Pathophysiology Exam 3

Rheumatic Disorders, Cardiovascular System, Neoplasia, Genetic and Congenital Disorders

ischemia

low oxygen delivery

infarction

tissue necrosis due to ischemia

thrombolus

blood clot

embolus

moving blood clot

pallor

abnormal paleness

paralysis

loss of muscle function and sensation

collateral circulation

alternative route of blood flow due to blocked or narrowed arteries

syncope

fainting

malaise

general feeling of unease or discomfort

claudictation

pain in legs due to walking, resolves at rest

sclerosis

hardening or thickening of body tissue

sclerodactyly

thickening and tightness of the skin of the fingers or toes

ankylosing

progressive stiffening of a joint

polyarticular

affecting multiple joints

autoantibodies

antibodies targeting the body's own tissues.

what is the pathophysiology of rheumatoid arthritis?

autoimmune disorder. antibody complexes attract WBCs with phagocytic enzymes that destroy cartilage resulting in join inflammation and destruction

Is rheumatoid arthritis symmetric or asymmetric?

symmetric

how is osteoarthritis different from rheumatoid arthritis?

wear and tear. typically asymmetric

what is the pathophysiology of systemic lupus erythematosus (SLE)?

autoantibodies damage tissue

what is a hallmark symptom of SLE?

butterfly rash

what is the pathophysiology of systemic sclerosis?

autoimmune. excessive collagen production in skin and internal organs

crest syndrome (type of systemic sclerosis)

calcinosis, raynaud phenomenon, esophageal dysmotility, sclerodactyly,

what are symptoms of systemic sclerosis?

tighten and thicken skin typically on the face, renal, heart, respiratory failure.

ankylosing spondylitis

chronic inflammatory disease of the vertebral column & sacroiliac joints. vertebral bodies become square.

patient has a crooked spine, an extended neck, and pain that started in the lower back. what is the diagnosis?

ankylosing spondylitis

primary gout

overproduction of uric acid and production of urate crystal deposits in kidney and joints

gout attack

sudden, painful, redness and tenderness in a joint. commonly the big toe.

dyslipidemia

abnormal lipid levels

how are lipids used in the body?

energy, cell membrane structure, blood clotting, myelin sheath, lipoproteins

xanthomas (cholesterol deposits) along tendons is a hallmark of what condition?

primary dyslipidemia

atherosclerosis

hardening of arteries due to lipid plaques from high cholesterol

what is vasculitis?

inflammatory injury and necrosis of blood vessels

I'm typically caused by radiation, toxins, infection, and cold.

vasculitis

what is acute arterial occulsion?

sudden interruption of arterial flow to tissues/organs. embolism lodges into small vessels

what are the 7Ps?

pain, pallor, pulselessness, paralysis, paresthesia, polar, and pistol shot.

what do the 7Ps indicate?

acute arterial occulsion

what is peripheral artery disease?

atherosclerosis in peripheral arteries (legs and feet)

what is raynaud disease?

vasospasm of small arteries and arterioles leading to pallor and numbness in fingers and toes

what is an aortic aneurysm?

dilation of blood vessel. may rupture.

what symptoms are in a thoracic aneurysm?

stroke like symptoms, back, neck and chest pain, difficulty swallowing

what symptoms are in an abdominal aneurysm?

typically nothing but can have ischemia to feet and legs, abdominal pain, back pain, emboli to legs

varicose veins

dilated or stretched veins in legs

what is chronic venous insufficiency?

persistent high BP causing fluid leaks in vessels

I have edema, think bluish brownish skin, necrosis of fat tissue, muscle atrophy, ulcers, and venous stasis dermatitis

chronic venous insufficiency

what is deep venous thrombosis

obstruction of venous flow leading to increased venous pressure

what is orthostatic hypotension?

drop in BP when changing to upright position

angina

chest pain to due to temporary mycocardial infarction

diastole

relaxation phase. heart chambers fill with blood

systole

contraction phase

asystole

absence of activity. flat line

what is the pathophysiology of pericarditis?

inflammation occurs then pericardial capillaries dilate and allow proteins and fluid to enter resulting in fibrin exudate which forms scar tissues

what is acute pericarditis?

