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Patho > Test three > Flashcards

Test three Flashcards

1
Q

hemodynamic hallmark of htn

A

persistently increased SVR

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2
Q

risks of htn

A

age
alc/tobacco
diet (sodium)
obesity
low socio-econ status
stress
men under 55; women over 64
black
sedentary
DM
high serum lipids
contraceptives

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3
Q

examples of 2ndary htn

A

coarctation of aorta
renal artery stenosis
Cushing
cirrhosis
neuro disorders, like brain injury
sleep apnea
pregnancy

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4
Q

clinical manifestation of htn

A

fatigue
activity intolerance
dizziness
palpitations
angina
dyspnea

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5
Q

complications of htn

A

target organ diseases affecting heart, brain, vasculature, kidney, and eyes

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6
Q

What does atherosclerosis in subclavian artery do?

A

causes false low read on side where narrowing occurs

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7
Q

Things to remember when taking BP

A

-feet on floor, sitting up
-take 2 readings on arm with highest BP, 1 min apart
-document if using forearm
-use proper cuff size

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8
Q

Nurse teaching ab htn care

A

Take BP at home! –> teach them how to and what is normal
-take it first thing in the morning and then at night b4 bed

Stress adherence to meds and decreasing risk factors

Beware of high-sodium antacids, appetite suppressants, and cold/sinus drugs

Avoid hot baths, lots of alc, and strenuous exercise w/in 3 hrs of taking vasodilation drugs

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9
Q

Drugs for htn

A

Adrenergic inhbiting agents - decrease SNS by working on peripherally and on vasomotor cento to inhibit NE release or block adrenergic receptors on blood vessels

ACE inhibitors - prevent AI to AII; reduce vasoconstriction and NA+/H2O retention

A-II receptor blockers- prevent A-II from binding to blood vessel walls

CCBs - increase Na excretion and cause vasodilation by stopping Ca+ from entering cells

Direct vasodilators- relax smooth muscle and reduce SVR

Diuretics - reduce plasma volume and reduce vascular response to catecholamines

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10
Q

htn drug side effects

A

-orthostatic htn
-dry mouth
-sex problems
-frequent voiding

*careful with NSAIDs

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11
Q

htn crisis manifestations

A

hypertensive encephalopathy
-headache, nausea/vomiting, seizures, confusion, coma, eyes

renal insufficiency

Cardiac decompensation
-MI, HF, pulmonary edema, chest pain, dyspnea

Aortic dissection
-chest and back pain, reduced/absent peripheral pulse

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12
Q

Road to CAD

A

endothelial injury + inflamation –> atherosclerosis –> CAD

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13
Q

Risks for CAD

A

age
men under 75; women over 75
whites
genes
lipids
Bp > 140/90
DM
tobacco
inactivity
waist over 40 or 35
BMI over 25
Possibly glucose, psych and hcy

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14
Q

CRP

A

protein made by the liver
nonspecific marker of inflammation
increased in ppl with CAD
a/w unstable plaqes and oxidation of LDL cholesterol

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15
Q

lipid measurements risks

A

cholesterol > 200
triglycerides > 150
LDL > 100
HDL < 60

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16
Q

Developmental stages of atherosclerosis

A

Endothelial injury
-htn, tobacco, hyperlipidemia, hcy, DM, infection, toxins

Fatty streak
-lipids infiltrate smooth muscle

Fibrous plaque
-collagen covers fatty streak
-lumen is narrowed
-blood flow is reduved

Complicated lesion
-plaque rupture
-thrombus formation (platelet adhesion)
-vessel occlusion

17
Q

clinical manifestation of CAD

A

Angina - manifestation of reversible myocardial ischemia
dyspnea and orthopnea
edema
nocturea
cough

18
Q

Drugs that restrict lipoprotein production

A

Statins - block synth of cholesterol and increase LDL receptors in liver (monitor liver enzymes and creatine kinase for toxisity and rhabdomyolysis)

Niacin - decreases synthesis of VLDL and LDL
(flushing (aspirin), pruritis, GI issues, orthohypo, hcy (folic acid))

Fibric acid derivatives - decrease hepatic synth of VLDL
(increases effects of warfin and antihyperglycemic drugs –> also statin myopathy)

Omega 3 fatty acids for super high triglycerides

19
Q

Drugs that increase lipoprotein removal

A

Bile acid sequestrants - increases conversion of cholesterol to bile acids to reduce total cholesterol and LDL
(GI side effects; reduced absorption of other drugs)

injected PCSK9 inhibitors - lower LDL
(used with diet and max statin)

20
Q

Drugs that decrease cholesterol absorption

A

Ezetimibe (Zetia)
decreases absorption of dietary and biliary cholseterol
-combine with statins
-don’t use if your livers fucked up

21
Q

Antiplatelet therapy

A

low does aspirin or Clopidogrel

22
Q

Prinzmetal’s angina

A

occurs at rest in response to coronary artery spasm
happens in ppl with migrains, Raynauds, smoking, or stress
a/w cold weather

23
Q

Triggers for angina in those with chronic angina

A

physical exertion
temp extremes
stess
heavy meals
tobacco
stimulants (coke or amphetamines)

