Metaplasia

mature cell type is replaced by a different mature cell type

Atrophy

Decrease in the size of cells; results in reduced tissue mass

Dysplasia

Cells that vary in size and shape within a tissue

Hyperthrophy

Increase in cell size; results in enlarged tissue mass

Signs

Objective (can be observed or measured)

Symptoms

Subjective (felt and reported by the patient)

Manifestations

Signs and symptoms of disease

Complications

New secondary or additional problems/ New problems caused by the disease or its treatment.

Occurrence

Tracked by incidence and prevalence

• Incidence: Number of new cases during a specific time period.
• Prevalence: Total number of existing cases (new + old) at a given time.

What factors/injuries can cause cell death?

Physical damage

• Excessive heat or cold, Radiation exposure

Mechanical damage

• Pressure or tearing of tissue

Chemical toxins

• Exogenous: from environment; Endogenous: from inside the body

Microorganisms

• Bacteria and viruses, for example

Abnormal metabolites

• Genetic disorders, Inborn errors of metabolism, and altered metabolism

Nutritional deficits and Imbalance of fluids or electrolytes

Remember TIPS:

1. Toxins
2. Infections
3. Physical Injury
4. Serum Deficit Injury

How to differentiate an multiorgan disorder and syndrome?

• Multiorgan Disorder: A disorder that damages or affects two or more organ systems.
• Syndrome: A collection of signs and symptoms that tend to occur together.

Relation b/t plasma protein and osmotic pressure.

• Plasma proteins (especially albumin) create osmotic (oncotic) pressure.
• Osmotic pressure pulls water into the bloodstream and keeps it inside blood vessels.
• ↑ Plasma proteins → ↑ Osmotic pressure → Water stays in blood vessels.
• ↓ Plasma proteins → ↓ Osmotic pressure → Water moves into tissues → Edema (swelling).

Relation b/t capillary hydrostatic pressure and osmotic pressure, and permeability

• Capillary hydrostatic pressure pushes fluid out of the capillary into the tissues.
• Osmotic (oncotic) pressure (created by plasma proteins, especially albumin) pulls fluid into the capillary.
• Capillary permeability determines how easily fluid and proteins can pass through the capillary wall.
• ↑ Permeability → More fluid and proteins leak into tissues → Edema (swelling).
• ↓ Permeability → Less leakage → Fluid stays in the bloodstream.

Typical sign of dehydration.

• Decreased skin turgor and dry mucous membranes
• Sunken eyes
• Sunken fontanelles in infant
• Lower blood pressure, rapid weak pulse
• Increased hematocrit
• Increased temperature
• Decreasing level of consciousness
• Urine―low volume and high specific gravity

What is the third-spacing?

• Third-spacing is the abnormal movement of fluid from the bloodstream into spaces where it cannot be used (such as the tissues or body cavities).
• Blood vessels lose fluid → Blood volume decreases
• Fluid becomes trapped in the interstitial space or body cavities
• Can lead to edema, low blood pressure, and decreased tissue perfusion

Hypoatremia and its common cause

Hyponatremia = Low sodium (Na⁺) in the blood.

Causes include:

• Losses from excessive sweating, vomiting, diarrhea
• Use of certain diuretic drugs combined with low-salt diet

Hormonal imbalances

Insufficient aldosterone

Adrenal insufficiency

• Excess ADH secretion
• Diuresis
• Excessive water intake

Three mechanisms to compensate for serum PH?

• Buffer pairs in the blood respond to pH changes immediately
• Respiratory system can alter carbonic acid levels to change pH
• Kidneys can modify the excretion rate of acids and absorption of bicarbonate ions to regulate pH

1. Most significant control mechanism
2. Slowest mechanism

Hypokalemia

Low potassium in the blood

Causes include:

• Definition: Serum K+ < 3.5 mEq/L
  • Excessive losses caused by diarrhea
  • Diuresis associated with some diuretic
  drugs
  • Excessive aldosterone or
  glucocorticoids
  ◦ Example: Cushing syndrome
  • Decreased dietary intake
  ◦ May occur with alcoholism, eating
  disorders, starvation
  • Treatment of diabetic ketoacidosis with
  insulin

Cause of warmth/redness of inflammation

• Direct physical damage

◦ Examples: cut, sprain

• Caustic chemicals

◦ Examples: acid, drain cleaner

• Ischemia or infarction
• Allergic reactions
• Extremes of heat or cold
• Foreign bodies

◦ Examples: splinter, glass

• Infection

Systemic effects of inflammation

• Mild fever (pyrexia)
  ◦ Common if inflammation is extensive
  ◦ Release of pyrogens
• Malaise
  ◦ Feeling unwell
• Fatigue
• Headache
• Anorexia

Long-term effects of using glucocorticoids

• Atrophy of lymphoid tissue; reduced hematopoiesis
  ◦ Increased risk of infection
• Catabolic effects
  ◦ Increased tissue breakdown; decreased protein synthesis
• Delayed healing
• Delayed growth in children
• Retention of sodium and water because of aldosterone-like affect in the kidney

What is a serous exudate?

