Adv Patho Exam 1 Flashcards

(241 cards)

1
Q

What are the core distinctions between Prokaryotes and Eukaryotes?

A
  • Prokaryotes: no true nucleus, no membrane-bound organelles
  • Eukaryotes: true nucleus, membrane-bound organelles (nucleus, mitochondria, ER, Golgi)

Structural differences drive selective drug targeting (e.g., prokaryotic translation/cell wall enzymes).

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2
Q

Describe the DNA structure in Prokaryotes and Eukaryotes.

A
  • Prokaryotic DNA: single circular chromosome in cytoplasm, classically no histones
  • Eukaryotic DNA: multiple linear chromosomes packaged with histones in a nucleus

Different ribosomes and enzymes explain why many antimicrobials spare human cells.

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3
Q

Define differentiation in cellular biology.

A

Differentiation = gene-expression program that produces specialized structure/function

Do not confuse differentiation with proliferation: many mature cells specialize but do not divide.

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4
Q

What are the major cellular functions related to movement and conductivity?

A
  • Movement: skeletal muscle moves limbs; smooth muscle propels contents of hollow organs
  • Conductivity: transmission of electrical impulses; prominent in neurons and cardiac muscle

Core mechanism: ion gradients and channels (Na+, K+, Ca2+) support excitability and contraction.

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5
Q

What is the difference between absorption and secretion?

A
  • Absorption: uptake of nutrients/substances (intestinal and renal epithelia)
  • Secretion: synthesis and release (mucus, hormones, enzymes) via ER-Golgi-vesicle trafficking

Both are essential cellular functions.

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6
Q

List the functions of the plasma membrane.

A
  • Defines boundary
  • Selective permeability maintains internal composition
  • Supports recognition, communication, and cell shape

Membrane integrity is a major point-of-no-return concept in cell injury.

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7
Q

What are the key components of membrane lipids?

A
  • Phospholipids (abundant)
  • Cholesterol (stability/fluidity)
  • Glycolipids (recognition)

Amphipathic lipids form a bilayer: hydrophilic heads outward, hydrophobic tails inward.

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8
Q

What are the types of membrane proteins?

A
  • Transmembrane
  • Cytosolic (inner leaflet)
  • Lipid-anchored
  • Peripheral

Functions include receptors, channels, carriers, pumps, enzymes, and adhesion.

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9
Q

Define ligand binding mechanics.

A

Specificity depends on shape and charge complementarity

Binding is typically reversible via weak noncovalent forces (H-bonds, electrostatic, van der Waals, hydrophobic).

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10
Q

What are the outcomes of receptor binding?

A
  • Activates or inhibits signaling cascades
  • Alters enzyme activity, membrane permeability, gene expression, survival/apoptosis decisions

These responses are crucial for cellular function.

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11
Q

What is the role of cell adhesion molecules (CAMs)?

A

Bind cells to each other and/or to ECM

Four families: integrins, cadherins, selectins, immunoglobulin superfamily (IgSF).

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12
Q

What are the types of cellular communication?

A
  • Contact-dependent signaling
  • Autocrine/paracrine signaling
  • Endocrine signaling
  • Neural/synaptic signaling

Maintains homeostasis and coordinates growth, division, differentiation.

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13
Q

What is metabolism?

A

All chemical reactions sustaining life; provides energy and building blocks

Catabolism breaks down fuels to generate ATP; anabolism uses energy to build macromolecules.

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14
Q

What is the significance of ATP in cellular processes?

A

ATP stores/transfers energy temporarily for cellular work

Powers muscle contraction, active transport, and macromolecule synthesis.

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15
Q

Define ischemia and its impact on cellular injury.

A

Ischemia: reduced blood flow leading to low oxygen supply

O2 loss causes mitochondrial ATP production drops, leading to cell swelling and potential death.

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16
Q

What are the mechanisms of cellular injury?

A
  • Decreased ATP production
  • Formation of free radicals/ROS
  • Increased intracellular calcium
  • Membrane damage
  • Protein misfolding (ER stress)
  • DNA damage

These mechanisms can lead to reversible or irreversible injury.

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17
Q

What is the difference between necrosis and apoptosis?

A
  • Necrosis: unregulated, inflammatory
  • Apoptosis: programmed, energy-dependent

Both are forms of cellular death but differ in processes and outcomes.

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18
Q

What is dysplasia?

A

Abnormal changes in cell size, shape, and organization (atypical hyperplasia)

Potentially precancerous; common in cervix, endometrium, respiratory and GI linings.

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19
Q

What are the clinical patterns of tonicity?

A
  • Isotonic: no net water shift
  • Hypotonic: water moves into cells -> swelling/lysis risk
  • Hypertonic: water moves out of cells -> cell shrinkage

Tonicity explains CNS symptoms in dysnatremias via brain cell swelling/shrinking.

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20
Q

What are the features associated with cellular injury?

A
  • Plasma and lysosomal membrane rupture
  • Rapid ATP depletion
  • Mitochondrial swelling

Leakage of cellular contents triggers inflammation and activates macrophages.

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21
Q

What are the three patterns of gangrenous necrosis?

A
  • Dry gangrene
  • Wet gangrene
  • Gas gangrene

Each type has distinct characteristics and causes, such as ischemia or infection.

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22
Q

Define apoptosis.

A

Programmed and energy-dependent cell death; maintains cell population balance

Typically less inflammatory than necrosis.

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23
Q

What are the triggers for pathologic apoptosis?

A
  • Severe injury beyond repair capacity
  • ER stress from misfolded proteins
  • Viral infection with cytotoxic T cell killing
  • Duct obstruction leading to atrophy

These triggers can lead to cell death when the cell is unable to recover.

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24
Q

What happens with dysregulated apoptosis?

A
  • Too little apoptosis -> survival of abnormal cells (cancer/autoimmunity risk)
  • Too much apoptosis -> tissue loss (e.g., neurodegeneration, MI, stroke)

Balance in apoptosis is crucial for maintaining healthy tissue.

