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CONDENSED Exam 3 Patho Study Guide 2023
The systemic circulatory system is a closed system
Anything that affects one part of this close system, it will affect the rest of the close system (makes sense). L= Lung and R= Rest of Body
● Right Heart: Pulmonary circulation and pumps blood through the lungs- no 02
● Left Heart: Systemic circulation and pumps blood through the body
○ Flow of fluid and blood depends on
■ Pressure differences between the ends of a vessel
● Blood pressure keeps the vessels open-too high causes problems (ex. hypertension-heart failure)
■ Vessel resistance to fluid flow
● Small vessels have more resistance ○ Arterioles have more smooth muscle > vasoconstriction ● Longer vessels have more resistance ● More viscous fluids have greater resistance ○ Polycythemia: thicker blood - increased hematocrit increases resistance
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● Arteries have higher resistance
■ Adequate volume to fill the blood vessel
○ Total Peripheral Resistance: pressure the blood must overcome to keep moving ● Heart’s job is to pump blood, oxygen, hormones, etc. through the body ○ Heart is main source of hydrostatic pressure (pushing) - when ventricles contract it takes a lot of pressure to move the blood forward ○ Heart is unique because it can generate its own action potentials
■ SA Node (primary pacemaker) > AV Node > Purkinje Fibers
Cardiac cycle LUV-DUB sounds when ventricles contracts and the shutting of cardiac valves ( tricuspid, pulmonary, mitral, and aortic (semilunar ) ○ Systole: Ventricles Contracts (squeezes)- blood pushes against AV valves and the valves shut after letting blood through to be distributed to the rest of the body
■ Afterload (if really high, heart works harder to overcome the systemic
vascular resistance (aorta and the rest of the systemic circulation), and if this continues, the heart will eventually fail-result in left Heart failure) : resistance from the aorta and the vascular system the Left heart must overcome to push blood from the left ventricle into the aorta, and to the rest of the body. What cause afterload to increase : hypertension, medications that causes vasoconstriction, etc. ○ Diastole: Ventricle Relaxes ( blood fills in ) - after blood flows out through AV valves, the semilunar valves closed to let blood fill back up
■ Preload : Venous return-Filling pressure of the heart at the end of
diastole- Preload is venous return to the heart to fill during diastole. ○ Pulse pressure: Difference between the systolic and diastolic blood pressures ○ Mean arterial pressure: average pressure during ventricular contraction and relaxation
■ Good indicator of perfusion - goal of 60mm/Hg at a minimum ( Under 60 is bad )
■ Diastolic BP + Pulse Pressure / 3
○ Blood pressure: pressure of blood upon blood vessels walls
■ BP = CO x Total peripheral resistance
Cardiac output Volume of blood ejected from heart /minute - ~4-8L/min ● CO = Heart Rate x Stroke Volume - THINK LEFT VENTRICLE
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● Mechanisms of Blood Pressure Regulation ○ Autonomic Nervous system
■ SNS : Fight or flight - increase HR, conduction & contraction, vasoconstriction
■ PNS : Rest and digest - decrease HR, conduction, and contraction
○ Baroreceptors : Sensitive to changes in pressure/stretch on blood vessels - set set point
■ Not everyone has the same set point
■ If you don’t have much volume, you won’t stretch artery much - low pressure
means sensor will ask for “more” and initiate vasoconstriction to raise pressure, increase heart rate and cause release of ADH to get us back to homeostasis ○ Hormonal Regulation: RAAS
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○ Renal regulation of BP: when BP falls, glomerular filtration rate falls
■ Primarily regulated through extracellular fluid volume
■ Promotes sodium / water retention
Veins Low pressure system High capacity (stores a lot of blood) Thin walls Main job: return blood to heart by: One way valves
- Low extremities work more
- Areas w.o valves: thoracic veins, abdominal(IVC) Muscle contractions (pumping legs) Arteries High pressure system Elastic Thick walls Main job: send blood to rest of body/organs SNS vessels - both vasodilation (to areas needing blood - heart, lungs, brain, skeletal muscle) and vasoconstriction (areas don’t need blood) Fight or flight ● Diseases of the veins ○ Varicose veins: dilated, tortuous veins
■ Etiology : blood pooled in veins and veins engorged in blood
● Can be caused from damage to valves OR gravity ● Valvular failure: valves pull apart overtime - distention
■ Risk Factors:
● Prolonged sitting or standing ● Intra Abdominal pressure increase, blocks blood from moving up ● Ascites, obesity, pregnancy - more girth/pressure/weight to push against ○ Chronic venous insufficiency: inadequate venous return over a long period of time
■ Manifestations:
● Venous HTN: Sustained increase in venous blood pressure ● Circulatory stasis