Serous exudate is a thin, watery, clear or pale yellow fluid that leaks from blood vessels during inflammation.

• Contains water, electrolytes, and a small amount of protein
• Has few cells
• Common in mild inflammation or early stages of injury

RICE (mechanism of them)

• Rest: Prevents further injury and allows healing.
• Ice: Causes vasoconstriction (narrows blood vessels), reducing blood flow, swelling, pain, and inflammation.
• Compression: Limits fluid from leaking into tissues, reducing edema (swelling).
• Elevation: Raises the injured area above the level of the heart, promoting venous and lymphatic drainage to decrease swelling.

Sequence in a healing process of an injury

Hemostasis – Bleeding stops.

• Blood vessels constrict.
• Platelets form a clot.

Inflammation – Cleans the wound.

• White blood cells remove bacteria and damaged tissue.
• Signs: Redness, heat, swelling, pain.

Proliferation – Rebuilds tissue.

• New blood vessels form (angiogenesis).
• Fibroblasts produce collagen.
• Granulation tissue develops.
• Wound begins to close.

Remodeling (Maturation) – Strengthens the tissue.

• Collagen is reorganized.
• Scar tissue matures.
• Tensile strength increases (but usually never reaches 100% of the original tissue).

What is a Colles’ fracture?

fracture of the distal radius (near the wrist) that usually occurs after falling on an outstretched hand (FOOSH).

• Location: Distal radius
• Common cause: Fall on an outstretched hand
• Classic deformity: "Dinner fork" (or "silver fork") deformity because the wrist bends upward
• Most common in: Older adults, especially those with osteoporosis

Procallus or fibrocartilaginous callus

The procallus, also called the fibrocartilaginous callus, is the second stage of bone healing.

• Forms within days after a fracture.
• Fibroblasts produce collagen.
• Chondroblasts produce fibrocartilage.
• Creates a soft callus that bridges the broken bone ends.
• Stabilizes the fracture but is not yet strong bone.

How Duchenne’s muscular dystrophy is inherited?

Duchenne muscular dystrophy is inherited in an X-linked recessive pattern.

• Caused by a mutation in the dystrophin gene on the X chromosome. Mostly affects males because they have only one X chromosome (XY).
• Females (XX) are usually carriers and often do not have symptoms because they have a second normal X chromosome.

Basic pathology of rheumatoid arthritis

• Synovitis: marked inflammation, cell proliferation
• Pannus formation
  ▫ granulation tissue spreads
• Cartilage erosion
  ▫ creates unstable joint
• Fibrosis
  ▫ calcifies and obliterates joint space
• Ankylosis
  ▫ joint fixation and deformity develop if untreated.
• Frequently occur around the joints
• Atrophy of muscles
• Bone alignment shifts
• Muscle spasms caused by inflammation and
  pain
• Contractures and deformity develop.

What factors delay the healing of bone fractures?

• Amount of local damage
• Proximity of bone ends.
• Presence of foreign material or infection
• Blood supply to fracture site
• Systemic factors, such as age, nutrition, anemia

Fat emboli from a broken femur and its sequalae

Cause: A femur (long bone) fracture releases fat droplets from the bone marrow into the bloodstream.

• Fat emboli travel through the blood and often lodge in the lungs.

Sequelae (complications):

• Respiratory distress (hypoxemia, shortness of breath)
• Neurologic changes (confusion, altered mental status)
• Petechial rash (small red spots on the chest, neck, or axillae)
• Can develop fat embolism syndrome (FES), a potentially life-threatening complication.

Therapeutic measures of osteoporosis

• Dietary supplements: Calcium and vitamin D to support bone health.
• Fluoride supplements: May stimulate bone formation (used less commonly).
• Bisphosphonates: Slow bone breakdown by inhibiting osteoclasts.
• Calcitonin: Decreases bone resorption and may reduce fracture pain.
• Human parathyroid hormone (teriparatide): Stimulates new bone formation.
• Weight-bearing exercise: Strengthens bones and improves balance.
• Raloxifene or tamoxifen: Estrogen-like medications that help reduce bone loss.
• Other medications: New therapies are being studied.
• Surgery: May be used to reduce severe kyphosis or treat fractures.

Causes of Rickets

Result from deficit of vitamin D and phosphates

• Causes—dietary deficits, malabsorption, intake of phenobarbital, lack of sun exposure
• In children, leads to weak bones and other skeletal deformities
• In adults, may lead to soft bones, resulting in compression fractures

Characteristics of erythrocytes with pernicious anemia

Characterized by very large, immature, nucleated erythrocytes

• Carry less hemoglobin
• Shorter life span

Early general signs and symptoms of anemia

Less oxygen reaching tissues leads to:

• Fatigue
• Weakness
• Pallor (pale skin)
• Shortness of breath with activity
• Dizziness or lightheadedness
• Headache
• Increased heart rate (tachycardia)
• Decreased exercise tolerance

Blood pressure change in patients with polycythemia vera and why?

Blood pressure: Usually increases (hypertension).

