency

93
Q

Aortic valve stenosis

A

valve does not open enough, caused by
calcification, bicuspid valve
•S/S: Murmurs, sob, heart failure, edema, exercise intolerance, angina,
syncope

94
Q

Aortic valve insufficiency

A

incompetent “leaky valve” caused by
rheumatic fever, endocarditis, Marfan, failure of prosthetic valve
S/S• Sob, edema

95
Q

Pericarditis

A

Is an inflammation of the heart; can be caused of a number of things: an infection, inflammatory proces, surgery, drugs, cancer
Sometimes people dont know they have pericarditis ……chest pain is a s/s.. it can be anything with chest pain.. use the
pain on inspiration should signifies that its pericarditis or pain while laying flat

96
Q

If a patient has chest pain how do i know its from ACS, Pericarditis or lung problems?

A

pain on inspiration that means it could be pericarditis or pain laying flat; coughing
Use a echo (sonogram of the heart) also do a ESR blood test (a systemic marker of inflammation)

97
Q

Acute pericarditis

A

signs and symptoms result from pericardial/ Acute pericarditis is inflammation of the pericardium (the flexible two-layered sac that envelops the heart) that begins suddenly, is often painful, and causes fluid and blood components such as fibrin, red blood cells, and white blood cells to enter the pericardial space.
inflammation less than 2 weeks pot infection, virus (coxsackievirus),
SLE, drugs, cancers
• Chest pain, friction rub, fever, increased pain with inspiration and
coughing
• Diagnosis- echo
• Treatment- depends on cause, nsaids (decrease inflammation like ibroprophen, Motrin ect ), steroids (also decreases inflammation), for recurrent - colchicine

98
Q

Pericardial effusion

A

When there is fluid in the heart muscle.. the problem with this..if its big enough put pressure on the heart muscles and the heart wont be able to contract… infection, trauma, cancer can cause it/ Accumulation of fluid in the pericardial cavity, usually inflammatory or
infectious, could be caused by CA (cancer and carcinoma), cardiac surgery or trauma

May cause no symptoms, or chest pain, sob, if large can cause low blood pressure
• Treatment- diuretics (water pills to get rid of the excess fluid), NSAIDs, steroids, colchicine, pericardial window (cutting a slit through the heart muscle and put a drain in and it drains out the fluid)

If the heart gets to big, it turns into cardiac tamponade (worsening effusion, causes pressure on heart, it can not fill.

Decreased BP, tachycardia, pulsus paradoxis- decrease in SBP> 10
mmHg with inspiration- pericardial window

99
Q

Cardiac tamponade

A

Worsening pericardial effusion; a large effusion that is compressing the heart; its not allowing the heart to expand and contract. The CO decrease, BP decrease.
Lower BP with tachycardia. This is an emergency, heart will fail

100
Q

Hypertrophic Cardiomyopathy (HOCM)

A

Is when the septum (middle muscle of the heart) becomes thicker. It put people at risk for developing impaired filling arrhythmias (one of the most common types of cardiomyopathy)
Causes of sudden death in young athletes
• Autosomal dominant disorder
• Chest pain, sob, syncope
• Diagnosis- echo cardiac MRI, loop recorder (like a EKG carry around and monitor), DNA testing
• Treatment- BB (beta blocker), defibrillator

101
Q

Congestive heart failure

A

The heart is not pumping adequately and the person becomes fluid volume overload.
What causes heart failure?: MI/ heart attack, CAD, myocarditis (inflammation of the heart), VHD (valvular heart disease), congenital defects, pulmonary disorder (COPD)
Pleural effusions are commonly seen in patients with congestive heart failure.

Risk factors: ASHD (arteriosclerosis heart disease), DM, HTN, increased age, smoking, ETOH

102
Q

Heart failure

A

Is when the heart is not pumping adequately. A person can have heart failure without havin congestive heart failure.

