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Pathophysiology 212 > Chapter 18 > Flashcards

Chapter 18 Flashcards

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1
Q

What are the 3 layers of an artery?

A
  1. tunica intima: endothelial cells (exchanging)
  2. tunica media: smooth muscle cells (constriction/dilation)
  3. tunica externa: collegen and elastic fibers (support/strength)
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2
Q

What is hyperlipidemia? What who lipids are insoluble in plasma and encapsulated by lipoproteins?

A

Abnormally high levels of fatty lipids

- Cholesterol and triglycerides

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3
Q

What are dietary lipids absorbed as?

A

chylomircrons

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4
Q

Name the 5 types of lipoproteins?

A
  1. Chylomircrons (2% protein)
  2. VLDL (55-65 TG, 10 C, 5-10 P)
  3. LDL (10 TG, 50 C, 25 P)
  4. IDL
  5. HDL (5 TG, 20 C, 50 P)
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5
Q

Describe the role of low density lipoprotein receptors in removal of cholesterol from the blood?

A
  • 60% go to the liver receptors and get engulfed
  • 40% go to the adrenal cortex and gonads and get engulfed. They have the same cells as the liver and get used as steroid hormones.
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6
Q

What are lipid blood levels raised by?

A
  • Nutrition
  • Genetics (lack of LDL receptors?)
  • Other diseases
  • Medications (beta blockers, estrogen)
  • Metabolic disorders
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7
Q

What is atherosclerosis?

A

Formation of fatty lesions in the intimal lining of the arteries. (Hardening)

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8
Q

What are non-modifiable and modifiable risk factors for atherosclerosis?

A

NM: increasing age, male/post menopausal women, family hx, genetically modified alterations in lipoprotein and cholesterol metabolism

M: Smoking, obesity, HT, hyperlipidemia, DM

C reactive protein, hyperhomocystimia, increased serum lipoprotein (non traditional risks)

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9
Q

How does tobacco use contribute to atherosclerosis?

A
  • increases blood lipid levels
  • damages epithelium
  • enhances thrombosis formation
  • increases blood thickness
  • increases circulating catecholamines
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10
Q

What is the role of inflammation in the development of atherosclerosis and how can it be assessed?

A

CRP is an acute inflam. phase reactant synthesized in the liver, getting a baseline can predict future complications, High CRP= predict cardiovascular risks

As LDL accumulates in the arterial walls, it signals epithelial cells to latch onto WBC circulating in the blood>the immune cells penetrate the wall and trigger an inflam. response>LDL become “foam cells”>form a fatty streak>growth continues=fibrous capsule>substances released by the foam cells can cause capsule to rupture=blood clot=block flow/heart attack

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11
Q

What are stable and unstable plaques?

A

Stable: thick fibrous capsules, partially block vessels, don’t tend to from clots/ emboli

unstable: thin fibrous, may rupture causing clots, may completely block artery, clot may break free

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12
Q

What vessels are affected by atherosclerosis? What changes are occurring?

A

Abdominal aorta, iliac, proximal coronary, thoracic aorta, femoral, popliteal, internal carotid

-narrowing of vessels, production of ischemia, obstruction, thrombosis, larger vessels = weakening wall, thrombosis, medium= ischemia

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13
Q

Explain the types of atherosclerosis. Fatty streak, fibrous plaque, complicated lesion

A
  • form foam cells, thin, flat, yellow, becomes thick and long
  • grey-white, lipid, smooth muscle, scare tissue and calcification, thickening of intima, predisposes to thrombus formation= decrease blood flow
  • fully developed
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14
Q

What is peripheral artery disease and its risk factors?

A

Atherosclerosis distal to the aortic arch

-male, >60, smokers, DM

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15
Q

What are the manifestations of PAD?

A
  • intermittent claudication (pain when walking)
  • calf pain and numbness
  • thinning of skin and s/c tissue
  • decreased blood supply (pale, cool, brittle, weak/absent pulses, hair loss, rubor)
  • leg colour blanches when elevated
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16
Q

What are complications of PAD? How is it diagnosed?

A
  • ulceration, gangrene, ischemic pain at rest, tissue necrosis
  • BP changes in legs, pulse changes, doppler U/S (detects BP and pulses), MRI, spiral CT, contrast angiography, inspection of limbs
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17
Q

What is the treatment of PAD?

