School

Diverticular Disease Diagnosis

• acute is determined by examination of the stool for blood, evaluation of blood samples for anemia and signs of active infection, or inflammation, ruptured sacs using ultrasound, magnetic resonance imaging or CT scan

• Once acute episode resolved, will need colonoscopy to emulate the diverticula

Diverticular Disease Pathophysiology

Diverticula: small, bulging pouches (weaken areas) that form the lining of your digestive system. (No to little symptoms from diverticula)

• Common in lower portion of the body large intestine (sigmoid colon)

Diverticulosis: common and10% of people over 40 and 50% of people over 60.

• More than one diverticulum is called diverticula.

  • Presence of diverticula is diverticulosis

  • Fecal matter in diverticula may promote development of infection known as diverticulitis

  • Chronic constipation is linked to development of Diverticular disease

• Slow movements of fecal matter leads to increased, prolonged pressure on the walls of large intestine (alters structure and function)

• Most people are unaware until they unaware until it leads to bleeding, infection, obstruction, ischemia of the affected area of the colon

  • Perforation can cause hemorrhage, abscess, sepsis and peritonitis

• Prevention involves dietary alterations to prevent constipated like a diet high in fiber or low in fat

Intestinal Obstruction

• Blockage prevents normal flow of intestinal contents through GI tract

• Types

  • mechanical

  • Functional

• Small Bowel Obstructon (SBO)

• Large Bowel Obstruction

Mechanical Obstruction

• occurs when something is physically blocking the intestine

  • Adhesions, hernias, polyps, tumors

• Blockage can be partial or complete

• Less commmon

  • Intussusception

  • Volvulus

  • Fecal impaction

Functional Obstruction

• Intestinal Musculature cannot propel content along the bowel

• Causes

  • Parkinson’s

  • Diabetes Mellitus

  • muscular dystrophy

  • Paralytic ileus

Continuing with the previous slide

Small Bowel Obstructon (SBO)

Intestinal contents, fluid, gas accumulate above the obstruction

Peritonitis

Swelling of the peritoneum

Small Bowel Obstruction Clinical manifestations

• Nausea/vomiting

  • Stomach contents, bile, fecal matter

• wavelike cramp pain

• May pass blood and mucous but no fecal matter, no flatus

• Dehydration, intense thirst

• Abdominal distension and pain

Large Bowel Obstruction

• accumulation of intestinal contents, fluid, gas proximal to the obstruction

• Serve distension and perforation can occur

  • Hard, board- like abdomen

  • Medical emergency

Large Bowel Obstruction Clinical Manifestations

• develops and progresses slowly

• Constipation may be only symptom

• Weakness, anorexia

• Vomiting fecal matter

Functional Fecal Incontinence

Repetitive voluntary or involuntary soiling (4+ years and older)

• Pathophysiology

  • Constipation

• Clinical Manifestations

  • Constipation, soiling once a month for at least 2 months

• Diagnosis

  • History/ physical, diet, developmental considerations, behaviors, food allergy

• Treatment:

  • Diet, increase fluids, mental health , scheduled time for defecation

Review: Diverticular Disease

• What is the condition ?

  • Diverticular disease occurs when small pouches, called diverticula, form in the wall of the colon. When these pouches are not inflamed, it is known as diverticulosis, and when they become infected or inflamed, it is called diverticulitis.

• What are the S/Sx?

  • Symptoms of diverticulosis are often mild or absent, but diverticulitis can cause left lower abdominal pain, fever, nausea, vomiting, and bowel changes such as constipation or diarrhea.

Review: Small Bowel Obstructions

What is the condition?

• blockage in the small intestine that prevents the normal movement of digestive contents. Common causes include adhesions from prior surgery, hernias, tumors, or inflammatory bowel disease.

What are the S/Sx?

• abdominal pain and cramping, bloating, nausea and vomiting, inability to pass gas or stool, and abdominal distention

What is the treatment?

• NPO (nothing by mouth), nasogastric tube insertion for decompression, IV fluids for hydration and electrolyte balance, and pain control.