inflammation of pericardium for less than 2 weeks

friction rub and chest pain that worsens when laying flat indicates what?

pericarditis

splinter hemorrhages and janeway lesions indicate what?

endocarditis

what is the pathophysiology of endocarditis?

infection of the inner heart surface causing vegetative growth that can form emboli and spread the infection leading to ischemia

what is rheumatic fever?

an immune mediated response affecting connective tissues of heart valves, blood vessels, joints, and skin

arthritis of large joints and aschoff bodies indicate what?

rheumatic fever

what is the major cause of rheumatic fever?

history of strep throat

stenosis

stiffening. won’t open well

regurgitation

leaky. won’t close well

what is hypertrophic cardiomyopathy?

thickened left ventricle that causes reduced stretching/filling, arrhythmias, and outflow obstruction

what is dilated cardiomyopathy?

thinned, dilated left ventricle that causes reduced pumping

what is myocarditis?

inflammation of heart muscle typically caused by infection or drugs

what is takotsubo cardiomyopathy?

broken heart syndrome. enlarged left ventricle that swells into an octopus shape. reversible

what is the frank starling mechanism?

increase filling and resistance stretches ventricles therefore strengthening contraction

acyanotic shunt

left to right. oxygenated blood leaks back into lungs

cyanotic shunt

right to left. deoxygenated blood flows to the body causing clubbed finger, syncope, squatting, and cyanosis

what is cardiogenic shock?

decreased CO due to pump failure. hypotenison, hypoxia, but adequate fluid. causes fluid retention and pulmonary edema

what is hypovolemic shock?

low blood volume due to fluid loss.

what is neurogenic shock?

type of distributive shock. decrease in sympathetic control of blood vessels. can’t contract and vasodilate causing hypotension and bradycardia.

what is septic shock?

type of distributive shock. sepsis. massive inflammatory response. hypotension, hyperglycemia, and low WBC function

what is obstructive shock?

type of distributive shock. obstruction of blood flow through vessels, heart, and lungs. starts are right heart failure then full shock.

cancer cachexia

state of losing fat and lean body mass

carcinogenesis

initiation and promotion of cancer through biological agents

anaplastic

complete loss of cell differentiation. no longer have specific function

metastasize

detached cancerous cells that spread through body

what are the three phases of carcinogenesis?

initiation, promotion, progression

what occurs during the initiation phase of carcinogenesis?

exposed cells are genetically changed and predisposed to malignancy

what occurs during the promotion phase of carcinogenesis?

cell division and growth. forming a pre-neoplastic group of cells. can be reveresed/removed

what occurs during the progression phase of carcinogenesis?

cells turn into aggressive, invasive, and malignant tumor cells

what does a D-Dimer test indicate?

venous thrombosis

what lab test helps evaluate heart failure?

BNP

severe valve disfunction causes what?

heart failure

what is a common cause of mitral valve dysfunction?

rheumatic fever

what are risk factors for atherosclerosis?

diabetes, male, smoking

what chromosomal abnormality occurs in Down Syndrome?

extra chromosome in trisomy 21

what occurs in the autosomal recessive disorder Phenylketonuria (PKU)?

lack of phenylalanine hydroxylase enzyme. cant break down protein.

what is the main symptom of PKU?

cant digest protein

what is Tay Sachs?

an autosomal recessive disorder that causes mutated HEXA gene allowing for accumulation of fatty substances in brain, spinal cord, and retina.

what is Turner syndrome?

missing X chromosome. webbed skin in neck area. in women

what is Klinefelter syndrome?

extra X chromosome (XXY). lack of facial hair, tall stature, breast development. in men.

how does cleft lip occur?

it is multifactorial. maternal infections, anti-seizure meds, genetic disorders.

compare and contrast unstable angina and NSTEMI?

both have myocardial ischemia. but, NSTEMI causes enough damage to release serum biomarkers while unstable angina does not.

what is acute coronary syndrome?

blocked artery. heart attack. medical emergency.

what is chronic ischemic heart disease?

blood flow to coronary arteries is limited due to narrowed or blocked arteries