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25
Define **autophagy**.
Self-degradative recycling process that helps survival during starvation or stress ## Footnote It removes damaged organelles/proteins.
26
What are the **functions** of autophagy?
* Maintains metabolism during nutrient deprivation * Removes dysfunctional organelles to reduce ROS accumulation * Relevant to aging, cancer prevention, neurodegeneration, cardiac and inflammatory disorders ## Footnote Autophagy plays a critical role in cellular health.
27
How does **aging** affect autophagy?
Autophagy declines with age, allowing damaged material to accumulate ## Footnote This contributes to protein aggregates and mitochondrial/DNA damage.
28
What are the **major fluid compartments** in the body?
* Intracellular fluid (ICF) * Extracellular fluid (ECF) ## Footnote ICF is key for metabolism, while ECF serves as a transport medium.
29
What are the **subdivisions** of extracellular fluid (ECF)?
* Interstitial fluid * Intravascular fluid * Transcellular fluids ## Footnote Each subdivision has specific roles in the body.
30
What is the difference between **filtration** and **reabsorption**?
* Filtration: fluid movement out of capillary into interstitium * Reabsorption: fluid movement from interstitium back into capillary ## Footnote Balance depends on hydrostatic and oncotic pressures.
31
List the **four Starling forces**.
* Capillary hydrostatic pressure pushes water out * Capillary oncotic pressure pulls water in * Interstitial hydrostatic pressure pushes water into capillary * Interstitial oncotic pressure pulls water out ## Footnote These forces determine fluid movement across capillary membranes.
32
What are the **mechanisms** of edema?
* Increased hydrostatic pressure * Decreased oncotic pressure * Increased permeability * Lymphatic obstruction ## Footnote Edema results from excessive interstitial fluid.
33
What are the **patterns** of edema?
* Localized vs generalized * Dependent edema * Pitting edema patterns ## Footnote Edema can affect wound healing and perfusion.
34
What is the **sodium-water linkage**?
Water follows sodium; sodium regulates ECF volume and osmotic balance ## Footnote Water balance is controlled by ADH; aldosterone and natriuretic peptides regulate sodium.
35
Describe the **RAAS sequence**.
* Low BP or sodium -> renin release -> angiotensinogen -> angiotensin I -> ACE -> angiotensin II ## Footnote Angiotensin II causes vasoconstriction and stimulates aldosterone and ADH.
36
What are **natriuretic peptides** and their function?
* ANP (atria) * BNP (ventricles) * Urodilatin (kidney) ## Footnote Released with increased volume/pressure, they cause vasodilation and increase sodium/water excretion.
37
What is the role of **chloride** in the body?
Major ECF anion; follows sodium and varies inversely with bicarbonate ## Footnote Helps maintain acid-base balance.
38
What triggers **ADH release**?
* Increased plasma osmolality (primary) * Decreased blood volume/pressure ## Footnote ADH increases water reabsorption in distal tubules/collecting ducts.
39
What are the **three lines of defense** in innate immunity?
* Surface barriers * Inflammation * Adaptive immunity ## Footnote These lines protect against pathogens and injury.
40
What are the **physical barriers** in the first line of defense?
* Tight junction epithelium (skin, GI, GU, respiratory) * Local inhibitory conditions (acidic environments, cooler skin, intact keratin) ## Footnote These barriers prevent pathogen entry.
41
What are the **key effects** of bradykinin?
* Vasodilation * Pain * Increased vascular permeability * Smooth muscle contraction ## Footnote Bradykinin is part of the kinin system activated during inflammation.
42
What are the **classic signs** of acute inflammation?
* Redness * Heat * Swelling * Pain * Loss of function ## Footnote These signs indicate the body's response to injury or infection.
43
What are the **four overlapping phases** of wound healing?
* Hemostasis * Inflammation * Proliferation/new tissue * Remodeling/maturation ## Footnote Each phase plays a crucial role in tissue repair.
44
What is the role of **B cells** in adaptive immunity?
Produce antibodies (humoral immunity) ## Footnote B cells are activated after innate defenses are breached.
45
What is the difference between **CD4** and **CD8 T cells**?
* CD4: helper T cells * CD8: cytotoxic T cells ## Footnote These cells have distinct roles in the immune response.
46
What are the **four types** of **cellular adaptation**?
* Atrophy * Hypertrophy * Hyperplasia * Metaplasia ## Footnote Each type of adaptation serves to maintain function and prevent injury.
47
Define **atrophy**.
Decrease in cell size, leads to smaller organ ## Footnote Can be physiologic (normal development) or pathologic (reduced workload, blood flow, etc.)
48
Define **hypertrophy**.
Increase in cell size, mainly in non-dividing cells ## Footnote Can be physiologic (normal demand) or pathologic (chronic overload).
49
Define **hyperplasia**.
Increase in number of cells caused by increased cell division ## Footnote Can be physiologic (normal response) or pathologic (abnormal proliferation).
50
Define **metaplasia**.
Reversible replacement of one mature cell type by another ## Footnote Protective but often causes loss of normal function.
51
What is **dysplasia**?
Abnormal growth pattern, considered precancerous ## Footnote Seen mostly in cervix, endometrium, and respiratory/GI linings.
52
What is **hypoxia**?
Lack of sufficient O2 inside cells ## Footnote Most common cause of cellular injury.
53
What is the most frequent cause of **hypoxia**?
Ischemia (reduced blood flow and O2 supply) ## Footnote Causes include loss of Hgb, reduced O2 in air, and poisoning of oxidative enzymes.
54
What happens to mitochondria during **hypoxia**?
Stop producing ATP ## Footnote The cell switches to anaerobic metabolism to make ATP from glycogen.
55
What is **reperfusion injury**?
Further injury after blood flow and O2 restored after ischemia ## Footnote Involves oxidative stress, nitrogen-based radicals, calcium overload, and inflammation.
56
What are **free radicals**?
Unpaired electron, unstable and highly reactive ## Footnote Sources include normal metabolism, radiation, and enzymatic metabolism of toxins.
57
What is **necrosis**?
Accidental/unregulated cell death after severe injury ## Footnote Causes include ischemia, toxins, and trauma.
58
What is **apoptosis**?
Programmed or regulated cell death ## Footnote Maintains balance and can be pathologic or dysregulated.
59
What is the **RAAS**?
Renin-Angiotensin-Aldosterone System ## Footnote Regulates blood pressure and fluid balance.
60
What triggers the release of **ADH**?