103
Q

CHF on right side

A

Have to do more testing; cant walk up to someone and tell them “oh you’re right sided heart failure”

Right sided: 
Peripheral edema 
• Ascites 
• JVD 
• Weight gain 
• Decreased urine output
 • Fatigue 
• tachycardia
104
Q

CHF on left side

A
  • Pulmonary edema
  • Shortness of breath
  • Pink frothy sputum
  • Rales
  • Orthopnea
  • Weight gain
  • fatigue
105
Q

Shock

A 
The heart not being able to pump blood throughout the body for it to get nutrients./ Failure of the circulatory system to deliver and adequate supply of
nutrients and oxygen to the body tissues 
There are different types of shock They are named what the cause is
VASODIALATION HAPPENS (BP drops)

S/S: shock typically looks the same, low BP and insufficient blood supply. We need to find out what’s causing the shock so we can fix it.
Early signs: bP goes down, tachycardia (to try to increase CO), fatigue, anxiety,tremors, as the shock progresses (DECOMPENSATED), we lose blood supply to certain areas (LIKE IN THE BRAIN) change of level of consciousness, respiratory acidosis, cant peruse the kidneys that decrease urine output, ischemic gut,

106
Q

Cardiogenic shock

A 
decrease Cardiac output and evidence of tissue
hypoxia in the presence of adequate intravascular volume- caused by
Heart failure (most often MI). 70% mortality / \
There is a failure of the heart to function properly; significant damage to the heart common cause is a MI.. heart muscles are weak and vent pump the blood out.. CFH cardiac output decreases.. the only way to fix this is. To improve the cardiac output. This is a high mortality// Cardiogenic shock is a life-threatening condition in which your heart suddenly can't pump enough blood to meet your body's needs. The condition is most often caused by a severe heart attack, but not everyone who has a heart attack has cardiogenic shock
107
Q

Hypovolemic shock

A

caused by loss of blood volume, either by
hemorrhage, dehydration or fluid shifts (third spacing) /
Low-volume; can be because of hemorrhaging cause low volume ; it can mean that they loss volume ; ex:: someone who s very sick and do. A fluid shift causes lose of volume decreases blood pressure ..universal blood is o- .. GIVE NORMAL SALINE / ISOTONIC…

108
Q

Neurogenic or Vasogenic shock

A

Think of vaso for vasodialation; massive vasodilation resulting from parasympathetic overstimulation or sympathetic under stimulation/

Means that the body is not constriction the blood vessels ..this means the systemic is not …….
Vasoconstriction med are given
What happens to BP, when blood vessels vasodialates, … the bP goes down. This can happens when thee parasympathetic system is over reacting or thee sympathetic system is not reacting enough. We

109
Q

Anaphylactic shock

A

massive vasodilation and peripheral pool
resulting from histamine release in allergic reactions /

when someone is exposed to an allergin and cause a systemic allergic reaction. The release of histamine and bradykin that causes massive vasodialatio; their blood pressure drops.
Use epinephrine to constrict these blood vessels

110
Q

Septic shock

A

massive vasodilation and increased permeability of
vessels with fluid volume shifts (third spacing) secondary to
inflammatory vascular response
/ massive vasodialation.. part of of the immune response.. give them fluid and cure the infection.

111
Q

Compensated stage (early stages of shock)

A

S&S: early, compensated stage. Compensatory mechanisms maintain
cardiac output and cellular oxygenation
• Pallor, restlessness, mild tachycardia, tachypnea, dry mouth,
sweaty palms, anxiety, may have slight hypotension and
normotensive

112
Q

DECOMPENSATED (progressive stage of shock)