A
  • protection of tissues
  • walking until pain= increases collateral circulation
  • avoid surface injury d/t slow healing
  • address cause
  • antiplatelet therapy (ASA)
  • Statins= vasodilator
  • surgery (femoralpopliteal bypass grafting)
  • percutaneous transluminal angioplasty and stenting
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18
Q

What is raynaud Phenomenon? State the difference between primary and secondary.

A

Intense vasospastic disorder of arteries and arterioles (usually fingers, less often toes)
P: symmetrical, without cause, no pain
S: non-sym, other disease/state of vasospasm (frostbite, hot/cold, vibration tools), intense pain, associated with PAD
- Usually women

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19
Q

What are the manifestations and treatment for raynaud phen. ?

A
  • tingling, numbness/aching, throbbing, pallor- cyanosis
  • avoidance of triggers, avoidance of vasoconstriction meds, vasodilation meds, sympathectomy (interruption of sympathetic nerve pathways)
  • decrease smoking and cold
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20
Q

What is an aneurysm? state the difference between true and false.

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A 
Abnormal localized dilation of blood vessel 
True: bounded by complete vessel wall 
-Berry (D) Saccular (P), fusiform (O) 
False: dissection or tear of wall 
-Dissecting, rupture
21
Q

What are risk factors for aortic aneurysm? diagnosed?

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A
  • atherosclerosis, trauma, infection, age

- ECG, U/S, MRI, CT

22
Q

What are the manifestations of a aneurysm?

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A 
Thoracic (substernal, back, neck pain) 
-trachea= stridor, cough, dyspnea
- laryngeal= hoarseness 
-esophagus= diff. swallowing 
- superior vena cava= facial/ neck edema 
Abd. aortic aneurysm (AAA) 
-pulsating mass if more than >4 cm 
- mild - severe abd. and back pain 
- lower back pain that radiates to legs
23
Q

Name complications of aneurysms.

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A
  • thrombi
  • compression (vasculature, nerves)
  • ruptures
24
Q

What is a dissecting aortic aneurysm? And risk factors?

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A

Hemorrhage into vessel wall- longitudinal tearing

-HT, 40-60 men, marfans, pregnancy, congenital defects of aortic valve, aortic coarctation/narrowing, blunt trauma

