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Systemic Disease (Wolfe) > Cardiovascular Disease > Flashcards

Cardiovascular Disease Flashcards

1
Q

What is the #1 cause of death in men and women in the US?

A

cardiovascular disorders

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2
Q

What are the top 3 cardiovascular disorders?

A

HTN, hypercholesterolemia, atherosclerosis

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3
Q

HTN stats

A

affects 1 in 3 adults and 50% are adequately controlled

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4
Q

What is the most common primary diagnosis in the US?

A

primary/essential HTN– aka silent killer

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5
Q

What is primary HTN?

A

the most common 95%; idiopathic, potential genetic or racial predilection; diet and lifestyle play an impact

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6
Q

What is secondary HTN?

A

increased bp secondary to another cause like medication, kidney, endocrine disorders, drug use

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7
Q

What is malignant hypertension?

A

call 911, end organ damage to cardiovascular system, CNS, or kidney

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8
Q

What is labile HTN?

A

BP that fluctuates repeatedly in response to emotional stress; HTN medications are normally not effective, instead Rx stress-relieving meds and monitor for 24 hrs

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9
Q

What is white coat syndrome?

A

can increase bp 20/10 mmHg; acute spike in bp due to the fact they know their bp is being taken

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10
Q

When does gestational HTN return to normal?

A

within 12 weeks of delivery (begins 1st trimester)

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11
Q

What are symptoms of acute HTN?

A

HA, nausea, vomiting, dizziness, sweating, loss of consciousness

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12
Q

What are some causes of acute hypertension?

A

exogenous etiologies: caffeine, nicotine, sodium intake, pregnancy, alcohol, medications; endogenous: tumor like adrenal gland tumor

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13
Q

Normal BP

A

<120 over <80

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14
Q

Elevated BP

A

120-129 and <80

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15
Q

Stage 1 BP

A

130-139 or 80-89

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16
Q

Stage 2 BP

A

> 140 or >90

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17
Q

Hypertensive crisis BP

A

> 180 and/or >120

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18
Q

T/F pt must be seated for 5 minutes before bp measurement

A

true

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19
Q

Every 20/10 mmHg increase in BP over 115/75, increases the risk for cardiovascular disease ___ fold

A

2 fold

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20
Q

HTN urgency

A

180/100 or greater, organ damage may occur; check for HA, SOB, nosebleeds or severe anxiety

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21
Q

HTN crisis

A

> 180/>120, organ damage WILL occur

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22
Q

What can a HTN crisis do to the body?

A

CVA, loss of consciousness, memory loss, MI, ESRD, aortic dissection, angina, pulmonary edema, eclampsia, blindness

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23
Q

What organs are primarily effected by HTN?

A

those with the most microvascular beds; brain, retina, heart, kidneys

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24
Q

What percent of HTN morbidity is from coronary artery disease?

A

50%

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25
Q

What percent of HTN morbidity is from cerebral vascular accident?

A

33%

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26
Q

What percent of HTN morbidity is from renal failure and end stage renal disease?

A

10%

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27
Q

What are HTN risk factors?

A

male, increased age, african american, family hx, sympathetic over-activity, sleep apnea, concomitant disease, lifestyle

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28
Q

Why is sympathetic over-activity an issue?

A

vasoconstriction, increased heart rate; from stress of pheochromocytoma which has the hallmark impending sense of doom

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29
Q

What diseases are concomitant to HTN?

A

dyslipidemia, diabetes

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30
Q

What lifestyle factors increase risk of HTN?

A

alcohol, obesity, sedentary lifestyle, smoking, salt intake

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31
Q

How do you calculate BMI?

A

weight (lbs)/height (in^2) x 703 OR kg/m^2

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32
Q

What is the BP equation?

A

BP = CO x VR
CO=cardiac output
VR= peripheral resistance

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33
Q

How do you calculate cardiac output?

A

CO = SV x HR which describes the amount of blood pumped by the ventricle per minute

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34
Q

What affects peripheral resistance?

A

blood volume and blood vessel size

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35
Q

What are some functions of angiotensin II?

A

up-regulates sympathetic tone, increases absorption of Na and Cl, excretion of Ca to increase volume of blood, stimulates aldosterone release from adrenal gland, arteriolar constriction, increase ADH from anterior pituitary

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36
Q

Increased BP creates a negative feedback loop to the kidney causing

A

reduced renin release

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37
Q

What does renin do?

A

transforms angiotensinogen to angiotensin I

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38
Q

What does ACE do?

A

converts angiotensin I to II

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39
Q

Where is ACE from?

A

surface of renal and pulmonary endothelium

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40
Q

What are manifestations of secondary HTN?

A

pitting edema, truncal obesity, foot ulcers, numbness of extremities, muscle weakness, tachycardia

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41
Q

What are lifestyle modifications of HTN?