  If the obstruction does not resolve or there is evidence of strangulation or perforation, surgical intervention is required to remove the blockage or repair the affected section of bowel.

Review: Large Bowel Obstructions

What is the condition?

• blockage in the colon that prevents the normal passage of intestinal contents. Common causes include colon cancer, diverticulitis, volvulus (twisting of the bowel), or strictures.

What are the S/Sx?

• abdominal distention, constipation or inability to pass gas, cramping abdominal pain, nausea and vomiting, and sometimes fever or signs of infection if complications occur.

What is the treatment?

• fluid and electrolyte replacement, bowel rest (NPO), nasogastric decompression, and addressing the underlying cause.

  Surgery may be required if there is complete obstruction, bowel ischemia, perforation, or malignancy.

Review: Functional Fecal Incontinence

• What is the condition?

  • A small bowel obstruction is a blockage in the small intestine that prevents the normal movement of food and fluids. It can be caused by adhesions, hernias, tumors, or paralysis of the bowel.

• What are the S/sx?

  • Common symptoms include crampy abdominal pain, vomiting, bloating, and inability to pass stool or gas.

Review of SBO and LBO

Review: Celiac Disease

Review: Mechanical Obstruction

Mobility and Functional Ability

• Discuss the two types of connective tissue found in the skeletal system

  • The skeletal system contains two types of connective tissue: bone and cartilage. Bone provides structure, support, and protection, while cartilage offers flexibility and reduces friction in joints.

• State the function of the parathyroid hormone, calcitonin, vitamin D in terms of bone formation and metabolism

  • Parathyroid hormone (PTH) increases blood calcium by stimulating bone resorption, calcitonin lowers blood calcium by inhibiting bone breakdown, and vitamin D promotes calcium absorption for bone mineralization.

• Describe the source of blood supply to the synovial joint

  • The synovial joint receives its blood supply from arterial branches surrounding the joint capsule, which form a network to nourish joint tissues and maintain healthy function.

Skeletal System (Connective Tissue)

• Bones (Rigid)

• Cartilage (Flexible)

• Connective Tissue Structure

  • Ligaments (bone to bone)

  • Tendons (bone to muscle)

Skeletal System Functions

• framework for attachment of muscles, tendons and ligaments

• Protects soft tissue and maintains soft tissue in proper position

• Provides stability for the body

• Maintains body shape

• Acts as a storage reservoir for calcium

• Contains the hematopoietic (formation of RBCs) connective tissue in which blood cells are formed (RBCs)

Classification of Bones

Long bones

• found in the upper and lower extremities

Short bones

• irregularly shaped bones located in the ankle and the wrist

Flat Bones

• composed of spongy bone between 2 layers of compact bone

• Found in areas such as the skull and rib cage

Regulation and Action of Parathyroid Hormone (PTH)

• PTH triggers release of calcium from bone

• Conserves calcium by the kidney

• Increases calcium in the intestine by activating Vitamin D

Hormonal Control of Bone Formation and Metabolism

• Parathyroid Hormone

• Calcitonin

• Vitamin D (dairy, lentils)

Tendons and Ligaments

• Dense connective tissue composed largely of intracellular bundles of collagen fibers arranged in the same direction and plane

• Limited blood supply

• Composted mainly of collagen (strong ad flexible protein)

• Attaches structures together

• Forms scar tissues

Joints

• areas where two or more bones meet

Classes of Joints

• based on movement and presence of a joint cavity

Joint Nourishment Supply

Blood Vessels

• direct or indirectly nourishes the majority of joint tissue

• Synovial membrane has a rich blood supply

Synovial Fluid

• supplies articulating cartilage

• Fluid is normally clear or pale yellow and does not clot

Trauma, Infection and Neoplasms Objectives

Discuss the types, clinical manifestations, and healing process of fractures

• closed, open, transverse, or spiral. Symptoms include pain, swelling, bruising, deformity, and loss of function. Healing happens in three stages: inflammation, callus formation, and remodeling.

