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Explain kidney/renal disease
- Increased fluid volume passes through the kidney -> impairment of filtration (microalbuimuria, hypertensive nephrosclerosis) -> reduction of BP will give improved renal function
- -Higher risk in DM and chronic renal disease Px
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Peripheral artery disease
- The insufficient tissue perfusion of extremities (lower extremities affected more than upper) due to existing atherosclerosis
- -Sxs: pulseless, paralysis, parethesia, pain, pallor
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Hypertension
- Elevated BP (>140/90 due to vasoconstriction and changed endothelial function) leading to target organ damage
- (>130/80 for DM or chronic kidney disease Px)
- -Optic nerve swelling, hemorrhages, exudates/cotton wool spots, macular star (malignant hypertension)
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Pharmacotherapy for hypertension that targets the kidneys?
Thiazide Diuretics, ACEi (Angiotensin conversting enzyme inhibitor), ARB (Angiotensin receptor blockers)
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Pharmacotherapy for hypertension that targets the heart?
Calcium channel blockers, beta blockers (BB)
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Coronary artery disease
- The number 1 killer in NA that affects men more than women. Is the accumulation of atheromatous plaques w/i artery walls of the myocardium -> less blood and O2 supply -> ischemia in myocardium
- -asymptomatic until >70% blocked (dyspnea, angina, palpitations, light-headed, faint, nausea)
- -Sxs increased by 4 Es: exertion, eating, excitement (stress), exposure to cold
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Coronary artery disease risk factors
- -hypercholesterolemia (elevated serum LDL esp)
- -smoking
- -hypertension
- -hyperglycemia (DM)
- -hereditary factors
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Tx of Coronary Artery Disease
- -cholesterol lowering meds
- -anticoagulants and aspirin (prevents clots)
- -thrombolytics (dissolve clots)
- -ACEi, BB, Calcium channel blockers (lower BP and heart workload)
- -nitroglycerin (vasodilators)
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Hollenhorst Plaque
- Cholesterol emboli that is normally dislodge from the carotid arteries and is trapped in a retinal artery
- -could have transient vision loss (~20mins) that will return when the vessel is unobstructed
- -A sign of severe atherosclerosis
- -could be a warning sign for stroke or TIA
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Angina Pectoris
- -chest pain caused by coronary artery disease or myocardial
- ischemia. Pain results from myocardial cells switching from aerobic to anaerobic metabolism-exacerbated with 4Es: exertion, eating, excitement (stress), exposure to cold -Sxs subside with rest and/or nitro
- -Tx: nitroglycerin to lower BP, alter diet, cease smoking, treat HT, DM, obesity, hyperlipidemia, Aspirin, BB (lower HR and contractility)
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Myocardial infarction
- -heart attack caused by coronary artery blockage and occlusion for >4-6 hrs -> irreversible myocardial necrosis (reperfusion may reverse some damage)
- -heart is dying
- -Sxs: chest pain, respiratory difficulty, anxiety, shock (lightheadedness, diaphoresis/sweating), nausea
- -50% do NOT display classic Sxs (older ppl, women, DM Px)
- -MONA: morphine, O2, nitro, aspirin
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Coarctation of the aorta
- -is a congenital defect in which the aorta b/t upper and lower body is narrow -> hypotension in legs and hypertension in arms and head, heart is stressed and damaged
- -Sxs: HA (high BP in upper body), leg pain (not enough blood)
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Pulmonary stenosis
- -is a congenital defect in which the pulmonary valve is narrower so the R ventricle works harder and hyptertophies but the lungs do not receive as much blood -> cyanosis (blue baby) and dyspnea
- -Tx: balloon valvuloplasty to enlarge the valve
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Patent ductus arteriosus
- -ductus arteriosus stays open 72 hrs after birth -> O2 rich and poor blood mix and the lungs have large blood volume load
- -Sxs: pulmonary hypertension, dyspnea, fatigue, poor feeding
- -Tx: PDA may spontaneously close, Indomethacin stimulates PDA closure, good nutrition, Surgery
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Tetralogy of Fallot
- -4 congential heart defects (pulmonary stenosis and R ventricular hypertrophy, ventricular septal defect, over-riding aorta)
- -most common cause of blue baby syndrome
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Heart Valve Disease