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○ Hypertension: consistent elevation of system arterial pressure
■ Most common primary diagnosis in the US - used to be just adults, not kids too
■ Primary (essential): genetics, race, age, diet, obesity, alcohol, insulin resistance
● Idiopathic: we don’t know what causes it - 90-95% of HTN cases ● Modifiable: alcohol (3+/day), salt intake, obesity, diabetes ● Nonmodifiable: family history, race, age, diabetes ○ African americans at higher risk
■ Secondary: caused by underlying disorder or med that raises
peripheral resistance or cardiac output ● Renal issues ● Corticosteroids - stress ● Pheochromocytoma: benign tumor that raises levels of epi/norepi ● Oral contraceptives - act like aldosterone ● Pregnancy ● Aortic coarctation
■ Isolated Systolic HTN: Sustained systolic BP > 140 mmHg w. diastolic < 90mmHg
● Most common in the elderly ● Linked to cardiovascular/cerebral issues ● Caused by: ○ Stiffening of large arteries ○ Decreased renal blood flow ○ Decreased baroreceptor sensitivity ○ Increased peripheral vascular resistance
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■ Complications: ● Long term damage of vessels leads to atherosclerosis ● Smooth muscle cells - hypertrophy and hyperplasia ● Heart issues: heart failure, angina, coronary artery disease, ventricular hypertrophy ● Brain issues: TIA, CVA (stroke), dementia ● Kidney issues: renal arteriosclerosis, renal failure/insufficiency ○ Many dialysis patients are on dialysis due to HTN or diabetes ● Eye issues: retinal vascular sclerosis, hemorrhage ■ Hypertensive crisis/urgency/emergency ● Systolic BP > 180 or Diastolic BP > 120 ○ Urgency: raise in BP, but not signs of other organ damage ■ We need to prevent organ damage ○ Emergency: obvious signs/symptoms of organ/tissue damage ○ Arteriosclerosis: abnormal thickening/hardening of vessel walls - increases pressure
■ Atherosclerosis: thickening/hardening caused by accumulation of lipids
● Body sees fatty material as foreign and starts inflammatory response ● Stiff vessels AND/OR plaque
■ Steps:
● Damage to a vessel ● Fatty Streak Development ● Migration of inflammatory mediators to the site ● Oxidation of LDL leading to more inflammatory mediators ● Body tries to create new inner lining to protect, but this hardens and becomes a complicated atherosclerotic lesion
■ Manifestations: inadequate perfusion, ischemia, necrosis
■ Causes:
● Coronary Artery Disease: increased pressure and decreased blood to the heart > heart attack (myocardial infarction) due to demand of O not being met ● Cerebrovascular disease: leads to stroke ● Peripheral arterial disease: extremities
■ Risk Factors:
● Modifiable:
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■ Resolves after 10 minutes with rest
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○ Diminished/absent lower extremities pulses, Coolness ○ Pallor when leg is elevated ○ Reactive hyperemia - redness of foot when limb is hung ○ Thin, shiny, taut skin ○ Hair loss & Brittle toenails ○ Ulcerations, gangrene ○ Erectile dysfunction ○ Paresthesia: shooting pain in extremity Heart failure ● unable to be an effective pump - ventricle cannot eject adequate cardiac output ○ Manifestations : low systemic arterial, low CO, poor renal and tissue perfusion, poor exercise tolerance, ventricular dysrhythmias
■ MAP drop to 50 means that the vital organs are not being perfused
○ Frank-Starlings Law : greater the stretch (preload) = greater contractile force of heart
■ This is good until it’s stretched too far for too long and fails
○ Risk Factors: CAD, HTN, pulmonary disease, cardiomyopathies, valvular disease ○ 2 Types of Heart Failure (kids are not divided into 2 types)
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○ Ventricular dilation: enlargement of heart chambers - stretch ○ Hypertrophy: increase muscle mass and cardiac wall thickness ● SNS: first and least effective, releases epi/norepi, increases HR ● R.A.A.S. & Released of ADH: increase h20 absorption - vasoconstriction ● Natriuretic Peptides: cardiac protective: released when heart is stressed ○ Promotes venous/arterial vasodilation - reduce preload/afterload ○ Enhances diuresis Rheumatic/Valvular Disease - 6 Questions ● Aneurysm: outpouching or sack-like local dilation in wall of a blood vessel (weakening) ○ Can occur in veins, but most common in arteries ○ Causes: atherosclerosis, congenital defect, infection, HTN ■ Aorta is most susceptible vessel to aneurysm ■ Thoracic/abdominal aneurysms are most deadly/risk rupture ● With this diagnosis, people are stabilized even w.out confirmation because it is a true emergency situation ○ Treatment: HTN control, use of drugs to lessen systolic blood ejection, resection of aorta and replacement with a graft ○ Aneurysms will grow larger as tension in vessel increases ○ True Aneurysms: bounded by a full weakened vessel wall, blood in vascular system ■ Fusiform: entire circumference of vessel involved and gradual dilation ■ Berry: small, spherical dilation of vessel at bifurcation - Circle of Willis typically ■ Saccular: extends over part of circumference of vessel, sac like ○ False aneurysms - “Dissecting aneurysm”: localized tear/dissection in inner wall of artery that causes hematoma and vessel enlargement ■ Bound only by outer layers