Differentiate the complications of fractures and musculoskeletal injuries.

• poor healing, misaligned bones, infection, compartment syndrome, and fat embolism. Muscle and soft tissue injuries can cause bleeding, chronic pain, stiffness, or abnormal bone growth in the muscle.

Discuss the differences between the etiologies and manifestations of osteomyelitis

• bone infection caused by bacteria spreading through the blood, nearby tissue, or trauma. Symptoms include bone pain, swelling, warmth, fever, and sometimes chronic drainage.

Describe four major causes of osteonecrosis

• trauma, long-term steroid use, alcohol abuse, or blood flow disorders like sickle cell disease.

Contrast osteogenic sarcoma, Ewing sarcoma, and chondrosarcoma in terms of most common age groups and anatomic sites affected

• Osteosarcoma: teens and young adults, usually in long bone ends.

• Ewing sarcoma: children/adolescents, often in long bone shafts or pelvis.

• Chondrosarcoma: adults 40–70, mostly in pelvis or shoulder bones.

Causes of Musculoskeletal Injuries

• Blunt tissue trauma

• Disruption of tendons and ligaments

• fractures of bony structures

• Falls most common cause of injury in patients 65 and older

Classifications of fractures

By cause:

• sudden injury

• Stress fractures

• Pathologic fractures (osteoporosis)

Location:

• proximal, midshaft, distal

Types

• open or closed (through the skin)

Signs of a fracture

• pain

• Abnormal mobility

• Deformity of the affected part

• Loss of function

• Swelling

• Tenderness at the site of bone disruption

4 stages of bone healing

Hematoma formation

• Days 1-5

Inflammatory phase

• days 5-11

Reparative

• days 11-28

Remodeling

• start at day 18 and may continue for many months or years

Factors delaying bone healing

• patients age (children heal faster than adults)

• current medications

• Debilitating disease (diabetes, rheumatoid arthritis)

• Local stress around the fracture site

• Circulatory problems

• Coagulation disorders

• Poor nutrition

Complications of Fractures

• Injury from bone fragments

• Pressure from swelling and hemorrhage (bleeding)

  • Fracture blisters, compartment syndrome

• Development of emboli (clots that move)

  • Fat emboli an thromboembolic

• increase protein for healing

• Increased blood sugar makes it harder to help and suppresses osteoblasts

Compartment Syndrome

• fluids are fracture blisters

• Severe pain that is out of proportion to the original injury or physical findings

• Fracture that swells that cuts off blood flow

Thromboemboli

• clot that goes to the artery on the way to the lungs (pulmonary embolism)

  • Symptom: shortness of breath

Disorders

• pulmonary embolism

• Deep vein thrombosis ( compress devices help)

Diagnostics

• venous Doppler ultrasound

• Lung scan

Fat Embolism Syndrome

• Long one/pelvic fracture→ fat globules entering circulation→ 1. Hypoxemia 2. Neurological abnormalities 3. Petechial rash

• Doesn’t blanch

Fat Embolism Syndrome Clinical Manifestations

• drowsy

• Confusion

• Encephalopathy

• Seizures

• Begins 12-72 hours after injury

• First symptoms include a subtle change in behavior

Original of Bone infections

• microorganisms introduced during injury

• Microorganisms introduced during operative procedures

• Microorganisms from the blood stream

Types of Osteomyelitis

Hematogenous Osteomyelitis

• originates with infectious organisms that reach the bone through the blood stream

  • Chills, fever, bacteremia

Contiguous Spread Osteomyelitis

• secondary to a contiguous force of infection

• Direct inoculation from an exogenous source or from an adjacent extra skeletal site

  • Most common

  • Persistent fever

  • Increased pain at surgical site

  • Poor wound healing

Chronic osteomyelitis

• Occur secondary to an open wound

  • May not have signs

  • Bone biopsy for diagnosis

  • New bone starts to form over dead bone

Osteonecrosis

causes

• mechanical disruption of blood vessels

  • Steroids or radiation

• Thrombosis and embolism

• Vessel injury

• Increased intraosseous pressure (compartment syndrome)

