Alterations in the Cardiovascular System Flashcards
1
Q
lymphatic capillaries openings are
A
larger than venous, because they pull in large proteins that can’t go back into veings
2
Q
lymphatics return
A
protein, lipids, cellular debris from interstitium to vasculature
3
Q
lymphedema occurs from
A
- stagnation of fluid in interstitium due to blockage
- inflammatory response (macrophages) or fibrosis
4
Q
s/s lymphedema
A
usually nonpitting edema
5
Q
primary lymphedema
A
congenital
6
Q
secondary lymphedema
A
damage to lymphatics due to non congenital causes
- filiariasis = mosquito born parasite that damages lymph vessels
- cancer or cancer tx
7
Q
cause of Chronic Venous Insufficiency (CVI)
A
vein or valve blockage/malfunction
8
Q
Risk Factors for CVI
A
female, pregnancey, obesity, aging, family hx, stasis
9
Q
s/s CVI
A
vericosity, itching, burning, muscle cramp, pitting edema,
10
Q
Virchow’s Triad
A
stasis, vascular injury, hypercoagulability
11
Q
examples of vascular injury
A
venepuncture, atherosclerosis, heart valve disease, surgery, trauma
12
Q
examples of circulatory stasis
A
A-Fib, Lft Ventricular syfunction, immobility, obesity
13
Q
s/s of DVT
A
pain, tenderness, swelling, erythema, none
14
Q
diagnosis of DVT
A
d-dimer, ultrasound
15
Q
complications of DVT
A
thromboembolus, post-thrombotic inflammatory syndrome
16
Q
arterial thrombus is caused by
A
activation of the coagulation cascade caused by the artherosclerotic roughening of the tunica intima
17
Q
types of thromboembolism
A
arterial, pulmonary emboli, air embolism, amniotic fluid, bacterial, fat, foreign material
18
Q
left hear delivers blood to
A
arteries
19
Q
pulmonary emboli source
A
most commonly from the deep veins of the thigh
right heart or venous circulation
20
Q
pathophys of pulmonary embolism
A
occlusion of part of pulmonary circulation => hypoxic vasoconstriction=>decreased surfactant=>release of neurohumoral response=>atelectasis in affected lung=> further hypoxemia=> pulmonary edema, HTN,shock, death
21
Q
s/s pulmonary embolism
A
tachypnea, dyspnea, chest pain, dead space, V/Q imbalances, decrease PaO2, pulmonary infarction, HTN, decreased CO, systemic Hypotension due to decreased blood flow from heart
22
Q
Superior Vena Cava Syndrome
A
venous distention in UE and head due to compression of SVC from lung cancer or lymphoma
23
Q
Aneurysms
A
walls are still intact but fluid leaks btn layers resulting in ballooning or bulging
24
Q
True Aneurysm
A
involve all 3 layers of the BV
fusiform, circumferential or dissecting
25
Pseudoaneurysm
extravascular hematoma that extends into the intravascular space
26
Risk factors for aneurysms
HTN
Atherosclerosis =erodes walls
inflammation = infection such as syphilis
collagen disorders = Marfan's, EDS
27
complications of HTN
retina damage, Lft ventricle hypertrophy, kidney failure
28
Blood Pressure
CO + Peripheral Vascular Resistance
29
Stroke Volume
amt of blood pumped out of the L ventricle per beat
| - affected by contractility, preload, and afterload
30
Cardiac Output
= Stroke Volume x HR
31
stage I HTN
130-139/80-89
32
stage II HTN
> 140/>90
33
mechanisms of vascular resistance
blood viscosity (water retention) and vascular diameter
34
two mechanisms for HTN
increased vascular resistance, increase CO
35
how does change in SNS affect HTN
Norepi is released and binds to alpha1 on BV and beta1 on heart = vasoconstriction and increase in HR = increase in CO and increase in vascular resistance
36
causes of Primary HTN
genetic + environment + neurohumoral
37
causes of Secondary HTN
systemic disease, renal artery disease, coarctation of aorta
38
malignant HTN
hypertensive crisis
rapidly progressive HTN = >180/>120
can lead to encephalopathy, and hypertensive emergency
39
Pulmonary HTN
Lft HF, hereditary, Phen-Phen, parenchymal lung disease
40
Juxtaglomerular Cells
release renin
41
mechanisms for renin release
> response to PG stimulus from macula densa cells
> response to activation of Beta Adrenergic receptors by increased activity of SNS
> response to barorecptrs directly sensing low blood pressure
42
macula densa cells
detects Na concentrations in distal tubule
43
Renin
converts Angiotensinogen into Angiotensinogen I
44
Angiotensinogen
hormone made by the liver secreted into blood stream
45
Angiotensinogen Converting Enzyme
