book- integumentary system Flashcards

(150 cards)

1
Q

melanocytes come from what embryo origin

A

neural crest cells

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2
Q

epidermis, dermal appendages, dermis and hypodermis embryologic origins

A

ectoderm= epidermis and dermal appendages

mesoderm= dermis and hypodermis

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3
Q

what type of epithelium is the epidermis

A

stratified squamous

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4
Q

4 cell types in epidermis

A

keratinocyte, melanocyte, langerhans cells, merle cells

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5
Q

layers of epidermis from bottom to top

A

stratum basale: basement; keratinocytes and melanocytes, site of mitosis

stratum spinous: partially keratinized

stratum granulosum: dead cells

stratum lucidum: dying cells (only in thick skin)

stratum corneum: fully formed keratin; highly flattened

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6
Q

keratinization

A

keratinocytes from basement membrane mature and harden as they move up and then die or shed (desquamate)

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7
Q

melanocytes

how do they become pigmented

A

contain eumelanins and pheomelanins

found near basement membranes

melanonsomes are transferred into nearby keratinocytes causing them to gain pigmentation

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8
Q

langerhans cells

function and where they are found

A

antigen presenting dendritic cells

Primarily in the stratum spinosum layer of the epidermis

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9
Q

merkel cells

A

for light touch in skin epidermis

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10
Q

dermoepidermal junction (basement membrane)

A

hemidesmosome: structure found in keratinocytes that connect them to basement membrane

basal laminate: contains laminate lucida (with anchoring proteins) and lamina densa (cross linking fibrils)

Type IV collagen (main structural protein of lamina densa)
Laminin (connects keratinocytes to collagen)
Integrins (cell surface receptors on keratinocytes)
Anchoring fibrils (Type VII collagen) link basement membrane to dermis

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11
Q

papillary layer and reticular layer of the dermis

A

papillary: capillaries, lymphatic and nerves in network of elastic fibers and collagen. nerves end in meissner’s corpuscles

reticular layer: vascular plexi, lymphatics, nerves, appendages (hair follicles, sweat glands, sebaceous glands) in network of elastic fibers and collagen

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12
Q

hair follicles get goose bumps via

A

arrector pili muscle

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13
Q

sebaceous gland is what type of gland

A

branching type-acinar gland that produces sebum

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14
Q

pilosebaceous unit

A

hair follicle, sebaceous gland and arrector pili muscle

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15
Q

eccrine (merocrine) sweat gland type of cell

A

simple tubular gland with simple cuboidal epithelium found over most of body

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16
Q

apocrine sweat glands

A

an eccrine sweat gland that’s only in axillary, pubic and perianal areas

associated with body odour (watery sweat plus bacterial flora)

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17
Q

hypodermis (subcutaneous)

A

mostly adipose

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18
Q

hairless areas

A

very thick skin i..e penis, palms, soles, labia Minora, nipples; have sebaceous glands in sweat pores

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19
Q

sebaceous glands density

A

high in nose, forehead, back, chest, arms. absent in palms and soles

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20
Q

sweat glands/ eccrine glands are highest in

A

palms and soles

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21
Q

lipid bilayer

A

phospholipids with proteins and cholesterol

phospholipids are amphipathic

phospholipid head is polar, charged and hydrophilic; attracts water

cholesterol in between phospholipids for membrane fluidity

carbs; glycolipids and glycoproteins for cell-cell recognition

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22
Q

integral, peripheral and secreted proteins in membrane

A

integral: span entire membrane

peripheral: one side, anchored by electrostatic interactions with membrane phospholipids

secreted: transported into circulation ie. hormones like insulin

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23
Q

4 intercellular junctions

A

tight junctions, adherent, desmosomes, gap junctions

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24
Q

basal and apical surface junctions

A

[ Apical surface ]
| Tight Junctions –> Seal, barrier (claudin, occludin)
| Adherens Junctions –> Cell-cell adhesion (E-cadherin + actin)
| Desmosomes –> Strong cell-cell adhesion (desmogleins + IF)
| Gap Junctions –> Communication (connexins, ion passage)

[ Basal surface ]
| Hemidesmosomes –> Anchor to basement membrane (IF + integrins)
| Focal Adhesions –> Anchor to ECM (actin + integrins)

