HSCI 4662 Exam Study Guide

Flashcards for HSCI 4662 Final Exam

Type 1 Diabetes (T1D)

Autoimmune destruction of pancreatic β-cells, resulting in no insulin production. Onset often in childhood/adolescence.

Type 2 Diabetes (T2D)

Insulin resistance combined with β-cell dysfunction. Strongly linked to obesity and lifestyle. Typically adult onset but increasingly seen in youth.

Gestational Diabetes (GDM)

Diabetes that occurs during pregnancy due to hormonal changes inducing insulin resistance. Typically resolves post-partum but increases future T2D risk.

Metabolic consequences of T1D

Hyperglycemia, ketoacidosis, muscle wasting, lipolysis.

Metabolic consequences of T2D

Hyperglycemia, dyslipidemia, increased hepatic glucose production, hyperinsulinemia initially.

Metabolic consequences of GDM

Hyperglycemia affects fetal development, increased risk for macrosomia, neonatal hypoglycemia.

Long-term hyperglycemia consequences (Adults)

Retinopathy, nephropathy, neuropathy, cardiovascular disease.

Long-term hyperglycemia consequences (Fetuses)

Macrosomia, hypoglycemia at birth, congenital abnormalities.

Mechanisms of Damage from Hyperglycemia

Advanced glycation end-products (AGEs), oxidative stress, sorbitol pathway, chronic inflammation, endothelial dysfunction.

Signs/Symptoms of Metabolic Syndrome

Central obesity, hypertension, hyperglycemia, elevated triglycerides, low HDL.

Risks associated with Metabolic Syndrome

T2D, cardiovascular disease, stroke.

Diagnostic Tests for Metabolic Syndrome

Fasting glucose, lipid panel, waist circumference, blood pressure measurement.

Short-Term Effects of Hyperglycemia

Polyuria, polydipsia, fatigue, blurred vision.

Long-Term Effects of Hyperglycemia

Neuropathy, nephropathy, retinopathy, increased infection risk, poor wound healing, CVD.

HbA1c

Glycated hemoglobin; reflects average blood glucose over ~3 months. Normal: <5.7%, Prediabetes: 5.7–6.4%, Diabetes: ≥6.5%. Helps monitor long-term glucose control.

Biguanides (e.g., Metformin)

Oral medication that decreases hepatic glucose output.

Sulfonylureas

Oral medication that increases insulin secretion.

DPP-4 Inhibitors

Oral medication that increases incretin hormones.

SGLT2 Inhibitors

Oral medication that increases glucose excretion via urine.

Thiazolidinediones

Oral medication that increases insulin sensitivity.

Alpha-glucosidase Inhibitors

Oral medication that decreases carbohydrate absorption.

DCCT study impact

Showed that tight glucose control reduces risk of microvascular complications (retinopathy, nephropathy, neuropathy) in T1D. Changed standard of care to emphasize intensive insulin therapy.

Moderate alcohol use (Diabetes)

Can cause hypoglycemia (especially in T1D), particularly on an empty stomach.

Heavy alcohol use (Diabetes)

Worsens insulin resistance, raises triglycerides, liver damage.

Obesity's effect on diabetes development

Increases insulin resistance by promoting chronic low-grade inflammation, increased free fatty acids, and ectopic fat deposition. Visceral fat is particularly associated with metabolic dysfunction.

Ethnicity's effect on diabetes development

Certain ethnic groups such as African Americans, Hispanic/Latino Americans, Native Americans, and Asian Americans have higher risks for T2D at lower BMIs.

Hunger

Physiological need for food, regulated by the hypothalamus (e.g., low blood glucose, ghrelin release).

Appetite

Psychological desire to eat, influenced by emotions, habits, sensory stimuli, and social cues.

Hormonal signals affecting food intake

Ghrelin, insulin, leptin

How is food intake regulated?

Central Regulation: Hypothalamus integrates signals (ghrelin, leptin, insulin, PYY). Peripheral Signals: Stomach distension, blood nutrient levels, gut hormones. Reward System: Dopamine pathways reinforce eating behavior.

Ghrelin

Increases appetite (hunger hormone).

Leptin

Decreases appetite; secreted by fat cells; resistance common in obesity.

ob/ob mice

Lack leptin gene → severe obesity due to uncontrolled eating.

db/db mice

Have leptin but lack leptin receptor → also obese. Demonstrate critical roles of leptin in appetite and weight regulation.