A

• Cardiovascular: if heart does not get enough ) O2, ischemia causes
decreasing O2, revert to anaerobic metabolism causing respiratory acidosis
buildup of lactic acid. This causes decrease in output, making situation work. Reduced brain function causes blood vessels to dilate and BP drops, HR rises
• Brain: decreased O2 poor brain function LOC decreases
• Pulmonary: poor Cardiac output results in pulmonary edema,
Renal: reduced cardiac output causes poor glomerular filtration,
oliguria or anuria, prolonged ischemia can cause permanent renal
damage
• GI: decreased circulation causes decreased or absent peristalsis
(paralytic ileus). Abdominal distention, vomiting may result.
Prolonged ischemia to the bowel may cause permanent damage
• Skin: becomes cold, clammy, and mottled. Extremities may develop
necrotic spots if ischemia is prolonged, weak or absent peripheral
pulses
• Blood: may develop DIC (disseminated intravascular coagulopathy)the clotting factors start to leave the blood/ Fibrin and clotting factors settle out of the blood, cause micro emboli (outsides of the blood and the person starts to bleed)
Circulating blood lacks clotting factors, increasing risk of bleeding.
Often an end stage complication/ too late… survival rate is very low.

113
Q

Vasculitis

A

An inflammation of the vasculature/ blood vessels. It can occur anywhere but
The most common is in the temporal arteries. Aka Giant Cell (Temporal) Arteritis

114
Q

Giant cell (temporal) Arteritis

A

A type of vasculitis (inflammation in the temporal arteries/ blood vessels)
• Presents with Headache and tenderness over superficial temporal
artery
• Treatment with steroids
• If it gets too bad and get to the ophthalmic artery, can lead to blindness
Cure it be decreasing inflammation; steroids

115
Q

Arterial disease of extremities

A
  • Peripheral Artery disease (PAD)
  • thromboangiitis obliterans (buerger disease )
  • raynaud’s phenomenon
116
Q

Peripheral Artery disease (PAD)

A
  • an arterial disease in the extremities; atherosclerosis in the legs..
    obstruction of large arteries that supply peripheral structures
    • Often found in lower extremities
    • Results from atherosclerosis, inflammation, embolism
    • Risk factors (same as atherosclerosis): DM, smoking, CAD, obesity, if you have atherosclerosis in heart, high risk of having it in legs and vice versa.
    • Manifestations- claudication (pain in legs while walking; cramping in legs) , cool extremities, angina in legs, weak pulses, smaller
    muscles, sparse hair (barley hair on lower extremities)
    • Treatment- walking, treat risk factors, antiplatelet (ASA, clopidogrel)
    peripheral vasodilators (cilostazol), PCI, surgery, put a stent in leg
117
Q

Thromboangiitis Obliterans (Buerger disease)

A

An arterial disease in the extremities; This. Is not that common; We have inflammation in hands and feet; heavy smokers (ages <35); have periods of inflammation, pain, intermittent claudication in arch of the foot and digits, redness, cool extremities.
Increased sensitivity to cold
• Stop smoking, no nicotine, vasodilation
we want to decrease vasoconstriction by avoiding nicotine and medication that help dilate those lil arteries in hands and feet.

118
Q

Raynaud’s phenomenon

A

An arterial disease of the extremities. More common in females than it is in males; common overall. Intense vasospasms of arteries and arterioles in the hands (less often
feet)
• Usually healthy young women, exposure to cold or strong emotions
causes vasoconstriction in the fingers
• Manifested- pale skin to cyanosis, sensation of cold, then period of
hyperemia- throbbing, redness and paresthias
• Treatment- avoid smoking, cold (wear gloves because its cold), stress, avoid vasoconstrictors (cold medications),
occasionally vasodilators/

Person has an intolerance to cold; when they are cold, can be 65 degrees, not necessarily 25degrees, they get constriction of their blood vessels, particarlly their hands and feet, and start to see discoloration; you see hands strat to become white (cyanotic); when they finally get those hands warm, those are termites will dialate and get hyperemia (rush of blood to capillaries).

119
Q

Aortic Aneurysm/Dissection

A

Aneurysm can occur in any artery. Aneurysm is an out pocketing of the blood pressure. There are different types. /weakened area in the wall of a blood vessel resulting in an abnormal widening or ballooning greater than 50% of the vessel’s normal diameter (width). An aneurysm may occur in any blood vessel, but is most often seen in an artery rather than a vein./
• Aneurysm is a false outpouching or sack-like dilation of the wall of a
blood vessels
• True aneurysm is bound by complete vessel wall, false aneurysm has
a localized dissection or tear- only bound by outer layers of vessels

120
Q

What is the difference btwn TRUE and FALSE Aneurysm.