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● Valvular Dysfunction: may be congenital or acquired ○ Most common in mitral/aortic valves ○ Causes: rheumatic heart disease, inflammation, endocarditis, syphilis, HTN ○ Two types: narrowing of valves so it won’t open properly OR distortion of valves ■ Stenosis: constricted, narrowed opening - blood can’t flow easily ● Leads to hypertrophy of cardiac muscle and increase cardiac work ● hear a murmur of blood shooting through narrowing opening ● Mitral stenosis: impaired flow from L atrium to L ventricle ○ Leads to atrial dilation/hypertrophy, dysrhythmias and eventually R ventricular heart failure ● Aortic Stenosis: left ventricle outflow obstruction ○ Leads to increase in L ventricular pressure and hypertrophy ○ Caused by calcification of normal aortic valve or congenital ○ Reduction to ¼ of size and progressively increases pressure overload of L ventricle ■ Regurgitation (incompetent): backflow of blood due to valves not closing 100% ● hear a murmur of blood leaking through valve when it should be closed ● Aortic regurgitation (insufficiency): leads to volume overload ○ Allows heart to compensate and maintain stroke volume with an increase end-diastolic volume/stretch of fibers ● Mitral regurgitation: backflow from L ventricle to L atrium ○ Extra blood volume in L atrium leads to afib and eventually increases pulmonary pressure - rigid/thick valve ○ Results in diminished stroke volume ○ Mitral valve prolapse: 1/both valve cusps float upwards and become leafy and floppy valves - can be an autosomal trait ● Tricuspid valve regurgitation: backflow of R ventricle into R atria ○ May be caused by dilation/failure of R ventricle ○ Often caused by pulmonary HTN ● Acute rheumatic fever: systemic inflammatory diseases - exaggerated immune response to strep ○ Occurs a few weeks post strep - lesions develop in heart/vessels/joints/SubQ ○ Prevention: treatment of strep throat - antibiotics/antiinflammatories ● Rheumatic heart disease: 10% of those with rheumatic fever will develop disease ○ Inflammation of 3 layers of heart/valves (myocarditis, endocarditis, pericarditis) ○ Can cause permanent scarring of heart valves, dysfunction of valves, heart failure Diabetes - 20 questions ● Fuel Sources: ○ Glycogenolysis:
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■ When glucose levels fall, liver converts stored glycogen to glucose ○ Gluconeogenesis: ■ Liver uses noncarbs (amino acids, glycerol, lactic acid) to make glucose ■ Fatty acid breakdown - causes ketones to be released and leads to ketoacidosis ● Pancreas ○ Exocrine: secrete pancreatic & digestive enzymes from pancreatic acini ○ Endocrine: secret hormones from islets of langerhans ■ Alpha cells: glucagon - maintain blood glucose in between meals/fasting ● Increase glucose by breaking down stored glycogen ■ Beta cells: insulin & amylin - increases satiety & inhibits glucagon ■ Delta cells: somatostatin - inhibits release of insulin/glucagon ○ Insulin: lowers blood glucose levels by moving glucose to muscle/liver/fat cells ■ Insulin transports glucose into cells (Without it, glucose cannot enter) ● Diabetes Mellitus: state of hyperglycemia resulting from impair insulin secretion, action or BOTH ○ Type 1: Absolute insulin deficiency - “Insulin Dependent Diabetes” ■ Most often in people < 30 ■ Autoimmune destruction of pancreatic beta cells ■ Type 1B Idiopathic: small # people with Type 1 that show NO autoimmune issue ■ Risk factors: ● HLA-DO/HLA-DR - antigens from genes that when person exposed to viral infection, kills beta cells - most people DO NOT develop diabetes ■ Onset: may be present for months-years before symptoms occur, onset is rapid ■ Symptoms: sudden weight loss, Polydipsia (thirst), polyuria, polyphagia (hunger) ○ Type 2: pancreas doesn’t make enough insulin - “ Noninsulin dependent” ■ Typically in people > 40 (but now children too) ■ Progressive disorder where body is resistant to it’s own insulin ■ More common than type I - 90-95% ■ Risk factors: obesity, sedentary lifestyle, family history (2-4x risk), african americans & native americans ● Adiponectin: protein hormone released that increases insulin sensitivity ● Metabolic Syndrome: increases risk for type II ○ Increase glucose, increase BP, abdominal obesity, increased triglycerides, low HDL. If 3+ of 5 of these risk factors =metabolic syndrome diagnosis ■ Onset: gradual, may have for years without symptoms ■ Symptoms (typically nonspecific) : polyuria, polydipsia, weight loss, fatigue, vision, pour wound healing,, paresthesia ● Glucosuria - causes osmotic diuresis that enhances water/electrolytes to go with glucose and kidneys filter more frequently to rid body of them ■ #1 cause of blindness is diabetes
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○ Acute Complications
