Pathophysiology Exam 2

When the nurse is obtaining a health history for a client with mitral valve stenosis, which question should the nurse ask?

"Did you ever have strep throat during childhood?"

Pathophysiology of artherosclerosis

- risk factors cause damage to the endothelium and tunica intima of arteries -damage allows foam cells to invade tunica intima and form fatty streaks - smooth muscle cells of tunica media form fibrous capsules of collagen and elastin, and lay down calcium deposits ----> becomes plaque - plaque builds up and causes ischemia of the artery, which leads to complications

acute episode afib

-Afib RVR (rapid ventricular rate) -ventricular rate is 150 or higher -HR too fast = decreased CO Clinical manifestations: -syncope -fatigue -SOA Immediate treatment: -Cardioversion -IV meds to slow R

Hypertensive crisis

-BP is 180/120 or greater Clinical manifestations: -severe headache -blurred vision -altered mental status -chest pain -SOA Complications: -Hemalogic stroke -confusion -retinopathy -cardiac ischemia -acute renal failure

Heart failure

-Heart is too weak and is unable to pump blood -Blood backs up and causes congestion -Leads to fluid overload (peripheral or pulmonary)

How does hypertension increase afterload?

-High pressure in the arteries and aorta increases the amount of pressure that the heart has to overcome -An increased amount of pressure added onto the already existing afterload makes it more difficult for the heart to eject blood -Can lead to blood "falling back" and not making it to the rest of the body ---> heart failure

Left Ventricular Dysfunction (Left-sided Heart Failure)

-Left side of heart = Lungs -The left side of the heart is connected to the lungs -The left side of the heart pumps oxygenated blood into the arterial circulation -Because the heart is failing, blood "falls" back into the lungs -Causes the lungs to become congested -Results in pulmonary edema (patient is "drowning" in their own fluids) Causes: -Acute MI in the left main coronary artery or left anterior descending artery -Valve dysfunction (aortic stenosis) -Cardiomyopathy -Hypertension Results of Impairment of the Left Ventricle: -Diminished cardiac output -Decreased ejection fraction -Blood accumulates in the left ventricle, left atrium, and pulmonary circulation -Results in pulmonary congestion Clinical Manifestations: -DROWNIN pneumonic

Long term complications of hypertension

-Left-sided heart failure -coronary artery disease -CVA -Peripheral artery disease -retinopathy (blindness) -chronic kidney disease

Heart failure education

-Monitor electrolyte lvlvs while taking diuretics -Low NA+ diet (helps decrease fluid) -Elevate HOB (helps with diuresis) -Daily weight (same time , scale and clothes) - report increase of >2-3 lbs in one day

Why does athersclerosis cause narrowing of vessels?

-Plaque attaches to the linings of vessels -Decreases the compliance of the vessels, making it more difficult to stretch -results in the narrowing of the blood vessels

afterload

-Resistance that the blood experiences as it leaves the ventricle -Pressure that the blood faces as it is trying to eject from the heart

preload

-Stretching of the ventricles -The volume of blood in the ventricles causes the stretch of myocardial muscle fibers -Occurs at diastole -Determined by venous return

latent TB infection

-T cells and macrophages surround organisms in granulomas and limit spread -DO NOT have active disease and CAN NOT spread it to others

rheumatoid arthritis

-T-cell mediated response to immunologic trigger -RF reacts with IgG to form immune complexes at the joint -results in damage/destruction to joint cartilage CM: -anemia -fatigue -neuropathy -renal -fibrotic lung

Why does left-sided heart failure cause pulmonary congestion?

-The heart is not pumping as well on the left side so the blood backflows and accumulates in the LV, LA, and pulmonary veins -This impairs gas exchange

Right Ventricular Dysfunction (aka right sided heart failure)

-The right side of the heart is connected to the venous circulation -The right side of the heart receives unoxygenated blood from the venous system -Blood becomes congested and goes back into venous circulation Causes: -Left-sided heart failure; Causes fluid overload and increased pressure ---> increased pressure = increased work for the heart ---> blood backs up into the right side of the heart and causes Right-sided heart failure -COPD; the heart is failing because the pressure in the lungs is too high -Valve dysfunction (tricuspid or pulmonic) Results of impairment of Right Ventricle: -Reduced BF into venous circulation and the left side of the heart -Decreased cardiac output -Increased pressure in the RV, RA, and systemic venous circulation Clinical manifestations: SWELLING pneumonic

How is preload determined?

-Venous return (the amount of blood returning to the heart) -Preload is determined by the stretch of the heart due to the volume of blood within the heart -No venous return = No preload

Bradycardia

-a type of arrhythmia -slow heart rate -low CO; SA node is not firing correctly, Abnormal conduction between atria and ventricle -may need a pacemaker

Tachycardia

-a type of arrhythmia -fast heart rate - not enough diastolic time for the filling of ventricles -decreased CO -Can be fatal

Afib

-a type of arrhythmia -rapid disorganized atrial activation causing uncoordinated atrial contraction and ventricular response Causes: -Cardiac: HF, valve disease, MI, CAD, HTN -Other: drug abuse, PE, hyperthyroidism Patho: -SA to AV should be a SMOOTH pathway, but SA loses its function --> heart tries to compensate and generate its own impulses--> this leads to a bunch of signals coming to AV node from all over--> leading to very irregular ventricular contractions --> more ventricular contractions = a higher heart rate

pleural effusion

-abnormal accumulation of fluid in the pleural space Causes: -malignancy -infection -heart, renal, liver failure -procedures CM: -repiratory distress -hypoxemia Treatment: -remove fluid