Concentrated plasma or decreased blood volume/pressure ## Footnote ADH increases water reabsorption in distal tubules and collecting ducts.
61
What is **edema**?
Excess fluid in interstitial space ## Footnote Can result from increased capillary hydrostatic pressure or decreased oncotic pressure.
62
What is the role of **albumin** in the body?
Maintains oncotic pressure in plasma ## Footnote Essential for fluid balance between blood and interstitial spaces.
63
What is **autophagy**?
Self-digestion and recycling within the cell ## Footnote Helps remove damaged organelles and misfolded proteins.
64
What is the **normal intake** of sodium per day?
5-6g/day ## Footnote Sodium regulates ECF volume and osmotic balance.
65
What are the **three components** of extracellular fluid (ECF)?
* Interstitial * Intravascular * Transcellular ## Footnote Each component serves different functions in the body.
66
What is the **function** of natriuretic peptides?
Cause vasodilation and enhance Na and H2O excretion ## Footnote Act as natural antagonists to RAAS.
67
What is the role of **ADH / Vasopressin** in the body?
* Increases water reabsorption in distal tubules and collecting ducts * Secreted by posterior pituitary * Triggered by concentrated plasma or decreased blood volume/pressure ## Footnote ADH plays a crucial role in regulating water balance in the body.
68
What are the **triggers for ADH release**?
* Concentrated plasma * Decreased blood volume * Decreased blood pressure ## Footnote These triggers help maintain fluid balance and blood pressure.
69
What are the **vasopressin receptors** and their locations?
* V1: in blood vessels * V2: in distal collecting ducts ## Footnote V1 receptors are activated by high doses of vasopressin, while V2 receptors are involved in water reabsorption.
70
What is **hypernatremia** and what does it produce?
Produces hypertonicity ## Footnote Hypernatremia is characterized by an elevated sodium concentration in the blood.
71
What are the types of **hyponatremia**?
* Hypovolemic: total body fluid loss with greater Na loss * Euvolemic: pure Na deficit or H2O retention * Hypervolemic: increased Na and H2O with greater H2O retention ## Footnote Each type of hyponatremia has different underlying causes and implications.
72
What is the **Bicarbonate-Carbonic Acid Buffer System** ratio?
Normal ratio is HCO3- : H2CO3 is 20:1 ## Footnote This system helps maintain pH balance in the body.
73
What are the **three lines of defense against pH imbalance**?
* Buffers: instant response * Respiratory control: minutes * Renal control: hours to days ## Footnote These mechanisms work together to maintain acid-base balance.
74
What is **metabolic acidosis** and its rapid causes?
* Increased nonvolatile acids * Loss of HCO3- * Reduced renal acid excretion * Rapid causes: lactic acidosis, hypoxia, shock ## Footnote Metabolic acidosis can lead to significant physiological disturbances.
75
What are the **causes of metabolic alkalosis**?
* H+ loss * HCO3- gain * Causes: vomiting, diuretics, hyperaldosteronism, excessive alkali intake ## Footnote Metabolic alkalosis can result from various conditions affecting acid-base balance.
76
What is the effect of **acidosis** on potassium levels?
H+ enters cells and K+ exits ## Footnote This shift can lead to hyperkalemia in acidosis.
77
What is the effect of **alkalosis** on potassium levels?
H+ exits cells and K+ enters ## Footnote This shift can lead to hypokalemia in alkalosis.
78
What are the **mechanisms of self-defense** in the endocrine system?
* Hormones guide development * Control growth and development * Coordinate reproductive systems * Help adapt to emergencies/stress ## Footnote The endocrine system plays a vital role in maintaining homeostasis.
79
What are the types of **hormonal communication**?
* Autocrine: acts on itself * Paracrine: acts on nearby cells * Endocrine: travels through blood to distant cells ## Footnote These communication methods define how hormones exert their effects.
80
What is the **feedback loop** mechanism in hormone regulation?
* Negative feedback: high hormone levels stop further release * Positive feedback: hormone release increases further secretion ## Footnote Feedback loops are crucial for maintaining hormonal balance.
81
What is the difference between **water-soluble** and **lipid-soluble hormones**?
* Water-soluble: circulate freely, short half-lives * Lipid-soluble: bind to carrier proteins, longer half-lives ## Footnote This distinction affects how hormones act and their duration of action.
82
What is **hypochloremia** and its common causes?
* Cl <97mEq/L * Often occurs with low Na or elevated bicarbonate * Causes: sodium deficit, diuretics, vomiting ## Footnote Hypochloremia can indicate underlying metabolic disturbances.
83
What are the **four types** of **cellular adaptation**?
* Atrophy * Hypertrophy * Hyperplasia * Metaplasia ## Footnote Each type of adaptation serves to maintain function and prevent injury.
84
Define **atrophy**.
Decrease in cell size, leads to smaller organ ## Footnote Can be physiologic (normal development) or pathologic (reduced workload, blood flow, etc.)
85
Define **hypertrophy**.
Increase in cell size, mainly in non-dividing cells ## Footnote Can be physiologic (normal demand) or pathologic (chronic overload).
86
Define **hyperplasia**.
Increase in number of cells caused by increased cell division ## Footnote Can be physiologic (normal response) or pathologic (abnormal proliferation).
87
Define **metaplasia**.
Reversible replacement of one mature cell type by another ## Footnote Protective but often causes loss of normal function.
88
What is **dysplasia**?
Abnormal growth pattern, considered precancerous ## Footnote Seen mostly in cervix, endometrium, and respiratory/GI linings.
89
What is **hypoxia**?
Lack of sufficient O2 inside cells ## Footnote Most common cause of cellular injury.
90
What is the most frequent cause of **hypoxia**?
Ischemia (reduced blood flow and O2 supply) ## Footnote Causes include loss of Hgb, reduced O2 in air, and poisoning of oxidative enzymes.
91
What happens to mitochondria during **hypoxia**?
Stop producing ATP ## Footnote The cell switches to anaerobic metabolism to make ATP from glycogen.
92
What is **reperfusion injury**?
Further injury after blood flow and O2 restored after ischemia ## Footnote Involves oxidative stress, nitrogen-based radicals, calcium overload, and inflammation.
93
What are **free radicals**?
Unpaired electron, unstable and highly reactive ## Footnote Sources include normal metabolism, radiation, and enzymatic metabolism of toxins.
94
What is **necrosis**?
Accidental/unregulated cell death after severe injury ## Footnote Causes include ischemia, toxins, and trauma.
