patho exam 1

Which three stages make up the General Adaptation Syndrome (GAS)?

Alarm, Resistance, Exhaustion.

What releases corticotropin-releasing hormone (CRH) and why?

The hypothalamus releases CRH to initiate the stress response.

What does adrenocorticotropic hormone (ACTH) stimulate?

ACTH stimulates the adrenal cortex to secrete cortisol.

Which hormones are released from the adrenal medulla during acute stress, and what do they do?

Epinephrine and norepinephrine increase heart rate, blood pressure, and redirect blood flow to vital organs and muscle; epinephrine also promotes bronchodilation and raises blood glucose.

What is the primary metabolic role of cortisol in stress?

Cortisol maintains blood glucose through gluconeogenesis.

What defines the Exhaustion stage of the General Adaptation Syndrome (GAS)?

Depletion of physiologic reserves with failure of compensatory mechanisms and increased risk of illness.

What is the hypothalamic–pituitary–adrenal (HPA) axis?

A coordinated pathway—hypothalamus (CRH) → anterior pituitary (ACTH) → adrenal cortex (cortisol)—that regulates the stress response.

Define allostasis and allostatic load.

Allostasis is “stability through change”; allostatic load is the cumulative “wear and tear” from repeated or chronic stress responses.

How does chronic stress typically affect adaptive immunity?

It suppresses T-cell and B-cell function (reduced production and activation).

What happens to natural killer (NK) cell activity with chronic stress, and why is that important?

NK cell activity decreases, reducing surveillance against virally infected and malignant cells.

What is meant by cytokine dysregulation in chronic stress?

An imbalance of pro- and anti-inflammatory signaling that leads to either excessive inflammation or inadequate responses.

Name two clinical red flags of stress-related immune impairment.

Frequent infections and poor wound healing.

What is central tolerance in the immune system?

Deletion of self-reactive T and B lymphocytes during development in the thymus and bone marrow.

What is peripheral tolerance in the immune system?

Suppression or anergy of self-reactive lymphocytes that escaped central deletion, preventing autoimmune responses.

Define autoimmunity in one sentence.

Autoimmunity is loss of self-tolerance, causing immune attack on the body’s own tissues.

Give one example of a disease with autoantibodies and name the autoantibody.

Systemic lupus erythematosus (SLE) with anti–double-stranded DNA (anti-dsDNA) antibodies.

What is rheumatoid arthritis (RA) and a hallmark symptom pattern?

RA is an autoimmune synovitis; hallmark is symmetric small-joint pain and morning stiffness.

What is multiple sclerosis (MS) and a common presenting feature?

Autoimmune demyelination in the central nervous system; common features include optic neuritis or sensory changes.

What is type 1 diabetes mellitus (T1DM) at the immune level?

Autoimmune destruction of pancreatic beta (β) cells leading to insulin deficiency.

What is severe combined immunodeficiency (SCID)?

A primary (congenital) immunodeficiency with profound T-cell and B-cell dysfunction leading to severe, recurrent infections.

What is the difference between primary and secondary immunodeficiency?

Primary is congenital (e.g., SCID); secondary is acquired (e.g., human immunodeficiency virus (HIV), chemotherapy, glucocorticoids).

What is acquired immunodeficiency syndrome (AIDS) and how is it defined?

AIDS is advanced HIV infection defined by a CD4+ T-cell count <200 cells/mm³ or an AIDS-defining illness.

What does a CD4+ T-cell count indicate in human immunodeficiency virus (HIV) care?

The degree of immune function and risk for opportunistic infections.

What does an HIV viral load measure and why is it important?

The amount of circulating HIV RNA; it monitors response to antiretroviral therapy (ART).

Name one opportunistic infection strongly associated with AIDS and its affected organ.

Pneumocystis jiroveci pneumonia (PJP/PCP) affects the lungs.

What immune mechanism mediates Type I hypersensitivity?

Immunoglobulin E (IgE)–mediated mast-cell degranulation (immediate reaction).

What is the priority nursing action in anaphylaxis (Type I hypersensitivity)?

Administer intramuscular epinephrine and secure the airway.

What is the immune mechanism in Type II hypersensitivity?

Immunoglobulin G (IgG) or immunoglobulin M (IgM) binding to host cell antigens with complement or antibody-dependent cellular cytotoxicity (ADCC).

Give one classic example of Type II hypersensitivity.

Acute hemolytic transfusion reaction.

Which process underlies Type III hypersensitivity?

Deposition of circulating antigen–antibody immune complexes with complement activation (e.g., SLE, post-streptococcal glomerulonephritis).