aneurysms

-abnormal bulge in vessels -can happen to any artery or vein

orthostatic hypotension

-abnormal drop in BP after standing

arrhythmias

-abnormal heart rhythms -uncoordinated heart muscle contractions Causes: -electrolyte imbalances -decreased oxygen delivery to cardiac cells -structural damage to the heart -medications/drugs

pulmonary arterial HTN

-abnormal pressure elevation within arterial complex of lungs -usually a secondary condition CM: -dyspnea with exertion -fatigue -syncope -HF

pericardial effusion

-accumulation of fluid in the pericardial cavity -rapid effusions are critical! -this is a CM of acute heart failure

pulmonary edema

-acute HF exacerbation Patho: -too much fluid in the body -heart can't pump effectively -fluid moves into alveoli in the lungs -causes impaired gas exchange Cause: -poor compliance with treatment plan -worsening disease Clinical manifestations: -productive cough (frothy sputum) -SOA -Rapid pulse -cyanotic -confusion -coarse crackles Treatment: -excrete fluid -oxygen therapy

Complications of heart failure

-acute heart failure exacerbation -arrhythmias and sudden cardiac death -chronic kidney disease (not enough CO = not enough perfusion) -liver damage (congestion of fluid) -decreased quality of life

true aneurysm

-all layers of the blood vessel walls bulge or one side bulges

Lung cancer

-arise from epithelial lining of major bronchi - 2 types; non-small cell, small cell Risk factors: smoking, second-hand smoke, environmental CM: -cough -hemoptysis -dyspnea -weight loss -anorexia -weakness -sweats -fever

neurovascular assessment

-assess long bones; change in shape or alignment, rapid swelling = neurovascular compromise -circulation; skin color, temp, pulses, capillary refill -movement -sensation; numbness or pain

chronic afib

-asymptomatic -palpations/fatigue -blood pools in atria and causes blood clots = blood clots travel = stroke Long-term maintenance: -anticoagulants -Meds to control HR (they prevent ventricles from responding as often and as random to numerous signals)

congestive heart failure (CHF)

-backup of fluid into lungs and/or peripheral tissues secondary to HF

ventilation without perfusion

-blood circulation is blocked, but there is still breathing happening -unable to pass O2 to blood from alveoli EX: DVT

perfusion without ventilation

-blood is circulating, but NO breathing is happening -airway is blocked, so NO O2 received and NO CO2 dropped off -shunting occurs -EX: asthma

metabolic acidosis

-body shifts from aerobic to anaerobic metabolism -lactic acid accumulates in the blood; pH drops Diagnosis: -ABGs

osteoblasts

-bone producing cells -respond to parathyroid hormone

shunting

-changing blood flow to certain areas

COPD

-chronic obstructive pulmonary disease -inflammation and destruction of lung parenchyma/central airways causing irreversible expiratory airflow limitation 2 conditions: -chronic bronchitis -emphysema

cardiac tamponade

-compression of the heart caused by large pericardial effusion -restricts heart expansion; LV has decreased filling, RV cannot accept enough blood accumulation of fluid in pericardial sac --> pericardial effusion --> restricts expansion of the heart --> decreases BF/perfusion --> shock Clinical Manifestations: -tachycardia; heart is working harder to pump more blood because there is a low CO -jugular vein distention -hypotension -muffled heart sounds; heart is pumping through fluid -circulatory shock; because there is no bood flow Diagnosis: Echo

RAAS compensatory mechanism

-decreased CO = decreased perfusion = low oxygen -stimulates renin -increases water retention, which increases preload ---> can lead to Right-sided7 heart failure

Why is it common for heart failure patients to have arrhythmias?

-decreased O2 delivery to cardiac cells, d/t poor perfusion from a failing heart -structural damage of the heart; heart is failing and doesn't pump correctly

hypoxemia

-deficient amount of oxygen in arterial blood -aerobic metabolism ceases; anaerobic metabolism takes over Causes: -inadequate O2 in air -respiratory disorders -dysfunction of CNS -alteration in circulation

Frank-Starling Mechanism

-does NOT work longterm -The heart increases the stretch of myocardial fibers so they can fill with more blood, which will then increase the preload -Overtime the stretching will increase the oxygen demand increased contractility = increased myocardial work = increased oxygen demands

modifiable risk factors for artherosclerosis

-dyslipidemia -hypertension -smoking -obesity -high cholesterol -diabetes

Volume overload leads to...

-elongation and thinning of myocytes -heart attempts to stretch myocardial fibers to increase the force of contraction (frank-starling mechanism) ---> stretching thins the fibers and makes them lose elasticity --> leads to fluid overload

Risk factors for hypertension

-family hx -race -age-related -insulin resistance -high sodium intake -obesity -excessive alcohol consumption -stress -smoking -diet high in cholesterol

Compensatory mechanisms of heart failure

-frank-starling mechanism -sympathetic nervous system -RAAS

Cardiac conduction system

-heart generates its own electrical impulses -action potentials = excitation/activation of the cardiac muscle

complications of COPD

-hypercapnia and hypoxemia cause pulmonary vascular shunting and vasoconstriction -increased vascular resistance - pulmonary arterial HTN develops - R side of heart pushes against high pressure in pulmonary arteries -Right ventricle atrophies -R-sided heart failure (cor pulmonale)

ARF

-impaired gas exchange due to pump, lung failure, or both 2 types: - hypoxemic resp failure (COPD, pulmonary edema, interstitial lung disease, pneumonia) -hypercapnic/hypoxemic resp failure ( drug overdose, TBI, spinal cord injury, muscular dystrophy)

hypercapnia

-inadequate ventilation leads to excessive carbon dioxide in the blood -arises when compensatory mechanisms are inadequate -produces respiratory acidosis CM: -SOB -diaphoresis -tachypnea -abdominal breathing -cyanosis -resp acidosis

sympathetic nervous system compensatory mechanism

-increases CO (CO = SVxHR) -Increases the HR in an attempt to increase CO, yet this increases BP overtime and causes HTN -HTN increases afterload and is a cause of L-sided heart failure!!!