95
What is **apoptosis**?
Programmed or regulated cell death ## Footnote Maintains balance and can be pathologic or dysregulated.
96
What is the **RAAS**?
Renin-Angiotensin-Aldosterone System ## Footnote Regulates blood pressure and fluid balance.
97
What triggers the release of **ADH**?
Concentrated plasma or decreased blood volume/pressure ## Footnote ADH increases water reabsorption in distal tubules and collecting ducts.
98
What is **edema**?
Excess fluid in interstitial space ## Footnote Can result from increased capillary hydrostatic pressure or decreased oncotic pressure.
99
What is the role of **albumin** in the body?
Maintains oncotic pressure in plasma ## Footnote Essential for fluid balance between blood and interstitial spaces.
100
What is **autophagy**?
Self-digestion and recycling within the cell ## Footnote Helps remove damaged organelles and misfolded proteins.
101
What is the **normal intake** of sodium per day?
5-6g/day ## Footnote Sodium regulates ECF volume and osmotic balance.
102
What are the **three components** of extracellular fluid (ECF)?
* Interstitial * Intravascular * Transcellular ## Footnote Each component serves different functions in the body.
103
What is the **function** of natriuretic peptides?
Cause vasodilation and enhance Na and H2O excretion ## Footnote Act as natural antagonists to RAAS.
104
What is the role of **ADH / Vasopressin** in the body?
* Increases water reabsorption in distal tubules and collecting ducts * Secreted by posterior pituitary * Triggered by concentrated plasma or decreased blood volume/pressure ## Footnote ADH plays a crucial role in regulating water balance in the body.
105
What are the **triggers for ADH release**?
* Concentrated plasma * Decreased blood volume * Decreased blood pressure ## Footnote These triggers help maintain fluid balance and blood pressure.
106
What are the **vasopressin receptors** and their locations?
* V1: in blood vessels * V2: in distal collecting ducts ## Footnote V1 receptors are activated by high doses of vasopressin, while V2 receptors are involved in water reabsorption.
107
What is **hypernatremia** and what does it produce?
Produces hypertonicity ## Footnote Hypernatremia is characterized by an elevated sodium concentration in the blood.
108
What are the types of **hyponatremia**?
* Hypovolemic: total body fluid loss with greater Na loss * Euvolemic: pure Na deficit or H2O retention * Hypervolemic: increased Na and H2O with greater H2O retention ## Footnote Each type of hyponatremia has different underlying causes and implications.
109
What is the **Bicarbonate-Carbonic Acid Buffer System** ratio?
Normal ratio is HCO3- : H2CO3 is 20:1 ## Footnote This system helps maintain pH balance in the body.
110
What are the **three lines of defense against pH imbalance**?
* Buffers: instant response * Respiratory control: minutes * Renal control: hours to days ## Footnote These mechanisms work together to maintain acid-base balance.
111
What is **metabolic acidosis** and its rapid causes?
* Increased nonvolatile acids * Loss of HCO3- * Reduced renal acid excretion * Rapid causes: lactic acidosis, hypoxia, shock ## Footnote Metabolic acidosis can lead to significant physiological disturbances.
112
What are the **causes of metabolic alkalosis**?
* H+ loss * HCO3- gain * Causes: vomiting, diuretics, hyperaldosteronism, excessive alkali intake ## Footnote Metabolic alkalosis can result from various conditions affecting acid-base balance.
113
What is the effect of **acidosis** on potassium levels?
H+ enters cells and K+ exits ## Footnote This shift can lead to hyperkalemia in acidosis.
114
What is the effect of **alkalosis** on potassium levels?
H+ exits cells and K+ enters ## Footnote This shift can lead to hypokalemia in alkalosis.
115
What are the **mechanisms of self-defense** in the endocrine system?
* Hormones guide development * Control growth and development * Coordinate reproductive systems * Help adapt to emergencies/stress ## Footnote The endocrine system plays a vital role in maintaining homeostasis.
116
What are the types of **hormonal communication**?
* Autocrine: acts on itself * Paracrine: acts on nearby cells * Endocrine: travels through blood to distant cells ## Footnote These communication methods define how hormones exert their effects.
117
What is the **feedback loop** mechanism in hormone regulation?
* Negative feedback: high hormone levels stop further release * Positive feedback: hormone release increases further secretion ## Footnote Feedback loops are crucial for maintaining hormonal balance.
118
What is the difference between **water-soluble** and **lipid-soluble hormones**?
* Water-soluble: circulate freely, short half-lives * Lipid-soluble: bind to carrier proteins, longer half-lives ## Footnote This distinction affects how hormones act and their duration of action.
119
What is **hypochloremia** and its common causes?
* Cl <97mEq/L * Often occurs with low Na or elevated bicarbonate * Causes: sodium deficit, diuretics, vomiting ## Footnote Hypochloremia can indicate underlying metabolic disturbances.
120
All living organisms are made of _______.
cells ## Footnote Cells are divided into Prokaryotic and Eukaryotic types.
121
Eukaryotic cells include which types of organisms?
* Animals * Plants * Fungi * Protozoa * Most algae ## Footnote Eukaryotic cells are larger and more organized than prokaryotic cells.
122
What does the term **Eukaryote** mean?
true nucleus ## Footnote 'Eu' means true, and 'karyon' means nucleus.
123
Prokaryotic cells are characterized by which features?
* Smaller and simpler structure * No nucleus * No organelles * Genetic material is free in the cytoplasm * DNA is a single circular chromosome * No histone proteins ## Footnote Prokaryotic cells include bacteria.
124
Eukaryotes have _______ chromosomes, while prokaryotes have _______.
multiple linear; one circular ## Footnote Histones are present in eukaryotes but absent in prokaryotes.
125
What are the **major cellular functions**?
* Movement * Conductivity * Metabolic Absorption * Secretion * Excretion * Respiration * Reproduction * Communication ## Footnote These functions are essential for maintaining cellular health and homeostasis.
126
Muscle cells are responsible for _______.
movement ## Footnote Skeletal muscles move bones and limbs, while smooth muscles move contents in hollow organs.
127
Cells can transmit electrical impulses as a response to _______.
stimulation ## Footnote Nerve cells and heart muscle cells show strong conductivity.
128
What is the function of **lysosomes** in cells?
remove waste products ## Footnote Lysosomes digest large molecules into waste that exits the cell.
