Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
168 Cards in this Set
- Front
- Back
|
Define atherosclerosis
|
fatty fibrous lesions in intimal layer of medium to large arteries; insidious process (20-40 yrs)
|
|
|
Modifiable risks for atherosclerosis
|
hyperlipidemia, HTN, smoking, DM, homocysteins, lipoproteins, CRP
|
|
|
Nonmodifiable risks for atherosclerosis
|
Age, gender (male), family Hx
|
|
|
What is C-reactive protein?
|
serum marker for systemic inflammation
|
|
|
Why is CRP not indicative of only atherosclerosis?
|
any other factor causing inflammation throughout the body can raise levels of CRP
|
|
|
An increase in lipoproteins causes formation of what?
|
foam cells
|
|
|
What is homocysteine?
|
animal protein metabolite
|
|
|
Relevance of homocysteine and atherosclerosis
|
dose related (ingesting more animal products increases risk of fatty plaques) and must have adequate levels of B6, B12, and folate to metabolize is efficiently
|
|
|
Describe a fatty streak
|
usually born with it; thin fatty streak on intimal surface, begins to dissipate over time; does not usually lead to necrosis/ischemia
|
|
|
Describe a fibrous atherosclerotic plaque
|
proliferation of vascular smooth muscle cells (similar to scar tissue), develops a lipid core
|
|
|
Describe a complicated lesion
|
very high risk plaque formation; may break off and cause clotting/obstruction, hemmorrhage, etc.
|
|
|
Describe the process of unstable lesion formation
|
hyperlipidemia/LDLs-> collection of monocytes in subendothelial layer-> monocytes become macrophages -> macro. release free radicals, oxidizing LDLs -> endothelial destruction, attraction of platelets/WBCs, smooth muscle proliferation -> ingestion of oxidized LDLs by macrophages = foam cells -> necrosis of foam cells = unstable lesion
|
|
|
Define aneurysm
|
atrophy of medial (muscular) layer of an artery
|
|
|
Difference b/t "true" and "pseudo" aneurysms
|
"true" include the entire vessel wall while "pseudo" is a localized dissection/tear in inner wall
|
|
|
Manifestations of aneurysms
|
may be asymptomatic, mild/mod. back pain
|
|
|
Manifestations of abdominal aneurysm
|
pulsing mass L of umbilicus, pain (back, post. legs)
|
|
|
Manifestations of thoracic aneurysm
|
(less common) dysphagia, pain (neck, high back), dyspnea, stridor, brassy cough, JVD, facial/neck edema
|
|
|
Ways to diagnose an aneurysm
|
angiograph, MRI, CT
|
|
|
Describe Arterial Peripheral Vascular Disease
|
atherosclerotic obstruction of medium arteries; causing pain, ischemia, impaired functioning, necrosis, infarct
|
|
|
Describe Chronic arteriosclerosis obliterans
|
usually bilateral (femoral/popliteal), found in men ages 60/70, chronic, slow progressing atherosclerosis of lower extremities
|
|
|
Manifestations of chronic arterial peripheral vascular disease aka arteriosclerosis obliterans
|
intermittant claudication progressing to pain at rest, diminished pulses, bruit, pallor w/elevation, hyperemia w/dependency, loss of hair on extremities, thin skin, little subcutaneous tissue, darkened areas on lower extremities, ulcers, gangrene
|
|
|
Manifestations of acute arterial peripheral vascular disease
|
very rapid onset of s/s by thrombosis formation; severe pain, numbness/tingling in extremities, line of demarcation, no pulse, cyanosis/mottling (later), neuromuscular dysfunction, possible loss of limb
|
|
|
7 "P"s of APVD
|
Pistol, Pallor, Polar, Pulselessness, Pain, Parasthesias, Paralysis
|
|
|
Treatment of APVD
|
thrombolytics, thrombectomy
|
|
|
Describe Raynaud's disease/phenomenon
|
sudden, intense vasospasm of arteries, usually in hands, fingers, sometimes toes
|
|
|
Primary Raynaud's
|
unknown etiology, found in young women, seldom causes necrosis
|
|
|
Secondary Raynaud's
|
sequela of previous vascular disease (frost bite, trauma, chronic arterial occlusions)
|
|
|
Possible triggers for Raynaud's
|
exposure to cold, emotional stress
|
|
|
Manifestations of Raynaud's
|
Pallor->cyanosis->hyperemia (white to blue to red), numbness, tingling, cool to the touch, short-term parasthesia, eventually reestablishment of color and bloodflow
|
|
|
Describe varicose veins
|
dilation of superficial veins or venous valve incompetence, resulting in blood refulx and tortuous swollen veins
|
|
|
Risks for varicose veins
|
prolonged standing, family Hx, obesity, pregnancy
|
|
|
Describe DVT
|
thrombophlebitis in deep or superficial veins
|
|
|
Risks for DVT
|
immobility, dehydration, advanced malignancy, varicose veins, pelvic or leg trauma/surgery, post partum, oral contraceptives (esp. w/smoking), hypercoagulability
|
|
|
What is hypercoagulability?
