Bone Injuries and Disorders, Study Guides, Projects, Research of Pathophysiology

A comprehensive overview of various bone injuries and disorders, including alveolar hyperventilation, increased airway resistance, decreased pulmonary compliance, obstructed pulmonary artery, soft tissue injuries (contusions, strains, sprains), joint injuries (dislocations, subluxations), fractures (hip fractures), osteopenia, osteoporosis, and osteomalacia/rickets. It covers the causes, clinical manifestations, and treatments for these conditions. The document delves into the bone matrix composition, the role of vitamins and minerals in bone health, and the mechanisms behind bone remodeling and mineralization. It also discusses the complications and risk factors associated with these bone-related issues. This detailed information can be valuable for healthcare professionals, students, and individuals interested in understanding the complexities of bone health and injury management.

Typology: Study Guides, Projects, Research

2024/2025

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EXAM 2 PATHOPHISIOLOGY – CV, Resp,
Musculoskeletal
1. Discuss pathophysiology of coronary artery
disease (CAD).
Coronary Arteries: Supply blood to the heart
oAtherosclerosis – plaque formation on artery walls
Plaque formation starts forming in early adulthood
Usually forms in the bigger vessels
Coronary artery beds, aorta, carotids, vertebral, renal,
femoral
Protrudes into lumen, partially or completely obstructing
blood flow
Leading factor in cardiovascular disease
Fibrotic plaques become calcified, hemorrhagic,
ulcerated, or thrombosed
Injury of Endothelial cells in tunica intima- inflammatory
process begins
LDL cholesterol invades tunica intima layer
Macrophages “eat up” LDL & die (foam cells)
Foam cells accumulate; build fatty layers (fatty streaks)
Smooth muscle cells of tunica media migrate to fatty
streaks
Form fibrous cap (collagen & elastin) over fatty streaks
and lays down calcium deposits (PLAQUE structure)
Process repeats, artery becomes stiff, plaque narrows
lumen & decreases blood flow (less O2 to tissue)
Acute Coronary Disease
Plaque is a problem (atherosclerosis)
Unstable plaque – ruptured and thrombus
Stable plaque – obstructs blood flow
Plaque vulnerability to rupture: size of lipid core; lack of stabilizing smooth muscle cells;
presence of inflammation; stability and thickness of fibrous caps
2. Describe the pathophysiology of the different types of angina.
CHRONIC STABLE ANGINA: Predictable
Imbalance between blood flow and the metabolic demands of myocardium
Physical exertion, emotional stress, exposure to cold
oSteady constricting, squeezing, or suffocating sensation
oIncreases in intensity at onset and end of episode
oRelieved with rest and nitroglycerin
oDelay of more than 5-10 minutes for relief is a sign of more severe ischemia!
PRINZMENTAL ANGINA (variant angina):
Coronary artery Spasm
Happens at rest; usually at night
UNSTABLE ANGINA:
Acute coronary syndrome
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EXAM 2 PATHOPHISIOLOGY – CV, Resp,

Musculoskeletal

1. Discuss pathophysiology of coronary artery

disease (CAD).

  • Coronary Arteries: Supply blood to the heart o Atherosclerosis – plaque formation on artery walls ▪ Plaque formation starts forming in early adulthood ▪ Usually forms in the bigger vessels ❖ Coronary artery beds, aorta, carotids, vertebral, renal, femoral ▪ Protrudes into lumen, partially or completely obstructing blood flow ▪ Leading factor in cardiovascular disease ▪ Fibrotic plaques become calcified, hemorrhagic, ulcerated, or thrombosed ▪ Injury of Endothelial cells in tunica intima- inflammatory process begins ▪ LDL cholesterol invades tunica intima layer ❖ Macrophages “eat up” LDL & die (foam cells) ❖ Foam cells accumulate; build fatty layers (fatty streaks) ▪ Smooth muscle cells of tunica media migrate to fatty streaks ❖ Form fibrous cap (collagen & elastin) over fatty streaks and lays down calcium deposits (PLAQUE structure) ▪ Process repeats, artery becomes stiff, plaque narrows lumen & decreases blood flow (less O2 to tissue) Acute Coronary Disease ▪ Plaque is a problem (atherosclerosis) ❖ Unstable plaque – ruptured and thrombus ❖ Stable plaque – obstructs blood flow ▪ Plaque vulnerability to rupture: size of lipid core; lack of stabilizing smooth muscle cells; presence of inflammation; stability and thickness of fibrous caps