- The valves are affected so that their is stenosis (less blood flow) or regurgitation (backflow)
- -left side valves are more commonly affected (mitral and aortic)
- -Sxs: none, weakness, fatigue, syncope, tachycardia, chest discomfort, dypsnea, heart murmurs, swelling feet, pulmonary edema
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Bacterial endocarditis
- inflammation of the endocardium (inner membrane of the heart muscle and valves) due to bacteria pooling
- -Sxs: stroke, gangrene, roth spots, conjunctival petechiae, chronic renal failure, hemorrhagic lesions
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Rheumatic heart disease
- The chronic heart valve damage that occurs after Rheumatic Fever that could eventually lead to heart failure
- Polyarthritis, carditis, skin lesions, Syndenham's chorea due to stroptococcal infection (strep throat in upper respiratory), pancarditis (esp for the heart valves, mitral valve)
- -Tx: Ab, steroids, Aspirin (anti-inflam), digitalis and diuretics if heart failure occurs, valve surgery
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Pericarditis
- inflammation of the pericardium due to infection, RA, lupus, truama, MI, tumor or radiation or idiopathic
- Sxs: chest pain (worsened when lying down, coughing or swallowing and relieved by sitting forward), cardiac tamponade (heart compression), fever
- Tx: NSAIDs, steriods (pain and inflammation), Ab (for infective causes)
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Arrythmias
- Heart rate is irrgular/fluctation
- -tachycardia (>100 beats/min)
- -bradycardia (<60 beats/min)
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Atrial fibrillation
- -atria quiver instead of beating effectively -> blood isn't pumped completely out of atria -> may pool and clot -> risk of stroke
- -tx: reassurance for minor cases, drugs, defibrillator, coumadin (anticoagulant), digoxin (stimulates L ventricle contraction, Verapamil (CCB slows HR), Lopressro (BB slows HR,vasodilation), pacemaker
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Ventricular fibrillation
- Ventricles quiver due to electrocution, drowing or MI -> heart pumps little blood
- -more serious heart arrrhythmia, death in minutes
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Mxyoma
- primary benign cardiac tumor
- -Tx: monitor if small and no Sxs, Surgery if flow problems and arrhthmias
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Angiosarcoma
- primary malignany cardia tumor
- -Tx: open heart surgery
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Congestive heart failure
- when the heart pumping is insufficient to supply enough blood/O2 to the body -> fluid build up in lungs and tissues and heart enlarges and beats faster
- -most commonly due to CAD
- -L sided heart failure -> pressure builds in lungs, pulmonary edema, dypsnea, cough and fatigue
- -R sided heart failure -> pressure builds in veins -> edema in organs, nauseated, no appetite, renal failure
- -exertion increases Sxs
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Congestive heart failure Tx
- -stop smoking, limit alcohol, limit fluid intake**, maintain good diet, control HT, manage DM
- -diuretics (for edema), digitalis (inotropic makes heart contrat stronger and slows HR), nitroglycerin (vasodilator), CCB BB ACEi ANGIIblockers (decrease BP)
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Calcium channel blockers
-helps decrease arrhythmias
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Beta Blockers
-slows HR and dilates vessels
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ACEi
helps keep vessels open
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Angiotensin II receptor blockers
helps keep vessels open
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Giant Cell Arteritis
- Inflammation of the large and medium vessels (esp temporal artery) that impairs blood flow and increases the risk of embolis
- -Dx: elevated ESR, temporal artery biopsy
- -Sxs: HA, scalp tenderness, Jaw claudication pain, pain and stiffness worst in MORNING, Arteritic anterior ischemic optic neuropathy
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Arteritic Anterior ischemic optic neuropathy
- bilateral vision loss that is due to giant cell arteritis causing damage to the blood vessels supplying the optic nerve, leading to ischemia and death of the nerve
- -optic disc is swollen, pale and Px has flame-shaped hemorrhages, cotton-wool exudates, GCA Sxs (HA, jaw claudication, temporal tenderness, stiffness worse in morning)
- Tx: treat GCA with prednisone (corticosteroid that will reduce inflammation) and Plavix (blood thinners)
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Non-arteritic anterior ischemic optic neuropathy