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25
tight junctions adheres junctions desmosomes gap junctions hemidesmosomes what is the main protein?
TJ: Claudins, occludins adherens: e-cadherin desmosomes: cadherins gap junctions: connexions hemidesmosomes: integrins
26
actin filaments (cytoskeleton)
Structure: Thin, flexible filaments made of actin Function: -Cell movement (e.g. lamellipodia, filopodia) -Shape maintenance -Muscle contraction -Cytokinesis Dynamic: Very dynamic, uses ATP Associated motor protein: Myosin
27
microtubules (cytoskeleton)
Structure: Hollow tubes made of α/β-tubulin dimers Function: -Intracellular transport (tracks for kinesin and dynein) -Mitotic spindle in cell division -Cilia and flagella movement Dynamic: Highly dynamic, uses GTP Motor proteins: Kinesin (outward), Dynein (inward)
28
intermediate filaments (cytoskeleton)
Structure: Rope-like fibers made of various proteins (e.g. keratin, vimentin, lamins) Function: -Provide mechanical strength -Maintain cell integrity -Anchor organelles and form nuclear lamina Dynamic: More stable, no energy needed Motor protein: None
29
primary active transport vs secondary active transport
primary: ATP to drive substances against gradient (i.e. Na/K ATPase) secondary: one substance moving with its gradient provides energy to move another substance against its gradient (i.e. Na/glucose transport). no ATP needed
30
endocytosis, pinocytosis and exocytosis
Endocytosis is the process by which a cell engulfs external material by enclosing it in a vesicle. Pinocytosis is a form of endocytosis where the cell nonspecifically takes in extracellular fluid and dissolved solutes. Exocytosis is the process of vesicles fusing with the plasma membrane to release substances outside the cell.
31
osmosis
diffusion of water across semi-permeable membrane from high to low concentration
32
isotonic, hypotonic, and hypertonic (osmosis)
isotonic: same concentration of solutes as normal ECF hypotonic: less solute; cell swells hypertonic: more solute; cell shrinks
33
membrane potential
The electrical potential difference across a cell membrane, due to unequal distribution of ions (especially Na⁺, K⁺, and Cl⁻) and selective ion permeability. Typically, the inside of the cell is negative compared to the outside (e.g., –70 mV in neurons).
34
ionic equilibrium (equilibrium potential)
The membrane voltage at which there is no net movement of a specific ion across the membrane because the electrical gradient balances the concentration gradient. Calculated using the Nernst equation. Each ion (e.g., K⁺, Na⁺) has its own equilibrium potential, and the actual membrane potential depends on the combined effect of all permeable ions (via the Goldman equation).
35
concentrations of Na+, K+, Cl-, Ca2+
higher outside: Na+, Ca2+, Cl- higher inside: K+
36
resting membrane potential and basis of RMP
-70mV via Na/K ATPase; 3 Na out, 2 K in
37
steps in an action potential
Resting Potential (–70 mV) - The neuron is at rest; Na⁺/K⁺ pump maintains high K⁺ inside, high Na⁺ outside. - Membrane is more permeable to K⁺ → inside is negative. Depolarization - Voltage-gated Na⁺ channels open → Na⁺ rushes into the cell. - Membrane potential becomes positive (up to +30 mV). Peak - Na⁺ channels inactivate, and voltage-gated K⁺ channels open. Repolarization - K⁺ exits the cell → membrane potential becomes negative again. Hyperpolarization (Undershoot) - K⁺ channels stay open a bit too long → membrane becomes more negative than resting. - Returns to resting potential via Na⁺/K⁺ ATPase and K⁺ channel closure.
38
propagation of action potential also axon
continuous: non-myelinated saltatory: myelinated; nodes of ranvier causes AP to jump and be faster, also high concentration of Na+ channels
39
synaptic transmission and degradation of dopamine
COMT in the synapse does 10% of breakdown MAO does rest and is in the presynaptic terminal
40
synaptic trasnmission; pre and post synaptic neuron
1. Action potential reaches the axon terminal of the presynaptic neuron. 2. Voltage-gated Ca²⁺ channels open, and Ca²⁺ enters the terminal. 3. Ca²⁺ triggers exocytosis of neurotransmitter vesicles into the synaptic cleft. 4. Neurotransmitters bind to receptors on the postsynaptic neuron’s membrane. 5. This causes either depolarization (excitatory) or hyperpolarization (inhibitory) of the postsynaptic neuron. 6. Neurotransmitters are then removed (by reuptake, degradation, or diffusion) to end the signal. 🔄 Roles: Presynaptic neuron: Sends the signal; releases neurotransmitters. Postsynaptic neuron: Receives the signal; responds via receptor activation.
41
core body temperature
average: 36.2 (98.2) 35.6-37.8 (96-100)
42
basal metabolic rate
metabolic rate when person is at mental and physical rest (but not sleeping), at room temperature and fasted for 12 hours
43
shivering
hypothalamic heat promoting center is activated; controlling muscle tone to increase tone of skeletal muscles; involuntary shuddering contractions
44
solute in sweat
sodium chloride
45
regulation of body temperature center? brain region?