2. Describe the pathophysiology of the different types of angina.

CHRONIC STABLE ANGINA: Predictable ➢ Imbalance between blood flow and the metabolic demands of myocardium ➢ Physical exertion , emotional stress, exposure to cold o Steady constricting, squeezing, or suffocating sensation o Increases in intensity at onset and end of episode o Relieved with rest and nitroglycerin o Delay of more than 5-10 minutes for relief is a sign of more severe ischemia! PRINZMENTAL ANGINA (variant angina): ➢ Coronary artery Spasm ➢ Happens at rest; usually at night UNSTABLE ANGINA: ➢ Acute coronary syndrome

➢ May occur more frequently, occur more easily at rest, feel more severe, or last longer

3. Compare acute and chronic coronary syndromes.

Unstable Angina

  • Ischemia (lack of blood flow) to cause symptoms, no signs of heart damage (Can also occur at rest) Non-ST-Elevation Myocardial Infarction (NSTEMI)
  • Ischemia severe to cause symptoms and raise cardiac markers (labs) ST-Elevation Myocardial Infarction (STEMI)
  • Ischemia severe to cause symptoms, raise cardiac markers (labs), and result in EKG changes (ST-elevation) - Necrosis of myocardial tissue

4. D

e s c r i b e

  • Acute Pericarditis

the pathophysiology of the

pericardial disorders.

Distortion of valve Does not CLOSE properly Blood flows backwards Mitral Valve Regurgitation and Prolapse Blood leaks back into left atrium Leads to impairment of left ventricle, ↑ in atrial pressure, and p Mitral Valve Prolapse: floppy mitral valve – balloons back into left atrium during systole With and without regurgitation oNarrowing of valve orifice oDoes not OPEN properly oNot enough blood flows through the valve Mitral Valve Stenosis Caused by Rheumatic fever Impair filling of left ventricle Leads to blood pooling in left atrium and thrombus formation Stenosis Regurgitation Valvar Dysfunction

Incompetentaortic valve allows blood flow Heart compensates with left ventricular hy Leads to heart failure Rheumatic fever Congenital abnormalities Infec

Aortic Regurgitation – Causes:

Aortic Stenosis – Causes: Congenital malformations of leaflets (bicuspid) Age-related calcifications Increased resistance to ejection of blood from left ventricle into aorta Heart compensates with lef t ventricular hypertrophy (enlargement) Eventually leads to heart failure Signs and Symptoms of Valvular Disorders ➢ Exertional dyspnea ➢ Orthopnea (short of air when laying down) ➢ Paroxysmal nocturnal dyspnea (wake up short of breath) ➢ Angina ➢ Syncope - fainting ➢ Palpitations ➢ Weakness ➢ Fatigue ➢ Pathologic heart murmur ➢ Extra heart sounds Some of the valve disorders are asymptomatic until the disease process becomes severe. Valves can be replaced with mechanical valves or tissue valve (human or animal donor). This is done via open heart surgery or transcatheter. If Rheumatic Fever/Rheumatic Heart Disease (RHD) -

  • Immune-mediated,

Afterload –

  • Force that contracting heart muscle must generate to eject the blood from the filled ventricles
  • Factors Affecting Afterload:
    • Obstruction
    • Vascular resistance
    • Hypertension
    • Polycythemia
    • Medications Impairment of the left ventricle (LV):
  • Diminished CO
  • Decreased EF
  • Pulmonary congestion Impairment of the right ventricle:
  • Reduced blood flow into pulmonary circulation
  • Reduced blood flow to the left side of the heart
  • Often of consequence of LV failure

8. Explain compensatory mechanisms of myocardial dysfunction.

Compensatory Mechanisms of heart failure - To increase circulating volume in a reduced EF:

  • Neurohormonal pathways are activated:
  1. SNS releases norepinephrine and epinephrine
  • Increased HR and contractility
  • Increased BP (increased afterload)
  • Aggravates ischemia, potentiates arrhythmias, promotes remodeling (thickening)
  1. Renin is released due to decreased perfusion of the kidneys
  • Stimulates RAAS and increases sodium and water retention (increased preload)
  1. Vasopressin is released from the hypothalamus
  • Water reabsorption (increased preload)
  • Initially, these processes help compensate
  • Long term = deleterious effects:
  • LV remodeling
  • Dilation
  • Hypertrophy (enlarging)

9. Compare right and left sided heart failure and differences

in clinical manifestations.

