Block I: Veins/Arteries/BP Flashcards
varicose veins usually involve the [] vein
saphenous
[] is superficial vein in which blood has pooled
varicose vein
what are 3 characteristics of varicose veins
- distended
- tortuous
- palpable
what system is dysfunctional in varicose veins?
valvular, muscluar
what is the pathophysiology behind varicose veins
- increased hydrostratic pressure
- damaged valves cannot maintain normal venous pressure
- increase pressure arises, creating more complications
- -tortous veins, edema
what are some risk factors for varicose veins
- standing for long periods of time, physical labor
- constricting clothes
- crossing leg at knees
i. e. trauma or gradual vein distention
what are some complications for varicose veins
- chronic venous insufficiency
[] results from progression of varicose veins due to sustained inadequate venous return
chronic venous insufficiency
describe the pathway to chronic venous insufficiency
- venous HTN
- circulatory stasis
- tissue hypoxia
- inflammatory reaction
- venous stasis ulcers and dermatitis
what circulation becomes to sluggish to meet metabolic needs (such as chronic venous stasis) what can result
- hypoxia, lack of nutritents
- faulty removal of metabolic waste
- cell death & necrosis (ulcers)
- -infection risk, from ulcer + poor circulation impairs delivery of immune cells
what are some treatments for varicose veins?
- leg elevation
- compression stockings
- exercise
- endovenous ablation
- US guided foam sclerotherapy
- surgical ligation and vein stripping
[] is a blood clot that is attached to a vessel wall
thrombosis
[] is a blood clot that has detached from vessel walls
thromboembolus
[] is a detached blood clot (thromboembolus) that occludes a pulmonary artery
pulmonary emboli
[] are clots found in large veins, primarily in lower extremeties
deep vein thrombosis
[] can cause obstruction of venous flow and increased venous pressure
DVT
what are the components of Virchow’s Tried and what do they mean []
- venous stasis
- venous endothelial
- hypercoaguable stages
indicate patient’s risk to DVT
what can cause venous statsis
- immobility
- obesity
- prolonges leg dependency
- age
- HF
what can cause venous endothelial damage
- trauma
2. medications
what can cause hypercoaguable stages
- inherited d/o
- malignancy
- pregnancy
- oral BC
- hormone replacement
- antiphospholipid symdrome
[] is a significant risk of DVT, why?
Hopsitalization
- surgery, trauma
- being bedridden
- having spinal cord injury
it is important to do what after a procedure
get up and walk to prevent DVT!
what prophylactic DVT measures may be given to a hospitalized patient
- low molecular weight herparin
- antithrombin agents
- warfarin
- pneumatic devices
- inverio vena cava filter
describe the pathopysiology of a DVT
- acc. clotting factors and platelets -> thrombus formation in vein (stasis will help promote)
- inflammation may cause local symptoms, usualy insidius
- if significnat obstrucion to venous flow occurs, increased pressure in vein behind clot may lead to edema of extremity
persistent venous outflow obstruction leads to []
post thrombotic syndrome
chronir, persistent pain, edema, ulceration
what is post thrombotic symdrone
chronic, persistent pain, edema, and ulceration of effected limb
complication of DVT
what are some tests you might order for a patient you suspect to have a DVT
- D-dimer (NOS, shows break down of clot and thats it)
- CT
- MRI
- US
how might you treat a DVT pt.
- low mol. wt. heparin
- unfractionated IV heparin
- antithrombin agents
- SQ heparin
- thrombolytic therapy
- aspirin
- inferior vena cava filter
[] is a progressive occulsion of superio vena cava that leads to venous distention in upper extremities and head
superior vena cava syndrome
what is the leading cause of superior vena cava syndrome
bronchogenic cancer (70%)
other causes: lymphomas, mets of other cancers
what are some bening causes of SVCS, how often do these occur?
30% benign causes
- invasive therapies
- thrombosis
- histoplasmosis
- tuberculosis
- cystic fibrosis
- benign tumors
SVC is usually [] pressure
LOW, easily compressed
what anatomical structure abuts the SVC and may obstruct venous return to R atria if enlarged (by tumor)
right mainstem bronchus
what surrounds the SVC which can pose a risk for obstruction if involved in cancer?
lymph nodes and right mainstem bronchus
a patient has swelling of face, chest, other parts of body
- venous distention above SVC
- HA
- dizziness
- cough
what may you suspect?