Hormones involved in Fasting (Short term)

↑ Glucagon, cortisol, growth hormone, ↓ Insulin

Hormones involved in Starvation (Prolonged)

↑ Ketone bodies, ↓ Thyroid hormones (to conserve energy), Gluconeogenesis predominates.

Enzymes activities during Fasting

Glycogenolysis → gluconeogenesis → lipolysis

Enzymes activities during Starvation

↑ β-oxidation, ↑ ketogenesis, ↓ protein synthesis

Glutamine

Critical for maintaining intestinal mucosa during fasting/rest. Serves as a primary fuel for enterocytes and supports immune function in the gut.

Insulin

Origin: Pancreatic beta cells, Target: Liver, muscle, fat, Function: Lowers blood glucose, promotes storage

Glucagon

Origin: Pancreatic alpha cells, Target: Liver, Function: Raises blood glucose via glycogen lysis, gluconeogenesis

Cortisol

Origin: Adrenal cortex, Target: Liver, muscle, fat, Function: Stress response, increases gluconeogenesis, decreases protein synthesis

Epinephrine

Origin: Adrenal medulla, Target: Multiple tissues, Function: Increases HR, BP, lipolysis, glycogenolysis

Thyroid hormones (T3/T4)

Origin: Thyroid gland, Target: Most cells, Function: Regulates metabolism, development

Growth hormone

Origin: Anterior pituitary, Target: Liver, fat, muscle, Function: Growth, increase lipolysis, decreased glucose uptake

ADH (Vasopressin)

Origin: Posterior pituitary, Target: Kidneys, Function: Water retention

Aldosterone

Origin: Adrenal cortex, Target: Kidneys, Function: Sodium retention, potassium excretion

Negative Feedback (Hormones)

Hormone release is inhibited by its own effects (e.g., high cortisol inhibits ACTH/CRH release).

Tyrosine

Amino acid used to produce Epinephrine, norepinephrine, dopamine, thyroid hormones.

Peptide Hormones

Composed of chains of amino acids (e.g., insulin, glucagon, GH).

Steroid Hormones

Made from cholesterol (e.g., cortisol, aldosterone, estrogen, testosterone).

Role of Hypothalamus in hormone secretion

Regulates pituitary hormone secretion.

Role of Pituitary gland in hormone secretion

Releases tropic hormones that act on peripheral endocrine glands (e.g., thyroid, adrenal glands, gonads).

Adrenal Medulla function

Secretes catecholamines (epinephrine, norepinephrine); fast stress response.

Adrenal Cortex function

Secretes steroid hormones: Zona glomerulosa: Aldosterone, Zona fasciculata: Cortisol, Zona reticularis: Androgens

Exocrine pancreas function

Produces digestive enzymes (acinar cells → duodenum).

Endocrine pancreas function

Islets of Langerhans produce insulin (β-cells), glucagon (α-cells), somatostatin (δ-cells).

Active form of thyroxin

T3 (triiodothyronine) is the active form.

Iodine deficiency relation to Goiter

Iodine deficiency ↓ T3/T4 production → ↑ TSH → thyroid gland enlarges → goiter.

Hormones produced in Anterior Pituitary

ACTH, TSH, LH, FSH, GH, Prolactin

Hormones produced in Posterior Pituitary

Oxytocin, ADH (produced in hypothalamus, stored/released here)

Purpose of hypothalamus in hormone secretion

Produces releasing/inhibiting hormones (e.g., TRH, CRH, GnRH, GHRH), Controls pituitary function (master regulator)

High Blood Volume restoration mechanism

Atrial natriuretic peptide (ANP) released, leads to vasodilation and increased sodium/water excretion.

Low Blood Volume restoration mechanism

Activates RAAS, leads to vasoconstriction, increased sodium and water reabsorption.

RAAS system activation trigger

Low BP or sodium

RAAS system steps

Kidney releases renin -> Renin converts angiotensinogen to angiotensin I -> ACE (lungs) converts angiotensin I to angiotensin II. Angiotensin II then promotes Vasoconstriction and secretion of Aldosterone & ADH

Oncotic Pressure

Pulling force from plasma proteins (e.g., albumin); retains fluid in vessels.

Hydrostatic Pressure

Pushing force from blood pressure; drives fluid out of capillaries.

Albumin

Maintains oncotic pressure. Produced in the liver. Prevents leakage of fluid into interstitial space.