hypothalamus peripheral and central thermoreceptors heat promoting or heat loss reflexes via autonomic effector pathways
46
vasoconstriction and vasodilation
skin temp falls, hypothalamic heat center active, SNS vasoconstriction of skin, blood gets restricted to deep body areas when skin temp rises, hypothalamus activates PNS vasodilation fibers in skin to dilate and bring blood to superficial areas and allow for heat loss
47
which type of collagen impacted in Ehlers danlos syndrome
I, III, or V classical is type V
48
which type of collagen impacted in osteogenesis imperfecta
type I
49
which type of collagen impacted in aport syndrome, good pasture syndrome
type IV
50
ehlers- danlos syndrome
Ehlers-Danlos Syndrome is a group of heritable connective tissue disorders primarily affecting collagen synthesis or structure, leading to fragile, hyperextensible tissues. ✅ Key Features Hyperextensible skin Joint hypermobility (→ frequent dislocations) Easy bruising and fragile blood vessels Poor wound healing Atrophic "cigarette paper" scars 🔬 Cause Mutations affecting collagen types I, III, or V, or enzymes involved in collagen processing (e.g., lysyl hydroxylase) Inherited usually in an autosomal dominant or recessive pattern (varies by type)
51
types of collagen and their major locations
type I = skin, tendon, ligament, blood vessel, organ, bone type II= cartilage type III= reticular CT type IV = basement membrane type V= interstitial tissue, hair, placenta
52
fever endogenous pyrogenous that alter hypothalamic set point
IL1, Il6, TNF are endogenous pyrogens released from WBCs, injured tissue cells, or macrophages in the presence of infection or fever producing stimuli act on thermorecprtors in hypothalamus and alter their rate of firing mediated by local release of prostaglandins which alter central thermoreceptor function and initiate heat promoting mechanism and reset thermostat to higher temperature fever purpose: increase metabolic rate and speed up healing, possibly inhibit bacterial growth
53
collagen composition
rich in glycine and proline (and hydroxyproline) glycine is every 3rd residue
54
collagen synthesis steps
🏭 1. Transcription & Translation (in fibroblasts) mRNA → preprocollagen (single polypeptide chain with signal peptide) ⚙️ 2. Post-translational Modifications (in RER) Signal peptide removed → becomes pro-α chain Hydroxylation of proline and lysine → requires vitamin C, O₂, Fe²⁺ Glycosylation of hydroxylysine (with glucose/galactose) 🔗 3. Triple Helix Formation Three pro-α chains align → form procollagen triple helix Stabilized by disulfide bonds and hydrogen bonds 📦 4. Secretion Procollagen is transported to Golgi, then secreted outside the cell ✂️ 5. Extracellular Processing Procollagen peptidases cleave terminal propeptides → forms tropocollagen 🧱 6. Cross-Linking Lysyl oxidase (requires copper) forms covalent cross-links between lysine/hydroxylysine residues → forms collagen fibrils, then collagen fibers
55
key steps in collagen synthesis
pre-pro collagen made in RER by ribosomes hydroxylation of lysine and proline, glycosylation of amino acids triple helical structure pro collagen packed into Golgi apparatus for exocytosis peptidases cleave pro collagen into tropocollagen tropocollagen crosslinks at hydroxylysine residues= mature attach to cell membranes via integrals, fibronectins etc.
56
which enzyme to crosslink collagen and elastin fibers at hydroxylysine residues? which cofactors needed? if deficient what are the sx
protein-lysine-6-oxidase (PL6O) {aka lysol oxidase?} copper and vitamin C lathyrism, weak CT and bone formation, hyperextensible skin, weak ligaments
57
which enzyme to hydroxylate proline residues on collagen chains to form hydroxyproline cofactors needed?
pro collagen proline dioxygenase {prolyl oxidase?} iron and vitamin C
58
2 types of melanin
pheomelanin: orange/red/light brown pigment. more in women. nipples, lips, glans penis, vagina, red hair. carcinogenic when damaged by UV light eumelanin: dark pigment that absorbs UV light, black or brown
59
synthesis of eumelanin and pheomelanin what is the precursor
tyrosine --> dopaquinone via tyrosinase *tyrosinase (mono phenol monooxygenase is in melanocytes and neurons and needs copper as a cofactor; without it you get albinism) pheomelanin: dopaquinone combine with cysteine eumelanin: dopaquinoen converted into leucodopachrome
60
3 amino acids in glutathione what cofactors are needed
Glutathione (GSH) is a vital antioxidant tripeptide composed of glutamate, cysteine, and glycine. requires ATP and magnesium
61
glutathione synthesis
🔁 Steps of Glutathione Synthesis 1. γ-Glutamylcysteine Formation Enzyme: γ-glutamylcysteine synthetase (rate-limiting step) Reactants: Glutamate + Cysteine Requires: ATP 2. Glutathione Formation Enzyme: Glutathione synthetase Reactants: γ-Glutamylcysteine + Glycine Requires: ATP 🧬 Overall Reaction: Glutamate + Cysteine + Glycine + 2 ATP → Glutathione (GSH) + 2 ADP + 2 Pi
62
glutathione redox reaction