- Unilateral vision loss and optic disc changes that are due to atherosclerosis, HT, DM, MI
- -the optic nerve is spared
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Transient Ischemic Attack
- -temporary focal brain or retinal ischemia leading to temporary loss of function
- -warning that a full-on stroke may occur
- -Sxs: diplopia, vision loss, vestibular dysfunction, motor (weak, uncoordinated), sensory (numb, tingling), speech and cognitive dysfunction
- -Mx: blood tests, ECG, imaging w/i hours
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Causes of transient ischemic attacks
- -atherosclerosis
- -embolisms
- -arterial dissection
- -Giant cell arteritis
- -sympathomimetic drugs (cocaine)
- -mass lesions
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Cerebral vascular accident
- disruption of blood supply to or w/i brain causing death of brain cells (caused by cerebral thrombosis, embolism, arterial stenosis, hemorrhage)
- -Sxs: can't do STRoke (Smile, Talk, Raise both arms)
- -Tx: tPA clot buster (contraindicated for hemorrhagic CVA), surgery, treat underlying disease, rehab
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Aneurysmal vascular disease
- An abnormal bulge in a blood vessel wall (most common are thoracic and abdominal) that could lead to atherosclerotic plaque, thrombi and emboli, pain, aneurysm rupture (fatal)
- -Risk: HT, atherosclerosis, smoking, male, obesity, sedentary
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Varicose veins
- the incompetent valves allow blood to flow away from the heart leads to the formation of dilated, tortuous superficial veins -> risk of leg ulcers, CHF, DM
- -Sxs: asymptomatic, dull ache, warm to touch, edema, itch, heavy leg sensation leg fatigue
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Superficial Thrombophlebitis
- inflammation of superifical leg veins with thrombus
- -Risk factors: abnormal veins, blood clotting, stasis of blood
- -Sxs: vein is painful and tender to touch, firm and swollen, surround is warm and red
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Deep vein thrombosis
- thrombus in deep vein that could more easily break off than superficial vein thrombosis
- -Sxs: none, calf swelling, calf pain (noticable or worse when standing or walking)
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Deep vein thrombus Tx
- anticoagulant (heparin, warfarin)
- foot elevation
- thrombolytic
- analgesisc (pain)
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Clotting cascade
the conversion of soluble fibrinogen into insoluble fibrin via the intrinsic (plasma) and extrinsic (tissue) pathways that convert inactive proteins into catalytically active proteases
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Gilbert's syndrome
- excess free bilirubin in the blood leading to jaundice, abdominal pain, poor appetite, fatigue and weakness
- Tx: none, phenobarbital to reduce bilirubin if severe
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Bilirubin
- formed from the destruction of old rbcs and transported to the liver were it is excreted in the bile (for fat digestion) or urine (for excretion of waste)
- It is bad to have bilirubin not transported to the liver (indirect bilirubin that is non-functional)
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General liver disease presentation
- GI (appetite, ascites, ab pain, dark urine, stool)
- Aching joints and emaciation (build up of waste)
- pruritis in skin, spicer angiomas (infection and bvs break down)
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Hepatitis A
- Viral inflammation of the liver
- -travels through contaminated food or H2O
- -at risk during traveling, sex
- -Tx: avoid stressing liver (alcohol)
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Hepatitis B
- Viral inflammation of the liver
- -travels through infected blood
- -at risk during child birth, health care workers, hemodialysis, sex
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Hepatitis C
- Viral inflammation of liver
- -through direct contact with blood
- -at risk during child birth, health care workers, hemodialysis, sex
- -no vaccine
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Hepatitis D
- viral inflammation of the liver
- -only in ppl already infected with Hep B
- -at risk Px with Hep B or hemodialysis
- -get Hep B vaccine
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Hepatits E
- viral inflammation of liver
- -through contaminated food or H2O
- -no vaccine, but resolves on its own in several weeks to months
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Heptatis
- Inflammation of the liver due to virus, alcochol, or autoimmune causes
- -Sxs: fatigue, HA, jaundice, ascites, pain, low grade fever, loss of appetite, nausea, vomitting diarrhea
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Cirrhosis