A

weight reduction, mediterranean diet, sodium decrease, physical activity, moderation of alcohol

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42
Q

What is a normal BMI?

A

18.5-24.9

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43
Q

What are first line agents?

A

diuretics, ACE inhibitors, Angiotensin receptor blockers, Ca channel blockers

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44
Q

What are diuretics?

A

furosemide, hydrochlorothiazide

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45
Q

What are ACE inhibitors?

A

captopril

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46
Q

What are ARBs?

A

valsartan

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47
Q

What are Ca channel blockers?

A

diltiazem, nifedipine, verapamil

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48
Q

What are second line agents?

A

beta blockers, alpha agonist/antagonist, methyldopa, vasodilators

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49
Q

What is a beta blocker?

A

metoprolol

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50
Q

What are alpha agonist/antagonist?

A

clonidine/terazonsin

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51
Q

What is a vasodilator?

A

hydralazine

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52
Q

What is first line in African americans?

A

Ca channel blockers

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53
Q

What is first line in whites?

A

beta blocker

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54
Q

What is the effect of HTN on heart muscle?

A

increased work load and stronger stroke which can lead to left ventricular hypertrophy and congestive heart failure

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55
Q

What is bad news on an EKG?

A

inverted T wave means current or past MI

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56
Q

What are you looking for in an urinalysis?

A

RBCs, WBCs, protein or glucose in urine

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57
Q

On the bp cuff, if the white line on the cuff doesn’t overlap with the other white line, you need…

A

a larger cuff

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58
Q

What is the desirable total cholesterol level?

A

<200

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59
Q

What is the desirable LDL level?

A

<100

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60
Q

What is the desirable HDL level?

A

> 45

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61
Q

What is the desirable triglyceride level?

A

<150

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62
Q

What is homocysteine level measuring?

A

amino acid in blood that converts cholesterol to LDL… causes damage to arterial walls and blood clots

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63
Q

What is a normal homocysteine level vs increase risk for CVD?

A

normal <12 micro mol/L; risk 12 to 15

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64
Q

What is the treatment for elevated homocysteine?

A

B vitamins like folic acid/b9, cobalamin/b12 and pyridoxine/b6

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65
Q

What does C reactive protein measure?

A

inflammation, promoting globulin in blood that is produced when blood vessel walls become damaged

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66
Q

What is normal C reactive protein?

A

<0.11 mg/dL

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67
Q

What is high C reactive protein?

A

0.20 to 1.50 mg/dL

68
Q

What factors increase CRP?

A

HTN, BMI, smoking, metabolic syndrome, hyperglycemia, low HDL, high triglycerides, estrogen use, chronic infection, RA, genetic mutation

69
Q

What is the progression toward MI?

A

HTN –> CAD –> MI

70
Q

What is coronary artery disease?

A

atherosclerosis, coronary revascularization, heart failure, angina, MI

71
Q

What is the most fatal MI?

A

left ventricular ischemia aka widow-makers heart attack

72
Q

Define arteriosclerosis

A

the thickening and hardening of the walls of the arteries, occurring typically in old age; will happen to everyone but HTN increases the rate

73
Q

Define atherosclerosis

A

preventable; a disease of the arteries characterized by the deposition of plaques of fatty material on their inner walls, produce emboli

74
Q

When does arteriosclerosis start

A

shortly after birth, intervene as young as possible

75
Q

What is a fibro-atheroma?

A

larger atheroma with calcification

76
Q

What is peripheral vascular disease?

A

arteriosclerotic type disease of the femoral/popliteal artery of the distal portion of superficial femor

77
Q

What are symptoms of peripheral vascular disease?

A

intermittent claudication limited to the calf/foot

78
Q

What are signs of peripheral vascular disease?

A

affected area has hair loss, thinning of skin, decreased muscle mass, coolness to touch, good to fair femoral pulses, no popliteal or pedal pulse

79
Q

What are renal effects of HTN?

A

renal artery stenosis, renal insufficiency, decreased GFR

80
Q

What is the result of decreased glomerular filtration rate and tubular dysfunction?

A

hematuria and proteinuria

81
Q

What occurs when a renal artery has stenosis

A

focal restriction results in decrease blood supply to kidneys and renal necrosis… may develop neo

82
Q

What is the increased risk of stroke CVA from HTN?

A

4x increased risk

83
Q

Which CVA is more common, hemorrhagic or ischemic?

A

ischemic 87%

84
Q

What is HTN encephalopathy?

A

swelling of the brain with HA, nausea, vomiting, HTN retinopathy, CN palsy, altered mental status

85
Q

How many people with TIA will stroke?

A

1/3

86
Q

How long does a TIA last?