24
Q

pathophysiology of chronic angina

A

occurs when myocardial cells become hypoxic w/in 10 s of coronary occlusion

lactic acid irritates myocardial nerve fibers and transmits pain messages

25
Q

Characteristics of chronic angina pain

A

usually substernal, but can radiate
doesn’t change with position or breathing
lasts 5-15 mins
subsides when precipitating factor resolves

26
Q

Diagnostic studies for chronic angina

A

12-lead ECG

Echo –> patient lies on left side

Exercise test (no caffeine 24 hrs b4; no smoking or exercise b4; stop if chest pain, wild VS change, or ECG change)

Nuclear cardiology - IV dipyridamole to mimic exercise, then inject isotope and do imaging –> observe for SOB, dizziness, nasea

Labs - troponin, CK-MB, lipids, CRP

27
Q

Drug therapy for chronic angina

A

SA nitrates -dilate blood vessels (SL NGT can be used prophylactically)

Aspirin - inhibits cyclooxygenase to prevent clot formation

LA nitrates - reduces frequency of angina

ACE inhibitors - for those at high risk for cardiac event; can also reverse ventricular remodeling

BBs - for MI, LV dysfunction, or HTN –> decrease myocardial O2 demand

CCB - if can’t use BBs

28
Q

Coronary catheter and angiography and PCI

A

-radiation and dye to view coronary arteries
-take baseline creatinine first to monitor renal func
-premedicate with corticosteroids if allergic to dye
-hydrate if CKD
-NPO 6-12 hrs

PCI
-balloon angioplasty
-don’t do if 3 vessel CAD and/or significant left main coronary artery disease

29
Q

ACS parts

A

prolonged ischemia from decline of once stable atherosclerotic plaque

partial block = UA or NSTEMI
full block = STEMI

30
Q

UA pain vs MI pain

A

UA
-new in onset
-occurs at rest
-worsens

MI
- Severe and persistent
- doesn’t get better with nitrate or rest
-heaviness, pressure, burning, crushing, tightness
-20+ mins
-might have epigastric pain that antacids won’t help

31
Q

What to do with patient on the way to the hospital and once you get there?

A

-SL NTG and chewable aspirin
-morphine if they get to hospital w/o having these things

Start to consider coronary angiography and PCI
-ECG –> if STEMI, PCI w/in 90 mins
-thrombolytic if no cath lab (w/in 30 mins of arrival)

32
Q

PCI

A

first, cardiac catheterization to locate blockages, see collateral circulation, and evaluate LV function

Put BMS or DES into blocked artery

If bad LV function, possibly IABP and/or inotrope

**very few need CABG

33
Q

Thrombolytic Therapy

A

-for ppl with chest pain less than 12 or 24 hrs and STEMI
-GET BASELINE LABS and start 2-3 IV lines
-meds can be given in one IV bolus or over 30-90 mins
-serum cardiac biomarkers rapidly rise 3 hrs after
-start heparin bc risk of re-clotting

*Now you can move them to PCI facility
*complications = bleeding –> apply pressure or ice

34
Q

absolute contraindications to thrombolytic therapy

A

-intracranial hemorrhage ever
-known structural/vascular abnormality
-intracranial neoplasm
-stroke in past 3 months
-recent head or facial trauma
-recent intracranial or intraspinal surgery
-severe uncontrolled htn
-active bleeding
-suspected aortic dissection

35
Q

Surgery options for ACS

A

CABG
-requires sternotomy and CPB
-for left coronary artery, 3-vessel disease, DM, CKD, LV dysfunc

MIDCAB –> no sternotomy or CPB
-IMA is sutured to left anterior descending or right coronary artery

OFCAB
-sternotomy, but no CPB
-done on beating heart
-less blood loss, renal dysfunc, postop afib, and neuro issues

Transmyocardial laser revascularization
-for ppl with advanced CAD who aren’t candidates for traditional CABG
-laser makes channels in heart to let blood flow to ischemic areas

36
Q

Drug therapy after an MI

A

IV nitroglycerin
aspirin
BBs
anticoagulants (LMWH or UH)

glycoprotein IIb/IIIa inhibitors if PCI anticipated

ACE-i sometimes; CCBs if issues w/ BBs

37
Q

Nursing interventions for ACS

A
  1. Pain assessment using PQRST
  2. position patient upright and give O2 NO MATTER WHAT
  3. Establish IV line
  4. give NG, MORPHINE, and O2 for chest pein
  5. maintain ECG monitoring (PVC and Vfib after MI are common)
  6. assess vitals frequently along with I and O

**look for heart failure: dyspnea, tachycardia, pulmonary congestion, distended neck veins

38
Q

Phases of ACS recovery

A
  1. hospitalization
    -msy or may not be able to ambulate –> depends on severity
    -start with sitting up, ROM, self care, then work on walking
    -focus on pain, anxiety, dysrhythmias
  2. Early recovery
    -2-12 weeks in outpatient place
    -increase activity
    -teach ab risk factor reduction
  3. Late recovery
    - physical activity program
    -therapeutic lifestyle changes
    -some med supervision

Patho (44 decks)

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