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Patho key terms 1-3 > Cardiac day 1 > Flashcards

Cardiac day 1 Flashcards

1
Q

what are the three arterial layers?

A

Tunica adventitia, tunica media, and tunica intima

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2
Q

what is the tunica adventitia

A

Connective tissue

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3
Q

what is the tunica media?

A

smooth muscle

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4
Q

what is the tunica intima

A

interior linning of artery:
- basement membrane
- Endothelial cell

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5
Q

substances of the arterial wall

A

-Nitric oxide
-endothelin
-VEGF
-thromboxane A2
-prostacyclin
von williebrand factor

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6
Q

Nitric oxide

A

stimulates vasodilation

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7
Q

endothelin

A

stimulates vessel vasoconstriction

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8
Q

VEGF

A

-Vascular endothelial growth factor: stimulates growth of new blood vessels

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9
Q

Thromboxane A2

A

activates clotting

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10
Q

prostacyclin

A

inhibits clottting

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11
Q

Von williebrand factor

A

activates clotting

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12
Q

what is systole

A

the period during which the ventricles are contracting

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13
Q

What is diastole?

A

The period during which the ventricles relax and fill with blood.

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14
Q

What is the cardiac output equation?

A

CO= SV x HR

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15
Q

Cardiac output

A

Amount of blood pumped per minute

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16
Q

SV

A

amount of blood pumped from the ventricle in one contraction

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17
Q

Heart rate

A

is the frequency of blood ejection from the heart

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18
Q

Blood pressure

A

reflection of cardiac cycles (BP=CO x PVR)

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19
Q

Systolic blood pressure(SBP)

A

THE maximum pressure in arteries from the left ventricular contraction

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20
Q

Diastolic blood pressure

A

minimum from heart relaxation

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21
Q

what 4 types of mechanisms regulate BP

A

neural, humoral mechanisms, natriuresis, and acting on nephron

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22
Q

two types of Neural mechanism (short term)

A

Intrinsic and extrinsic

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23
Q

What is involved in Intrinsic neural mechanism (short term)

A

Baroreceptors and chemo receptors
- They influence HR and strength of cardiac contraction

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24
Q

what is involved in extrinsic neural mechanisms?

A

outside circulation through neural pathways like hypothalamus

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25
Q

Humoral mechanism

A
  • Rennin angiotensin
  • vasopressin
    -epinephrine and norepinephrine
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26
Q

Where in the kidneys is Renin released from?

A

Juxtaglomerular cells

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27
Q

Where is ACE derived from?

A

Lungs

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28
Q

The RAAS system stimulates the release of:

A

Aldosterone

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29
Q

what does Aldosterone stimulate and what are its affects.

A
  • Vasoconstriction which Increase blood pressure
  • sodium increases in the kidneys which water follows and increase stroke volume resulting in an increase in blood pressure.
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30
Q

what PRODUCES ADH?

A

Hypothalamus

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31
Q

What SECRETES ADH into the blood stream? what occurs? what happens to urine?

A

posterior pituitary
- kidneys reabsorb water and increase BP through increasing volume
-Urine becomes concentrated.

32
Q

what is natriuresis prompted by? and what does it release?

A

-Atrial natriuretic peptide (ANP)
- B-type natriuretic peptide (BNP)

33
Q

What mechanism responds to stretch within the ventricles? why?

A

BNP
- will respond if to much volume or to little.

34
Q

What does BNP control?

A

BNP controls renin levels and can increase or decrease RAAS ( Works as a inverse relationship)
-help regulate BP long term

35
Q

What occurs to nephrons during dieresis?

A

Increase urine output

36
Q

What occurs to nephrons during natriureses?

A

increase sodium and water excretion

37
Q

What is stage 2 hypertension?

A

BP ≥ 140/ 90

38
Q

what is stage 1 Hypertension

A

BP 130-139/80-89

39
Q

Normal BP

A

BP<120/80

40
Q

Elevated BP

A

120-129/<80

41
Q

Hyper tension (epi, CM, COMPLICATIONS)

A

-epi: age, gender, race, family history, smoking, inactivity, genetics, obesity
CM: asymptomatic
Complications:
-Heart: MI, ANGINA, HF
-Brain: stroke, ischemic attack
-peripheral artery disease
- chronic kidney disease

42
Q

Orthostatic HTN ( etiology, patho)

A
  • etiology:
  • going from lying down to standing or sitting to standing
  • hypovolemia
    -bed rest
    medications
    Patho: When postural change occurs the body is unable to pump blood back to the body. (typically temporary)
  • BARORECEPTORS will notice decrease pressure in BV and increase HR to stabilize BP
43
Q

Key points of the venous system?

A
  • one way valves in large veins
    -limited contractility (skeletal muscle pump)
    -decreased driving pressure
  • thin walled vessel
44
Q

What moves blood in the veins?

A

Skeletal muscle
(when you walk the calf contracts and brings blood back up)

45
Q

The nurse is interviewing a client diagnosed with venous insufficiency. Which of the following statements by the client is consistent with this diagnosis?

A. “My feet are always cold and I can’t seem to keep them warm.”

B. “My legs and ankles have been really swollen lately.”

C. “I get pain in my legs whenever I walk a lot.”

D. “I’ve got this fungal infection on my toenail that won’t go away.”

A

B my legs and ankles have been really swollen lately .

46
Q

Chronic venous insufficiency (patho & epi)

A

Patho: inadequate venous return over. long period of time. causes venous hypertension, circulatory stasis, hypoxia
epi: varicose veins or valvular incompetence

47
Q

Chronic venous insufficiency CM

A

-EDEMA
-brown pigmentation caused by hemosiderin deposits from breakdown of rbcs
-venous ulcers: medially over ankle and lower leg can crack open and ooze out.

