Pathophysio Quiz 2

What are types of cellular injuries?

1. Reversible cellular injury

2. Irreversible cellular injury

What are the etiologies of cellular injuries?

1. Nutritional deficiencies / imbalances

2. Infectious agents and immunological response

3. Physical trauma, chemical injuries, radiation-induced injuries

4. Ischemia and hypoxic injury

Perfusion

Good blood flow; Delivery of oxygen, nutrients, and removal of waste

Ischemia

Inadequate blood flow causing tissue hypoxia and waste build up

Hypoxia

Results from ischemia, oxygen deprivation

What will happen to the cell?

1. Hypoxic tissue injury → oxygen decreases → decrease ATP

2. Sodium potassium pump fails and sodium enters cell

3. Cell swells and cell death occurs in normal perfsuion isn’t returned

What is reversible cellular injury characterized by?

Intracellular accumulation of substances such as fluids, fats, proteins, glucose, pigments, or minerals.

What causes intracellular accumulations?

1. Altered metabolism

2. Genetic disorders

3. Enzyme deficiencies.

What are examples of cellular accumulation?

1. Fat accumulation: caused by altered metabolism → build up fat globules in cell → fatty liver

2. Lack of enzyme: accumulation of endogenous material → lysosomal storage disease (Gaucher disease)

3. Pigment / minerals: ingestion of indigestible materials → build up exogenous materials

4. Abnormal proteins: mutation → build up of abnormal proteins

How can cells repair abnormal proteins?

Chaperones (reshape proteins) or ubiquitin (break into small pieces)

What is cellular adaptation?

Structural or functional change that cell undergoes in response to environmental stressors to allow them to survive and function better

What are the types of adaptive cellular response?

1. Normal

2. Hypertrophy

3. Metaplasia

4. Atrophy

5. Hyperplasia

6. Dysplasia

Hypertrophy

Increase in cell size and functional capacity due to increased demand

Metaplasia

Replacement of one cell type with another better suited to stress.

ex. esophageal cells changing to columnar cells in acid reflux.

Atrophy

Decrease in cell size and function

ex. muscle atrophy

What causes atrophy?

Disuse, denervation (lack of nerve stimulation), ischemia, nutrient starvation, loss of endocrine signals, persistent injury.

Hyperplasia

Increase in number of cells, increasing functional capacity. Cells response to increase demand by dividing

What causes hyperplasia?

1. Increased physiologic demand

2. Hormonal stimulation

3. Chronic irritation or injury

Dysplasia

Disorganized appearance of cells (size, shape, arrangement) due to adaptive effort gone astray; may progress to cancer (preneoplastic)

What are the types of irreversible cell injury?

1. Necrosis

2. Apoptosis

What is necrosis?

Irreversible cell injury with swelling, membrane/organelle breakdown, leakage of contents, and inflammation.

What are the types of tissue necrosis?

1. Coagulative

2. Liquefactive

3. Fat necrosis

4. Caseous necrosis

All caused by ischemia or toxic injury

What is coagulative necrosis?

Necrosis due to ischemia, tissue structure preserved.

ex. heart

What is liquefactive necrosis?

Necrosis from rapid cell death, often due to infection, forming pus (combination of WBCs and dead tissue)

ex. brain

What is fat necrosis?

Death of fat tissue

ex. pancreas.

What is caseous necrosis?

Cell death in lungs caused by tuberculosis

ex. lungs

What is gangrene?

Necrosis of large tissue area, results from interruption of blood supply to a particular part of body

What are the types of gangrene?

1. Dry gangrene

2. Wet gangrene

3. Gas gangrene

Dry gangrene

Coagulative necrosis characterized by blackened, dry, wrinkled tissue

Wet gangrene

Liquefactive necrosis often found in internal organs; fatal

Gas gangrene

Results from infection of necrotic tissue. Form gas containing bubbles

What is apoptosis?

Programmed cell death without inflammation; part of normal development or response to injury.

What are the two pathways that trigger apoptosis?

1. Signals inducing apoptosis

2. Intrinsic pathways

3. Cellular aging

How do signals induce apoptosis?

Withdrawal of survival signals that normally suppress apoptotic pathway

fas lingang → trigger death cascade

How does intrinsic pathway trigger apoptosis

Severe cell damage or to cellular DNA → increase in protein

What is the cellular basis of aging?

Progressive decline in cells’ ability to repair and divide due to cumulative environmental and metabolic damage.

What are the theories of aging?

1. Damage / error theory

2. Programmed senescence theory

What is the damage/error theory of aging?

Aging results from accumulated damage and limited cell repair capacity.

Aging results from accumulated damage and limited cell repair capacity.

Aging is genetically programmed; cells have finite replications due to telomere shortening.

What are the physiologic changes of aging?

1. Age-related decrease in functional reserve

2. Decreased ability to adapt to environmental demands

What is somatic death?

Death of the entire organism with cessation of heartbeat and respiration.

What are key features of somatic death?

1. Rigor mortis (0–6 hrs, then flaccidity 24–48 hrs),

2. Release of lytic enzymes in body tissues: postmortem autolysis

3. Brain death (no brainstem reflexes, flat EEG).

What are the layers of the skin?

1. Epidermis

2. Dermis

3. Hypodermis (subcutaneous fat)

What is the function of the skin?

1. Protective barrier for internal organs

2. Senses changes in temp, pressure, or pain

3. Regulates body temp

4. Excretes fluid and electrolytes (sweat)

5. Stores fat

6. Synthesize vitamin D

7. Provide site for drug absorption

What external factor is primary cause of age related changes of the epidermis?

Exposure to sunlight

What are the changes that happen in the epidermis?

1. Epidermis thins

2. Prickle cells have less orderly arrangement

3. Cells will reproduce more slowly

How does these epidermis changes manifest on the skin?