Blood flow

• other cortex receives supply form surrounding blood vessels

• Some sites have limited collateral circulation; interruption flow affects significant amount of bone tissue

Osteonecrosis Clinical Manifestations

• varies depend on extent of infarction

• Starts with pain with activity

• Progresses to pain at rest

Symptoms of Bone tumor (Neoplasms)

• pain

• Presence of a mass

• Impairment of function

Types of Malignant Bone Tumors

Osteosarcoma:

• aggressive and highly malignant

• Common in children and adolescents

• Most common: primary bone tumor

Ewing Sarcoma:

• Peripheral primitive neuroectodermal tumor (PNET)

• Often in those under 20 yerars old

Chondrosarcoma

• Malignant tumor originating from cartilage cells

• Common in adults

• Second most common primary bone tumor

• Slow growing

• Often painless

Treatment goals for metastatic bone disease

• preventing pathologic fractures

• Promoting survival with maximum functioning

• Allowing the person to maintain as much mobility and pain control as possible

What tumor types would most likely metastasize

Osteosarcoma

Metabolic Disorders

• Describe risk factors that contribute to to the development of osteopenia, osteoporosis, osteomalacia, and rickets, and relate them to the prevention of the disorder

  • Osteopenia and osteoporosis are caused by aging, low calcium or vitamin D intake, lack of exercise, smoking, excessive alcohol, and hormonal changes (especially low estrogen). Prevention includes a calcium- and vitamin D-rich diet, regular weight-bearing exercise, and avoiding smoking and excessive alcohol.

    Osteomalacia and rickets result from vitamin D deficiency, poor dietary calcium, kidney disease, or limited sunlight exposure. Prevention focuses on adequate vitamin D, calcium intake, and sunlight exposure.

• Discuss clinical manifestations and diagnostic criteria for osteopenia, osteoporosis, osteomalacia and rickets

Clinical manifestations:

• Osteopenia: mild bone loss, usually no symptoms, detected by bone density scans.

• Osteoporosis: fractures (especially hip, spine, wrist), loss of height, back pain, kyphosis; diagnosed by DEXA scan showing low bone density.

• Osteomalacia: bone pain, muscle weakness, difficulty walking; diagnosed by low vitamin D, low calcium/phosphate, and X-ray findings.

• Rickets (in children): bowed legs, delayed growth, skeletal deformities; diagnosed by clinical signs, low vitamin D, and X-rays showing soft bones.

Osteopenia

• reduction in bone mass greater than expected for age or sex

• Causes:

  • Decrease in bone formation

  • Inadequate bone mineralization (deossification)

Normal bone growth

• long bones grow in length, the deeper layer of cartilage cells in the growth plate multiply and enlarge, pushing articulation cartilage farther away from metaphysisand diaphysis of the bone

Osteoporosis

• skeletal disorder

  • Loss of bone mass and deterioration of architecture of cancellous bone with an increase in bone fragility and susceptibility to fractures

    • Loss of mineralized bone mass causes increased porosity of skeleton

  • Causes

    • Occur as result of endocrine disorder

    • Aging

Risk factors associated with osteoporosis and clinical manifestations

Personal Characterstics

• white

• Female

• Small bone structure

• Postmenopausal

• Family history

• Hump, decrease in height, predisposition in fractures

• Fractures in distal radius, fractured hip, compression fracture of vertebrae

Lifestyle

• sedentary, calcium deficient, excessive alcohol and caffeine intake, smoking

• Drug related

• Disease related

Diagnosis of Osteoporosis

• Bone Mineral density assessment

• Dual energy x ray absorptiometry of spine and hip

T score:

• compares your results to a healthy young adult 20-35 years old

Z score:

• results to a person of same gender and age as yourself

• -1.5 to -2.4 may indicate osteopenia

• Less than -2.5 may indicate osteoporosis

Disorders involving softening of bones

Osteomalacia:

• Inadequate mineralization of bone results from a calcium or phosphate deficiency or both

Rickets

• vitamin D deficiency, inadequate calcium absorption and impaired mineralization of bone in children

Osteomalacia Clincial manifestations

• affects height

• Bone pain

• Muscle weakness

• Fractures

Rickets Clincial Manifestations

• bone deformity

• Lumbar lordosis

• Bowing of legs

What condition results from loss of bone mass

osteoporosis

Rheumatic Disorders

• Describe the pathologic changes that may be found in joint of a person with rheumatoid arthritis

  • autoimmune disease causing inflammation of the joint lining (synovium), leading to swelling, pain, joint deformity, and erosion of cartilage and bone.