|
deficiency in plasma proteins: antithrombin III, protein C, protein S, ***factor 5 Leiden
|
|
|
Virchow's triad
|
blood stasis, endothelial injury, hypercoagulability
|
|
|
Manifestations of DVT
|
throbbing calf, homan's sign, warmth, fever, increased WBCs, venous doppler (diagnostic)
|
|
|
Define prehypertensive BP values:
|
Systolic: 120-139
Diastolic: 80-89 |
|
|
Diabetic values for hypertension:
|
Systolic: 130 & up
Diastolic: 80 & up |
|
|
Essential HTN
|
95% of cases; unknown etiology, possibly: fam Hx, insulin resistence, altered Na/H2O secretion, African American race, renin/angiotensin, baroreceptor failure, vascular responsiveness
|
|
|
Secondary HTN
|
5% of cases; renal disease, hyperaldosteronism, renal artery stenosis, cocaine/amphetamine use, sleep apnea
|
|
|
Complications of HTN
|
cardiovascular damage, accelerated atherosclerosis, MI, inc. resistance in systole -> greater workload -> LV hypertrophy (compensatory to inc. CO) -> LV dilation/failure, aortic aneurysm/dissection
|
|
|
HTN manifestations
|
NONE!
|
|
|
Values qualifying orthostatic hypotension
|
drop in systolic >20, and/or drop in diastolic >10
|
|
|
Orthostatic hypotension etiology
|
hypovolemia (diarrhea, vomiting, diuretics, blood loss), antihypertensives, aging (less responsive baroreceptors, Rx), prolonged bedrest (dec. volume, dec. venous tone, weak muscles), ANS disease (Parkinson's)
|
|
|
Orthostatic hypotension Manifestions
|
lightheadedness, syncope, incapacitation
|
|
|
Describe endocarditis
|
inflammation of inner lining of myocardium (usually bacterial)
|
|
|
Risks for endocarditis
|
artificial heart valve, valve disease, congenital heart defects, dental procedures, IV drug usage, damage of endocardial surface & portal of entry (lesions, dental cleaning, upper resp. infection)
|
|
|
Complications of endocarditis
|
vegetative lesions increase risk for blood clots, hemmorrhage, initating immune response (type III) causing arthritis, glomerular nephritis, renal failure etc., continual systemic release of bacteria can cause septicemia
|
|
|
Manifestations of Acute edocarditis
|
increased WBCs, fever spike, chills
|
|
|
Manifestations for subacute endocarditis
|
low-grade fever, gradual onset, malaise, weight loss
|
|
|
Chronic endocarditis
|
long-standing
|
|
|
General S/S of endocarditis
|
petechiae, splinter hemmorrhages, new/changed heart murmur
|
|
|
Diagnosis of endocarditis
|
+ blood cultures (optimum sampling during a chill- "shower of bacteria"), echo, TEE (looks at valve function)
|
|
|
Describe Rheumatic heart disease
|
caused by rheumatic fever, results in stenosis or insufficiency in aortic or mitral valves
|
|
|
Risck for Rheumatic heart disease
|
peak risk at age 5-15, usually follows pharyngitis with streptococcal infection
|
|
|
Manifestations of rheumatic heart disease
|
usually 10 yrs after strep. occurence, fever, abdominal pain, submandibular lymphadenopathy, inc. CRP, inc. WBC
|
|
|
Primary pericarditis
|
rare; viral infection of pericardial sac
|
|
|
Secondary pericarditis
|
caused by infection, AI disorder, renal failure, open heart surgery, SLE
|
|
|
Chronic pericarditis vs. Acute
|