A

< 24 hours but usually 15 mintues

87
Q

What are symptoms of a TIA?

A

vertigo, dizziness, light headedness, focal deficit, weakness contralateral, speech disturbance, visual disturbance

88
Q

What are the 3 types of ischemic CVA?

A

thrombotic 35% embolic 30% And lacunar/hypoxic 20%

89
Q

What is a thrombotic CVA?

A

plaque decreases the lumen aka stenosis

90
Q

What is an embolic CVA?

A

plaque/ fibrous cap is liberated and lodged in the artery

91
Q

What is lacunar and hypoxic CVA?

A

secondary to hypoxic events (fine vessels in the brain), difficult to dx

92
Q

What are signs of lacunar and hypoxic CVA?

A

INO and weird saccadic dysfunction

93
Q

What is the cause of a hemorrhagic CVA?

A

rupture of an intracranial artery

94
Q

How does damage occur in a hemorrhagic CVA?

A

hypoxia, hydraulic pressure, toxicity of blood to brain tissue

95
Q

What may hydraulic pressure cause?

A

herniation of the brain through the foramen magnum

96
Q

What are risk factors for hemorrhagic CVA?

A

HTN, vessel damage, aneurysm, trauma, vasculature malformation

97
Q

What is the strongest portion of the cranium?

A

the petrous portion of the temporal bone

98
Q

What is epidural?

A

between cranium and dura mater; trauma is the most common cause; 80% involve the middle meningeal artery

99
Q

Where is the most common location of damage for the middle meningeal artery?

A

the most temporal area of the skull (thinnest area) results in epidural hemorrhagic CVA

100
Q

What is subdural?

A

the most common type of hemorrhagic stroke, caused by acceleration injuries

101
Q

What is the highest risk factor group for subdural stroke?

A

alcoholics, blood thins and brain shrinks in alcoholics

102
Q

What is subarachnoid?

A

commonly caused by congenital malformations and berry aneurysms that lead to leaks in CSF and increased ICP= worse headache ever

103
Q

What age group is subarachnoid stroke more common in?

A

young patients

104
Q

What is the FAST acronym for stroke?

A

face asymmetry, arm hangs, speech slurred, time call 911

105
Q

How to differentiate bell’s palsy and stroke

A

bell’s palsy cannot raise their eyebrows

106
Q

Is bell’s palsy a lower or higher brainstem problem?

A

lower, idiopathic– leads to paralysis of half of the face

107
Q

What fibers does a stoke affect?

A

with brain lesion, retain ipsilateral fibers to upper portion of the face aka the patient can raise their eyebrows

108
Q

General stroke treatment

A

anti-platelet medication, cholesterol lowering statins and anti HTN meds

109
Q

Ischemic stroke treatment if within first 4 hours

A

clot-dissolving medicine tissue plasminogen activator (gold standard), ASA, endovascular device to remove clot

110
Q

Hemorrhage stroke treatment

A

endovascular procedure, surgery to secure aneurysm

111
Q

If a patient presents with a homonymous visual field defect respecting the vertical midline…

A

think CVA or cerebral lesion and perform a cranial nerve screening

112
Q

What is treatment of homonymous VF defect?

A

yoked prism base towards field defect

113
Q

Ocular effects of HTN

A

second only to diabetic retinopathy in prevalence

114
Q

What does the clinical presentation of ocular HTN depend on?

A

severity, duration and degree of control

115
Q

What are retinal vascular changes?

A

constriction, crossing changes, micro-aneurysms, and sclerosis

116
Q

What is HTN retinopathy?

A

hemorrhages, exudates, CWS, papilledema

117
Q

What is grade 1 HTN?

A

minimal vessel change, arterial narrowing

118
Q

What is grade 2 HTN?

A

sclerosis, thickened arterial wall, attenuated arteries, widened ALR, ciking/banking at AV crossings

119
Q

What is grade 3 HTN?

A

exudates, hemes, CWS, occlusions, micro-aneurysms and macro-aneurysms

120
Q

What is grade 4 HTN?

A

optic nerve head edema, macular edema

121
Q

T/F malignant hypertensive retinopathy correlates with severe systemic disease

A

true, 3 year survival of grade 4 ret is approximately 6% (worse than choroidal melanoma)

122
Q

T/F chronic hypertension w/ a significant elevation in diastolic pressure has been directly related to the narrowing of the caliber of the vessel

A

true

123
Q

What causes arterial attenuation?

A

arteries have a large tunica media and the more stressed they are the more muscular they become, this leads to rigidity and straightness

124
Q

What causes venous tortuosity?

A

venules have thin walls and are flimsy, increased pressure causes the venule to twist and turn

125
Q

What is vasoconstriction controlled by?

A

autoregulation

126
Q

What is the appearance of arterial attenuation?