48
Q

Thrombophlebitis

A

Blood clot with vessel inflammation

49
Q

Thromboembolus

A

traveling blood clot

50
Q

Venous thrombosis / deep vein thrombosis (DVT)

A

Blood clot in the vein generally in the legs due to poor circulation of the blood.
CM; tenderness, warmth, and edema
-Ultrasound used for diagnosis

51
Q

Triad of Virchow

A

venous stasis
-venous wall injury hypercoagulability

52
Q

Varicose Veins

A

dilated, tortuous superficial veins due to prolonged standing or venous pressure

  • eti- blood pooled in veins can be caused from dmg to valves or action of gravity.
    epi- prolonged standing, pregnancy, incompetent valves, intraabdomianl pressure
53
Q

Peripheral artery disease (PAD)

A

patho- decreased flow to peripheral arteries
- lower extremities most affected PAIN
-develops slowly
Etiology- ATHEROSCLEROSIS most common cause
EPI- smoking, >60 yrs, obesity, HTN
CM: Intermittent claudication
Diagnosis: pulse check, cap refill, ABI less than one, ultrasound

54
Q

The MOST common cause of peripheral arterial disease is?

A

atherclerosis

55
Q

True or False: Peripheral arterial disease leads to a decrease in rich oxygenated blood being delivered to the lower extremities, which leads to ischemia and necrosis of skin tissue.

A

true

56
Q

You’re assessing a patient’s health history for peripheral vascular disease. What signs and symptoms reported by the patient would indicate the patient may be experiencing peripheral arterial disease? Select all that apply:

A. “I often wake up at night with leg pain and have to dangle my leg out of the bed to ease the pain.”

B. “If I stand or sit too long my legs start to feel heavy and achy.”

C. “It hurts to elevate my legs.”

D. “Sometimes when I’m walking my legs start to cramp and tingle to the point where I can’t walk until the pain goes away.”

A

A,C,D

57
Q

PAD CM (THINK 5 P)

A

Perfusion reduction
- decreases pulses
Pain
-intermittent claudication
pallor
Paraesthesia
Palpable cool leg

ischemia in lower leg and hypoxia in cellular level

58
Q

Aneurysm

A

PATHO: Damage to the arterial lining usually r/t athersclosis. This weakens the wall and causes a localized bulging or dilation
ETI: Damage to the arterial lining usually r/t athersclosis , genetic or vascular disease/trauma
EPI: often found in men incidental
- most common aneurysm is Abdominal aortic (AAA)

59
Q

AAA CEREBRAL & Thoracic

A

AAA
-pain abdominal, back, flank pain GI disturbances: pulsatile masses
Cerebral: often silent, HA, Vision changes, seizures
Thoracic: chest pain, back pain, SOB, trouble swallowing

60
Q

aneurysms do what to blood flow

A
  • Turbulent blood flow and are susceptive to rupture
  • leads to hemorrhages
    Thrombus formation
    Dissection: collapse of vessel wall
61
Q

Bruit

A

turbulent blood flow often produces a whooshing sound
hear whoosing in carotid artery
ex. carotid stenosis caused by atherosclerosis plaque

62
Q

Raymounds syndrome

A
  • exaggerated reflex sympathetic stimulus causes vasoconstriction
  • increase platelet activation and aggregation
    -endothelial dysfunction, deficient NO and high levels of endothelien, angiotenin 1 all vasoconstrictors

-manifests as blanching of the the skin and numbness and coolness of the skin

63
Q

Dyslipidema

A
  • imbalance of lipid components
    • triglycerides, phospholipids, cholesterol
      LDL and HDL
64
Q

Atherosclerosis

A

deposit of fat into arteries

ETI- endothelial changes of increasing oxidizing free radicals

EPI- common in men, age 40 or more, smoking, obesity, hyperglycemia, hypercholesterolemia

65
Q

Arteriosclerosis

A

Hardening/thickening of arterial walls.

66
Q

Atherosclerosis Complications

A

When endothelium is injured blood flow is turbulent
-blood flow changes creating small areas of stagnant blood.

stagnant blood predisposes thrombus
- PAD
-STROKE
-RENAL ARTERY STENOSIS
-THROMI OR EMBOLOUS

67
Q

Angina

A

Chest pain
-pain in other ares from myocardial ischemia

68
Q

Heart attack

A

Ischemic heart attack
ACS (acute coronary syndrome)
-UNSTABLE ANGINA
-STEMI
-NSTEMI
Type 2 MI

69
Q

Unstable angina

A

Clinical and ECG findings without an elevated troponin marker level

70
Q

NSTEMI

A

Troponin elevation but no ST elevation

71
Q

STEMI

A

TROPONIN AND ST elevation

72
Q

ACS Metabolic Syndrome increase risk for CAD with:

A

At least three or more of the following
-high BG levels
-high BP
Increase circumference waist
-lod hdl
-high triglycerides

73
Q

ACS

A

cardiac muscle has ischemia= lack of sufficient muscle

CM: angina, chest pain crushing the left side radiating to the left arm
-pain radiating to jaw back neck arm
dyspnea
clenched fist on chest

74
Q

Chronic ischemic heart disease

A

fixed coronary obstruction that produces a difference between blood flow and metabolic demands
typically provided by exertion or emotional stress.
Relieved by medications or rest.

75
Q

Cardiac tests

A

-ecg
Cardiac catherization
stress test
ct
mri
TROPONIN
-rise within 3 hours of MI onset
elevated 7-10 days

Patho key terms 1-3 (8 decks)

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