Non moidifiable risk factors for artherosclerosis

-increasing age -male gender -post-menopausal women -genetic disorders of lipid metabolism

osteomylitis

-infection of the bone -commonly staph -causes bone destruction/abscess, the blood supply to bone is destroyed = necrosis CM: -chills, fever, edema, malaise, drainage, pain Treatment: -long-term antibiotics -surgery debridement -hyperbaric

cystic fibrosis

-inherited disorder causing gene mutation -abnormal fluid secretion by exocrine glands in the epithelial lining of resp, GI, and reproductive tract Diagnosis: - positive family hx, gene abnormality -airway obstruction -chronic inflammation Treatment: -no cure -open airways -mobilize secretions -pancreatic enzyme replacement

ejection fraction

-measurement of the volume percentage of blood ejected with each contraction (in the left ventricle)

osteopenia

-metabloic disease -abnormal reduction of bone density -part of the progression to osteoporsis

sudden injury fracture

-most common -falls, trauma

false aneurysm

-not actually an aneurysm!! -dissection (hole) in inner artery wall---> allows blood to pool in surrounding tissues and form a bulge

Clinical manifestations of hypertension

-often nothing/silent killer -headache -dizziness -blurred vision

Complications of atherosclerosis

-peripheral artery disease -aneurysms -thrombus; MI, stroke, CAD -hypertension (high BP)

unstable plaque

-plaque rupture and migration through a vessel -thrombus may cause occlusion in arteries of the heart, brain, limb -causes severe ischemia/infarction -very dangerous !!!

acute HF exacerbation

-pulmonary edema -peripheral edema

Heart

-pumps blood through the circulatory system -left side of heart moves blood to body and tissues -right side of heart moves blood to pulmonary system

calcitonin

-released by the thyroid when blood calcium is HIGH -inhibits the release of calcium from bone (inhibits osteoclast activity) -inhibits calcium and phosphate reabsorption by the kidney

influenza

-respiratory tract infection caused by an influenza virus -upper-airway infection; kills mucous-secreting epithelial cells which leads to holes between underlying basal cells, thus allowing extracellular fluid to escape (runny nose) -lower respiratory tract; cause shedding of bronchial/alveolar cell; promotes bacterial adhesion -transmission; inhalation of droplets CM: -viral pneumonia -sinusitis -bronchitis -bacterial pneumonia

secondary TB infection

-risk: HIV, immunocompromised -infection reactivated -gradual lung destruction CM: -fever -weight loss -fatigue -night sweats -cough -anemia -TB may erode into blood vessel

Parathyroid hormone (PTH)

-secreted when blood calcium is LOW -increases blood calcium by: bone resorption by osteoclasts ( releases calcium) kidney reabsorption intestinal absorption through vitamin D -decreases blood phosphate by: kidney reabsorption

stable plaque

-surrounded by fibrous tissue -causes progressive narrowing of artery ---> results in ischemia Ischemia: inadequate oxygenation and perfusion to distal tissue

Pressure gradient

-the only way perfusion can happen -high pressure (arterial) flows to low pressure (venous)

hypertrophy

-thickening of myocytes (heart muscle cells) -pressure overload causes HTN --> heart has to pump harder to overcome resistance --> the heart becomes bigger because it is a muscle --> bigger heart takes away ventricular space ---> decreases CO because there is no room for blood decreased ventricle size = impaired filling = decreased CO, EF, and increased oxygen demands of heart tissue

Function of the circulatory system

-transport system -circulates nutrients and oxygen to tissues -removes waste products

Order of bloodflow through the heart

1) Superior/Inferior Vena Cava 2) Right Atrium 3) Tricuspid Valve 4) Right Ventricle 5) Pulmonary Valve 6) Pulmonary Arteries (R and L) 7) Lungs 8) Pulmonary Veins (R and L) 9) Left Atrium 10) Bicuspid valve (mitral) 11) Left Ventricle 12) Aortic Valve 13) Aorta 14) Body tissues

RAAS system response to low BP

1) The body senses low blood pressure 2) Stimulation of the sympathetic nervous system occurs 3) The sympathetic nervous system stimulates kidneys and JG cells to release renin 4) Renin enters the bloodstream and activates angiotensinogen in the liver 5) Renin turns angiotensinogen into angiotensin I 6) ACE (angiotensin-converting enzyme) converts angiotensin I to angiotensin II 7) Angiotensin II makes smooth muscles contract which increases BP 8) Angiotensin II also stimulates aldosterone and the pituitary gland 9) Aldosterone signals kidneys to retain water and NA ---> increases blood volume, which then increases BP 10) Pituitary gland secretes ADH which makes kidneys retain water--> increases BV which then increases BP

compression fracture

2 bones crushed together; not a complete break, they are just wedged together

How long after a MI does the heart lose contractile function?

60 seconds

Which statement is true regarding atherosclerosis? Select all that apply. A. Endothelial cell injury begins the process of atherosclerosis B. Atherosclerosis results in the thickening and hardening of the vessel wall. C. Atherosclerosis can affect many vascular systems in the body D. Atherosclerosis is a plaque caused by neutrophils E. Atherosclerosis is an acute process of heart muscle degeneration.