129
What are the types of **membrane proteins**?
* Transmembrane proteins * Cytosolic proteins * Lipid-anchored proteins * Peripheral proteins ## Footnote Each type has distinct roles in cellular function.
130
What is the **glycocalyx**?
carbohydrate coating ## Footnote Formed by glycolipids and glycoproteins on the outer surface of the plasma membrane.
131
What are the **main components** of the Extracellular Matrix (ECM)?
* Fibrous Structural Proteins * Adhesive Glycoproteins * Proteoglycans and Hyaluronic Acid ## Footnote The ECM provides structural support and facilitates communication between cells.
132
Cell Adhesion Molecules (CAMs) are essential for _______.
tissue structure ## Footnote CAMs allow cells to bind to each other and to the extracellular matrix.
133
What are the **three main mechanisms** of cell adhesion?
* Extracellular Matrix (ECM) * Cell Adhesion Molecules (CAMs) * Specialized Cell Junctions ## Footnote These mechanisms help maintain tissue integrity and communication.
134
What are **tight junctions** responsible for?
preventing leakage ## Footnote Tight junctions act as barriers to diffusion between cells.
135
What is the **function of gap junctions**?
allow direct passage of ions and small signaling molecules ## Footnote They enable electrical and chemical communication between cells.
136
What are the **three phases of catabolism**?
* Digestion * Glycolysis and Oxidation * Citric Acid Cycle (Krebs Cycle) ## Footnote These phases are essential for breaking down food and producing energy.
137
Anaerobic glycolysis occurs when _______ is absent.
oxygen ## Footnote It produces lactic acid and is less efficient than aerobic respiration.
138
What is the **Na⁺–K⁺ pump** responsible for?
maintaining cell volume and excitability ## Footnote It uses ATP to transport sodium and potassium across the cell membrane.
139
What are the types of **chemical signaling**?
* Contact-Dependent * Paracrine * Autocrine * Hormonal (Endocrine) * Neurohormonal * Neurotransmitter Signaling ## Footnote Each type has different distances and mechanisms of action.
140
Cells can adapt to stress or environmental changes to _______.
survive ## Footnote Adapted cells are in a reversible state, maintaining function and preventing injury.
141
What are **stem cells** capable of?
* Self-renewal * Differentiation into specialized cells ## Footnote Stem cells are unspecialized cells that can give rise to various cell types.
142
What is the role of **cellular memory**?
maintain specialization across generations ## Footnote Cells remember their function due to specific gene expression patterns set during embryonic development.
143
What is the **definition** of **cellular adaptation**?
Cells can adapt to stress or environmental changes to survive ## Footnote Adapted cells are neither completely normal nor injured—they are in a reversible, in-between state.
144
What is the **goal** of cellular adaptation?
To maintain function and prevent injury ## Footnote When stress continues or becomes too strong, cell injury or death occurs.
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Name the **major types** of cellular adaptation.
* Atrophy * Hypertrophy * Hyperplasia * Metaplasia * Dysplasia ## Footnote These adaptations occur in response to various stressors.
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What does **atrophy** mean?
Decrease in cell size ## Footnote This leads to a smaller organ.
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What are the **two types** of atrophy?
* Physiologic atrophy * Pathologic atrophy ## Footnote Physiologic atrophy occurs during normal development, while pathologic atrophy is caused by reduced workload, use, blood flow, hormones, or nerve supply.
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What does **hypertrophy** mean?
Increase in cell size ## Footnote This results in an enlarged organ.
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What are the **three types** of hypertrophy?
* Physiologic hypertrophy * Pathologic hypertrophy * Compensatory hypertrophy ## Footnote Physiologic hypertrophy is caused by normal demand or hormones, while pathologic hypertrophy is due to chronic overload.
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What does **hyperplasia** mean?
Increase in the number of cells ## Footnote This is caused by increased cell division.
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What are the **two types** of hyperplasia?
* Physiologic hyperplasia * Pathologic hyperplasia ## Footnote Physiologic hyperplasia is a normal, beneficial response, while pathologic hyperplasia is abnormal and excessive.
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What does **dysplasia** mean?
Abnormal changes in cell size, shape, and organization ## Footnote It is often called atypical hyperplasia and represents a potentially precancerous change.
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What is **metaplasia**?
Reversible replacement of one mature cell type with another ## Footnote This change can better tolerate stress but often causes loss of normal function.
154
What is **ischemia-reperfusion injury**?
Further injury that occurs when blood flow and oxygen are restored after ischemia ## Footnote This can lead to oxidative stress and additional cellular damage.
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What are the **mechanisms** of ischemia-reperfusion injury?
* Oxidative stress * Nitrogen-based radicals * Calcium overload * Inflammation * Complement activation ## Footnote Antioxidants can help reduce damage by neutralizing reactive oxygen species (ROS).
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What are examples of **chemical agents** that cause injury?
* Highly toxic substances (e.g., arsenic, cyanide) * Environmental and industrial toxins * Alcohol * Social and street drugs ## Footnote Chronic exposure to these agents can lead to significant cellular damage.
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What is **necrosis**?
Cell death that occurs after severe and irreversible injury ## Footnote Major causes include ischemia, exposure to toxins, and physical injury.
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What are the **cellular features** of necrosis?
* Plasma and lysosomal membranes rupture * Rapid ATP depletion * Leakage of cellular contents ## Footnote These features lead to inflammation and further tissue damage.
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What is **gangrenous necrosis**?
Refers to large areas of tissue death ## Footnote It can be dry, wet, or gas gangrene, each with distinct characteristics.