• Compare rheumatoid arthritis and osteoarthritis in terms of joint involvement, level of inflammation and local and systemic manifestations

  • Osteoarthritis (OA) is a degenerative joint disease where cartilage wears down, causing bone spurs, joint space narrowing, stiffness, and pain, usually without significant inflammation.

• Describe pathologic joint changes associated with osteoarthritis

  • Comparison: RA often affects small joints symmetrically (hands, wrists) with high inflammation and systemic symptoms like fatigue and fever. OA usually affects weight-bearing or large joints asymmetrically (knees, hips), with mild inflammation and no systemic symptoms.

  • Pathologic changes in OA include cartilage loss, bone thickening, osteophyte formation, and joint space narrowing, leading to stiffness and reduced mobility.

Systemic inflammatory disease

• affects 1-2% of population

• Prevalence increases with age

• Elderly onset for rheumatoid arthritis is 65

Rheumatoid Arthritis Characteristics

• autoimmune

• Extra articular

• Articular

• Slow (insidious) onset with systemic manifestations

• Exacerbations and remissions

• Only few joints for brief durations but it may get worse

RA Clincial Manifestations

• fatigue

• Weakness

• Anorexia

• Weight loss

• Low grade fever

• Anemia

• PAIN

Diagnosis criteria for Rheumatoid arthritis

• morning stiffness for 1 hour for at least 6 weeks

• Swelling of 3 or more joints for 6 weeks

• Swelling or wrist, metacarpophalangeal or proximal joints for more than 6 weeks in your hands

• systemic joint swelling

• Rheumatoid nodules

• Serum rheumatoid factor (RH)

• history and physical

• Physical exam

• ESR

Osteoarthritis

• RA causes it

• Degenerative joint disease

• Localized or generalized syndromes

• Secondary OA has known underlying cause

  • Congenital or acquired defects of joint,structures, trauma, infection, metabolic disorders or inflammatory disease

Pathogenesis of Osteoarthritis

• progressive loss of articular cartilage

• Synovitis

• Osteophytes

  • Bone spurs

Causes of Osteoarthritis

• post inflammatory diseases

• Post traumatic disorders

• Anatomic disorders

• Metabolic disorders

• Neuropathic arthritis

• Heredity disorders of collagen

• Age

• Obesity

Osteoarthritis Manifestations

• history, physical, x rays, labs

• Joint pain

• Stiffness

• Limitation of motion

• Joint instability

• Deformity

What describes the primary pathophysiological process in osteoarthritis

progressive loss of articular cartilage with osteophyte formations

How Rheumatoid arthritis leads to joint deformities and reduced mobility

• autoimmune

• Attacks synovial joint

• Chronic inflammation

• Pannus formation (abnormal tissue growth)

• Cartilage destruction

• Erosion

• Joint deformity

Compartment syndrome

• increased pressure within a loved muscle compartment

Case Study

Ventilation and Diffusion

• Ventilation is the mechanical process of air moving into and out of the lungs,

• diffusion is the passive movement of gases across the alveolo-capillary membrane from an area of high pressure to low pressure

Acid Base Balance

Differentiate between acids and bases including ph measurements

• acids are substances that release hydrogen ions

• Bases are substances that acceptt hydrogen ions or release hydroxide ions

Compare the roles of buffer systems in regulation of acid base balance

• buffer systems keep blood pH stable

• Bicarbonate buffering system is most important, balancing acids and bases through CO2 regulation by the lungs and bicarbonate control by the kidneys