secreted by the lungs
| converts Angiontensinogen I into Angiotensinogen II
46
Angiotensinogen II
increases SNS activity
H2O retention by kidneys
Aldosterone secretion by Adrenal Cortex
Arteriole Vasoconstriction increasing BP
Post Pituitary release of Vasopressing/ADH
ADH increases H2O reabsorption which increases circulating volume
47
Aldosterone
released from the adrenal cortex by stimulation from Ang II, responsible for signalling kidneys to retain H2O, Na, and excreting K
48
Antidiuretic Hormone(ADH)/Vasopressin
Released from the posterior pituitary in response to Ang II ==> retain water by kidneys
49
Angiotensin Converting Enzyme (ACE)
enzyme found on mostly on the surface of the lungs and some on the kidneys
=> responsible for cleaving Ang I into Ang II
=> destroys bradykinin
50
bradykinin
potent humoral modulator that is a powerful vasodilator
51
naturetic hormones
activate excretion of Na into the urine
control renal sodium excretion and induce diuresis
improve renal blood flow/filtration
supress aldosterone and SNS
52
obesity leads to increased Primary Hypotension thru
```
increased adipokines (leptin)
overactive SNS and RAAS
Insulin Resistance - endothelial injury and inflammation
```
53
preemclampsia
HTN in pregnancey and proteinuria after 20 weeks
54
Primary Orthostatic Hypotension
neurogenic conditions
55
Secondary Orthostatic Hypotension
medications, dehydration
56
examples of vasculitis
inflammation of vessels due drugs, infection or autoimmune => thrombangitis obliterans, Kawasaki, temporal arteritis
57
Temporal arteritis/Giant Cell Arteritis
T cell and macrophages attack arteries of the brain
58
risk for Temporal arteritis/Giant Cell Arteritis
postmenopausal and scandinavian decent
59
S/S Temporal arteritis/Giant Cell Arteritis
HA, Vision changes, tenderness, jaw pain
60
Thromboangiitis Obliterans/Buerger's Disease
autoimmune vasculitis where inflammation blocks peripheral arteries of LUE
=> strongly associated with smoking and male gender
61
two categories of Raynaud's
Primary Idiopathic Raynaud's Disease
| Secondary Raynaud's Syndrome => hypersensitivity rxn associated with connective tissue diseases
62
Raynaud's
Vasospastic response in the small arteries /arterioles of fingers
63
Criteria for Kawasaki Disease
Vasculitis seen in children need 5/6
> fever for 5 days
> bilateral conjuctival injection w/o exudate
> changes in oral mucous such as strawberry tongue
> polymorphous rash
> cervical lymphadenopathy
> changes in the extremities/peripheral edema
64
coronary artery stenosis can be a result of
Kawasaki Disease
65
Acute Kawasaki
fever, conjunctivitis, strawberry tongue, rash, lymphadenopathy, irritability
66
Subacute Kawasaki
Begins when fever ends, ends when clinical signs resolve
Child is most at risk for coronary artery aneurism
Peeling of palms and soles, thrombosis
67
Convalescent Kawasaki
continued elevation of erythrocyte sedimentation rate and platelet count, coronary artery stenosis, arthritis, thickening of the tunica intima
68
mucocutaneous lymph node syndrom
Kawasaki Disease
69
leading cause of coronary artery and cerebrovascular disease
Artherosclerosis
70
atheroma
plaque development through the accumulation of lipid laden macrophages
71
foam cells
macrophages that have consumed oxidized LDLs from microtears in tunica intima
72
fatty streaks
accumulation of fatty streaks on BP roughened BV wall
73
what happens to fatty streaks
calcify into fibours plaques, that are prone to rupture that can result in thrombus that may occlude artery
74
HTN and Angiotensin
=> HTN creates microtears in BV endothelium due to shear pressures
=> HTN results in the release of ANGII
=> ANG II
> endothelial disfunction
> decreases apoptosis
> increases artherosclerosis
> increases thrombosis by increasing platelet aggregation and increasing vasoconstriction
> increases smooth muscle cell growth and migration
75
PAD Peripheral Artery Disease
type of atherosclerosis in arteries that supply extremities
76
S/S of PAD
intermittent claudication, diminished pulses
77
Ankle Brachial Index
BP taken at ankles and calves to see if there is a differential = PAD
78
intermittent claudication
leg pain during exercise due to narrowing of arteries
79
How does endothelial dysfunction cause atherosclerosis?