Edema

Fluid accumulates in interstitial space due to: ↑ hydrostatic pressure (e.g., CHF), ↓ oncotic pressure (e.g., low albumin), Capillary leakage (inflammation)

Ascites

Accumulation of fluid in peritoneal cavity (common in liver disease due to hypoalbuminemia and portal hypertension).

Factors involved in control of urine volume

ADH levels (increases water reabsorption), Aldosterone (increases sodium/water reabsorption), Blood volume and pressure, Hydration status and plasma osmolality

Aging effect body fluid

↓ muscle mass, ↓ total body water, ↓ Thirst sensation, ↓ kidney concentrating ability, ↑ Risk of dehydration and electrolyte imbalance

Functions of Hemoglobin

Transports oxygen from lungs to tissues. Transports CO₂ from tissues to lungs. Buffers blood pH.

Hemoglobin structure

Tetramer: 2 α and 2 β subunits (in adults). Each subunit contains a heme group with iron that binds one O₂ molecule (4 O₂ per hemoglobin).

Right Shift of Hemoglobin Oxygen Saturation Curve

↓ O₂ affinity = easier O₂ release; ↑ CO₂, ↑ H⁺ (↓ pH), ↑ temperature, ↑ 2,3-BPG. Occurs during exercise or in tissues

Left Shift of Hemoglobin Oxygen Saturation Curve

↑ O₂ affinity = harder O₂ release; ↓ CO₂, ↓ H⁺ (↑ pH), ↓ temp, ↓ 2,3-BPG, fetal hemoglobin. Occurs in lungs or with fetal hemoglobin

Adult Hemoglobin (HbA)

α₂β₂

Fetal Hemoglobin (HbF)

α₂γ₂; HbF has higher O₂ affinity → facilitates oxygen transfer from mother to fetus.

Isohydric shift

Process by which CO₂ is transported in the blood without significantly changing the pH, thanks to buffering systems in red blood cells (RBCs); Facilitates CO₂ transport from tissues to lungs, Maintains blood pH homeostasis during respiration & Supports the Bohr effect.

Respiratory Acidosis

Cause: Hypoventilation (COPD, drug OD); Primary Issue: ↑ CO₂ → ↓ pH

Respiratory Alkalosis

Cause: Hyperventilation (anxiety, high altitude); Primary Issue: ↓ CO₂ → ↑ pH

Metabolic Acidosis

Cause: Diarrhea, ketoacidosis, renal failure; Primary Issue: ↓ HCO₃⁻ → ↓ pH

Metabolic Alkalosis

Cause: Vomiting, diuretics; Primary Issue: ↑ HCO₃⁻ → ↑ pH

Bicarbonate buffer system

Ratio of HCO₃⁻ : H₂CO₃ = 20:1 at normal pH (7.4).

Phosphate buffer system

Ratio of HPO₄²⁻ : H₂PO₄⁻ = 4:1; Active in renal tubules and intracellular fluid.

Role of respiratory center in acid base balance

Medulla oblongata regulates ventilation. Increased CO₂ stimulates breathing (to exhale CO₂, raise pH). Decreased CO₂ reduces breathing (to retain CO₂, lower pH).

Types of energy in the body

Chemical Energy, Mechanical Energy, Thermal Energy, Electrical Energy

ATP-PCr System

Provides immediate energy for short bursts of high-intensity activity (e.g., sprinting).

Glycolytic System

Breaks down carbohydrates to produce ATP for moderate-duration, high-intensity efforts.

Oxidative System

Utilizes oxygen to generate ATP for prolonged, lower-intensity activities.

Components of energy expenditure

Resting Metabolic Rate (RMR), Physical Activity, Thermic Effect of Food (TEF)

Factors that affect energy expenditure

Age, Sex, and Body Composition, Genetics, Hormones, Physical Activity Level

How to delay onset of fatigue

Training, Nutrition, Hydration

Direct Calorimetry

Measures heat output from the body.

Indirect Calorimetry

Estimates energy expenditure by analyzing respiratory gases.

RQ

Ratio of CO₂ produced to O₂ consumed, indicating which macronutrients are being metabolized; RQ = 1.0: Primarily carbohydrate metabolism, RQ = 0.7: Primarily fat metabolism

Creatine benefits

Beneficial for high-intensity, short-duration activities like sprinting and weightlifting. It aids in rapid ATP production, enhancing performance.

Key players in immune defense

White Blood Cells (Leukocytes)

Impact of nutrients on immune system

Vitamin C, Vitamin D, Zinc, Probiotics