What is the timeline and mediator for Type IV hypersensitivity?

Delayed (24–72 hours), T-cell–mediated (no antibodies).

What is the mechanism of nonsteroidal anti-inflammatory drugs (NSAIDs)?

Inhibition of cyclooxygenase (COX) enzymes, reducing prostaglandin synthesis (analgesic, antipyretic, anti-inflammatory effects).

What is a key difference between COX-1 and COX-2 inhibition?

COX-1 inhibition increases gastrointestinal bleeding/ulcer risk; COX-2–selective inhibition reduces GI risk but may increase cardiovascular risk.

Name a common indication and a major risk for ibuprofen (an NSAID).

Indication: pain/inflammation/fever; risk: gastrointestinal irritation/ulcer and renal impairment.

What is the core anti-inflammatory mechanism of glucocorticoids?

Suppression of pro-inflammatory cytokines (e.g., interleukin-1 (IL-1), interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-α)) and eicosanoid pathways via gene regulation.

Why must long-term glucocorticoid therapy be tapered?

To avoid adrenal insufficiency due to suppression of the hypothalamic–pituitary–adrenal (HPA) axis.

List two high-yield adverse effects of chronic glucocorticoid use.

Hyperglycemia and increased infection risk (others: osteoporosis, mood/sleep changes, skin thinning).

How does acetaminophen relieve pain and fever, and what is a key safety limit?

Central cyclooxygenase (COX) inhibition (no peripheral anti-inflammatory effect); maximum daily dose is 4 grams (lower with liver disease or alcohol use).

Define the Alarm stage of the General Adaptation Syndrome (GAS) in one line.

Sympathetic surge and adrenal hormone release that rapidly mobilize energy and perfusion.

What two simple bedside findings can suggest stress-related immune suppression?

Recurrent infections and delayed wound healing.

Which stress hormone primarily causes bronchodilation and increased blood glucose?

Which stress hormone primarily drives vasoconstriction to maintain blood pressure?

What percentage of total body water is intracellular fluid (ICF)?

About two-thirds of total body water

What percentage of total body water is extracellular fluid (ECF)?

About one-third of total body water is extracellular.

What are the three types of extracellular fluid (ECF)?

Interstitial fluid, intravascular fluid (plasma), and transcellular fluid (CSF, pleural, synovial, GI fluids).

What is hydrostatic pressure?

The pressure that pushes water out of capillaries into tissues.

What is oncotic pressure?

The pressure (mostly from albumin) that pulls water back into capillaries from tissues.

What is the main cause of edema?

An imbalance between hydrostatic and oncotic pressures, or lymphatic obstruction.

What health conditions can cause edema?

Heart failure, kidney disease, cirrhosis, burns, lymphatic blockage.

How does edema happen physiologically?

Increased capillary pressure, decreased plasma proteins, or impaired lymph drainage cause excess fluid to accumulate in the interstitial space.

What hormone increases water reabsorption by the kidneys?

Antidiuretic hormone (ADH or vasopressin).

What hormone increases sodium and water retention?

Aldosterone.

What hormones reduce blood volume and pressure?

Natriuretic peptides (ANP, BNP, urodilatin).

What is the main function of sodium (Na⁺)?

Regulates water balance, blood pressure, and supports nerve/muscle activity.

What is the normal sodium range?

135–145 mEq/L.

What health conditions can cause hyponatremia?

SIADH, diuretics, heart failure, kidney disease, psychogenic polydipsia, vomiting, diarrhea.

How does hyponatremia happen physiologically?

Lowers extracellular osmolality, causing water to enter cells and swell — especially brain cells.

What health conditions can cause hypernatremia?

Dehydration, diabetes insipidus, high fever, profuse sweating, diarrhea without adequate water intake.

How does hypernatremia happen physiologically?

High extracellular sodium draws water out of cells, causing cellular dehydration and CNS symptoms.

What is the main function of potassium (K⁺)?

Maintains intracellular electrical neutrality and supports nerve and muscle activity, especially in the heart.

What is the normal potassium range?

3.5–5.0 mEq/L.

What health conditions can cause hypokalemia?

Vomiting, diarrhea, diuretics, alkalosis, insulin therapy.

How does hypokalemia happen physiologically?

K⁺ is lost or shifted into cells, lowering serum levels and hyperpolarizing cells → decreased excitability.

What ECG changes occur with hypokalemia?

Flattened T waves, U waves, and increased risk of arrhythmias.

What health conditions can cause hyperkalemia?