Glutathione cycles between reduced (GSH) and oxidized (GSSG) forms to neutralize free radicals and maintain cellular redox balance. Glutathione peroxidase uses 2 GSH to reduce hydrogen peroxide (H₂O₂) or organic peroxides Glutathione reductase then regenerates GSH from GSSG using NADPH 📌 Purpose: - Prevents oxidative damage to lipids, DNA, and proteins - Maintains function of critical sulfhydryl (-SH) groups in enzymes
63
glutathione detoxification function (antioxidant)
Glutathione participates in phase II liver detoxification, conjugating with harmful substances to make them water-soluble and excretable. 🔬 How It Works: Enzyme: Glutathione-S-transferase (GST) Reaction: GSH binds to electrophilic xenobiotics or toxins 📌 Examples: Detoxifies acetaminophen metabolites, pesticides, carcinogens water soluble; eliminate in urine GST is a selenium dependent enzyme
64
glutathione redox and detoxification give the mechanism and key enzyme
redox: reduce ROS/ peroxides --> enzymes: glutathione peroxidase, glutathione reductase detoxification: conjugates toxins for excretion --> enzymes: glutathione- S- transferase (GST)
65
source and mechanism of non-vitamin antioxidant: carotenoids
Carotenoids → Source: Found in colorful fruits/vegetables (e.g., carrots, tomatoes); → Mechanism: Scavenge singlet oxygen and neutralize lipid peroxyl radicals to protect cell membranes.
66
source and mechanism of non-vitamin antioxidant: flavinoids
Flavonoids → Source: Abundant in berries, green tea, and dark chocolate; → Mechanism: Donate electrons to neutralize free radicals and inhibit oxidative enzymes (e.g., xanthine oxidase).
67
source and mechanism of non-vitamin antioxidant: glutathione
Glutathione → Source: Synthesized endogenously in the liver from glutamate, cysteine, and glycine; → Mechanism: Reduces hydrogen peroxide and lipid peroxides via glutathione peroxidase and conjugates toxins for detoxification.
68
source and mechanism of non-vitamin antioxidant: alpha-lipoic acid (ALA)
Alpha-Lipoic Acid (ALA) → Source: Synthesized in mitochondria and found in spinach, broccoli, and meats; → Mechanism: Regenerates other antioxidants (like vitamins C and E), chelates metals, and scavenges a broad range of free radicals both in lipid and aqueous environments.
69
source and mechanism of non-vitamin antioxidant: CoQ10
→ Source: Synthesized endogenously in the mitochondria and found in organ meats, oily fish, and whole grains; → Mechanism: Functions in the mitochondrial electron transport chain to generate ATP and acts as a lipid-soluble antioxidant, protecting membranes and mitochondrial lipids from oxidative damage.
70
normal microflora in the human body
👄 Mouth/Oral Cavity Dominant Flora: Streptococcus spp. (e.g., S. mutans, S. salivarius), Actinomyces, Neisseria Note: Anaerobes like Fusobacterium and Prevotella in gingival crevices 👃 Nose and Nasopharynx Dominant Flora: Staphylococcus epidermidis, Corynebacterium, Streptococcus Note: Staphylococcus aureus may be transiently present 🟤 Skin Dominant Flora: Staphylococcus epidermidis, Corynebacterium, Propionibacterium acnes (now Cutibacterium acnes) Note: Influenced by moisture, oil, and location 🫁 Lower Respiratory Tract (lungs, trachea) Normal Condition: Typically sterile Note: Upper respiratory tract (nasopharynx) has flora, but ciliary action keeps lower tract clear 🧠 CNS Normal Condition: Sterile 🍽️ Stomach Dominant Flora: Few microbes due to acidity, but Lactobacillus and Helicobacter pylori may be present 💩 Intestines Small Intestine: Lactobacillus, Enterococcus, Streptococcus Colon (Large Intestine): Dominated by anaerobes like Bacteroides, Clostridium, Eubacterium, and facultative anaerobes like E. coli 👩‍⚕️ Genitourinary Tract Urethra: Staphylococcus epidermidis, Enterococcus, Corynebacterium Vagina (pre-puberty/post-menopause): Mixed flora including Streptococcus, Staphylococcus Vagina (reproductive age): Dominated by Lactobacillus spp. (maintain low pH by producing lactic acid)
71
adsorption
aka viral attachment; receptors or lectin (glycoprotein to glycopreotin) interactions
72
tissue tropism
affinity of a microbe for a particular tissue or cell
73
how e coli binds to bladder mucosa
type I pili; binds terminal D-mannose moieties of mucosal glycoproteins --> UTI
74
how infections can spread in the body
flagella direct mechanical penetration into tissue (i.e. hyaluronidase enzyme in strep) chemotaxis (move along chemical gradient) lie dormant in WBC to be transported some enveloped viruses spread by inducing syncytial bridges between cells (i.e. HSV)
75
how HIV spreads
hides inside helper T cells
76
replication process of viruses and bacteria is regulated by
nutrient availability exponential growth (at first with ample nutrients) stationary growth (host adapts and restricts nutrients like sequestration of iron) death; when nutrients are scarce
77
stages of viral replication