Left Side Heart Failure (congestive heart failure) Right Side Heart Failure (Cor Pulmonale)

Systolic or diastolic ventricular dysfunction

Decreased left ventricular emptying

Increased volume and pressure in left ventricle

Increased volume and pressure in left atrium

(increased preload)

Increased volume in pulmonary veins

Increased volume in pulmonary capillary bed

Fluid transudation (the process of passing

through a membrane, pore or interstice) from capillaries to alveoli ↓

Alveolar space fluid

Pulmonary Edema

Increased pulmonary vascular resistance

Right ventricular failure

Increased pulmonary vascular resistance

Decreased right ventricular emptying

Increased volume and pressure in right

Ventricle (end-diastolic volume and

Preload increases)

Increased volume and pressure in right

atrium

Increased volume and pressure in the

great veins

Increased volume in the systemic venous

circulation

Increased volume in distensible organs

Increased capillary pressure

Peripheral edema and serous effusion

( fluid fills the inside of body cavities) Clinical Manifestations

  • • • • • • • • • • Fluid retention and edema
  • Increased capillary pressures
  • Nocturia d/t increased CO and renal blood flow with increase blood flow to heart in supine position
  • Respiratory manifestations
  • Pulmonary congestion worsens in recumbent position Left Heart Failure Right Heart Failure
  • Decreased cardiac output
  • Activity intolerance
  • Pulmonary congestion (edema)
  • Cyanosis and hypoxia
  • Cough with pink frothy sputum
  • Orthopnea
  • Paroxysmal nocturnal dyspnea
  • Congestion of peripheral tissues
  • Dependent edema and ascites
  • Liver congestion and impaired liver function
  • GI congestion with weight loss, GI distress, and anorexia
  • Left HF can lead to Right!
  • 1 out 2 pts are rehospitalized within 60 days of hospital discharge

10. Discuss the pathophysiology and resulting complications of circulatory shock.

Myocardial Contractility:

  • Also known as inotropy
  • Contractile performance of the heart
  • Actin and myosin filaments of the heart muscle to interact and shorten against a load
    • Requires ATP and calcium ions
  • Na+/Ca+ exchange pump and Ca+ pump
    • Both of these pumps work to transport calcium out of the cell Frank-Starling Law/Mechanism: ↑ contractility = ↑myocardial work = ↑ myocardial 0₂ demand Intrinsic factors:
  • Myocardial response to stretch before contraction
  • Increased afterload after a contraction begins
  • Response to heart rate changes Extrinsic factors:
  • Neurohormonal
  • Chemical & pharmacological
  • Pathologic conditions Neurohormonal: the sympathetic nervous system, the aldosterone renin-angiotensin system, vasopressin, endothelin (vasoconstrictors), vasodilator systems such as the endothelial relaxation factor, prostaglandins and the bradykinin-kallikrein system Factors affecting contractibility:
  • Oxygen availability
  • Electrolytes (calcium, K+, magnesium)
  • pH (acidosis, alkalosis)
  • Inotropes (positive and negative)
  • Medications that change the force of contraction of the heart
  • Positive = heart pumps more blood with each beat
  • Negative = decrease the heart rate
  • Catecholamines (stress & anxiety)
  • Epinephrine and norepinephrine (sympathetic nervous system) SHOCK:
  • Circulatory failure = hypo perfusion of organs and tissues
  • Insufficient O2 and nutrients for cellular function
  • Cellular metabolism moves from aerobic to anaerobic metabolism
  • Limited amounts of ATP produced
  • Normal cellular function cannot be sustained
  • Compensatory mechanisms
  • Sympathetic nervous system
  • RAAS
  • Complications: Resp failure, kidney failure, multi-organ failure Acute respiratory distress syndrome (ARDS): Respiratory failure with need for mechanical ventilation Acute kidney injury (AKI): Impaired renal perfusion Gastrointestinal complications: Ischemia Disseminated Intravascular Coagulation (DIC): Widespread activation of the coagulation system Multiple Organ Dysfunction Syndrome (MODS): Failure of multiple organs (30-100% death rate) Clinical Manifestations of Shock:
  • Tachycardia/bradycardia
  • Hypotension
  • Oliguria (decreased urine output)
  • Cool and clammy skin OR warm skin
  • Central and peripheral cyanosis
  • Respiratory distress
  • Angioedema (anaphylaxis)
  • Itching and uritcaria (hives) (anaphylaxis)
  • Neurologic changes Types of shock ----
  • Hypovolemic: Acute loss of 15% or more of circulating blood volume
  • Cardiogenic: Acute MI (most common)
  • Obstructive: Pulmonary embolism (most common)
  • Distributive shock: Neurogenic, anaphylactic, septic