A B C

Which clinical manifestations would the nurse assess for in a client with pulmonary HTN? Select all that apply. A. Peripheral edeam B. Jugular venous distention C. Systemic HTN D. Bilateral rhonci E. Dyspnea on exertion

A B E

An nurse is educating a patient with newly diagnosed Raynaud's disease about triggers. Which of the following should the nurse include in her education? Select all that apply A. cold weather B. bee stings C. caffeine D. smoking E. irritating fabrics

A C D

A nurse is educating a new grad on short-term control mechanisms for blood pressure. Which of the following should she include in her education? A. Angiotensin II regulation in RAAS system B. Fluid regulating in the RAAS system C. Parasympathetic system D. Sympathetic stimulation E. retention/excretion mechanism of kidneys F. Baroreceptors

A C D F

The nurse is caring for 4 patients. After receiving the report, who should she see first?

A 60 y/o male who has started complaining of acute onset of pain in the lower leg, he can't move it, and it's turning white

The nurse is caring for a client with a pathologic fracture. Which statement best describes this fracture?

A fracture that happens at the site of an abnormality already in that bone.

RAAS system

A system that manages low or high BP to maintain homeostasis

Dyslipidemia

Abnormally elevated cholesterol or fats (lipids) in the blood.

severe complications of fractures

Acute compartment syndrome: Patho: -decrease in compartment size; constrictive casts -increase in compartment volume; bleeding, inflammation -increased pressure; compromises circulation, death of nerves and muscle cells -permanent LOF -muscle necrosis CM: -5ps 1) pain 2) paresthesia 3) pallor 4) pulselessness 5) poikilothermia Treatment: -notify physician -goal; reduce pressure

A nurse is precepting a new grad to the cardiac unit. While educating about atherosclerosis, which comment made by the new grad indicates teaching was successful?

Atherosclerosis is caused by the inflammatory response in a blood vessel

A nurse is caring for a patient with an abdominal aortic aneurysm. During morning rounds, she discovers that the patient is complaining of severe back pain. Upon assessment, she discovered the patient's abdomen was distended, and their BP was 69/40. What should the nurse do? A. Call a code blue B. Prepare the patient for emergency surgery C. Start an IV and administer recovery fluids D. Give a blood pressure-raising agent

B

The nurse is caring for a client with a suspected pneumothorax. Which clinical manifestations should the nurse expect in this client? Select all that apply. A. Fine crackles B. Dyspnea C. Use of accessory muscles D. Low SpO2 E. Absence of breath sounds

B C D E

What are risk factors for developing osteoarthritis? Select all that apply. A. Caucasian race B. Obesity C. Smoking D. Poor diet E. Older age

B E

Why do atypical acute MI patients typically wait to come to the hospital?

Because the symptoms are often misunderstood as just not "feeling well" Symptoms aren't as severe; EX patient may not have chest pain

Why are neurovascular check very important?

Because they are used to determine if any impairment exists after cast application and reduction of the fracture. -fracture can cut through blood vessel and cause internal bleeding

How does the RAAS increase blood volume?

By stimulating the pituitary gland and aldosterone Pituitary gland: secretes ADH which makes kidneys retain water Aldosterone: signals kidneys to retain water and NA

The nurse is caring for a client with aortic stenosis. Which clinical manifestations should the nurse monitor for in this client? Select all that apply. A. hypotension B. bounding pulse C. synocope D. dry cough E. heart failure

C, E

PE

CM: small: intermittent SOA, exercise intolerance large: sudeen onset: severe chest pain, respiratory distress, LOC, shock, often fatal

Which is a cause of right ventricular failure?

COPD

blue blower

COPD: chronic bronchitis cor pulmonale

pink puffers

COPD: emphysema dyspnea, use of accessory muscles, barrel chest

The nurse is caring for a client with an uncontrolled systolic blood pressure of 200 mg Hg. The nurse knows the client is at risk for which complication?

Cerebral artery rupture

asmthma

Chronic inflammatory disorder of the airways -intermittent airflow obstruction; reversible -Type I hypersensitivity; IgE mediated 2 categories: Atopic (allergies) Non-atopic (non-allergenic): exercise-induced asthma Patho: -IgE activation causes inflammatory response in airways; leads to excessive mucous production, mucosal edema, bronchoconstriction -progressive airway obstruction -prolonged expiration CM: -wheezing -coughing -mucus production -use of accessory muscles -low SPO2 -Pt c/o dyspnea, chest tightness, anxiety

Which condition is a complication of HTN?

Congestive heart failure

systole

Contraction of the heart

Pneumonic for clinical manifestations of Left sided Heart Failure

D= dyspnea (Shortness of breath) R= rales (crackles in the lungs) O= orthopnea (SOA when laying down) W= Weakness and fatigue (b/c of decreased cardiac output) N= Nocturnal dyspnea (SOA at night) I= Impaired gas exchange N= Nagging cough (pink, frothy sputum)

myocardial infarction (MI) damage

Damage of the infarct depends on... -location and extent of occlusion -amount of heart tissue supplied by CA vessel -duration of occlusion -metabolic needs of affected tissue -the extent of collateral circulation

The nurse is monitoring a client with a respiratory disorder. What clinical manifestations are commonly associated with respiratory disorders?

Dyspnea and cough

Example of shunting

EX: pneumonia -alveoli filled with fluid so they are unable to participate in gas exchange with blood -causes local or regional hypoxia which triggers vasoconstriction (shunting) -blood is then redirected to areas with better ventilation

tension pneumothorax

Emergency!!! -air enters pleural space, but cannot exit -intrapleural pressure increases tension on the heart and great vessels causing mediastinal shift CM: -severe respiratory distress -acute hypoxemia -tracheal deviation Treatment: -release pressure

T/F: An acute MI is relieved by rest or nitro

False

What is the primary function of the respiratory system?

Gas exchange

Which immunoglobulin contributes to the patho of asthma?

IgE

The nurse is caring for a client with pulmonary edema and hypoxemia. How does pulmonary edema cause hypoxemia?