🦠 Stages of Viral Replication 1. Attachment (Adsorption) → Virus binds to specific receptors on the host cell surface. 2. Penetration (Entry) → Virus enters the host cell via endocytosis or membrane fusion. 3. Uncoating → Viral capsid is removed, releasing the viral genome into the host cell cytoplasm or nucleus. 4. Replication (Genome Synthesis) → Viral genome is replicated using host or viral enzymes (differs for DNA vs. RNA viruses). 5. Transcription and Translation (Protein Synthesis) → Viral mRNA is transcribed and translated to produce structural and non-structural proteins. 6. Assembly (Maturation) → New viral particles are assembled from replicated genome and synthesized proteins. 7. Release → New virions exit the host cell by: - Lysis (common in non-enveloped viruses) - Budding (common in enveloped viruses)
78
passive vs active defenses in host cells to virus
passive: mechanical barrier like skin, placenta and mucosa. usually preventative active: WBC, antibodies, cytokines, complement
79
purpose of complement cascade and the final thing that's made to do the killing
Enhances the ability of antibodies and phagocytes to clear microbes. Promotes inflammation. Directly lyses pathogens via the membrane attack complex (MAC). 💥 Major Functions: Opsonization: C3b coats pathogens to enhance phagocytosis. Cell Lysis: MAC punches holes in membranes. Inflammation: C3a and C5a recruit immune cells (chemotaxis) and increase vascular permeability. Clearance: Helps remove immune complexes and apoptotic cells.
80
three activation pathways in complement cascade
Classical Pathway → Triggered by antigen-antibody complexes (IgG or IgM). Lectin Pathway → Triggered by mannose-binding lectin (MBL) binding to microbial sugars. Alternative Pathway → Triggered by spontaneous hydrolysis of C3 and interaction with pathogen surfaces.
81
classical complement pathway
→ Triggered by antigen-antibody complexes (IgG or IgM).
82
lectin complement pathway
→ Triggered by mannose-binding lectin (MBL) binding to microbial sugars.
83
alternative complement pathway
→ Triggered by spontaneous hydrolysis of C3 and interaction with pathogen surfaces.
84
central step in the compliment pathway
C3 convertase is formed → cleaves C3 into C3a and C3b. C3b opsonizes pathogens; C3a promotes inflammation. All pathways converge at C5 convertase, leading to MAC formation (C5b–C9).
85
how do bacteria avoid phagocytosis
mutation of antigens, polysaccharide capsules, producing toxins that damage phagocytic cells
86
what can viruses not do
produce toxins
87
latency of viruses
integrate into host genome and avoid immune detection
88
how do viruses avoid host immune system
pass through syncytial bridges, decrease expression of antigen, alter antigen expression (i.e. antigenic drift of influenza)
89
parasites
large size hinders immune attack thick outer covering antigenic variability, resistant to host leukocyte toxins, release immunosuppressive toxins and enzymes
90
acute vs chronic infection
acute: fever, muscle aches, flu like i.e strep, UTI, chicken pox chronic: slower; vague sx i.e. AIDS, hep B, mononucleosis
91
latent and carrier states
latent: no sx; can flare i.e. herpes simplex, EBV carrier state: with or without sx; spread infection to others
92
iatrogenic and nosocomial infection
iatrogenic- from medical intervention nosocomial= hospital
93
mucus membranes have what to help with healing
immune cells and secretory IgA for surveillance (dendritic and langerhans cells) submucosal lymphoid tissue (peers patches) in site of antigen processing and activation of T helper, killer or suppressor lymphocytes
94
3 steps of hemostasis
vascular spasm; vasoconstriction platelet plug formation exposed collagen; platelets adhere via vWF; form a bridge. adhesion using ADP and serotonin
95
inhibitor and stimulator of platelet aggregation
thromboxane A2 (TXA2) to stimulate platelet aggregation prostacyclin (PGI2) to inhibit platelets aggregation
96
types of wound healing; primary, secondary and tertiary intention
1. Primary Intention (First Intention) Definition: Wound edges are clean, well-approximated (closed) — e.g., surgical incision with sutures. Healing: Minimal tissue loss, minimal scarring. Features: Fast healing Low infection risk Minimal granulation tissue ---------- 2. Secondary Intention Definition: Wound edges are not approximated; wound left open and heals naturally. Healing: Occurs by granulation tissue formation, wound contraction, and epithelialization. Features: More inflammation More granulation tissue and scarring Higher risk of infection Slower healing (e.g., pressure ulcers, large traumatic wounds) ----------- 3. Tertiary Intention (Delayed Primary Closure) Definition: Wound is initially left open due to contamination or risk of infection, then closed surgically later. Healing: Combines elements of primary and secondary intention. Features: Moderate scarring Higher infection risk than primary Used for contaminated wounds or surgical wounds reopened due to infection
97
contact dermatitis
Etiology: Exposure to irritants (e.g. soaps, acids) or allergens (e.g. nickel, poison ivy). Presentation: Red, itchy rash at the contact site; may have vesicles or crusting.
98
atopic dermatitis
Etiology: Genetic predisposition; associated with atopy (asthma, allergic rhinitis). Presentation: Chronic, relapsing itchy rash; dry, scaly skin on flexures (adults) or face/extensors (infants).
99
seborrheic dermatitis