Damage to the endothelium upsets the balance between vasoconstriction and vasodilation and initiates a number of events/processes that promote or exacerbate atherosclerosis; these include increased endothelial permeability, platelet aggregation, leukocyte adhesion, and generation of cytokines
80
macrophages release enzymes to digest oxidated LDL and toxic oxygen radicals create oxidative stress
atherosclerosis
81
LDL is primarily responsible for
delivering cholesterol to tissues
82
excess LDL enters blood arteries
causing inflammation
83
can be improved by diet and exercise
HDL
84
Lp(a)
similar to LDL but has an apolipoprotein(a) attached
85
Lp(a) may increase
Coronary Heart Disease and inhibit thrombolysis
86
goal levels of LDL
<100-130
87
goal levels of HDL
> 40 men
| > 50 women
88
function of cholesterol
hormone synthesis, cell membrane, bile acid synthesis
89
Hyperlipidemia
elevated cholesterol, TG, or LDL
90
Dyslipidemia
Hyperlipidemia and lo HDL
91
apolipoprotein
protein taxi for cholesterol, w/o which cannot bind to liver receptor and be taken in for processing
92
type of hyperlipidemia that increases patient's risk for pancreatitis
secondary hypertriglyceridemia
93
cardiac leading cause of death
coronary artery disease = atherosclerosis of coronary arteries
94
modifiable risk factors of CAD
obesity, HTN, diet, diabetes mellitus
95
Risk Factors for CAD
adipokines, CKD, pollution, meds, CA calcification, inflammation, microbiome
96
Consisting of four defects, TOF is a congenital cardiac defect that:
Allows desaturated blood to enter the systemic system without passing through the lungs
97
A stricture is present in the aorta which leads to restricted blood flow to the lower part of circulation. BP in head and UL’s is high, whilst that in the LL’s is low.
Coarctation of the Aorta
98
most common cyanotic congenital cardiac defect
Tetralogy of Fallot
99
Tet spells
Near occlusion of the right ventricular outflow tract with profound cyanosis
100
Children with cyanotic congential heart disease often
squat, this kinks the femoral artery increasing peripheral resistance. This in turn increases left-sided ventricular resistance which lessens the burden of right-eft shunt.
101
normally ductus arteriosus closes and becomes
ligamentum arteriosus
102
Coarctation should be suspected in
an asymptomatic child with hypertension
103
decrease in the systolic BP on standing by 20 mmHg
Orthostatic Postural Hypotension
104
Causes for Orthostatic Hypotension
dysfunction of baroreceptors
elderly
beta blockers
105
angina is a symptom
of CAD
106
angina pectoris is similar to
intermittent claudication
107
pain from angina and intermittent claudication is caused by
lactic acid build up from hypoxia in tissues
108
transient myocardial ischemia types
Stable Angina = predictable chest pain
Unstable Angina = new onset or change in old pattern
Prinzmetal Angina = vasospasms causing unpredictable angina
Silent Ischemia = no detectable symptoms
109
atherosclerosis is so pervasive that it is threatening to occlude bloodflow to heart
> life threatening
> acute coronary syndrome
> unstable angina
110
Non-STEMI
no significant ST segment elevation
early MI
subendocardial ischemia
injury reversible
111
ST elvevation MI
Ischemia of heart muscle has gone through wall = transmural
| Significant ST segment elevation
112
T Wave Inversion
Ischemia
113
ST Segment Elevation
Myocardial Injury
114
Q Wave Depression
Infarction/Necrosis
115
Mr. PM As MVP
Mitral Regurgitation, Physiologic Murmur, Aortic Stenosis, Mitral Valve Prolapse - Systolic Murmurs
116
ARMS
Aortic Regurgitation, Mitral Stenosis - Diastolic Murmurs
117
first 24 hrs after MI
arrythmias, cardiogenic shock
118
3 days after MI
inflammation of pericardium,inflammatory response due to hypoxia and cell death
119
3-14 days after MI
scar begins, mushy tissue and easily reinjured, AVOID STRESS
120
2 weeks and beyond
remaining muscle picks up slack and grows
121
risk factors for heart failure
ischemic heart disease/MI, HTN, congenital disorders