Renal failure, tissue trauma, acidosis, potassium-sparing diuretics, Addison’s disease.

How does hyperkalemia happen physiologically?

Increased extracellular K⁺ depolarizes cell membranes, disrupting repolarization and conduction — especially in the heart.

What ECG changes occur with hyperkalemia?

Peaked T waves, widened QRS, bradycardia, and risk of cardiac arrest.

What is the main role of calcium (Ca²⁺)?

Supports bone structure, nerve transmission, muscle contraction, and blood clotting.

What is the normal calcium range?

8.8–10.5 mg/dL (total).

What health conditions can cause hypocalcemia?

Hypoparathyroidism, vitamin D deficiency, pancreatitis, massive transfusion (citrate), renal failure.

How does hypocalcemia happen physiologically?

Low serum Ca²⁺ increases neuronal membrane excitability → spontaneous depolarization and tetany.

What signs are associated with hypocalcemia?

Chvostek sign, Trousseau sign, muscle twitching, spasms, seizures.

What health conditions can cause hypercalcemia?

Hyperparathyroidism, bone cancer, prolonged immobilization, vitamin D toxicity.

How does hypercalcemia happen physiologically?

Elevated Ca²⁺ increases the threshold for depolarization, decreasing neuromuscular excitability.

What symptoms are seen in hypercalcemia?

Constipation, muscle weakness, lethargy, kidney stones, shortened QT interval.

What is the main role of magnesium (Mg²⁺)?

Stabilizes nerve and muscle cells, regulates cardiac conduction, and serves as an enzymatic cofactor.

What is the normal magnesium range?

1.8–3.0 mg/dL.

What health conditions can cause hypomagnesemia?

Alcoholism, diarrhea, malnutrition, diuretics, uncontrolled diabetes.

How does hypomagnesemia happen physiologically?

Low Mg²⁺ removes inhibitory control on calcium channels, increasing neuromuscular excitability.

What symptoms are seen in hypomagnesemia?

Tremors, seizures, hyperreflexia, torsades de pointes.

What health conditions can cause hypermagnesemia?

Renal failure, excessive magnesium intake (antacids/laxatives), tumor lysis syndrome.

How does hypermagnesemia happen physiologically?

Suppresses acetylcholine release and neuromuscular activity → weakness, bradycardia, respiratory depression.

What is phosphate’s primary role in the body?

Energy production (ATP), bone mineralization, and buffering of acids and bases.

What is the normal phosphate range?

2.5–5.0 mg/dL.

What health conditions can cause hypophosphatemia?

Alcohol abuse, refeeding syndrome, DKA recovery, malabsorption, respiratory alkalosis.

How does hypophosphatemia happen physiologically?

Low phosphate reduces ATP production, impairing muscle and organ function, especially in diaphragm and heart.

What health conditions can cause hyperphosphatemia?

Chronic kidney disease, tumor lysis syndrome, hypoparathyroidism, rhabdomyolysis.

How does hyperphosphatemia happen physiologically?

Excess PO₄³⁻ binds to Ca²⁺, forming insoluble salts, reducing free calcium and promoting soft tissue calcification.

What is the normal arterial blood pH?

7.35–7.45.

What is the normal PaCO₂ range?

35–45 mmHg.

What is the normal bicarbonate (HCO₃⁻) range?

21–28 mEq/L.

What causes metabolic acidosis?

DKA, renal failure, diarrhea, lactic acidosis, toxin ingestion.

How does metabolic acidosis happen physiologically?

Acid accumulates or bicarbonate is lost → blood pH drops; lungs try to compensate with hyperventilation.

What causes metabolic alkalosis?

Vomiting, NG suction, diuretic use, excess bicarbonate intake.

How does metabolic alkalosis happen physiologically?

Loss of H⁺ or gain of HCO₃⁻ raises pH; respiratory compensation causes hypoventilation to retain CO₂.

What causes respiratory acidosis?

COPD, hypoventilation due to CNS depression, sedatives, airway obstruction.

How does respiratory acidosis happen physiologically?

CO₂ retention increases carbonic acid, lowering pH; kidneys compensate over time by retaining HCO₃⁻.

What causes respiratory alkalosis?

Hyperventilation due to anxiety, pain, fever, or sepsis.

How does respiratory alkalosis happen physiologically?

Excess CO₂ loss raises pH; causes cerebral vasoconstriction and electrolyte shifts (e.g., hypocalcemia).

What is Kussmaul breathing and when is it seen?

Deep, labored breathing seen in metabolic acidosis, especially diabetic ketoacidosis.