Impairs alveolocapillary diffusion

rest pain

In PAD patients... burning, tingling, or numbing sensation d/t decreased BF

dependent rubor

In PAD patients... patient skin is always red/magenta d/t decreased BF

What occurs 20-40 minutes after a MI?

Irreversible cell death (necrosis)

A community health nurse is educating the public about an acute MI. Which piece of education would she want to include in the presentation?

It takes around 20-40 mins for heart necrosis to occur

Mechanisms of Blood Pressure Regulation

Largely controlled by kidneys; fluid regulation with the Renin-angiotensin-aldosterone system (RAAS)

The nurse is caring for a client with pulmonary edema. For what other disorder would the nurse prioritize when assessing the client?

Left-sided heart failure

What causes bone death in a client with osteomyelitis?

Localized ischemia

Pericardium

Membrane surrounding the heart

High afterload causes ________ work for the heart? (more or less?)

More

What is the trigger for angina?

Myocardial ischemia

Why does atherscleosis cause carotid artery bruit?

Narrowing of the arteries creates turbulent blood flow = bruit

A patient presents to the ED with complaints of severe headache, blurred vision, confusion, and shortness of breath. Upon assessment, his blood pressure is 198 / 121. What is the priority intervention?

Obtain a prescription for IV antihypertensive

PAD vs PVD

PAD: -affects arteries -an oxygen/perfusion issue b/c arteries transport oxygen -poor or absent pulse -cool skin -ulcers: dry, round, red -dry, shining surrounding skin -skin pale when elevated -skin rubor when dependent -elevation decreases perfusion and causes pain -gravity helps perfusion PVD: -affects veins -NOT an oxygen issue b/c the arteries are still functioning, while the veins are not -present pulses -warm skin -ulcers: irregular, copious serous exudate -edema and skin weeping -surrounding skin brown/blue -varicose veins are common -elevation helps perfusion -standing causes edema

Disorders leading to poor perfusion

PE pulmonary HTN

pericarditis

Patho: -An infection --> histamine release --> increases vascular permeability --> leads to leaky vessels --> increases fluid is pericardium = pericardial effusion Clinical Manifestations: -chest pain that worsens with deep breath (sharp,abrupt) -pericardial friction rub (leathery sound) -EKG changes -Pt will find relief when sitting up and leaning forward Complications: -pericardial effusion -cardiac tamponade

Raynaud's phenomenon

Patho: -Episodic vasospastic disorder of small cutaneous arteries Causes: -unknown primary cause -secondary cause is most commonly autoimmune -precipitated by triggers; cold, caffeine, smoking, vibration clinical manifestations: -ischemic phase: pallor and numbness -hyperemic phase: red, throbbing pain Treatment: -avoid triggers -medications

Peripheral venous disease (PVD)

Patho: -Valve incompetence (blood leaks back down the legs) Clinical manifestations: -Edema -necrosis of subcutaneous fat -secondary lymphatic insufficiency -stasis dermatitis (brown/blue skin) -venous ulcers Diagnosis: -ultrasound Treatment; -Compression socks -lower extremity elevation -venous ablation

TB

Patho: -airborne infection caused by Mycobacterium tuberculosis -destruction results from hypersensitivity immune response Transmission; -coughing, sneezing, and talking = resp droplets Risk factors: -living under crowded and confined conditions = immunocompromised Diagnosis: + Tb test

peripheral artery disease (PAD)

Patho: -atherosclerosis narrows arteries in legs and feet; decreases BF Clinical manifestations: -claudication pain (calf pain) -thinning skin -skin cool to touch -weak or no pulse -dependent rubor Complications: -rest pain -ulcers -gangrene -amputation Treatment: -stent -bypass graft

hypertrophic cardiomyopathy

Patho: -autosomal dominant heart disease -LV hypertrophy; septum thickens and blocks blood flow to aorta--> decreases CO because it creates resistance --> if it fully covers the aorta, then it blocks blood from flowing from LV to aorta = NO CO = sudden cardiac death Clinical manifestations: -asymptomatic -angina -SOA -Syncope episodes -Arrhythmias Complications: -sudden cardiac death -afib -stroke (slow BF --> leads to clotting--> clots can form in ventricles/aorta and go to the brain) -heart failure

Osteoporosis

Patho: -decrease in bone matric and mineralization -reabsorption exceeds formation = loss of bone mass -fracture easy -bone brittle and fragile Risk factors: -hormonal; estrogen loss in females -aging -low weight -sedentary lifestyle -diet; low in calcium and vitamin D -race -smoking/alcohol CM: -kyphosis of the dorsal spine -shortened height -sharp, acute back pain after bending and lifting

Mitral valve regurgitation

Patho: -incomplete closure of mitral valve Causes: -MI -Aging Clinical manifestations: -murmur -left sided heart failure Complications: -Rise in LA pressure -pulmonary edema -decrease in CO -HF

atelectasis

Patho: -incomplete lung expansion Types: -compression (tumoe, pleural effusion, pneumothorax) -absorption (hypoventilation, anesthesia) -surfactant impairment (ARDS, mechanical ventilation) Risk factors: -post op complication CM: -tachypnea -tachycardia -dyspnea -cyanosis -hypoxemia -diminished lung expansion -the absence of breath sounds

aortic stenosis

Patho: -incomplete opening; closing leads to increased resistance --> heart grows in size --> decreases CO (hypertrophy) Causes: -age-related calcification -congenital malformations Clinical manifestations: -murmur -syncope -left-sided heart failure Complications: -left-sided heart failure

Pneumonia

Patho: -infection/inflammation causes excess fluid and edema = poor gas exchange -classified according to the source of infection Risk factors: -recent exposure to a virus -tobacco use -chronic lung disease -aspiration -mechanical ventilation -Immunocompromised -atelectasis; immobility CM: early: malaise/fever, severe shaking, fine crackles progression: purulent sputum, pleuritic chest pain, resp distress