1. Age spots / liver spots: uneven distribution of melanin

2. Seborrheic keratosis: build up of old skin cells

What are the changes that happen in the dermis & subcataenous tissue?

1. Dermis becomes less elastic

2. Collagen fibers become cross-linked and rearranged into thick bundles (skin folds on itself)

3. Decresed subcutaneous fat (fat under skin)

4. Decreased perfusion (blood flow to skin from shorten capillary loops)

What changes happen to hair?

1. Hair thinning for both sexes after 40

   1. Male inherit baldness trait from mother (x-linked)

2. Loss of melanocytes in hair follicles → gray / white hair

3. Woman have increase facial hair post menopause due to loss of estrogen

What changes that happen nails?

1. Become dull, brittle, hard, and thick

2. Diminished vascular supply to nail bed

3. Increase in longitudinal striations can cause splitting of nail surface

4. Common fungal infection—onychomycosis

What are the changes that happen to glands?

1. Decrease in number of sebaceous glands and sebum secretion → drier, coarser skin

2. Decrease size, number, and function of sweat glands → less efficient evaporative heat loss

What are the changes to the integumentary system?

1. Protective function declines

2. Skin injured easily; heals slowly

3. Decreased sensation and loss of effective vasoactivity due to decline in sensory nerves and blood vessels

4. Vasculature more fragile

What are common vascular lesions?

1. Senile purpura

2. Venous stasis

3. Cherry angioma

4. Venous lakes

Sensile purpura

Spontaneous bruising; can be indicative of bleeding in the skin

Venous stasis

Blood starts pulling to lower extremities, can change appearance of skin over time

Cherry angioma

Overgrowth of capillaries, but not problematic

Venous lakes

Chronic vein ruptures that causes pooling of the vein. Commonly found in face and lips due to UV exposure

What are primary skin lesions?

1. Macule

2. Patch

3. Papule

4. Plaque

5. Vesicle

6. Bulla

7. Pustule

Macule

Lesion less than 1cm in diameter and is flat; continuous with surface around it, just a color change.

ex. freckle

Patch

Lesion larger than 1cm that is flat; area of color change'

ex. certain birthmarks

Papule

Raised lesion (can be felt), but less than 1cm in diamater

ex. moles

Plaque

Raised lesion larger than 1cm in diameter

Vesicle

Lesion smaller than 1cm with fluid filled bubble

ex. herpes

Bulla

Lesion bigger than 1cm with fluid filled bubble

ex. burns

Pustule

Smaller lesions with visible white head on it (pus)

ex. acne

What are the secondary lesions?

1. Excoriation

2. Lichenification

3. Scar

Excoriation

Scratch marks

Inchenification

Chronic thickening of skin as a result of repeated scratching

ex. eczema

Scar

Primary lesion developed into a scar

What are the distributions of secondary lesions?

1. Diffuse

2. Localized

3. Discrete

4. Confluent

5. Linear

Diffusion

Scattered lesions

Localized

Cluster of lesions

Discrete

Lesions are separated from one another

Confluent

Overlapping lesions

Linear

Lesions occurring in aline

What are the common infectious skin conditions?

1. Bacterial

2. Viral

3. Fungal

What are the bacterial infectious conditions?

1. Impetigo

2. Syphilis

3. Cutaneous abscess

Impetigo (staphylococci)

Common staph infection in children. Starts an red itchy sore (cluster of vesicle) that ruptures and heals as a crusty, yellow scab

What is the treatment for impetigo?

Topical antibiotic (mupirocin)

Syphilis (treponema pallidum)

Sexually transmitted bacterial infection that has three stages: primary stage, secondary stage, and latent stage

What is the primary stage in syphilis?

Painless ulcers forming on surface of tongue

What is the secondary stage in syphilis?

Wide spread skin lesions

What is the latent stage in syphilis?

Stage of no symptoms but can reactivate

What is the treatment for syphilis?

Antibiotic (penicillin)

Cutaneous abscess (MRSA)

Infection of skin from break in skin

What is the treatment for cutaneous abscess?

1. Incision & drainage

2. Oral antibiotics if MRSA (methicillin resistant staph aureus)

What are the viral infectious conditions?

1. Verrucae

2. Herpes simplex (oral / genital)

3. Chicken pox (varicella)

4. Herpes zoster

Verrucae

Human papilloma virus; sexuall transmitted warts that can be linked to the development of cancer

Herpes simplex

Two types:

1. Type 1: oral herpes, cold sores around mouth

2. Type 2: genital herpes, painful vesicular lesions

What is the treatment for herpes simplex?

Antiviral medication that may reduce severity / duration and supress recurrence but can’t be cured

Chicken pox

Starts as a macule and progresses into a vascular lesion.

What is the treatment for chicken pox>

Preventable with childhood vaccine

Herpes Zoster

Shingles; Stage 2 of chicken pox with painful lesions. Common in unvaccinated person who hasn’t had chicken pox and progresses to shingles.

Treatment for herpes zoster

Antiviral medication (acyclovir / valacyclovir). Will shotern course of outbreak but won’t get rid of it

What are the fungal infectious conditions?

1. Tinea corporis

2. Tinea cruris

3. Tinea pedis

4. Tinea unguium

Tinea corporis

Fungal infection of body, also known as ringworm

Tinea cruris

Fungal infection of inner thigh, common in men

Tinea pedis

Athletes foot; fungal infection of foot

Tinea unguium (onychomycosis)

Fungal infection of nail; really hard to treat and medication is toxic for liver

What is the treatment for fungal infectious conditions?

1. Dry skin out (warm, moist environments favorable for fungal infections)

2. Topical antifungals (clotrimazole) that may require many weeks to month to fully treat