Pumping action of atria/ventricles dyssynchronous

“fibbing” of the atria Types: Chronic Acute with Rapid Ventricular Rate (HR > 150) Consequences: Chronic: Blood pools in the atria = blood clots = travel Rapid ventricular rate: HR too fast = decreased CO Fatigue, SOA, syncope Treatment: Immediate: Cardioversion or IV gtt Long term maintenance: Anticoagulants Medications to control HR (goal < 110 bpm)

Myocardial Infarction:

  • Damage depends on:
    • Uncoordinated heart muscle contractions
    • Altered movement of impulses
    • Causes of arrhythmias:
      • Electrolyte imbalances
      • Decreased oxygen delivery to cardiac cells
      • Structural damage
      • Medications/street drugs

Atrial Fibrillation

o Location and extent of occlusion

o Amount of heart tissue supplied

by vessel

o Duration of occlusion

o Metabolic needs of

affected tissue

o Extent of collateral circulation

  • Leads to:
    • Conversion of aerobic to anaerobic metabolism
  • 60 seconds: Loss of contractile function
  • Minutes: Ischemic area ceases to function
  • 20-40 minutes: Irreversible cell death (necrosis)

TYPICAL

  • Severe chest pain (constricting, suffocating, crushing)
  • Substernal pain that radiates to the left arm, neck, or jaw
  • Prolonged chest pain not relieved by rest or nitroglycerin
  • Shortness of breath

ATYPICAL

  • Women more likely
  • Fatigue and weakness
  • Feeling of impending doom
  • Anxiety
  • Epigastric distress, nausea, vomiting

Treatment of MI: MONA morphine oxygen nitrogen

aspirin RESPIRATORY:

  • Infections/Cancer
    • Common cold
      • More than 100 viruses cause the common cold, rhinovirus most common
      • Invades tissues of upper respiratory tract
      • Histamine /prostaglandins etc. release, initiate inflammatory response
        • Mucosa swelling, goblet cells increase mucus production

Clinical manifestations:

  • Sinus pain, nasal congestion, runny nose, sneezing, watery eyes, scratchy

throat, headache, low grade fever

Complication: Otitis Media

  • Eustachian tube blockage due to swelling
  • Bacterial growth

Rhinosinusitis

  • Inflammation of

nasal passages &

sinuses due to

allergy/virus/bacteria

  • S. Pneumoniae
  • H. influenza
  • Typical: bacterial-alveoli
  • Lobar: entire lobe
  • Bronchopneumonia: patchy -more than one

lobe

  • Atypical: Viral- involves interstitium
    • Risk Factors
      • Recent exposure to virus
      • Tobacco use/Substance abuse
      • Chronic lung disease
      • Aspiration risk
      • Mech. ventilation
      • Immune compromised/Age
      • Atelectasis- Inactivity/Immobility
    • Diagnostic Testing
      • Elevated WBC/Sputum C&S
      • Arterial Blood Gases
      • Chest X-Ray: consolidation
        • Tuberculosis
          • World’s foremost

cause of death from a

single infectious agent

(Causes26% of

avoidable deaths in

developing countries)

  • Airborne infection

caused by

Mycobacterium

tuberculosis

  • Aerobic;

Protective waxy

capsule; Can

stay alive in “suspended animation” for years

  • May infect any organ of body but lungs most common
  • Treatment: multidrug regimen for 6 months or longer
    • Develops drug resistance

Ghon focus containing:

  • Macrophages
  • T cells
  • Inactive TB bacteria

Nodules in lung tissue and

lymph nodes.