most commonly acute; chronic associated with TB, systemic infection, or fungal infection
|
|
|
Most common viral causes of pericarditis
|
Flu, EB, HIV
|
|
|
Acute manifestations of pericarditis
|
2-6 wks; sharp, radiating chest pain, elevated ST, friction rub
|
|
|
Convalescent manifestations of pericarditis
|
months; fatigue
|
|
|
Pericarditis complications
|
pericardial effusion (resulting in dec. CO, low BP), cardiac tamponade (causing compression of LV)
|
|
|
Cardiac tamponade manifestations
|
pulses paradoxus (decrease 10< in SBP w/inspiration), hypotension, JVD, muffled heart sounds, tachycardia, dyspnea
|
|
|
Heart areas supplied by LAD coronary artery
|
L ventricle, L ant. interventricular septum, L ant. papillary muscle
|
|
|
Heart areas supplied by Circumflex coronary artery
|
L later wall of L ventricle, posterior surface of the heart, (10-15% SA node)
|
|
|
Heart areas supplied by R coronary artery
|
posterior heart, (90%) SA node, posterior papillary muscles, posterior interventricular septum
|
|
|
Peripheral cardiac catheterization
|
measures R heart pressure, pulmonary artery pressure, and pulmonary wedge pressure
|
|
|
Brachial/Femoral artery catheterization
|
measures L heart pressure; inject dyes to see arteries
|
|
|
Time frame for irreversible damage to myocardium when O2 demand > supply
|
30-60 min.
|
|
|
Stable angina
|
stable plaque in 1 or more coronary arteries; chronic
|
|
|
Manifestations of stable angina
|
transient ischemia, fixed lesion, cold, stress and activity exacerbates s/s, referred chest pain relieved by rest or NTG, radiating pain to L arm, predictable pain, T wave inversion, transient ST depression, lactic acid buildup/acidosis
|
|
|
Variant angina/Printzmetal's
|
No lesions, angina caused by coronary artery spasm; chronic
|
|
|
Manifestations of Printzmetal's/variant angina
|
awaken from sleep w/angina, clean coronaries
|
|
|
Unstable angina
|
acute coronary vasoconstriction (usually b/c cocaine use) or rupture of unstable plaque or anemic individual with stable angina
|
|
|
Manifestations of unstable angina
|
acute onset, s/s at rest, with or w/o ST depression, squeezing pain lasting minutes, spread of pain, SOB, fainting, N & V, diaphoresis, anxiety, impending doom
|
|
|
Describe NSTEMI
|
prolonged ischemia resulting in subendothelial infarct with some salvagable muscle
|
|
|
Chemical markers released with NSTEMI
|
CK, CKMB, troponin I
|
|
|
Norm values for chemical markers of NSTEMI
|
CK; male 55-170, female 30-135
CKMB; 0% troponin I; <6 |
|
|
Advantage of using troponin I marker for Acute Coronary Syndrome diagnosis
|
elevated levels stay in bloodstream for days; much longer than other markers
|
|
|
Advantage of using CKMB marker for Acute Coronary Syndrome diagnosis
|
specific for cardiac muscle damage
|
|
|
EKG changes for STEMI
|
ST elevations >1mm, with or w/o T inversion
|
|
|
Describe STEMI
|
differentiated from NSTEMI b/c ST elevation; subendocardial infarct, also has release of chemical markers
|
|
|
Describe Q wave MI
|
transmural infarct; necrosis extends through the myocardial wall
|
|
|
Diagnostic tools for Q wave MI
|
ST elevation, chemical markers, pathologically wide Q waves >0.04 sec.