A

A pseudoaneurysm, or false aneurysm of the vessels, occurs when a blood vessel wall is injured and the leaking blood collects in the surrounding tissue. It is sometimes called a false aneurysm. In a true aneurysm, the artery or vessel weakens and bulges, sometimes forming a blood-filled sac.
look at pic

121
Q

Abdominal Aortic Aneurysm

A

AKA AAA; most common- usually develop after 50, are associated with severe atherosclerosis, occur more frequently in men, HTN, and smokers
• Usually asymptomatic, >4cm can be palpable, >5 cm undergo repair
- Don’t do anything until it reaches 5cm.

122
Q

Thoracic Aneurysm

A

Not as common; usually due to Marfan syndrome.

123
Q

Aortic Dissection (aneurysm)

A

There is different types
-Type A
-The B
S/S: usually hear a snap or ripping pain. May start to see BP high in the beginning and then starts to decline. Need to get to hospital for a quick repair. We want the hood pressure to not be too high and not be too low.
Sometimes there is a difference in BP in arms and legs. (Normally the bP in legs and arms are close)/
abrupt excruciating pain, described as
tearing or ripping, in the beginning medium to high bp, later loss of pulse and bp in one or both arms
• This is medical emergency, stabilize BP, surgical repair

124
Q

Type A Aortic Dissection

A

VERY SERIOUS/ MOST SERIOUS AND MOST COMMON
Involves the Aorta of the body, if it ruptures GET HELP! There is a very rapid decline in healt; you need to get it fixed quickly.

125
Q

Type B Aortic Dissection

A

distal to subclavian artery and do not involve ascending aorta; Doesn’t cause many problems, but need to watch them.

126
Q

Congenital heart defects

A

Patent Ductus Arteriosus
ASD
VSD
Tetralogy of fallot

127
Q

Patent Ductus Arteriosus (PDA)

A

A congenital heart defect; this is when we are born the aorta and pulmonary artery are connected by the PDA after a couple days, its supposed to close off and its not connected anymore. However when it DOESNT CLOSE OFF, that means that there is a PDA and what happens is the oxygen rich and oxygen poor blood mix and cause failure to thrive, and cause significant issues with the baby.

128
Q

Arterial septal defect (ASD)

A

ALSO A Congenital defect; atrial septal defect, opening in atrial septum (PFO) /
The septum is the wall of the two sides of the heart.
*With ASD, there is a hole in the septum
look at pic

129
Q

Difference btwn HOCM (hypertrophic cardiomyopathy) and ASD (arterial septal defect)

A

HOCM is the THICKENING of the septum (hence hyper)

ASD there is a hole in the septum.

130
Q

Ventricular septal defect (VSD)

A

ventricular septal defect- symptoms depend on size, most asymptomatic/
There’s a whole btwn the two ventricles
Most of the time people dont know that they have it.

131
Q

Tetralogy of Fallot

A

This is a congenital disorder, where there is MULTIPLE DISORDERS within the heart. Ex: have a VSD 2.the aorta is going to shift (transposition of great arteries); it will go over the left ventricle and going to communicate inside the VSD, 3. THEN the pulmonary artery is going to have stenosis; this means that the right ventricle is going to pump harder and harder to get past that harder, which will cause right ventricular hypertrophy.

  • The person is going to have significant trouble with cardiovascular perfusion because the vessels being in the wrong spot and the hypertrophy.
  • Most children cyanosis because of this.
132
Q

Transposition of great arteries

A

The switching of vessels; aorta arise from RV, pulmonary

arteries LV

133
Q

Coarctation

A

of the aorta- narrowing in a portion-weak femoral,
popliteal and dorsalis pedal pulse, lower blood pressure in legs
/ when the aorta it’s self have blockages of it or narrowing of it;and that causes changes of the BP in upper and lower extremities.
/ A narrowing of the large blood vessel (aorta) that leads from the heart.
Coarctation of the aorta is usually present at birth (congenital), and may occur with other heart defects.