25
What are manifestations of dissecting aortic aneurysm?
- Excruciating pain anterior chest & back - Blood pressure (initially high, later may be unobtainable in one or both arms) - Syncope (black out) - lower extremity hemiplegia, paralysis - heart failure if aortic valve involvement
26
What is the diagnosis and treatment of dissecting AA?
D: physical exam, aortic angiography, transesophageal ECG, CT, MRI T: medical (stabilize BP, pain, anxiety), Surgery (resection, prosthetic graft)
27
What is arterial, systolic, diastolic BP, pulse pressure, mean arterial BP?
- ejection of blood from left ventricle to aorta - highest pressure (during contraction) - lowest pressure (during relaxation) - difference b/w systolic and diastolic - average pressure in the arterial system during ventricular contraction and relaxation
28
Explain how CO and peripheral vascular resistance interact in determining BP?
The product of the 2 = BP | - BP= CO (blood ejected from the heart) x peripheral vascular resistance (change in viscosity and radius of arterioles)
29
Explain the determinants of BP (short term and long term).
Short term: neural and humoral mechanisms (during exercise or threatening events) Long term: kidneys retain or excrete water and sodium to regulate vascular volume (ECV)
30
Explain neural mechanisms.
- medulla and pons gets a message from the body and regulates BP and pulse - parasympathetic impulses to heart slows HR - sympathetic impulses to heart and blood vessels= incr. HR and vasoconstriction - baroreceptors/stretch receptors sense incr. in pressure (intrinsic) - chemoreceptors sense change in carbon monoxide (intrinsic) - diffuse reactions d/t pain, cold (extrinsic)
31
Explain humoral mechanisms.
``` Renin angiotension aldosterone system -released in response to SNS activity, decreased volume -converts I-II causing vasoconstriction Vasopressin (ADH) Epinephrine - potent vasoconstrictor ```
32
What are the risk factors for PRIMARY HT?
- family hx - race - age - life style (high salt, fat intake, cholesterol, excessive alcohol, smoking, stress)
33
What are the risk factors for SECONDARY HT?
- diabetes - kidney disease - adrenal cortical disorders (facilitates salt and H2o retention) - pheochromocytoma (produce and release cate.) - narrowing of aorta - drugs - -obstructive sleep apnea - oral contraceptives (volume explanding estrogen and progesterone = sod. retention)
34
What are modifications to treat/ prevent HT?
-weight loss, exercise, decrease salt intake and alcohol, quit smoking, diuretics, beta blockers (dec. HR), ACE inhibitors (dec. vasoco.), calcium channel (dec. movement of Ca), vasodilation (relaxation of muscles)
35
Define systolic HT and relate to circulatory changes that occur with aging.
- stiffening of the large arteries - decreased baroreceptor sensitivity - incr. peripheral vascular resistance - decr. renal blood flow - elastin fibres are replaced with collagen fibres
36
Name some target organ damages
Heart: MI, heart failure, angina, L hypertrophy Brain: aneurysm, stroke, dementia, encephalapathy Kidney: HT nephropathy, chronic renal failure Liver Lungs Eyes: HT retinopathy Blood: elevated sugar levels
37
What is hypertensive crisis? What are symptoms?
Elevated BP with future target organ damage - >180/>110 - Emergency is DBP >120 with target damage and vascular damage - arterial spasms, papilledema, headache, restlesness, confusion, stupor, motor and sensory deficits, visual disturbances
38
Define orthostatic hypotension. State some of the causes.
Sustained drop in BP d/t change in body position 500-700 ml of blood shift to lower body - reduced blood volume - pharmaceuticals - Aging: loss of skeletal muscles (decr. blood volume, inability to raise HR, decr. skeletal muscle pumps) - bed rest/imm.: reduced BV, failure of vasocon., weakness of skel. muscles
39
State the manifestations and diagnosis of Orthostatic hypotension?
Manifestations: visual changes, dizziness, syncope, ataxia, weakness, light headed (drop in systole =20 and diastole= 10) Diagnosis: lying/standing BP with 2-3 minute wait, use of tilt table
40
The venous circulation is a low pressure system. Describe venous return of the blood from the lower extremities, function, and effects of gravity.
blood from the skin and sub cut. tissues in legs collect in superficial veins> communicating veins>deep venous channels>heart - leg muscle moves venous blood from lower extremities to heart - walk= incr. flow in deep venous channels - contraction= valves prevent back flow and blood goes into deep veins - relaxation= valves open, blood from superficial veins move to deep veins
41
What is varicose veins? State the difference between primary and secondary.
Dilation (lumpy) veins Primary: originate in superficial saphenous veins (standing, pregnancy, abd. pressure, heavy lifting) Secondary: impaired flow in deep veins d/t other disease (DVT, fistulas, malformations, tumour, pregnancy)
42
What is the patho of Chronic venous insufficiency? What are the causes?
Incr. venous pressure= dilation and stretching of vessel walls= full weight of the venous column of blood is transmitted to the leg veins - Venous HT causing stretching, impaired blood flow (edema, ischemia, necrosis, breakdown of RBC. brown pigmentation)
43
What is DVT? and what are the risk factors?
Thombus (in vein) and inflammation (in vessel wall) (superficial or deep veins) Risks: Virchow's Triad (venous stasis, vascular trauma, hypercoagulation)
44
Explain venous stasis in DVT.
- bed rest/immobility= decr. flow, pooling - SC injury (spinal cord) - acute MI/CHF/ Shock= impaired cardiac function - obstruction= incr. viscosity d/t dehydration
45
Explain Vascular trauma in DVT.
- venous catheters - surgery (ortho) - trauma/ infection/ # hip
46
Explain Hypercoagulability in DVT.
- genetics - stress/ trauma - pregnancy= incr. fibrogen, prothrombin, coag. factors - oral contraceptives - dehydration= incr. concentration of clotting fct. - cancer= coagulation may be produced by tumour cells
47
State the manifestations of DVT.
- often no asymptomatic - pain - inflammation (fever, malaise, incr. WBC), swelling - tenderness
48
State the treatment of DVT.
- prevent thrombus formation - anticoagulation - elevate limbs and bedrest (until 0 swelling/tend.) - ambulation with elastic stockings - heat (relieve vasospasm and inflam.)

Pathophysiology 212 (4 decks)

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