• Why? Polycythemia vera causes the body to produce too many red blood cells, making the blood thicker (more viscous).
• Thicker blood increases resistance to blood flow, so the heart must pump harder, leading to higher blood pressure.

DIC presentation and related mechanisms

• Involves both excessive bleeding and clotting
• Excessive clotting in circulation
• Thrombi and infarcts occur.
• Clotting factors are reduced to a dangerous level.
• Widespread, uncontrollable hemorrhage results.
• Very poor prognosis, with high fatality rate
• Complication of many primary problems
• Obstetrical complications, such as abruptio placentae
• Infections
• Carcinomas
• Major trauma

Von Willebrand disease (cause)

• Von Willebrand disease (vWD) is an inherited bleeding disorder caused by a deficiency or dysfunction of von Willebrand factor (vWF).
• vWF helps platelets stick to damaged blood vessels (platelet adhesion). vWF also carries and protects clotting factor VIII.
• Without enough functional vWE, blood clotting is impaired, leading to prolonged bleeding.

Multiple myeloma (what kind of malignant cells are involved?)

Malignant plasma cells in the bone marrow.

Visual field and visual signal pathway

Visual field: The area you can see when looking straight ahead.

Visual signal pathway:

1. Light enters the eye and hits the retina.
2. The retina converts light into nerve signals.
3. Signals travel through the optic nerve.
4. Some nerve fibers cross at the optic chiasm.
5. Signals continue through the optic tract.
6. Signals reach the thalamus (lateral geniculate nucleus, LGN).
7. Signals travel through the optic radiations.
8. Signals reach the visual cortex (occipital lobe), where vision is interpreted.

Cerebrovascular accident and prognosis

• Cerebrovascular accident (CVA) = Stroke.
• Occurs when blood flow to part of the brain is blocked or a blood vessel ruptures, causing brain cells to die.
• Prognosis: Depends on the size and location of the stroke and how quickly treatment begins. Early treatment improves recovery. Some people recover well, while others may have permanent weakness, speech problems, or paralysis.

Typical signs of TIA

• Directly related to location of ischemia
• Intermittent short episodes of impaired function (e.g., muscle weakness in arm or leg)
• Visual disturbances
• Numbness and paresthesia in face
• Transient aphasia or confusion may develop.
• Repeated attacks may be a warning sign for obstruction related to atherosclerosis

Pathophysiological changes of Parkinson’s disease

Dopamine-producing neurons in the substantia nigra degenerate (die). This causes low dopamine levels in the brain.

Low dopamine leads to impaired movement control.

Common effects:

• Tremor
• Muscle rigidity
• Slow movement (bradykinesia) Poor balance and posture

Neuron degenerated in amyotrophic lateral sclerosis

• In ALS, motor neurons degenerate (die).
• Upper motor neurons in the brain and Lower motor neurons in the brainstem and spinal cord

This causes:

Muscle weakness, Muscle wasting (atrophy), and Paralysis

Characteristics of cerebral palsy

Cerebral palsy is a non-progressive brain disorder that affects movement, muscle tone, and posture.

Characteristics:

• Muscle weakness
• Muscle stiffness (spasticity) or abnormal muscle tone
• Poor coordination and balance
• Difficulty walking or controling movements
• Symptoms are present early in life and do not worsen over time (the brain injury is non-progressive)

Treatment of mayasthenia gravis

• Anticholinesterase agents
• Temporary improvement of neuromuscular transmission
• Glucocorticoids
• Suppression of immune system
• Immunosuppressants
• Plasmapheresis
• Removal of antibodies from the blood
• Thymectomy

How to differentiate Osteoarthritis and rheumatoid arthritis (basic pathology and presentation)?

Osteoarthritis (OA):

• Wear-and-tear joint disease
• Cartilage breaks down
• Pain worsens with activity
• Usually affects weight-bearing joints
• Often one side or asymmetrical

Rheumatoid Arthritis (RA):

• Autoimmune disease
• Immune system attacks the synovium (joint lining)
• Causes inflammation, pannus, and joint destruction
• Usually affects both sides (symmetrical)
• Morning stiffness is common

Broca and Wernicke’s aphasia

Broca's aphasia (Expressive aphasia):

• Can understand speech
• Cannot speak fluently (slow, broken speech)
• Knows what they want to say but has difficulty saying it

Wernicke's aphasia (Receptive aphasia):

• Cannot understand spoken or written language
• Speech is fluent but doesn't make sense
• Often unaware that their speech is incorrect

Features of Sickle cell anemia, iron deficiency anemia, beta-thalassemia minor, pernicious anemia

• Sickle cell anemia: Abnormal sickle-shaped red blood cells that block blood vessels and break down easily.
• Iron deficiency anemia: Not enough iron to make hemoglobin small, pale red blood cells (microcytic, hypochromic).
• Beta-thalassemia minor: Inherited decrease in beta-globin production mild anemia with small red blood cells.
• Pernicious anemia: Vitamin deficiency in large red blood cells (macrocytic anemia) and possible nerve problems.