A

reduced caliber of retinal arterioles, nicking/banking possible

127
Q

T/F focal constrictions are most commonly seen in patients with a diastolic BP greater than 100mmHg

A

true, secondary to acute rise in bp

128
Q

Will focal constrictions disappear with reduction in bp?

A

possibly, they’re due to hypertonus not atherosclerosis

129
Q

What causes sclerosis?

A

prolonged HTN, this is irreversible damage and thickening of the arterial wall, best observed 1DD out

130
Q

What is the appearance of sclerosis?

A

attenuation of arterioles, thickening of ALR, nicking and banking at AV crossings

131
Q

What is the normal arterial to vein ratio?

A

2/3

132
Q

What is the normal ALR?

A

1/3

133
Q

What does compression of the retinal vein at their common sheath with arteries lead to?

A

BRVO

134
Q

What is a micro-aneurysm?

A

small out-pouch of a venule wall, may be the direct result of an increase in pressure from a sclerosed arteriole

135
Q

Where are micro-aneurysms located?

A

usually near AV crossings and often associated with CWS, best seen with IVFA

136
Q

Appearance of micro-aneurysm and dot-blot hemes on IVFA?

A

micro-A light up while dot-blot hemes show up as darkened areas

137
Q

What is exudation from?

A

prolonged HTN or abrupt acute episode; tight junctions are damaged and blood + hard exudates leak into retina

138
Q

What is a CWS?

A

sign of ischemia of the NFL

139
Q

What is the most common etiology of BRVO?

A

vascular occlusion from complication of sclerosis in HTN

140
Q

What is a fusiform retinal macro-aneurysm?

A

spindle shaped, typically associated with exudation

141
Q

What is a saccular retinal macro-aneurysm?

A

shaped like a small sac, more likely to result in hemorrhage

142
Q

What is HTN encephalopathy?

A

optic nerve swelling + hemes secondary to acute spikes in bp; bilateral disc edema and venous engorgement

143
Q

What is acute HTN?

A

rapid rise in BP leading to arteriolar constriction and damage to small vessel endothelium causing leakage of plasma protein into the posterior retina and a breakdown fo the BRB resulting in hard exudate formation

144
Q

What is a macular star?

A

leakage of plasma into macular area in a radiating pattern, lipid exudates in the OPL

145
Q

What grade is macular star?

A

technically grade 3

146
Q

What is HTN choroidopathy?

A

grade 3/4; necrosis of choroidal capillaries and arterioles, elschnig spots

147
Q

What are elschnig spots?

A

round, deep, grayish-yellow spots that become hyper-pigmented over time; RPE infarction

148
Q

What are vascular sources of emboli?

A

cholesterol plaque at bifurcation of ECA and ICA

149
Q

What are cardiac sources of emboli?

A

calcification of cardiac valves; chalk white, non-refractile, permanent, central artery

150
Q

What are fibrin and endogenous sources of emboli?

A

atrial fibrillation, infectious endocarditis, acute MI

151
Q

What is a hollenhorst plaque?

A

cholesterol, yellow-golden color, refractile, small, multiple, near arterial branches, transient

152
Q

How to evaluate for Hollenhorst plaque?

A

bruit eval, carotid doppler and bifurcation of ICA/ECA

153
Q

What is a calcific plaque?

A

chalky while, large, non-refractile, near ONH

154
Q

How to evaluate for calcific plaque?

A

cardiology consult for echocardiogram to r/o valvular stenosis

155
Q

What is a fibrinoplatelet?

A

capsule shaped, fuzzy, plug-like

156
Q

What is fibrinoplatelet associated with?

A

auto-immune, hyper coagulable, vegetative

157
Q

What is a talc emboli?

A

multiple tiny, glittering, grouped around macula from IV drug abuse

158
Q

What is a fat emboli?

A

purtscher’s retinopathy, from long bone fracture, acute pancreatitis, or post-liposuction

159
Q

What is a tumor emboli?

A

metastatic neoplasm

160
Q

How to diagnose a retinal emboli?

A

ophthalmoscopy, carotid auscultation

161
Q

How to treat a retinal emboli?

A

ocular digital massage, aspirin therapy, breathe into paper bag, paracentesis

162
Q

Why do you breathe into a paper bag with a retinal emboli?

A

increased CO2 dilates retinal vasculature

163
Q

How to perform a carotid auscultation?

A

palpate carotid pulse at carotid triangle and listen with bell at carotid triangle

164
Q

Bruit sounds at <50, 50-90 and >90?

A

<50% stenosis = no sound; 50-90% swishing sound; >90% no heart beat sound

165
Q

When do you perform a carotid endarterectomy?

A

if >70% stenosed and symptomatic

Systemic Disease (Wolfe) (10 decks)

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