Etiology: Overgrowth of Malassezia yeast; often worsens with stress or cold weather. Presentation: Greasy, yellow, scaly plaques on scalp (dandruff), eyebrows, nasolabial folds, chest.
100
nummular dermatitis
Etiology: Unknown; often related to dry skin or irritants. Presentation: Coin-shaped, well-demarcated itchy red plaques, typically on extremities.
101
generalized exfoliative dermatitis
Etiology: Severe eczema/psoriasis, drug reactions, malignancy (e.g. cutaneous T-cell lymphoma). Presentation: Widespread redness and scaling; may include fever, chills, lymphadenopathy.
102
stasis dermatitis
Etiology: Chronic venous insufficiency with poor lower limb circulation. Presentation: Erythema, scaling, hyperpigmentation on lower legs; may lead to ulcers.
103
lichen simplex chronicus (neurodermatitis)
Etiology: Chronic scratching/rubbing due to itch-scratch cycle, often stress-related. Presentation: Thickened, leathery plaques with exaggerated skin markings; common on neck, wrists, ankles.
104
nevocellular nevus
circumscribed hyperpigmented macules, papules or nodules moles/ nevi
105
vitiligo
autoimmune destruction of melanocyte sx: patchy areas of depigmented skin, chalk white appearance under wood's light
106
eczema key features and which surface it presents on
redness, unclear margins, scaling, pruritic, lichenification caused by scratching or rubbing flexor surfaces
107
drug related dermatitis
inflammatory maculopapular or vesicular rash related to allergic or metabolic reactions to drugs
108
photodermatitis
inflammatory skin rash (vesicular or maculopapular) from heightened sensitivity to UV light
109
erythema multiforme where? sx? cause? timeline?
sudden inflammatory eruption; symmetric erythematous, oedematous, or bulbous lesions of skin and mucus membranes on distal extremities and face systemic sx: malaise, arthralgia, fever causes could be infectious (i.e. herpes simplex) or drug induced usually lasts a couple weeks are recur in spring or fall for several years
110
urticaria (hives) what type of hypersensitivity
flattened, fluid filled vesicles, with extreme pruritus allergic; type I hypersensitivity
111
acne rosacea
idiopathic inflammatory usually in face esp. females, Middle Ages, stress, sun, food allergies sx: erythema on face, telangiectasia, papule or pustules, usually central face and lateral cheeks and forehead are spared. exacerbated by alcohol, stress and vasodilators
112
lichen planus
4 Ps: pruritic, polygonal shaped, pink/purple papule affect skin is thin and easily torn; pain and irritation cause unknown; likely cross reaction of microbes (esp dysbiosis) leaky gut, food allergies vulva, uncircumcised penis, extra genital sites
113
psoriasis
autoimmune erythematous plaques with silver scaling from hyperkeratosis causes and risk factors: leaky gut, food allergies, stress, dysbiosisi, strep pyogenes cross reaction, western life, low vitamin D sx: extensor surfaces of elbows and knees. thickening, pitting and destruction of nails, predisposed to psoriatic arthritis
114
extensor vs flexor surface skin conditions
ezcema= flexor psoriasis= extensors
115
guttate psoriasis
on palms and soles (silver scales, hyperkeratosis)
116
koebner phénomenon in which skin condiiton
psoriasis The Koebner phenomenon (also called the isomorphic response) is the appearance of new skin lesions in areas of trauma or injury in patients with certain skin diseases.
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epidermolysis what gene mutation
epidermolysis bullosa is due to mutation in keratin gene; leading to lack of connection between dermis and epidermis skin is fragile and has recurrent blisters benign autoimmune bullous eruption; immunoglobulins directed against the basement membrane of epidermis; mostly type XVII collagen of hemidesmosomes tense bull, negative nikolskys sign (bullae dont spread with pressure), lesions on extremities esp. flexural folds, annular dusky erythematous oedematous lesions
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pemphigus vulgaris which gene impacted
autoimmune attack on desmoglein 1 and 3; interfere with keratinocyte adhesion irreversible broncholitis obliterans infection of rupture blisters painful intraepidermal bullae starting around mouth, positive nikolskys sign (blisters spread when pressed)
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albinism
autosomal recessive; x linked (mostly in males) partial or total loss of pigmentation
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Ehlers danlos syndrome
collagen synthesis disorder; autosomal dominant or recessive types classic type 1: type V collagen synthesis --> skin laxity type 2: mild type 3: joint laxity and hypermobile type 4: autosomal dominant; type III collagen, high risk of aortic aneurysm
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actinic (solar) keratosis
sharply delineated paths (flat) or plaque (raised) or sun damaged skin. on back of hands or face. can evolve into squamous cell carcinoma. keratocanthomas= rapidly growing papules on sun exposed skin; turn into centrally umbilicate volcano like nodules that rgress in a year self resolving variant of squamous cell carcinoma