|
|
|
S/S of acute MI
|
severe chest discomfort unrelieved by NTG, impending doom, diaphoresis, ECG change, N&V, GI symptoms, arm fatigue, tachycardia, hypotension, restless, dysrhythmia
|
|
|
Different s/s for women with acute MI
|
atypical chest pain description
|
|
|
Different s/s for elderly with acute MI
|
complaints of SOB, not chest pain
|
|
|
Compensatory mechanisms with MI
|
tachycardia (SNS temp. inc. contractility), generalized vasoconstriction, Renin/Angiotensin (inc. preload), ventricular dilation and hypertrophy
|
|
|
typical ejection fraction
|
66%
|
|
|
components of stroke volume
|
preload (volume), afterload (resistence), and contractility (pump strength)
|
|
|
Describe Heart Failure
|
inability of the heart as a pump to meet requirements
|
|
|
Cardiac reserve
|
increased CO w/increased activity; usually 4.5-8 L/min.
|
|
|
Compensation for HF
|
kidneys; SNS release epi/norepi to vasoconstrict, RAAS, natriuretics; ventricular hypertrophy, Frank-Starling mechanism
|
|
|
Negatives for compensatory mechanisms for HF
|
eventually depleted sources of epi/norepi, with vasoconstriction comes increase workload
|
|
|
Benefits of compensatory mechanisms for HF
|
Inc. BP will inc. afterload, shunting to heart & brain, increased venous return (preload), positive inotropics (increased contractility)
|
|
|
ANP
|
released by atria with increased stretch & pressure, produces transient diuresis, moderate K loss
|
|
|
BNP
|
stored/released by ventricular cells in response to increased pressure & stretch, produces transient diuresis
|
|
|
Normal renal blood flow
|
25% of CO
|
|
|
Effects of RAAS
|
release of renin which marks release of angio I ->angio II, which causes vasoconstriction (inc. afterload), and release of aldosterone which marks retention of Na/H2O, increasing preload
|
|
|
Effects of Myocardial hypertrophy
|
short term fix to increase CO and contractility; long term causes dec. chamber size/filling, inc. wall tension, and ischemia
|
|
|
Describe systolic HF
|
decreased contractility due to ischemia, anemia, or valve insufficiency
|
|
|
Describe diastolic HF
|
decreased size of ventricles by ischemia, mitral stenosis, or hypertropic cardiomyopathy
|
|
|
Effects of both systolic and diastolic HF
|
edema, pulmonary effusion (crackles)
|
|
|
L-sided HF Manifestations
|
pulmonary edema/crackles, DOE, orthopnea, PND, nonproductive cough, rales, pink & frothy sputum, tachycardia, Afib, thready pulse (1+), pulsus alterans, S3 gallop, pallor, cool extremities, late cyanosis, fatigue, late confusion
|
|
|
Lab values for L-sided HF
|
inc. BUN/Creatinine, dec. Na in urine (dilutional hyponaturemia), inc. urine specific gravity
|
|
|
Causes of R-sided HF
|
end stage lung disease- "cor pulmonale", valve dysfunction (stenosis/regurgitation), R ventricular MI, L-sided HF