• Protein buffers (albumin and hemoglobin) bind or release H+

• Phosphate buffers act mainly inside cells and in urine

Identify origin of acid base disturbance

• problems with the lungs or metabolism (kidney and tissues)

• Respiratory disturbances: caused by changes in CO2 due to ventilation problems

• Metabolic disturbances: changes in HCO3- due to kidney function or metabolic processes

Interpret acid base imbalances via arterial blood gas lab values

• pH: 7.35-7.45

• PaCO2: 35-45 mmHG (respiratory function)

• HCO3- (bicarbonate) 22-26 mEq: reflects metabolic function

• PaCO2 is abnormal: respiratory cause

• HCO30: metabolic cause

Discuss common causes and clinical manifestations of metabolic and respiratory acidosis and metabolic and respiratory alkalosis

• Metabolic Acidosis

  • Kidney failure

  • Decrease pH, decrease HCO3-

  • Rapid breathing and confusion

• Respiratory acidosis

  • Hypoventilation (COPD)

  • decrease pH, increase PaCO2

  • Headache

• Metabolic alkalosis

  • Vomiting

  • increase pH and increase HCO3-

  • Muscle cramping

• Respiratory Alkalosis

  • Hyperventilation

  • increase in pH, decrease in PaCo2

  • Dizziness

Acid Base Balance

• Regulation of acids and bases is critical for metabolic activities

• Narrow ph range is required for function of cells, tissues, and organs

  • Ph 7.35-7.45

  • More h+ more acidic

  • More OH more alkaline

  • High pH is alkalosis

  • low pH is acidosis

PH balance

• represents negative logarithm of H+ ion concentration

• PH is inversely related to H+ ion concentration

  • Low pH indictates high concentration of h+ ions

  • High pH indicates a low concentration of H+ ions

Anion Gap

• Increase in anion gap= metabolic acidosis

• Cation - anion

H+ cations can be exchanged with K

• H⁺ increases in the blood (acidosis), H⁺ moves into cells and K⁺ moves out to maintain electrical neutrality_

• Showing unmeasurable anions in plasma that replace bicarbonate in metabolic acidosis

pH regulators

Chemical buffer systems of body fluids

• combine with excess acids or bases to prevent large changes in pH

• H20+CO2 < - > H2CO3 <- > H+ + HCO3-

Lungs

• control elimination of CO2

Kidneys

• Eliminate H+ and both reabsorb and generate new HCO3-

Bicarbonate Buffer System

• most important buffering system for your body

• Weak acids or bases in the body fluids exchange for strong acids or bases to help neutralize

Potassium Hydrogen Exchange System

• Excess H+ can be exchanged for K+ across the cell membrane

Chemical Buffering System

• largest system

• Amphoteric: acid or case

• Albumin: intracellular proteins and plasma globulins combine with H+ ions (It helps maintain blood pH by binding hydrogen ions (H⁺) when the blood becomes too acidic)

  • Example of plasma protein buffer

Respiratory Buffer System

• Chemoreceptors and peripheral chemoreceptors sense changes in PaCO2 and pH

• INCREASED ventilation DECREASES PaCO2

• DECREASED ventilation INCREASES PaCO2

Blood gases

• Rise in PaCo2

  • Central chemoreceptors

• Rise in PaCO2, Fall in PaO2, Fall in pH

  • Peripheral chemoreceptors

• excess H+ increased ventilation to prevent acidosis

• Not enough H+ decreased ventilation to prevent alkalosis

• Rapid acting

• Not sufficient to completely normalize pH by itself

Renal Buffer System

3 mechanisms of action

1. Reabsorbs of HCO3- (bicarbonate and blood is filtering through the kidney)

2. Produces new HCO3-

   1. H+ combines with phosphate or ammonia to create new HCO3- when homeostasis is reached, excess H+ is excreted

3. Excretes acids from protein and lipid metabolism

   1. Phosphate and ammonia buffering systems excrete excess H+

• Primary source for retaining/creating bases

• Takes hour to begin adjusting pH can last days

• Complements plasma and respiratory buffering systems for adjusting pH

Review

What causes changes in respirations

• chemical receptors in continuous chemoreceptors and peripheral detecting changes in CO2

