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Pathophysiology 212 > Chapter 18 > Flashcards

Chapter 18 Flashcards

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.

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?

A
  • atherosclerosis, trauma, infection, age

- ECG, U/S, MRI, CT

22
Q

What are the manifestations of a aneurysm?

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.

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

What is a dissecting aortic aneurysm? And risk factors?

A

Hemorrhage into vessel wall- longitudinal tearing

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

25
Q

What are manifestations of dissecting aortic aneurysm?

A
  • 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
Q

What is the diagnosis and treatment of dissecting AA?

A

D: physical exam, aortic angiography, transesophageal ECG, CT, MRI

T: medical (stabilize BP, pain, anxiety), Surgery (resection, prosthetic graft)

27
Q

What is arterial, systolic, diastolic BP, pulse pressure, mean arterial BP?

A
  • 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
Q

Explain how CO and peripheral vascular resistance interact in determining BP?

A

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
Q

Explain the determinants of BP (short term and long term).

A

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
Q

Explain neural mechanisms.

A
  • 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
Q

Explain humoral mechanisms.

A 
Renin angiotension aldosterone system 
-released in response to SNS activity, decreased volume 
-converts I-II causing vasoconstriction 
Vasopressin (ADH) 
Epinephrine 
- potent vasoconstrictor
32
Q

What are the risk factors for PRIMARY HT?

A
  • family hx
  • race
  • age
  • life style (high salt, fat intake, cholesterol, excessive alcohol, smoking, stress)
33
Q

What are the risk factors for SECONDARY HT?

A
  • 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
Q

What are modifications to treat/ prevent HT?

A

-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
Q

Define systolic HT and relate to circulatory changes that occur with aging.

A
  • stiffening of the large arteries
  • decreased baroreceptor sensitivity
  • incr. peripheral vascular resistance
  • decr. renal blood flow
  • elastin fibres are replaced with collagen fibres
36
Q

Name some target organ damages

A

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
Q

What is hypertensive crisis? What are symptoms?

A

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
Q

Define orthostatic hypotension. State some of the causes.

A

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
Q

State the manifestations and diagnosis of Orthostatic hypotension?

A

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
Q

The venous circulation is a low pressure system. Describe venous return of the blood from the lower extremities, function, and effects of gravity.

A

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
Q

What is varicose veins? State the difference between primary and secondary.

A

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
Q

What is the patho of Chronic venous insufficiency? What are the causes?

A

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
Q

What is DVT? and what are the risk factors?

A

Thombus (in vein) and inflammation (in vessel wall)
(superficial or deep veins)
Risks: Virchow’s Triad (venous stasis, vascular trauma, hypercoagulation)

44
Q

Explain venous stasis in DVT.

A
  • bed rest/immobility= decr. flow, pooling
  • SC injury (spinal cord)
  • acute MI/CHF/ Shock= impaired cardiac function
  • obstruction= incr. viscosity d/t dehydration
45
Q

Explain Vascular trauma in DVT.

A
  • venous catheters
  • surgery (ortho)
  • trauma/ infection/ # hip
46
Q

Explain Hypercoagulability in DVT.

A
  • 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
Q

State the manifestations of DVT.

A
  • often no asymptomatic
  • pain
  • inflammation (fever, malaise, incr. WBC), swelling
  • tenderness
48
Q

State the treatment of DVT.

A
  • 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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