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What is **apoptosis**?
Programmed and energy-dependent form of cell death ## Footnote It maintains balance in cell populations and occurs in both normal and pathological conditions.
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What is **autophagy**?
Self-degradative and recycling process ## Footnote It helps the cell survive during starvation or stress.
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What are the **functions of autophagy**?
* Maintains metabolism during nutrient deprivation * Removes dysfunctional organelles * Plays a role in aging, cancer prevention, neurodegenerative diseases ## Footnote Autophagy is crucial for cellular health and longevity.
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What are the **mechanisms of exchange** between plasma and interstitial fluid?
* Hydrostatic pressure * Osmotic/oncotic pressure ## Footnote These forces regulate fluid movement in and out of capillaries.
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What is **edema**?
Excessive accumulation of fluid in the interstitial spaces ## Footnote It results from fluid movement from capillaries or lymphatic vessels into surrounding tissues.
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What are the **four major mechanisms** responsible for edema?
* Increased capillary hydrostatic pressure * Decreased capillary oncotic pressure * Increased capillary membrane permeability * Lymphatic channel obstruction ## Footnote Each mechanism contributes to fluid imbalance in tissues.
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What is the **Renin-Angiotensin-Aldosterone System (RAAS)**?
A hormone system that regulates blood pressure and fluid balance ## Footnote It is triggered by low blood pressure or sodium levels.
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What is **hyponatremia**?
Low sodium levels in the blood ## Footnote Treatment involves addressing the underlying cause and may include water restriction or hypertonic saline.
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What is **hypochloremia**?
Serum chloride less than 97 mEq/L ## Footnote Often occurs with hyponatremia or elevated bicarbonate in metabolic alkalosis.
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What is **metabolic acidosis**?
A condition characterized by increased nonvolatile acids or loss of bicarbonate ## Footnote Rapid causes include lactic acidosis, while slower causes include renal failure.
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What is the **serum chloride** level considered low?
Less than 97 mEq/L ## Footnote Often occurs with hyponatremia or elevated bicarbonate in metabolic alkalosis.
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Name three **associations** with low serum chloride.
* Sodium deficit from restricted intake * Diuretics * Vomiting ## Footnote These factors can contribute to low serum chloride levels.
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What is the **management** for low serum chloride?
Treat the underlying cause ## Footnote Addressing the root issue is essential for correction.
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What are the **mechanisms** of **metabolic acidosis**?
* Increased nonvolatile acids * Loss of HCO₃⁻ * Reduced renal acid excretion ## Footnote These mechanisms lead to a decrease in blood pH.
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What are **rapid causes** of metabolic acidosis?
* Lactic acidosis (hypoxia, shock) ## Footnote Rapid onset conditions can lead to significant acid accumulation.
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What are **slower causes** of metabolic acidosis?
* Renal failure * DKA/starvation ketoacidosis * Toxin/acid ingestion * Chronic diarrhea (HCO₃⁻ loss) ## Footnote These conditions develop over time and contribute to acid-base imbalance.
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What happens during **compensation** in metabolic acidosis?
* Buffers consume H⁺ * K⁺ shifts out of cells * Ionized calcium increases ## Footnote These physiological responses help to mitigate the effects of acidosis.
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What is the **respiratory compensation** for metabolic acidosis?
Kussmaul respirations (deep, rapid) to reduce PaCO₂ ## Footnote This type of breathing is a response to acidosis.
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What is the **anion gap** formula in metabolic acidosis?
Anion gap ≈ (Na⁺ + K⁺) − (Cl⁻ + HCO₃⁻) ## Footnote Normal anion gap is about 10–12 mEq/L.
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What does an **elevated anion gap** indicate?
Accumulation of unmeasured anions (lactate, ketoacids, toxins, renal failure) ## Footnote This suggests a more severe metabolic acidosis.
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What are the **clinical signs** of metabolic acidosis?
* Headache * Lethargy * Confusion * Coma * GI upset * Dysrhythmias * Hypotension ## Footnote These symptoms reflect the systemic effects of acidosis.
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What is the **ABG** finding in metabolic acidosis?
pH < 7.35, HCO₃⁻ < 22 mEq/L ## Footnote These values confirm the diagnosis of metabolic acidosis.
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What is the **treatment** for metabolic acidosis?
* Treat cause * Correct volume and electrolytes * Buffer therapy for severe acidemia (pH ≤ 7.1) ## Footnote Addressing the underlying cause is crucial for effective management.
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What are the **mechanisms** of **metabolic alkalosis**?
* H⁺ loss * HCO₃⁻ gain ## Footnote These mechanisms lead to an increase in blood pH.
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What are common **causes** of metabolic alkalosis?
* Vomiting or NG suction (HCl loss) * Diuretics * Hyperaldosteronism * Excessive alkali (sodium bicarb) * Massive transfusion (citrate) ## Footnote These factors contribute to the development of metabolic alkalosis.
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What is **hypochloremic metabolic alkalosis**?
Low Cl⁻ sustains HCO₃⁻ retention ## Footnote This condition is characterized by low chloride levels.
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What is the **compensation** mechanism for metabolic alkalosis?
Hypoventilation retains CO₂ (limited by oxygen need) ## Footnote This response helps to balance the increased pH.
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What are the **clinical signs** of metabolic alkalosis?