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dysplastic nevus
irregular and indistinct border, multiple colours, lack symmetry; can progress to malignant melanoma not a normal mole/nevi
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seborrheic keratosis
benign neoplasm in eldery on head, trunk, extremities sharply delineated papule with pasted on appearance non pigment papules develop into large, greasy, darkly pigmented plaques "stuck on" appearance primarily on face, trunk and upper extremities
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most common skin tumor
basal cell carcinoma
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basal cell vs squamous cell carcinoma
basal: pearly papule on sun exposed skin, almost never metastasizes squamous: locally invasive but rarely metastasizes. from sun exposure (sometimes chemical carcinogens or radiation). scaling, indurated, ulcerated nodule and may start out as actinic keratosis
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melanoma
from excessive sun exposure begins with growing radially, lymphcytic response is prominent, doesnt not metastasize ; easily cured later grows vertically down into tissue and may metastasize
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bacteria causing acne vulgaris
propioni-bacterium acnes
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acne vulgaris
plugged sebaceous glands and propionic-bacterium acnes infection western life, high fat and sugar diet, PCOS open comedones (black head), closed comedones (white heads), pustules, nodules, cysts or papule. on face, upper trunk and upper arms. worse premenstrual, better in dry and sun
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candidiasis diagnostic feature
c. albicans is an oval yeast; stains gram-positive is in normal flora of GI, URT, female genitals can grow into pseudohypae diagnostic: can grow a germ tube in serum risks: immunosuppression, antibiotics candidate vaginitis thrush (oral candidiasis): white patches on erythematous base that can be scraped off chronic mucocutaneous candidiasis: multiple erythematous, pustular or thick lesions on face
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cellulitis
pyogenic disease; starts in localized area (i.e. wound) then spreads through underlying tissue can be lifethreatening and cause septicaemia acute bacterial infection of the dermis and subcutaneous tissue from strep or staph sx: swelling, red hot skin, peau d'orange appearance, fever or chills, lymphangitis, lymphadenopathy, tachycardia, hypotension, headache, leukocytosis
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cause of cellulitis
staph or strep
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erysipelas
Erysipelas is a superficial bacterial skin infection involving the upper dermis and lymphatic vessels, characterized by sharply demarcated, raised borders and bright red skin. commonly causes by streptococcus pyogenes pyogenic, more superficial that cellulitis, but can progress to it lymphangitis, well defined edges, shiny, red, swollen and tender. vesicles or bullae can develop
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erythema infectiosum/ parvovirus B19 (fifth disease)
incubation then mild flu sx then slapped cheek rash appears then legs and arms get lacy or macular pattern worse with stress, temp, exercise parvovirus B19 is a DNA virus
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erythema nodosum
in the deep dermis and subcutaneous fat tissue with red tender nodules pretibial region or arms in kids; usually from strep nodules resemble bruises, associated with arthralgia ------------- Erythema nodosum is an inflammatory condition of the subcutaneous fat (a type of panniculitis) resulting in tender, red nodules, usually on the shins.
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folliculitis main cause?
inflamed hair follicles; from staphylococcus aureus or other skin flaura pustules around hair follicle, common in beard
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HSV1 vs HSV2 (herpes simplex virus)
HSV1: oral, latent in trigeminal ganglia HSV2: genital, latent in sacral ganglia HSV-1 typically causes oral herpes (cold sores) and is transmitted through saliva or oral contact, establishing latency in the trigeminal ganglion. HSV-2 primarily causes genital herpes, spreads through sexual contact, and remains latent in the sacral dorsal root ganglia.
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impetigo cause?
skin infection via staphylococcus aureus perioral or chin vesicles form honey coloured crust highly infectious
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methicillin-resistant staphylococcus aureus (MRSA)
antibiotic resistant; esp hosptals and immunosuppressed highly virulent spread to organs and blood --> sepsis secretes toxic shock syndrome toxin necrotizing disease; skin, lungs or other tissue
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molluscum contagiosum
from molluscipox virus, DNA virus that incubates for 2-8 weeks pearly nodules, cheesy matter self limiting