|
|
|
Manifestations of R-sided HF
|
JVD, positive HJ reflux, hepatomegaly, ascites (fluid in lungs), peripheral edema/weight gain, nocturia
|
|
|
Labs for R-sided HF
|
inc. bilirubin, AST/ALP, PTT
|
|
|
Diagnotics for HF
|
inc. BNP/ANP, inc. endothelin-1(R sided), echo (watch wall motion), EF<40% (L sided)
|
|
|
Class I HF
|
well controlled, normal activity
|
|
|
Class II HF
|
ordinary activity results in fatigue, palpations, dyspnea, angina
|
|
|
Class III HF
|
symptoms caused by less than ordinary activity
|
|
|
Class IV HF
|
symptoms at rest
|
|
|
Etiology of secondary cardiomyopathy
|
MI, pregnancy, virus, HTN
|
|
|
dilated CMP
|
progressive hypertrophy & dilation of ventricle; impaired pumping
|
|
|
etiology of dilated CMP
|
ischemia, alcohol, myocarditis, genetics, idiopathic
|
|
|
Manifestations of dilated CMP
|
crackles, dysrrhythmia, pulmonary edema, risk of thromboembolism
|
|
|
hypertrophic CMP
|
idiopathic ventricular hypertrophy happening in young adults causing sudden death & ineffective diastolic filling
|
|
|
Manifestations of hypertrophic CMP
|
murmur, dyspnea
|
|
|
restrictive CMP
|
rigid ventricular walls, little expansion, common in Asia & Africa; maybe caused by amyloidosis
|
|
|
Manifestations of restrictive CMP
|
orthopnea, fatigue
|
|
|
peripartum CMP
|
LV dysfunction in last mo.-> 5 mo. postpartum, results in poor prognosis (1/2 will not recover, 18-56% mortality)
|
|
|
Risks for peripartum CMP
|
hormonal change, increased maternal age, African American, multifetal pregnancy, preeclampsia, gestational HTN
|
|
|
Mitral stenosis etiology
|
inflammation, endocarditis, congenital defects, papillary muscle dysfunction (from MIs), LA hypertrophy
|
|
|
Manifestations of Mitral stenosis
|
diastolic murmur, DOE, tachycardia, Afib, irregular pulse
|
|
|
Mitral regurgitation etiology
|
rheumatic HD, ruptured chordae tendons, mitral valve prolapse, papillary muscle dysfunction (MIs)
|
|
|
Manifestations of mitral regurgitation
|
pulmonary edema, pan/holosystolic murmur, palpatations, Afib, DOE, fatigue
|
|
|
Etiology of Aortic stenosis
|
rheumatic HD, congenital valve defect, elderly/atherosclerosis
|
|
|
Manifestations of aortic stenosis
|
angina, syncope, LV failure, systolic murmur, fatigue, exertional hypotension
|
|
|
Etiology of aortic regurgitation
|
endocarditis, rheumatic HD, trauma, aortic dissection
|
|
|
Manifestations of aortic regurgitation
|
diastolic murmur, early: palpatations, fatigue, DOE, inc. pulse pressure; late: angina, HF
|
|
|
Etiology of Asthma
|
airway obstruction, hypersensitive bronchi, exposure to inhaled/ingested irritants or inflammation
|
|
|
Extrinsic asthma
|
non-allergic
|
|
|
Intrinsic asthma
|
allergic; inflammatory triggers
|
|
|
Early asthmatic response (10-20 min.)