134
Q

Erythrocytes (RBC)

A

The most common blood cell.
Nonnucleated, thin and biconcave disc (larger surface area for O2
diffusion and allows O2 to diffuse rapidly in and out of cell
Function:
• Transport Oxygen to tissues (hemoglobin carries four O2 molecules) • Transport CO2 • Participates in acid-base balance
/ their job is to transport oxygen, co2, and participates in acid base balances.

135
Q

What does hemoglobin depends on?

A

Depends on the the availability of iron to make hemoglobin. If we dont have enough iron in the body, cant develop enough hemoglobin and develop an anemia chronic disease.

136
Q

What is the difference between hemoglobin and erythrocytes?

A

Hemoglobin is the protein pigment that gives blood its red color. RBC is also known as Red blood corpuscles or erythrocytes. They are the common type of blood cell in vertebrates. Their main function is to supply oxygen to all the body cells.

137
Q

Erythropoiesis

A

RBC production. ; kidneys produce erythropoietin patients that have kidney disease, can be anemic because they are not producing enough erythropoietin.
• Until age 5 all red blood cells are produced in red bone marrow then gradually declines
• By age 20 mainly takes places membranous bones of vertebrae, sternum, ribs,
and pelvis
• Governed by O2 needs (kidneys sense low O2 produce erythropoietin)
• Lifespan 4 months (120 days)

The kidneys are partially in charge of how much blood we have. If the kidneys see that we dont have enough oxygen they would say “hmmm… i need to increase more erythropoietin to increase the production of RBC”.
-When the rbc are dying off and not producing enough, we produce anemia

138
Q

ERYTHROPOIETIN

A

In order to make red blood cells, the body maintains an adequate supply of erythropoietin (EPO), a hormone that is produced by the kidney. EPO helps make red blood cells.

139
Q

Anemia

A 
Low level of RBC, Hemoglobin or both 
Can result from :
• Blood loss (bleeding)
• Destruction (hemolysis)
• Deficient RBC production due to lack of nutrients or
bone marrow failure
140
Q

Effects of anemia

A

• Pallor or skin, mucous membranes, conjunctivae, nail beds are all pale!
• Tachycardia, palpitations, experience chest pain, low BP
• In hemolytic anemia- (someone have rbc breaking down) that builds into hyperbilirubinemia (high bilirubin in the blood) which causes jaundice and gall stones… this sometimes happens with newborns because they are not getting enough fluids; and stick them in front of window to get sunlight and helps bring them back to normal until they are able to drink breast milk.
-
• Anemia R/T ineffective hematopoiesis (RBC destruction in BM)- high
levels or iron in gut, iron overload and eventual damage to endocrine
organs and heart / in other words, if somone has destruction of the RBC in the bone marrow this can cause high levels of iron; when there are high levels of iron in gut this can lead to liver and heart problems, which can be potentially deadly.

141
Q

Blood loss anemia

A

Symptoms depends on how rapidly they lose their blood
If the body is losing gradually… the body can adapt
As oppose to someon who had a accident and lose blood rapidly.. the body cant adjust and go into shock.
The slower the loss.. the less dramatic the symptoms will
**Where do we lose blood overtime?: heavy mensturals, and GI systems
• Depends on rate of blood loss (rapid – shock), slower symptoms
progressive
• Can lead to iron deficiency- slowing reproduction of RBC
• Chronic blood loss (GI, menstruation leads to iron- deficiency anemia)

142
Q

Hemolytic anemia

A
  • Pre-mature destruction of RBC/ RBC break down, retention of Iron (if destroyed to early, Thant means we are losing more rbc than we produce)
  • Fatigue, dyspnea .. remember anemia have low blood cells, sob, low o2, dysapnea, sometimes chest pain.
  • Examples: sickle cell, Thalassemia’s
143
Q