COPD: emphysema

Patho: -inflammatory response; destruction of lung tissue, loss of lung elasticity, enlargement of distal airspaces, loss of elastic recoil (lungs collapse during expiration = can't get air out aka air trapping) --> hypercapnia Think PINK for CM Pink skin, pursed lip breathing Increased chest (barrel chest) No cough Keep on tripoding (using accessory muscles) Complications: Frequent infections Risk for pneumothorax

DVT (deep vein thrombosis)

Patho: -injury to the vessel occurs -inflammatory response/clotting cascade is initiated -thrombus grows in the direction of blood flow Clinical manifestations: -unilateral swelling -pain -warmth -redness

chronic stable angina

Patho: -intermittent imbalance; "comes and goes" -coronary blood flow and metabolic demands of the myocardium -*NOT a total occlusion---> ischemia* Precipitated by (caused by): -physical exertion -exposure to cold -emotional stress Relief: -rest -nitro tabs

infective endocarditis

Patho: -invasion of valves/endocardium by microbial agent (staph aureus) -formation of vegetation and destruction of underlying cardiac tissue (vegetation holds the valve in place and doesn't allow it to close) Risks: -prosthetic heart valves and implantable valves -immunosuppression Clinical manifestations: -high fever/chills -new heart murmur -emboli Treatment: -antibiotics

unstable angina

Patho: -possible MI!! -ischemia enough to cause symptoms in the patient Symptoms: -Severe chest pain -SOA -other symptoms of a MI Relief: -nothing!

Osteoarthritis

Patho: -progressive loss of articular cartilage and synovitis -no cure CM: -pain -stiffness -limitation of motion -joint instability -deformity Risk factors: -age -gender -obesity -race -mechanical stress

ARDS

Patho: -severe inflammatory process causing diffuse alveolar damage -results in sudden, progressive pulmonary edema -stiffens lungs and impairs gas exchange -rapid onset: 12-18 hours Causes: -multiple; aspiration, infections, sepsis, smoke, drowning CM: -rapid, shallow breathing, crackles, resp failure, impaired gas exchange

Acute Peripheral Arterial Occlusion

Patho: -unstable plaque or clot obstructs artery --> leads to a lack of blood supply to an extremity -results in tissue death (gangrene) Clinical manifestation: -the 7ps Treatments: -thrombolytic therapy (blood thinners) -embolectomy (removal of clots)

Abdominal Aortic Aneurysm

Patho: -weakness of the abdominal aorta allows the vessel to stretch , which can then rupture Clinical manifestations PRIOR to rupture: -asymptomatic -pulsating mass -bruit Clinical manifestations POST rupture: -massive hemorrhage -hypovolemic shock (d/t low blood volume) -severe back pain

7Ps

Pistol shot (acute onset) Pain Pallor (cyanosis; d/t poor BF) Pulse absent below occlusion (because the artery is blocked) Paresthesia (numbness/tingling) Paralysis Poikilothermia (cool, d/t poor BF)

diastole

Relaxation of the heart -When the ventricles are passively filling with blood

Cause of Rheumatoid heart disease

Rheumatic fever

Pneumonic for clinical manifestation fo Right sided Heart Failure

S= swelling of legs, liver, and GI W= weight gain (b/c of fluid overload, occurs rapidly) E= edema L= large jugular vein (b/c of fluid overload and blood congestion in venous circulation) L= lethargy I= Irregular heart rate N= Nocturia G= Girth (ascites, aka abdominal swelling)

The nurse is caring for a client with a tear to an ankle ligament. What term is used to describe this injury?

Sprain

risk factors for DVT

Stasis, endothelial injury and hypercoagulability (Virchow's triad)

myocardial infarction (MI) interventions

Surgical: -cath lab -surgery

stroke volume

The amount of blood ejected from the heart with each beat

The nurse just received the patient's angiography results and it shows they have a false aneurysm. The nurse knows which of the following is correct about false aneurysms.

The artery has dissected causing blood to pool into the middle layer of the vessel

How is smoking a risk factor for artherosclerosis?

The chemicals inhaled when smoking causes damage to the heart and blood vessels ----> makes one more susceptible to plaque buildup

high preload and low afterload =

The heart will have an easier time pumping blood throughout the body and keeping up with the demand

Blood pressure

The pressure exerted by the blood upon the walls of the blood vessels

How can strep throat cause rheumatic fever and rheumatic heart disease?

The same bacteria that causes strep causes theses diseases. Strep can spread from the throat to the heart

How is obesity a risk factor for artherosclerosis?

Those who are obese often have high BP, high glucose levels, abnormal lipid levels, and inflammation ----> all are risk factors for atherosclerosis

A nurse is caring for a patient with PAD. When assessing the patient, which of the following would be an abnormal finding?

Toenails beginning to turn black and a wound on the bottom of the foot

Clinical manifestations of an acute MI?

Typical: -severe chest pain -radiates; left arm, neck, or jaw -C/O shortness of breath -the feeling of impending doom -anxiety Atypical: -women are more likely; especially diabetic and elderly -C/O fatigue and weakness -epigastric distress, nausea, vomiting -the feeling of impending doom -anxiety

The nurse is caring for a client diagnosed with asthma. The nurse understands that adequate control of the disorder is necessary due to which pathophysiologic process?