Caseous necrosis inside

nodules.

Calcium may deposit in the

fatty area of necrosis.

Visible on x-rays.

Miliary TB lesions look like

grains of millet in the tissues.

Meat inspection was introduced

to keep them out of the food

supply. Pasteurization of milk

was introduced to keep TB out

of the milk supply.

Secrete hormonally active products

Risk factors: Smoking number one risk factor 80-90% of lung cancers due to tobacco use, Lung

cancer very rare before the WW I, Exposure to second hand smoke, Exposure to industrial

substances, Mining/smelting/chemical /petroleum/air pollution, Cigarettes + asbestos 6-10X

higher, Ionizing radiation (rare)

Paraneoplastic manifestations:

SIADH, Cushing’s syndrome,

thrombophlebitis Various endocrine,

neuromuscular, cardiovascular and

hematologic symptoms.

Treatment:

No treatment benefit for long term-survival. In

addition, chemotherapy may help to relieve

symptoms in patients who experience

significant symptoms from their disease.

Depends on Stage.

  • Disorders of Ventilation and Gas Exchange
    • Hypoxemia: Low blood oxygen
      • (^) Inadequate/reduction of arterial oxygen (PO 2 )
      • (^) Cause:
        • (^) Inadequate O 2 in air, resp. disorders, dysfunction of CNS, alteration in circulation
        • (^) Mechanisms of respiratory system leading to Hypoxemia
        • (^) Hypoventilation, impaired/inadequate circulation, mismatch ventilation and perfusion
        • (^) More than one cause may contribute
        • (^) Brain and heart very sensitive to hypoxia
        • (^) Treatment hypoxemia: correct cause ▪ Reduced or deoxygenated Hgb in small blood vessels causing bluish color of skin/mucous membranes ▪ Modified by cutaneous pigment, skin thickness, quantity of Hgb ▪ Central Cyanosis - Cause: deoxygenated Hgb in arterial blood ▪ Evident on tongue and lips ▪ Peripheral Cyanosis: Results from vasoconstriction or diminished peripheral blood flow

❖ Cold exposure, shock, heart failure, peripheral vascular disease

❖ Evident tip of nose, ears, extremities

CM of Hypoxemia:

  • Mild hypoxemia produces few manifestations because Hgb saturation still > 90% when

PO 2 only 60 mmHg

o Sympathetic nervous system initiates compensatory mechanisms

▪ Increase HR & BP, peripheral vasoconstriction,

  • Increasing hypoxemia more profound effects:

o Respiratory distress-dyspnea, use of accessory muscles, cyanosis

o Aerobic metabolism ceases; anaerobic metabolism takes over

o Formation of lactic acid leads to metabolic acidosis

  • Agitated behavior,

uncoordinated

muscle movements,

euphoria, impaired

judgment,

convulsions,

delirium, cyanosis

is late sign, stupor,

coma, death

  • Lack of O 2
  • Body shifts from aerobic to

anaerobic metabolism

which forms Lactic acid

  • Lactic acid accumulates in the

blood; ph drops

  • Diagnosis:
    • Arterial Blood Gases:

Direct measurement of

oxygen content in blood

- Hypoxia - inadequate tissue oxygenation at the cellullar level and is a life-threatening

condition

  • Results from a deficiency in oxygen delivery or oxygen use at the cellular level
  • Can be life threatening and cause fatal dysrhythmias

Early Signs Late signs

❖ Restlessness

❖ Confusion

❖ Anxiety

❖ Difficulty concentrating

❖ Elevated blood pressure

❖ Increased heart rate

❖ Increased respiratory rate

❖ Dyspnea – difficult or labored breathing

❖ Decreased level of consciousness

❖ Decreased activity level

❖ Decreased respiratory rate as patient

fatigues

❖ Hypotension –BP will lower

❖ Bradycardia - slow heart rate (<60)

❖ Acidosis (pH < 7.35)

❖ Cyanosis