• If there’s too many H+ ions what will the respiratory system do

  • Increase respirations

• What does the kidney produce to neutralize acids

  • Bicarbonate

Acid Base Imbalances

• Respiratory or Metabolic in origin

  • Respiratory disorders are due to an alternation in CO2

    • An increase in CO2= respiratory acidosis

    • A decrease in CO2= respiratory alkalosis

• Metabolic disorders are due to an alternation in HCO3-

  • An increase in HCO3-= metabolic alkalosis

  • A decrease in HCO3-= metabolic acidosis

Arterial Blood Gas Sampling

• Arterial stick performed By MD/RT/RN

  • Arterial puncture at radial (most of the time), brachial, femoral

  • Indwelling arterial catheter

• Measures pH, acid-base balance and oxygenation status

• Allen’s test

ABG Pneumonic

Acid Base Mnemonic (ROME)

• Respiratory…Opposite

  • PH increases, PCO2 decreases= alkalosis

  • PH decreases, PCO2 increases= acidosis

• Metabolic…Equal

  • PH increases, HCO3 increase =alkalosis

  • pH decreases, HCO3 decreases= acidosis

Practice 1

PH: 7.30 (acidosis)

CO2: 50 mmHg (respiratory driven)

HCO3-: 24 meq (normal)

respiratory acidosis

Practice 2

PH: 7.50 (alkalosis)

CO2: 43 mmHg (normal)

HCO3-: 28 mEq (metabolic driven)

Metabolic alkalosis

Practice 3

pH: 7.31 (acidosis)

CO2: 36 mmHg (normal)

HCO3-: 12 mEq (metabolic driven)

Metabolic acidosis

Practice 4

PH: 7.48 (alkalosis )

CO2: 28 mmHg (respiratory driven)

HCO3-: 23 mEq (normal)

Respiratory alkalosis

Metabolic Acidosis

Causes

• diabetic ketoacidosis

• Lactic acidosis

• Drug and alcohol overdose

• Acute kidney injury

• Liver failure

• Hyperkalemia

• Diarrhea (lose base therefore acidosis)

Metabolic Alkalosis

Causes:

• prolonged vomiting (losing acid because stomach has acid)

• Diuretic use

• Hypokalemia, hypocalcemia, hypochloremia, hypomagnesemia

• Antacid abuse

• Inadequate renal perfusion

Respiratory Acidosis

Causes

• hypoventilation

• Over-sedation (retaining extra CO2)

• Brain stem dysfunction

• Obstructive sleep apnea

• Acute respiratory distress syndrome

• COPD

• Pneumothorax

Respiratory Alkalosis

Causes

• Hyperventilation

• Anxiety

• Acute respiratory distress syndrome

• Stroke

• Head injury

Altered Ventilation and Diffusion

• Explain the role of ventilation and diffusion in oxygen/carbon dioxide gas exchange

  • Ventilation: movement of air in and out of the lungs, bringing oxygen into the alveoli and removing carbon dioxide

    • Diffusion: O₂ moves from the alveoli into the blood and CO₂ moves from the blood into the alveoli, driven by concentration (partial pressure) differences across the alveolar-capillary membrane.

• Compare carbon dioxide and oxygen in maintaining homeostasis

  • Oxygen: cellular metabolism and energy production,

  • carbon dioxide: waste product that helps regulate blood pH through the bicarbonate buffer system.

  • Both gases must be balanced—too little O₂ (hypoxia) or too much CO₂ (hypercapnia) disrupts homeostasis and affects organ function.

• Describe the processes that can impair ventilation and diffusion

  • Ventilation and diffusion can be impaired by airway obstruction, lung diseases (e.g., COPD, asthma, pneumonia), chest trauma, pulmonary edema, or thickening of the alveolar membrane, all of which limit airflow or gas exchange between the lungs and blood.