Uncontrolled inflammation leads to increased bronchial hyperresponsiveness and eventual scarring.

spiral fracture

a fracture in which the bone has been twisted apart

stress fracture

a small crack in the bone that often develops from chronic, excessive impact

Community aquired pneumonia

a type of pneumonia that results from contagious infection outside of a hospital or clinic

compliance of vessels

ability to stretch

hospital aquired pneumonia

acquired during hospitalization

chronic hypoxemia

activates compensatory mechanisms: -increased ventilation; digital clubbing, cyanosis, dyspnea at rest -pulmonary vasoconstriction; improves V/Q matching for a SHORT time= shunts blood to a well ventilated area -increased production of RBC; kidneys sense low blood O2= release of erythropoietin

A nurse is caring for a patient in the cardiac unit. The patient suddenly shouts that they are having crushing chest pain, SOB, and pain radiating through their left shoulder. The nurse understands the patient is experiencing which complication.

acute MI

ventilation/perfusion match

adequate oxygenation of blood and removal of CO2 depends on perfusion of blood through pulmonary vessels and appropriate contact between ventilated alveoli and perfused capillaries of pulmonary circulation

pneumothorax

air in the pleural cavity Patho: -presence of atmospheric air (+) in pleural space (-) CM: Small: tachycardia or dyspnea Large: respiratory distress, acute hypoxemia, absence of breath sounds and chest movement on the affected side

Total Peripheral Vascular Resistance (PVR)

amount of force exerted on circulating blood by vasculature

infarction

area of ischemic necrosis in an organ produced by occlusion of arterial blood supply or venous drainage

Coronary artery disease (CAD)

atherosclerosis partially or fully obstructs vessels---> results in diminished blood flow to heart muscle

S1

atrial contraction

Veins carry blood...

back to the heart

Where does gas exchange occur?

between air in alveoli and blood in pulmonary circulation

thrombus

blood clot

bruit

blowing, swooshing sound heard through a stethoscope when an artery is partially occluded

open fracture

bone fracture that breaks through the skin

complete fracture

bone is broken all the way through

segmented fracture

bone is fractured in 2 places leaving a bone segment detached

incomplete fracture

bone is not broken all the way through

osteoclasts

bone resoprtion cells

dislocations

bones forced out of alignment

closed fracture

broken bone with no open wound

bone matrix

calcium, phosphate, vitamin D

claudication pain

calf pain

stage 3 of bone healing

callus formation

stage 4 of bone healing

callus reabsorbed/bone

What are systolic and diastolic determined by

cardiac output total peripheral vascular resistance

What is a clinical manifestation of atherosclerosis?

carotid artery bruit

Angina

chest pain

Types of afib

chronic acute episode

Types of hypoxemia

chronic and acute

primary hypertension

chronic elevation of blood pressure without evidence of other diseases

2 types of angina

chronic stable, unstable

Determinants of cardiac output

circulating blood volume force of heart contraction heart rate

acute hypoxemia

clinical manifestations: -neurologic response= restlessness, agitation, euphoria, impaired judgment -heart attempts to compensate= increased RR, tachycardia, increased CO, vasoconstriction, increased BP -decompensation (body gives up/can't keep up anymore) = decreased RR, bradycardia, hypotension, cyanosis, arrhythmias, metabolic acidosis -late neurological= convulsions, death, coma

cardiovascular system is a ________ system

closed means that an increased volume in vessels increases the pressure in the vessels

types of fractures

communication with the external environment: - open or closed degree of break: -complete or incomplete the character of fracture pieces: -comminuted -impacted -compression -transverse

Risk factors for aneurysms

congenital defect, atherosclerosis, hypertension, dyslipidemia, diabetes mellitus, tobacco, advanced age, trauma, and infection

pleural cavity

contains the lungs

MI leads to

conversion of aerobic to anaerobic metabolism (no blood is pumping, so no oxygen is coming to the heart --> heart uses anaerobic to maintain myocardial functionl)

decreased blood flow

decreased delivery of oxygen and nutrients

Cardiomyopathy

disease of the heart muscle

cardiomyopathy

disease of the heart muscle

Valvular heart disease

disorders involving valves of the heart that impact the heart's ability to pump blood effectively to the lungs or tissues of the body and cause the heart to work harder

COPD CM

early: -cough -increased RR and exercise dyspnea -wheezing late: -constant dyspnea, trapped air/prolonged expiration -barrel chest and use of accessory muscles -cyanosis -clubbing -pulmonary HTN/R side HF

COPD: chronic bronchitis

excessive mucous production, mucous plugging, and fibrosis Patho: -trigger causes inflammatory response; excessive mucous production/hypersecretion mucous, mucous plugging, fibrosis of bronchial wall, hypoxia/hypercapnia Think BLUE for CM Big and blue (cyanosis) Long term chronic cough with thick mucus Unusual lung sounds Edema d/t cor pulmonale

heart rate effects on BP

faster = high BP slower = low BP

systolic pressure

force of blood on vessel when the heart contracts

pathologic fracture

fracture caused by diseased or weakened bone

comminuted fracture

fracture in which the bone is broken into more than 2 pieces

arterial system carries blood...

from heart to tissues "away from the heart" 90% carry oxygenated blood, but pulmonary artery carries deoxygenated

stage 2 of bone healing

granulation tissue

episodic

happening in parts or segments; "comes and goes"

cardiac output

heart rate x stroke volume amount of blood pumped out of the ventricles in 1 minute

Stage 1 of bone healing

hematoma formation

primary gout

hereditary defect in uric acid metabolism -uric acid breakdown product purine metabolism -increased serum uric acid increases the risk of gout Causes: -increased synthesis of purine -increased purines in the diet -decreased excretion of uric acid Patho: -increased uric acid leads to the formation of urate crystals which deposits in joints -initiates local inflammatory response Risk: -males over 40 CM: -heat -decreased movement -redness -swelling -pain

secondary hypertension

high blood pressure caused by the effects of another disease

hypercholesterolemia

high levels of cholesterol in the blood

How is high cholesterol a risk factor for artherosclerosis?

high levels of cholesterol in the blood can form deposits (plaque)

How is diabetes a risk factor for artherosclerosis?