|
Type I rxn, release of histamine & ACh, bronchoconstriction, increased prod. & secretion of mucous
|
|
|
Late asthmatic response (4-8 hrs)
|
migration of basophils, eosinophils, and neutrophils; retention of secretions, airway obstruction/trapping; lasting days-wks
|
|
|
Asthma Manifestations
|
sudden dyspnea, chest tightness, expiratory wheezing, dry cough, hyperinflation, fatigue, wheezing halts in acute attacks getting worse
|
|
|
Diagnostic measures for asthma
|
pEF, forced exp. vol.; pt to know green zone (best flow), yellow, red zones
|
|
|
COPD
|
current and chronic obstruction in airway; chronic bronchitis and/or emphysema
|
|
|
Manifestations of COPD
|
excessive mucous production, productive cough, freq. resp. infection, DOE, prolonged exhalation, wheezing, crackles
|
|
|
Labs characterizing COPD
|
PCO2 > 50 (hypercapnea), PO2 < 60 (hypoxemia), inc. erythropoietin, Hgb > 20 (secondary polycythemia)
|
|
|
Cor Pulmonale
|
usually found in Pts with long-standing secondary pulm. HTN, often in conj. with R-sided HF
|
|
|
Manifestations of Cor Pulmonale
|
peripheral edema, hepatomegaly, ascites (fluid in lungs), red faced
|
|
|
Labs characterizing Cor Pulmonale
|
Inc. RBCs, secondary polycythemia (Hgb>20)
|
|
|
Emphysema
|
elargement of alveoli or alveolar ducts, or destruction of alveolar walls; causing decreased Ventilation
|
|
|
Etiology of emphysema
|
alpha 1 antiprotease deficiency, smoking, aging, air pollution, recurrent infection
|
|
|
alpha 1 antiprotease deficiency
|
autosomal recessive disorder causing deficiency in enzyme that protects the lungs from protease injury by microorganisms
|
|
|
Check valve obstruction
|
occlusion of ducts, allows inspiration, but traps air in alveoli upon expiration
|
|
|
Manifestations of valve obstruction
|
PINK PUFFERS; purse-lipped breathing, dyspnea, thin body, barrel chest, diminished breath sounds
|
|
|
Cystic fibrosis
|
autosomal recessive chromosome 7 disorder causing decreased prod. of CFTCR, decreasing Cl transport and Na/H2O reabsorption, inc. viscosity of secretions
|
|
|
Complications of CF
|
bronchiectasis, impaired cilliary function, frequent infection, malabsorption, steatorhea, diarrhea, cramping, inc. risk for diabetes
|
|
|
Diagnosing CF
|
+ sweat Cl test, failure to thrive, recurrect resp. infection; persistent cough, barrel chest, clubbing, oily stool, malnutrition, diabetes
|
|
|
Pulmonary Embolism
|
Perfusion declines with obstruction of pulm. artery
|
|
|
Risks for PE
|
immobility, BC, pregnancy, orthopedic/gynocologic surgery
|
|
|
PE manifestations
|
sudden dyspnea, chest pain, hypoxia w/o hypercapnea, tachypnea, tachycardia, impending doom
|
|
|
saddle embolism
|
blocks both lungs
|
|
|
diagnosis of PE
|
V/Q scan, spiral CT, inc. D-dimer, ABGs, venous ultrasound
|
|
|
Low V/Q
|
hypoventilation; pneumonia, atelactesis, COPD, chest wall abnormalities, guillain-barre, MD
|
|
|
High V/Q
|
PE
|
|
|
Hypercapnic Respiratory Failure
|
ventilation failure, hypoventilation, resp. acidosis
|
|
|
Manifestations of Hyper.Resp. Failure
|
h/a, conjuctiva hyperemia, flushed, confusion, coma
|
|
|
Diffusion Limitation
|
thickening of alveolar-cap membrane; PE, black lung; hypoxemia w/exercise
|
|
|
Manifestations of hypoxemia
|
PO2<50; prolonged expiration (1:3-1:4), retractions, cyanosis, purse-lipped breathing, restless, combative, anxious, confused, fatigue, tachycardia, HTN
|
|
|
ARDS
|
sudden, progressive respiratory failure associated with damage to and increased permeability of alveolar capillary membrane marked by profound hypoxemia, causing damage to type II cells, decreasing surfactant production and resulting in stiff, noncompliant lungs and hyaline membrane formation
|
|
|
ARDS etiology
|
lung injury, gram - sepsis, aspiration of gastric contents, major trauma (drowning, burns, emboli)
|
|
|
ARDS manifestations
|
dyspnea, tachypnea, cough, restlessness, clear lungs/fine crackles, alkalosis, hypoxemia, CXR, pulmonary HTN
|
|
|
ARDS complications
|
nosocomial pneumonia (ventilator), barotrauma (pneumothorax), stress ulcers, renal failure
|
