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Pathophysiology III > Block I: Veins/Arteries/BP > Flashcards

Block I: Veins/Arteries/BP Flashcards

1
Q

varicose veins usually involve the [] vein

A

saphenous

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2
Q

[] is superficial vein in which blood has pooled

A

varicose vein

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3
Q

what are 3 characteristics of varicose veins

A
  1. distended
  2. tortuous
  3. palpable
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4
Q

what system is dysfunctional in varicose veins?

A

valvular, muscluar

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5
Q

what is the pathophysiology behind varicose veins

A
  1. increased hydrostratic pressure
    - damaged valves cannot maintain normal venous pressure
    - increase pressure arises, creating more complications
    - -tortous veins, edema
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6
Q

what are some risk factors for varicose veins

A
  1. standing for long periods of time, physical labor
  2. constricting clothes
  3. crossing leg at knees
    i. e. trauma or gradual vein distention
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7
Q

what are some complications for varicose veins

A
  1. chronic venous insufficiency
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8
Q

[] results from progression of varicose veins due to sustained inadequate venous return

A

chronic venous insufficiency

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9
Q

describe the pathway to chronic venous insufficiency

A
  1. venous HTN
  2. circulatory stasis
  3. tissue hypoxia
  4. inflammatory reaction
  5. venous stasis ulcers and dermatitis
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10
Q

what circulation becomes to sluggish to meet metabolic needs (such as chronic venous stasis) what can result

A
  1. hypoxia, lack of nutritents
  2. faulty removal of metabolic waste
  3. cell death & necrosis (ulcers)
    - -infection risk, from ulcer + poor circulation impairs delivery of immune cells
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11
Q

what are some treatments for varicose veins?

A
  1. leg elevation
  2. compression stockings
  3. exercise
  4. endovenous ablation
  5. US guided foam sclerotherapy
  6. surgical ligation and vein stripping
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12
Q

[] is a blood clot that is attached to a vessel wall

A

thrombosis

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13
Q

[] is a blood clot that has detached from vessel walls

A

thromboembolus

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14
Q

[] is a detached blood clot (thromboembolus) that occludes a pulmonary artery

A

pulmonary emboli

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15
Q

[] are clots found in large veins, primarily in lower extremeties

A

deep vein thrombosis

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16
Q

[] can cause obstruction of venous flow and increased venous pressure

A

DVT

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17
Q

what are the components of Virchow’s Tried and what do they mean []

A
  1. venous stasis
  2. venous endothelial
  3. hypercoaguable stages

indicate patient’s risk to DVT

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18
Q

what can cause venous statsis

A
  1. immobility
  2. obesity
  3. prolonges leg dependency
  4. age
  5. HF
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19
Q

what can cause venous endothelial damage

A
  1. trauma

2. medications

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20
Q

what can cause hypercoaguable stages

A
  1. inherited d/o
  2. malignancy
  3. pregnancy
  4. oral BC
  5. hormone replacement
  6. antiphospholipid symdrome
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21
Q

[] is a significant risk of DVT, why?

A

Hopsitalization

  1. surgery, trauma
  2. being bedridden
  3. having spinal cord injury
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22
Q

it is important to do what after a procedure

A

get up and walk to prevent DVT!

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23
Q

what prophylactic DVT measures may be given to a hospitalized patient

A
  1. low molecular weight herparin
  2. antithrombin agents
  3. warfarin
  4. pneumatic devices
  5. inverio vena cava filter
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24
Q

describe the pathopysiology of a DVT

A
  1. acc. clotting factors and platelets -> thrombus formation in vein (stasis will help promote)
  2. inflammation may cause local symptoms, usualy insidius
  3. if significnat obstrucion to venous flow occurs, increased pressure in vein behind clot may lead to edema of extremity
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25
Q

persistent venous outflow obstruction leads to []

A

post thrombotic syndrome

chronir, persistent pain, edema, ulceration

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26
Q

what is post thrombotic symdrone

A

chronic, persistent pain, edema, and ulceration of effected limb

complication of DVT

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27
Q

what are some tests you might order for a patient you suspect to have a DVT

A
  1. D-dimer (NOS, shows break down of clot and thats it)
  2. CT
  3. MRI
  4. US
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28
Q

how might you treat a DVT pt.

A
  1. low mol. wt. heparin
  2. unfractionated IV heparin
  3. antithrombin agents
  4. SQ heparin
  5. thrombolytic therapy
  6. aspirin
  7. inferior vena cava filter
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29
Q

[] is a progressive occulsion of superio vena cava that leads to venous distention in upper extremities and head

A

superior vena cava syndrome

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30
Q

what is the leading cause of superior vena cava syndrome

A

bronchogenic cancer (70%)

other causes: lymphomas, mets of other cancers

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31
Q

what are some bening causes of SVCS, how often do these occur?

A

30% benign causes

  1. invasive therapies
  2. thrombosis
  3. histoplasmosis
  4. tuberculosis
  5. cystic fibrosis
  6. benign tumors
32
Q

SVC is usually [] pressure

A

LOW, easily compressed

33
Q

what anatomical structure abuts the SVC and may obstruct venous return to R atria if enlarged (by tumor)

A

right mainstem bronchus

34
Q

what surrounds the SVC which can pose a risk for obstruction if involved in cancer?