high levels of glucose in the blood can lead to plaque buildup

What causes fibrous plaque in artherosclerosis?

hypercholesterolemia and inflammation

How is hypertension a risk factor for artherosclerosis?

hypertension narrows blood vessels and causes damage ---> makes one more susceptible to atherosclerosis

pressure overload in the heart leads to...

hypertrophy

impaired ventilation and gas exchange results in....

hypoxemia and/or hypercapnia

Rheumatic heart disease

immunologic disorder -carditis occurs; inflammation of the endocardium, myocardium, pericardium, and valves -valves; inflammation damages calves and causes vegetation Clinical Manifestations: -mitral valve regurgitation -heart failure -new heart murmur -arrhythmias Treatment: -antibiotics -antiinflammatories -reduce long-term valve damage

common complications of fractures

impaired healing DVT infection peripheral nerve damage -pressure ulcers -joint contraction -muscle atrophy

exacerbation

increase in the severity of a disease or its symptoms

Health promotion in osteoporosis patients

increase... -sun exposure -vitamin D -weight-bearing exercise -diet -calcium intake -limit alcohol/caffeine/carbonated beverages

Why can infective endocarditis cause sepsis?

infection can travel through the heart to the bloodstream

Rheumatic fever

infectious disorder Cause: -group A streptococcus bacteria -systemic immune response Clinical manifestations; -sore throat, headache, fever -arthritis -subcutaneous nodules -rash -carditis

endocarditis

inflammation of the inner lining of the heart

myocarditis

inflammation of the myocardium

AV node

initiates ventricular conduction

sprain

injury to a ligament

endocardium

inner lining of the heart

How is dyslipidemia a risk factor for artherosclerosis?

leads to lipid deposits on arterial walls ---> lead to plaque buildup

Hypotension

low blood pressure = inadequate perfusion to organs/tissues Causes: -medications -dehydration (low BV) -infection/sepsis (vasodilation) -shock Clinical manifestations: -dizziness -syncope -decreased urine output (not enough BF to kidneys, so kidneys retain) Compensatory mechanisms: -RAAS

pericardium

membranous sac enclosing the heart

when ventilation and perfusion don't work together=

mismatch

force of heart contraction effects on BP

more force = high BP less force = low BP

circulating blood volume effects on BP

more volume = high BP less volume = low BP

tunica intima

most inner side of vessel where blood flows

ventilation

movement of air in and out of the lungs

complications of sprains and strains

muscle contractions adhesions

Myocardium

muscular, middle layer of the heart

myocardium

muscular, middle layer of the heart

MI

myocardial infarction

Aortic stenosis

narrowing of the aorta

No pressure

no perfusion

oblique fracture

occurs at an angle across the bone

transverse fracture

occurs straight across the bone

SA node

pacemaker of the heart sends signals to the AV node, which leads to the contraction of ventricles

clinical manifestations of fractures

pain swelling LOF numbness crepitus -deformity of affected part

subluxations

partial dislocation

Disorders leading to poor ventilation

pneumonia cystic fibrosis lung cancer pleural effusion

Determinants of stroke volume

preload and afterload

Classes of hypertension

primary and secondary

respiration

process of gas exhnage at cellular level

contractile function of the heart means...

pumping

Determinants of PVR

radius of arterioles compliance of arteries viscocity of the blood

ischemia

reduction in arterial flow to level that is insufficient to meet oxygen demands

stage 5 of bone healing

remodeling

What should the nurse watch for with a patient that currently has a DVT?

respiratory distress Clot is in venous systemm--> blood returns to the lungs --> clot can travel with the blood and enter the lungs --> PE

The nurse is caring for a client diagnosed with a deep vein thrombosis of the lower extremity. Which assessment should the nurse perform to evaluate for a potential complication?

respiratory rate

treatment for autoimmune rheumatic disorders

rest hot or cold packs PT joint support gentle exercise avoid stress avoind infections meds

cor pulmonale

right-sided heart failure arising from chronic lung disease

osteomalacia

softening of bone, with inadequate amounts of mineral (calcium) in the bone

types of pneumothorax

spontaneuos: rupture of lung bleb closed: air from lung (EX rib fracture) open: air from the atmosphere (EX penetrating chest wound) Tension: air trapped

2 types of plaque

stable unstable

valve disorders

stenosis and regurgitation

compliance of arteries effect on BP

stiff = high BP stretchy = low BP

categories of fractures

sudden injury fatigue/stress fracture pathologic fracture

coronary arteries

supply blood to the heart

SLE

systemic lupus erythematosus Patho: -type III hypersensitivity -immune complexes invade conenctive tissue CM: -arthritis -malar "butterfly" rash -photosensitivity -cardiac: CAD and HTN

progressive disease

takes a while to develop "doesn't happen overnight"

strain

tear in a tendon

How does endocarditis cause a murmur?

the formation of vegetations prevent the valves from closing all the way--> this causes a new sound--> new murmur

diastolic pressure

the pressure in the arteries when the heart relaxes between beats

fibrosis

the thickening and scarring of connective tissue, usually as a result of injury.

viscocity of the blood effect on BP

thick = high BP thin = low BP

occlusion

total blockage; no bloodflow

2 categories of aneurysms

true false

impacted fracture

two pieces of bone wedged together

regurgitation

valve does NOT CLOSE completely

stenosis

valve does NOT OPEN completely

radius of arterioles effect on BP

vasoconstriction= high BP vasodilation = low BP

S2

ventricular contraction

cause of aneurysm

vessel walls weaken and stretch, which then allow them to stretch too much and rupture

vasospastic

where small blood vessels near the surface of the skin have spasms that limit blood flow

ventilation and perfusion MUST _______

work together

long-term compensatory mechanisms...

worsens heart function