* Weakness * Cramps * Hyperreflexia * Hypocalcemia symptoms (paresthesias, tetany, seizures) * Shallow breathing * Dysrhythmias ## Footnote These symptoms reflect the systemic effects of alkalosis.
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What is the **ABG** finding in metabolic alkalosis?
pH > 7.45, HCO₃⁻ > 26 mEq/L; PaCO₂ often > 40 mmHg if compensating ## Footnote These values confirm the diagnosis of metabolic alkalosis.
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What is the **treatment** for metabolic alkalosis?
* Treat cause * Volume/Cl⁻ repletion with NaCl for hypochloremic states * K⁺ repletion * Address mineralocorticoid excess ## Footnote Correcting the underlying issue is essential for management.
190
What does the **first line of defense** in the immune system include?
* Physical barriers * Mechanical clearance mechanisms * Biochemical secretions * Human microbiome living on body surfaces ## Footnote These components work together to prevent pathogen entry.
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What are the **physical barriers** in the first line of defense?
* Tightly joined epithelial cells of skin, GI, GU, and respiratory tracts * Skin integrity limits pathogen entry * Local conditions inhibit growth (cooler skin temperature, acidic environments) ## Footnote These barriers are crucial for preventing infections.
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What are the **mechanical defenses** in the first line of defense?
* Mucociliary escalator * Shear and flow (urination) * Rapid clearance (vomiting and defecation) * Cell turnover (shedding of skin and mucosal cells) ## Footnote These mechanisms help to expel pathogens from the body.
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What are the **biochemical barriers** in the first line of defense?
* Secretions that trap or kill microbes (mucus, sweat, saliva, tears, earwax) * Sebaceous products (fatty acids and lactic acid) * Enzymes and antimicrobials within secretions ## Footnote These substances play a vital role in pathogen defense.
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What are **antimicrobial peptides** and proteins?
* Defensins from neutrophils and epithelial cells disrupt bacterial membranes * Collectins enhance microbial recognition and can activate complement ## Footnote These components are part of the innate immune response.
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What is the **human microbiome**?
Diverse microbes colonizing skin, eyes, mouth, nose, GI tract, upper airway, urethra, vagina ## Footnote The microbiome composition is individualized and shaped by various factors.
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What are the **benefits** of the microbiome?
* Digestion (enzymes for fatty acids and complex polysaccharides) * Metabolites (synthesis of vitamins) * Chemical defense (antibacterial compounds) * Niche competition (blocks pathogen attachment) * Immune education (promotes protective responses) ## Footnote The microbiome plays a crucial role in health and disease prevention.
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What can **disrupt** the microbiome?
* Broad-spectrum antibiotics * Dietary shifts * Toxins * Infections * Hospitalization * Critical illness ## Footnote Dysbiosis can impair immune function and colonization resistance.
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What is **dysbiosis** and its clinical relevance?
* Overgrowth examples: Candida albicans, Clostridioides difficile * Opportunists from the normal microbiome can cause disease when barriers or immunity fail ## Footnote Dysbiosis can lead to infections and complications.
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What are the **first line** body sites in action?
* Skin: acidic, dry, keratinized * Respiratory tract: mucus plus cilia * GI tract: gastric acid, digestive enzymes * GU tract: urine flow and osmolarity ## Footnote These sites are equipped with defenses to protect against pathogens.
200
What is **inflammation**?
A protective response to injury or infection in vascularized tissues ## Footnote Inflammation is triggered by various factors and involves guardian cells.
201
What is the **coagulation system**?
Forms a fibrin–platelet mesh to stop bleeding, trap pathogens, and create a scaffold for healing ## Footnote This system is crucial for wound healing and preventing infection.
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What are the **pathways** of the coagulation system?
* Extrinsic (activated by tissue factor) * Intrinsic (activated by negatively charged surfaces) * Both converge at Factor X → thrombin → fibrin ## Footnote These pathways are essential for clot formation.
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What does **bradykinin** do?
* Causes vasodilation * Increases vascular permeability * Induces pain * Smooth muscle contraction ## Footnote Bradykinin amplifies the inflammatory response.
204
What triggers **mast cell degranulation**?
* PRRs * Complement fragments * IgE crosslinking * Physical/chemical/thermal injury ## Footnote Mast cells release mediators that contribute to inflammation.
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What are the **new mediators** synthesized by mast cells?
* Leukotrienes * Prostaglandins * PAF * VEGF * PDGF ## Footnote These mediators play roles in inflammation and healing.
206
What are **systemic acute responses** to inflammation?
* Fever * Leukocytosis * Acute-phase reactants ## Footnote These responses indicate the body is fighting infection or injury.
207
What is the effect of **ischemia** on wound healing?
Less O₂ → cell death, infection risk, prolonged inflammation ## Footnote Ischemia can severely impair the healing process.
208
What are the effects of **obesity** on wound healing?
* Impaired leukocyte function * Higher infection risk * Lower growth factor production * More proinflammatory cytokines ## Footnote Obesity complicates the healing process.
209
What is the role of **adaptive immunity**?
Begins upon exposure to an antigen ## Footnote This immune response is specific and involves various immune cells.
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What are the roles of **effector cells** in adaptive immunity?
* B cells → plasma cells (secrete antibodies) * T cells → Tc cells (kill infected cells) * Th cells → regulate immune response * Treg cells → suppress excessive reactions ## Footnote These cells coordinate the immune response.
211
Where do **T lymphocytes** mature?
In the thymus ## Footnote T cells originate in the bone marrow but mature in this primary lymphoid organ.
212
What are the **classes of antibodies**?