A

lymph nodes and right mainstem bronchus

35
Q

a patient has swelling of face, chest, other parts of body

  • venous distention above SVC
  • HA
  • dizziness
  • cough

what may you suspect?

A

SVC, esp. if hx lung cancer

36
Q

how would you dx. a SVC patient

A
  1. chest XR
  2. dopler studies
  3. CT
  4. MRI
  5. US
37
Q

SVCS is a

a. vascular
b. oncologic

emergency

A

oncologic

38
Q

what is the treatment protocol for malignant SVCS

A
  1. radiation
  2. surgery
  3. chemo
  4. admin diuretic
  5. steroidal
  6. anticoagulant agent
39
Q

what is teratment protocol for non-malignant SVCS

A
  1. bypass sx
  2. thrombolysis
  3. balloon angioplasty
  4. placement intravascular stents
40
Q

[] refers to arterial pressure in systemic circulation

A

BP

41
Q

[] is measure of BP when heart constracts/beats

A

SBP

42
Q

[] is measure of BP when heart is relaxed/filling

A

DBP

43
Q

[] is consistent elevation of systemic arterial BP

A

HTN

44
Q

[] is the most common primary dx in US

A

HTN

45
Q

[] is elevated SBP with normal DBP

A

isolated systolic HTN, common in pt. 60+

46
Q

isolated systolic HTN is primarily due to []

A

diminished arterial compliance

47
Q

what are risks of isolated systolic HTN

A

4-fold risk

  1. MI
  2. LV hypertrophy
  3. renal dysfunction
  4. stroke
  5. cv mortality
48
Q

what % of HTN cases are idiopathic

A

95

49
Q

how might overactivity SNS cause HTN

A
  1. increased prod. catecholamines (epi/NE_
  2. increased HR -> systemic vasoconstriction
  3. RAAS
    - angiotensin II to constrict
    - aldoeterone to increase Na and water retention
50
Q

[] is overactive in HTN pt.

A

RAAS

51
Q

what effect does arteriolar remodeling have on CV

A

increase PR, caused by atherosclerosis and cardiac hypertorphy

52
Q

what medications oppose RAAS

A
  1. ACEI
  2. ARBS
  3. RENIN INH
53
Q

[] is the process of excretion of Na in urine via activation of kidneys when P rises

A

natiuresis

54
Q

[] is promoted by ventriculat and atrial natriuretic peptides (VNP, ANP) and C-type natruretic peptide (CNP_ and urodilatin

A

nariutesis

55
Q

[] opposed alodsterone

A

natruresis hormones

-EXCRETE Na instead of REABSORBING Na

can cause volume depletion

56
Q

what are the effects of ANP and BNP in HTN

A

Can cause

  1. ventricular hypertrophy
  2. atherosclerosis
  3. HF
57
Q

[] is the most common cause of secondary HTN

A

renal dysfunction/failure

58
Q

systemic disease that increase [] or []can cause secondary HTN

A
  1. peripheral vascular resistance

2. cardiac output

59
Q

between systolic and diastolic HTN, what is more pathological? Why?

A

SBP HTN, nore likely to cause end organ damage

-MI, stroke, kidney disease

60
Q

what 2 vitamins can cause HTN if you eat TOO LITTLE of them?

A
  1. K
  2. Mg
  3. Ca
61
Q

any condition that increased HR or stroke volume will cause []

A

increased CO

62
Q

any factors that increase blood viscosity or reduced vessel diameter will case []

A

increase PR

63
Q

what is complicated HTN?

A

HTN that is chronic and damages the walls of systemic BVs

  1. hypertrophy/hyperplasia
  2. fibrosis tunica intima
  3. fibrosis tunica media
  4. vascular remodelying

*significnat fibrosis affects blood flow to organs

64
Q

sustained increased preassure causes [] of itima

A

proliferations

65
Q

a diastolic BP of [] indicated hypertensive emergency

A

> 140 mmHG

66
Q

what usually triggers hypertensive emergency

A
  1. drugs used for general anesthesia
67
Q

what is a major complication of hypertensive crisis?

A

encephalopathy

68
Q

how is HTN dx?

A

2-3 separate occaisons of suscained increased BP

69
Q

what is masked HTN?

A

HTN that is low in office, high at home (opp. white coat HTN)

70
Q

what is the sodium intake goal?

A

2.4 g/day

71
Q

what vitamin should be increaased in HTN pt

A

K

72
Q

what compensates for orthostatic HTN

A

baroreceptors = prompt increase in HR and constriction of systemic arterioles

73
Q

what is the threshold for orthostatic hypotension

A

decrease in systolic and diastolic BP on standing

20mmHG or more

and by 10mmHg or more within 3 minutes of standing

74
Q

what can cause acutre orthostrasic hypotension

A
  1. meds.
  2. prolonged immobility
  3. starvation
  4. exhaustion
  5. volume depletion
75
Q

what can cause chronic orthostatic hypotension

A
  1. secondary

2. endocrine/metabolic d/o

76
Q

what are some normal compensatory mechanisms to protect from orthostatic hypotension

A
  1. increase SNS through streatch receptors
    - not super effective in maintaining stable BP
    - neurogenic causes
    - non-neurogenic causes
77
Q

[] is intermittend symptoms of orthostatic intolerance accompanied by excessive tachycardia without arterial hypotension

A

POTS

postural tachycardia syndrome

Pathophysiology III (5 decks)

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