Iron Deficiency Anemia

A

We need iron to make hemoglobin
If we not taking enough iron we are not going to make sufficient amount of hemoglobin. (This can happen to people who are vegan or vegetarian.)
Iron defincieny anemia:
Results form dietary deficiency, loss of iron through bleeding or
increased demand
• Leads to decreased hemoglobin synthesis and impaired O2 delivery
• Usual reason is chronic blood loss- GI, ulcers, polyps, cancer,
pregnancy
• S/S: Fatigue, dyspnea, tachycardia, pallor, brittle hair and nails, smooth
tongue, sores in corners of mouth, pica

144
Q

Megoblastic Anemia

A

Caused by vitamin B deficiency & folic acid deficiency.
- seen in vegans, people with gastric bypasses (not absorbing b12) may be prescribed B12
- b12 is found in all foods of animal origin
Vit B12 found in all foods of animal origin ( found in strict
vegetarians)
• Gastrectomy, ileal resection
-Rember defincieny in B12 causes spina bifilda in new borns.
• S/SFatigue, glossitis (sore tongue)
Folic acid deficiency:
• Green leafy veggies, fruit cereal and meats
• Caused by dietary deficiency and ETOH

145
Q

Aplastic Anemia

A

Reduction in everything! Reduction in RBC, WBC, PLT (platelets)/ Disorder of pluripotenial bone marrow results in reduction of RBC,
WBC, PLT

Sudden onset- weakness, fatigue, pallor, petechiae (lil red dots that occur), ecchymosis,
bleeding from nose, gum, vagina, susceptible to infection due to
decreased neutrophils (becoming immunocompromise)

Causes: people who are exposure to high doses of radiation (ex: people who have cancer and are undergoing chemotherapy), chemicals, chemo, AIDS,
viral hepatitis, mono

Treatment- stem cell replacement, RBC transfusions

146
Q

What type of chronic diseases lead to anemia?

A

• AIDS
• Osteomyelitis (infection of the bones)
• Cancers
• Autoimmune disorders (RA, IBS, SLE)
• Chronic Kidney disease (erythropoietin deficiency); If damaged not going to produce an amount of erythropoietin
• Treatment: treat underlying disease, epoetin, iron therapy (iron transfusions),
blood transfusions

147
Q

Polycythemia

A

The opposite of anemia….High levels of hematocrit (more than 50%); this happens during dehydration; which increases the concentration of blood products.
There are two different types :
Relative polycythemia: because someon is dehydrate; which causes higher concentration of blood products
Absolute polycythemia: more common; due to an increase to an increase to RBC; THIS ALSO HAS TWO TYPES

148
Q

Relative polycythemia

A

Dehydration, which causes a high level concentration of blood products.

149
Q

Absolute polycythemia

A

Increase RBC mass

There are two types:

-*PRIMARY- when someone has an increased RBC, WBC, PLT this typically occurs in someone who is over the age of 62.
They would have an enlarged spleen, HTN, PAIN AND ITCHNESS IN HANDS TOES, NIGHT SWEATS & WEIGHT LOSS (hyper metabolism), AND WE ARE WORRIED ABOUT BLOOD CLOTS because of the increased amounts of RBC, increase chance of thromboembolism

Treatment- phlebotomy (they often come in to take blood off; take blood away), ASA (give aspirin; known as an antiplatlet; prevent blood clots from sticking together)

*>SECONDARY: is a compensatory response; its related to someone who has low oxygen levels (ex: people who lives in high altitudes like Colorado; body will increase hemoglobin and hematocrit so they can have more oxygen to live in high altitudes that have less oxygen in atmosphere…also people with COPD have lower oxygen levels they may have increase in blood count)….////

Secondary- physiologic increase in erythropoietin
usually as a compensatory response
• High altitudes, COPD, Heart disease, smoking • Treatment- relieve hypoxia- by giving O2, treat pulmonary HTN

150
Q

how does respiratory disorders affect the heart

A

When oxygen is inhaled, it travels through the lungs and into the bloodstream. The blood then travels to the heart where it is pumped to the rest of the body. If your blood isn’t receiving enough oxygen from your lungs, the heart has to work harder to pump enough oxygen throughout the body

PATHO (5 decks)

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