- widespread nodules and fibrosis of liver due to hepatitis, chronic alcoholism, drugs, toxins, infections, Wilson's, galactosemia, hemochromatosis, glycogen storage diseases, congestive heart failure
- -leads to edema, ascites, bruisng and bleeding, jaundice, pruritis, gallstones, toxins in blood or brain, sensitivity to meds, portal hypertension
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Wilson's Disease
- genetic disease that increases copper absorption and decreases copper excretion
- -Sxs: liver (jaundice hepatitis, cirrhosis), CNS (tremors, coordination), blood and bones (anemia, osteoarthritis), kidneys (pee out lots of nutrients), Kayser-Fleischer ring
- -Tx: D-penicillamine/trientine hydrochloride (remove copper), zinc acetate (copper excretion), Vit B-6, low copper diet, liver surgery
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Multiple Sclerosis
- Auto-immune disease of the CNS (specifically the myelin)
- -Demyelination -> scar tissure (sclerosis)
- -Optic nerve commonly affected! MS disrupts conduction from eye to brain
- -Sxs: Vision, speech, constinence, STM, paralysis depression, anxiety
- -Tx: no cure, interferon Beta 1 drugs (slow progression), steroids (decrease relapse)
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Intranuclear ophthalmoplegia
- Median longitduinal fasciculus lesion -> supranueclear gaze palsy -> horizontal dysconjugate eye mov'ts (pursuits and saccades affected, poor adduction, poor abduction
- -Sxs: diplopia
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Parkinson's Disesase
- Free radical build up, triggers, and genertics -> progressive neurodegenerative CNS disease, loss of dopamine-producing cells in the substantia nigra -> mov't disorder, paralysis, shaking
- -Sxs: tremors, rigidity, bradykinesia, impaired coordination, dry eye, poor saccade convergence pursuits, reduced CSF
- -Tx: levodopa
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Huntington's Chorea
- AD inheritance (chromosome 4) of basal ganglia degeneration -> protein build-up, reduction of ACh and GABA, overaction of dopamine
- -No cure
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Amyotrophic Lateral Sclerosis (ALS)/Lou Gehrig disease
- fatal, progressive motor neuron disease
- -> upper (tight, stiff, hyperreflexia) and lower (cramps, twitches, weakness, fasciculations) motor neuron damage
- -ALS could be due to excess glutamate, autosomal dominant
- -No cure, riluzole (decreases glutamate, only slows progression)
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Myasthenia Gravis
- Neuromuscular junction disease where antibodies destory, alter, block AChR -> muscle weakness during periods of activity and improves after rest
- -Sxs: Diplopia, ptosis, facial expression, chewing, talking, swallowing
- -Dx: Blood test (AChR antibody), CT scan (EOM, thymus), Edrophonium chloride (blocks ACh breakdown temporarily)
- -Tx: Neostigmine (anti AChase), Prednisone (immunosuppressive, inhibits abnormal antibodies), thymectomy (remove thymus producing abnormal antibodies), plasmapheresis (remove abnormal antibodies)
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Muscular dystrophy
- skeletal muscle degeneration due to defective dystrophin protein that normally keeps muscle cells intact
- -Sxs: muscle weakness, loss, deformities, contracture, pseudohypertrophy, cardiac and respiratory arrest
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Marfan's Syndrome
- -inborn problem with protein metabolism (mutation in gene fibrillin-1)
- -elongation of bones, arachnodactyly, scoliosis
- -ectopia lentis, glaucoma, retinal detachement, blue sclera
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Galactosemia
- -inborn problem with converting galactose into glucose
- -galactose-free diet
- -hypoglycemia, bilateral cataract, cognitive dysfunction, renal and hepatic dysfunction
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Glycogen Storage Disease
- -inborn error of glycogen metabolism
- -hypoglycemia, elevated cholesterol, stunted growth and osteoporosis, clotting problems
- -Tx: provide glucose source, liver transplant
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Phenylketonuria (PKU)
- -most common inborn error of metabolism where phenylalanine is not metabolised because lack of phenylalanin hydroxylase (PAH) -> CNS damage, mental retardation
- -TX: low phenylalanine diet
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Tay-Sachs Disease
- -inborn error of lipid metabolism (absent Hex-A enzyme)
- -progressive CNS destruction (blindness, cognitive delay, demetia, deafness)
- -constricted fields (startle effect), and macular cherry red spot (pale, no vasculature)
- -fatal <5years
- -TX: none
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