SVC, esp. if hx lung cancer
how would you dx. a SVC patient
- chest XR
- dopler studies
- CT
- MRI
- US
SVCS is a
a. vascular
b. oncologic
emergency
oncologic
what is the treatment protocol for malignant SVCS
- radiation
- surgery
- chemo
- admin diuretic
- steroidal
- anticoagulant agent
what is teratment protocol for non-malignant SVCS
- bypass sx
- thrombolysis
- balloon angioplasty
- placement intravascular stents
[] refers to arterial pressure in systemic circulation
BP
[] is measure of BP when heart constracts/beats
SBP
[] is measure of BP when heart is relaxed/filling
DBP
[] is consistent elevation of systemic arterial BP
HTN
[] is the most common primary dx in US
HTN
[] is elevated SBP with normal DBP
isolated systolic HTN, common in pt. 60+
isolated systolic HTN is primarily due to []
diminished arterial compliance
what are risks of isolated systolic HTN
4-fold risk
- MI
- LV hypertrophy
- renal dysfunction
- stroke
- cv mortality
what % of HTN cases are idiopathic
95
how might overactivity SNS cause HTN
- increased prod. catecholamines (epi/NE_
- increased HR -> systemic vasoconstriction
- RAAS
- angiotensin II to constrict
- aldoeterone to increase Na and water retention
[] is overactive in HTN pt.
RAAS
what effect does arteriolar remodeling have on CV
increase PR, caused by atherosclerosis and cardiac hypertorphy
what medications oppose RAAS
- ACEI
- ARBS
- RENIN INH
[] is the process of excretion of Na in urine via activation of kidneys when P rises
natiuresis
[] is promoted by ventriculat and atrial natriuretic peptides (VNP, ANP) and C-type natruretic peptide (CNP_ and urodilatin
nariutesis
[] opposed alodsterone
natruresis hormones
-EXCRETE Na instead of REABSORBING Na
can cause volume depletion
what are the effects of ANP and BNP in HTN
Can cause
- ventricular hypertrophy
- atherosclerosis
- HF
[] is the most common cause of secondary HTN
renal dysfunction/failure
systemic disease that increase [] or []can cause secondary HTN
- peripheral vascular resistance
2. cardiac output
between systolic and diastolic HTN, what is more pathological? Why?
SBP HTN, nore likely to cause end organ damage
-MI, stroke, kidney disease
what 2 vitamins can cause HTN if you eat TOO LITTLE of them?
- K
- Mg
- Ca
any condition that increased HR or stroke volume will cause []
increased CO
any factors that increase blood viscosity or reduced vessel diameter will case []
increase PR
what is complicated HTN?
HTN that is chronic and damages the walls of systemic BVs
- hypertrophy/hyperplasia
- fibrosis tunica intima
- fibrosis tunica media
- vascular remodelying
*significnat fibrosis affects blood flow to organs
sustained increased preassure causes [] of itima
proliferations
a diastolic BP of [] indicated hypertensive emergency
> 140 mmHG
what usually triggers hypertensive emergency
- drugs used for general anesthesia
what is a major complication of hypertensive crisis?
encephalopathy
how is HTN dx?
2-3 separate occaisons of suscained increased BP
what is masked HTN?
HTN that is low in office, high at home (opp. white coat HTN)
what is the sodium intake goal?
2.4 g/day
what vitamin should be increaased in HTN pt
K
what compensates for orthostatic HTN
baroreceptors = prompt increase in HR and constriction of systemic arterioles
what is the threshold for orthostatic hypotension
decrease in systolic and diastolic BP on standing
20mmHG or more
and by 10mmHg or more within 3 minutes of standing
what can cause acutre orthostrasic hypotension
- meds.
- prolonged immobility
- starvation
- exhaustion
- volume depletion
what can cause chronic orthostatic hypotension
- secondary
2. endocrine/metabolic d/o
what are some normal compensatory mechanisms to protect from orthostatic hypotension
- increase SNS through streatch receptors
- not super effective in maintaining stable BP
- neurogenic causes
- non-neurogenic causes
[] is intermittend symptoms of orthostatic intolerance accompanied by excessive tachycardia without arterial hypotension
POTS
postural tachycardia syndrome