* IgG: Most common * IgM: First made during infection * IgA: Found in secretions * IgD: Receptor on B cells * IgE: Allergic reactions ## Footnote Each class has distinct functions in the immune response.
213
What is **neutralization** in antibody action?
Blocking viruses or toxins from binding to host cells ## Footnote This is a direct action of antibodies against pathogens.
214
What is the role of **IgE** in defense against parasites?
Binds to mast cells and basophils; triggers histamine release ## Footnote This response is crucial for combating large parasites.
215
What are the types of **hormonal signaling**?
* Autocrine * Paracrine * Endocrine ## Footnote These signaling methods help regulate body functions.
216
What is the **feedback system** for hormone levels?
* Negative feedback: high levels stop release * Positive feedback: increases secretion ## Footnote Feedback loops maintain hormonal balance.
217
What is the **half-life** of water-soluble hormones?
Short (seconds to minutes) ## Footnote Example: insulin lasts 3–5 minutes before breakdown.
218
Where are **hormone receptors** located?
* On the cell membrane (water-soluble hormones) * Inside the cytoplasm or nucleus (lipid-soluble hormones) ## Footnote The location determines the hormone's action inside the cell.
219
Where are **hormone receptors** located?
* On the cell membrane (for water-soluble hormones) * Inside the cytoplasm or nucleus (for lipid-soluble hormones) ## Footnote The receptor’s location determines how the hormone acts inside the cell.
220
What are the characteristics of **water-soluble hormones**?
* Cannot cross the membrane * Bind to surface receptors * Use second messengers to transmit signals * Responses are fast and short-acting ## Footnote Examples of second messengers include cAMP, cGMP, IP₃, calcium, and tyrosine kinase systems.
221
What are the characteristics of **lipid-soluble hormones**?
* Cross the cell membrane easily * Bind to cytosolic or nuclear receptors * Directly influence gene expression * Effects appear slowly but last longer ## Footnote Examples include cortisol, estrogen, testosterone, and aldosterone.
222
Where is the **hypothalamus** located?
At the base of the brain ## Footnote It is connected to the pituitary by the infundibulum (pituitary stalk).
223
What hormones does the **hypothalamus** produce?
* TRH (stimulates TSH release) * GnRH (controls FSH and LH) * GHRH & Somatostatin (regulate growth hormone) * CRH (stimulates ACTH release) * PIH (Dopamine) (inhibits prolactin) * PRH ## Footnote It also produces ADH and Oxytocin, which are stored in the posterior pituitary.
224
What is the function of the **posterior pituitary**?
* Stores and releases ADH * Stores and releases Oxytocin ## Footnote Release is controlled by neurotransmitters: glutamate stimulates, GABA inhibits.
225
What does **ADH** do?
* Maintains water balance * Increases water reabsorption in kidney tubules * Triggered by high plasma osmolality or low blood volume * Inhibited by alcohol and excess fluid intake ## Footnote At high doses, ADH acts as vasopressin, causing vasoconstriction and raising blood pressure.
226
What is the role of **Oxytocin**?
* Causes uterine contractions during labor * Promotes milk ejection during breastfeeding * Helps prevent postpartum bleeding ## Footnote Secreted in response to suckling or reproductive tract stimulation.
227
What does the **pineal gland** secrete?
Melatonin ## Footnote It regulates circadian rhythms, sleep, and puberty timing.
228
What is the function of **calcitonin**?
* Helps maintain calcium balance * Used to treat osteoporosis, Paget’s disease, hypercalcemia, and bone metastasis ## Footnote Procalcitonin, its precursor, rises in infection and inflammation and aids in diagnosis.
229
How is **thyroid hormone secretion** regulated?
* Negative feedback loop between hypothalamus, pituitary, and thyroid * TRH stimulates TSH release * TSH stimulates thyroid to release T3 and T4 * High TH levels inhibit TRH and TSH ## Footnote Cold, stress, and low T4 increase TRH and TSH secretion.
230
What are the actions of **TSH**?
* Increases thyroid hormone release from stored colloid * Stimulates iodide uptake and oxidation * Promotes synthesis of new thyroid hormone * Stimulates thyroid growth ## Footnote This includes cell enlargement and division.
231
What percentage of thyroid hormones produced is **T4** and **T3**?
* 90% T4 * 10% T3 ## Footnote In blood, most hormones are bound to thyroxine-binding globulin (TBG).
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What are the actions of **thyroid hormones**?
* Increase metabolic rate * Essential for growth and brain development * Affect protein, fat, and carbohydrate metabolism * Regulate heart rate and respiration ## Footnote They also influence skin, hair, and bone health.
233
What does **PTH** do?
* Stimulates osteoclast activity to release calcium into blood * Increases calcium reabsorption in kidneys * Enhances calcium absorption in intestines ## Footnote Chronic PTH elevation causes bone remodeling; low-dose PTH promotes bone formation.
234
What activates **vitamin D₃ (calcitriol)**?
Activated in the kidneys ## Footnote It enhances calcium absorption.
235
What triggers **insulin secretion**?
* Rising blood glucose * Parasympathetic input * Selected amino acids * Gut hormones ## Footnote Secretion is inhibited by hypoglycemia, sympathetic drive, high insulin, and prostaglandins.
236
What are the core actions of **insulin**?
* Promotes glucose uptake in muscle, fat, and liver * Stimulates glycogen, protein, and fat synthesis * Supports cellular uptake of K⁺, phosphate, and magnesium ## Footnote Insulin has anabolic effects.
237
What is the role of **somatostatin**?
* Modulates islet balance * Inhibits secretion of insulin, glucagon, and pancreatic polypeptide ## Footnote It fine-tunes carbohydrate, fat, and protein metabolism.
238
What do **incretins** do?
* Enhance glucose-dependent insulin * Suppress glucagon * Slow gastric emptying ## Footnote GIP and GLP-1 also help preserve β-cell mass and support insulin stores.
239
What does **gastrin** do?
* Stimulates gastric acid * May aid fetal islet development ## Footnote Ghrelin increases appetite and affects insulin sensitivity.
240
What are the main functions of **glucocorticoids**?
* Increase blood glucose via liver gluconeogenesis * Reduce glucose uptake by muscle and fat * Promote protein breakdown and lipolysis under stress ## Footnote Chronic stress can lead to muscle wasting, insulin resistance, and hyperglycemia.
241
What are the **anti-inflammatory effects** of glucocorticoids?
* Suppress T-cell proliferation * Block phospholipase A₂, prostaglandins, and cytokines * Stabilize lysosomes ## Footnote Prolonged use increases infection risk and delays healing.