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tinea (ringworm)
heat and moisture pruritic papules, broken hairs, thickened and broken nails dermatophyte that infects superficial keratinized structures; never deeper tissues nails, skin, hair spread via direct contact dx: hyphae and KOH solution of UV light (wood lamp)
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varicella zoster virus (VZV)
primary chickenpox; recurrent is shingles DNA enveloped herpes virus chickenpox: pruritic papulovesicular rash that turns into vesicles and pustules herpes zoster/ shingles: latent virus reactivated and have painful vesicles in course of sensory nerve (dermatone). nerve pain after vesicles disappear (postherpetic neuralgia). latent in dorsal root ganglia
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reye's syndrome
Definition: Reye’s syndrome is a rare, potentially fatal condition that causes acute encephalopathy and liver dysfunction (fatty liver), usually in children recovering from a viral illness. 🧫 Etiology & Risk Factors: Strongly associated with aspirin use in children during or after viral infections such as: Influenza Varicella (chickenpox)
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verrucae cause?
raised skin lesions from HPV many presentations depending on HPV serotypes i.e. plantar warts, carcinogenic -------------- Definition: Verrucae are benign epidermal growths caused by human papillomavirus (HPV) infection of the skin or mucous membranes. 🧫 Etiology: Caused by HPV, particularly: Verruca vulgaris (common wart): HPV types 2, 4 Verruca plana (flat warts): HPV types 3, 10 Verruca plantaris (plantar warts): HPV type 1 Condyloma acuminata (genital warts): HPV types 6, 11
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clostridium perfingens what is the toxin? what system does it effect? complication?
can be normal flora in GI; produces spores that are found in soil, air, water grows in traumatized tissues; war wounds, bike accident etc has alpha toxin lecithinase; pass along muscle bundle and kill them degradative enzymes ferment muscle sugars --> gas crepitations --> gas gangrene impacts vasculature --> necrosis enterotoxin in SI in large quantities dx; double zone of hemolysis on blood agar manifestations: food poisoning and gas gangrene (or myonecrosis; painful wound infection- crepitation from gas in tissues, cellulitis, blood tinged serous exudate that leads to shock and death)
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strep viridans
alpha hemolytic strains are in normal nasopharyngeal and gut flora sx: heart valves (endocarditis), blood (bacteremia), skin (abscesses). has a breakdown in normal defense like an infection or immunosuppression before damaging heart
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bacillus species gram positive or negative? bacillus anthracis bacillus cereus --> what do they cause and what toxin
gram positive rod, form spores b. anthracis: anthrax toxin; inhibit phosphokinase responsible for growth of human cells and cause edema cereus: food poisoning (rice and grains)
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bacillus anthracis
spore forming species; has anthrax toxin, exotoxin, antiphagocytic capsule contaminates wounds or mucus membranes cutaneous anthrax: eruption of erythematous papule into vesicular and ulcerate --> black eschar on edematous base --> malignant pustule --> sepsis pulmonary anthrax: inhale spores causes flu sx into pneumonia, cyanosis, neck and chest edema then death 0-------- Bacillus anthracis is a Gram-positive, spore-forming, rod-shaped bacterium that causes anthrax, a zoonotic disease affecting skin, lungs, and GI tract Cutaneous anthrax is the most common form and presents as a painless black eschar (necrotic ulcer) with surrounding edema and regional lymphadenopathy. Inhalation anthrax (also known as wool-sorter's disease) begins with flu-like symptoms but can rapidly progress to severe respiratory distress, mediastinal widening, and shock. Gastrointestinal anthrax occurs after ingesting contaminated meat and presents with abdominal pain, bloody diarrhea, and high mortality if untreated. Injectional anthrax, seen in IV drug users, causes severe soft tissue infection without eschar and can progress quickly to sepsis.
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pseudomonas aeruginmosa what 2 pigments does it secrete that are helpful for dx
aerobic gram negative rod. oxidizes sugars for energy instead of fermenting them (oxidase positive) 2 pigments for dx 1. procyanin (turn pus in infected wound blue) 2. pyroverdin (fluorescein; fluoresce yellow green under UV) smell like corn tortilla/ potatoes = fruity odour opportunistic infection; cause pneumonia if have cystic fibrosis or burn victims. also cause otitis externa and folliculitis
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key features of pseudomonas aeruginosa
Oxidase-positive Produces blue-green pigment (pyocyanin and pyoverdine) Fruity/grape-like odor pneumonia, otitis externa, folliculitis
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