• Explain why ventilation and perfusion must be matched

  • Ventilation (air reaching alveoli) and perfusion (blood reaching alveoli) must be matched (V/Q balance) so that adequate oxygen enters the blood and carbon dioxide is effectively removed. A mismatch such as in pulmonary embolism or airway obstruction reduces gas exchange efficiency and leads to hypoxemia.

• List 3 types of conditions in which hypoxia can occur

  1. Hypoxic hypoxia – due to low oxygen in the air or poor ventilation (e.g., high altitude).

  2. Anemic hypoxia – from low hemoglobin or impaired oxygen-carrying capacity.

  3. Circulatory (stagnant) hypoxia – due to poor blood flow (e.g., heart failure, shock).

• Discuss common causes and clinical manifestations of impaired ventilation and diffusion

  • Causes: COPD, asthma, pneumonia, pulmonary edema, pulmonary embolism, or chest injuries.

    Clinical manifestations: Shortness of breath (dyspnea), rapid breathing (tachypnea), cyanosis, confusion, fatigue, and abnormal blood gas values (low PaO₂, high PaCO₂).

A&P of the Respiratory System

• upper and lower airways

• Upper: nose, mouth, nasopharynx, and oropharynx

• Laryngeal pharynx connected the upper and lower airways

• Lower: trachea, bronchi, bronchioles and alveoli

Alveoli

• Alveolar capillary junction: oxygen and carbon dioxide are exchanged

• Type I alveolar cells: provide structure and air exchange

• Type II alveolar cells: secrete surfactant

Breathing

Ventilation: process of moving air into and out of the trachea, bronchi and lungs

Diffusion: process of moving and exchanging oxygen and carbon dioxide across the alveolar-capillary membrane

Perfusion: process of supplying oxygenated blood to the lungs and organ system via blood vessels

Respiration: cells throughout the body use oxygen aerobically to make energy

Ventilation

• acquire oxygen

• Removes carbon dioxide

• Cellular metabolism

• Intercostal muscles, diaphragm, sternocleidomastoid which aids in chest expansion and recoil

What makes us breathe

• drive to ventilate is stimulated by the respiratory control center in the brainstem in response to chemical messages in the body

• Respiratory control center comprises of neurons in the pons and medulla

Central Chemoreceptors

• detects CO2 changes

• Medulla and pons

• Central chemoreceptors

  • Most sensitive

  • Alter rate of breathing to adapt to higher or lower levels of CO2 in the body

  • Carbon dioxide is acidic therefore if blood is more acidic, the respiratory center increases the rate and depth of breathing to release excess carbon dioxide

Peripheral Chemoreceptors

• most sensitive oxygen levels in the arterial blood (PaO2)

• Located in the aorta and carotid arteries

• Trigger an increase of ventilation in response to low oxygen levels in the blood

Partial Pressure of Gases

• oxygen and carbon dioxide gases are countless particles in constant collison

• Force of these collisions forms a pressure

• Small amount of oxygen is dissolved and circulating in the plasma

• Dissolved portion creates a pressure in the plasma called partial pressure

• Partial pressure of oxygen in arterial blood is labeled PaO2

Oxygen Diffusion and Transport

As PaO2 (oxygen in plasma) rises, oxygen moves from the plasma into red blood cells

• oxygen is attracted to iron

• Oxygen binds to hemoglobin Forming oxyhemoglobin

• 1 hemoglobin carries 4 oxygen molecules

• Binding attraction continues until saturated

• oxygen saturation (SaO2) refers to amount of oxyhemoglobin

• 87-99% of O2 is combined with hemoglobin

• When fully saturated, O2 continues to diffuse and dissolve until partial pressure in arteries are equal to partial pressure of the O2 in the alveoli

• Diffusion stops until a change in PaO2 in sensed again

• dissolved O2 in the plasma is diffused into cells and used for cellular metabolism

• Blood moves and senses PaO2 and PaO2 passes the carotid and sends a message to the brain saying they need more oxygen. I actually have no idea what i am writing.