BIO-322: Fluid, Electrolyte, Acid-Base, and Hematologic Disorders

Comprehensive practice flashcards covering fluid and electrolyte imbalances, acid-base disorders, bleeding disorders, red blood cell conditions, and white blood cell neoplasms.

How is total body water distributed between the intracellular fluid (ICF) and extracellular fluid (ECF) compartments?

Approximately $2/3$ ($67\%$) of total body water resides in the ICF, while $1/3$ ($33\%$) resides in the ECF.

What two sub-compartments constitute extracellular fluid (ECF) and in what proportions?

Interstitial fluid makes up $80\%$ of the ECF, and blood plasma makes up the remaining $20\%$.

What four primary capillary forces govern fluid exchange between blood plasma and the interstitial space?

Capillary Hydrostatic Pressure (CHP), Capillary Osmotic Pressure (COP), Interstitial Fluid Hydrostatic Pressure (IFHP), and Interstitial Fluid Osmotic Pressure (IFOP).

How do the clinical manifestations of left-sided heart failure differ from right-sided heart failure?

Left-sided heart failure causes fluid backup into the lungs resulting in pulmonary edema, whereas right-sided heart failure causes fluid backup into systemic tissues resulting in peripheral pitting edema and ascites.

What effect does aldosterone have on renal electrolyte handling, blood volume, blood pressure, and urine output?

Aldosterone stimulates renal reabsorption of $\text{Na}^+$ (water follows passively) and excretion of $\text{K}^+$, which increases blood volume and blood pressure while decreasing urine output.

What physiological stimuli trigger the release of Anti-Diuretic Hormone (ADH / Vasopressin), and what is its primary effect?

ADH is triggered by increased serum osmolarity (detected by hypothalamic osmoreceptors) or decreased blood volume/pressure (detected by atrial stretch receptors); it increases water reabsorption in the renal distal convoluted tubules and collecting ducts.

How do laboratory findings and urine volumes contrast between Syndrome of Inappropriate ADH (SIADH) and Diabetes Insipidus (DI)?

SIADH presents with elevated ADH, dilutional hyponatremia, low serum osmolarity, high urine osmolarity, and low urine volume. DI presents with deficient ADH (or renal resistance), hypernatremia, high serum osmolarity, low urine osmolarity, and massive urine output ($8\,-\,12\,\text{L/day}$ compared to normal $1\,-\,2\,\text{L/day}$).

What specific EKG abnormalities characterize hypokalemia versus hyperkalemia?

Hypokalemia displays flattened or depressed T waves, ST segment depression, and prominent U waves; hyperkalemia displays wide QRS complexes, prolonged PR intervals, and tall, peaked T waves.

What are Chvostek's sign and Trousseau's sign, and what underlying electrolyte imbalance do they demonstrate?

Chvostek's sign is twitching of ipsilateral facial muscles elicited by tapping the facial nerve anterior to the ear. Trousseau's sign is carpopedal spasm induced by inflating a blood pressure cuff above SBP for $3\,\text{minutes}$. Both indicate hypocalcemia.

What classic mnemonic summarizes the clinical signs and symptoms of hypercalcemia?

"Bones (pain), stones (renal calculus), groans (abdominal pain/N/V), thrones (polyuria leading to dehydration), and psychiatric overtones (depression/confusion)", alongside hyporeflexia, muscle weakness, and a shortened ST segment on EKG.

What are the standard reference values for arterial blood pH, $P_{\text{CO}_2}$, and $\text{HCO}_3^-$?

Arterial blood pH is $7.35\,-\,7.45$, $P_{\text{CO}_2}$ is $35\,-\,45\,\text{mmHg}$, and $\text{HCO}_3^-$ is $22\,-\,26\,\text{mmol/L}$.

What is the normal physiological ratio of bicarbonate ($\text{HCO}_3^-$) to carbonic acid ($\text{H}_2\text{CO}_3$) in systemic arterial blood?

A $20:1$ ratio of bicarbonate to carbonic acid maintains normal physiological pH.

What equation is used to calculate the serum Anion Gap, and what is the normal reference range?

$\text{Anion Gap} = [\text{Na}^+] - ([\text{HCO}_3^-] + [\text{Cl}^-])$, with a normal range of $10\,-\,12\,\text{mEq/L}$.

What causes are included in the "MUDPILES" mnemonic for high anion gap metabolic acidosis?

Methanol, Uremia, Diabetic ketoacidosis, Propylene glycol/Phenformin, Isoniazid/Iron, Lactic acidosis, Ethylene glycol/Ethanol, and Salicylates.

How does the respiratory system compensate for metabolic acidosis compared to metabolic alkalosis?

In metabolic acidosis, the respiratory system compensates via hyperventilation (Kussmaul breathing) to blow off $\text{CO}_2$. In metabolic alkalosis, the respiratory system compensates via hypoventilation (slow, shallow breathing) to retain $\text{CO}_2$.

What three organic molecules are produced during fatty acid breakdown in Diabetic Ketoacidosis (DKA), and which one causes fruity breath?

Acetoacetic acid, $\beta$-hydroxybutyric acid, and acetone. Acetone is responsible for fruity breath.

How do arterial pH shifts affect serum levels of potassium ($\text{K}^+$) and ionized calcium ($\text{Ca}^{2+}$)?

Acidosis causes hyperkalemia (cell influx of $\text{H}^+$ displaces $\text{K}^+$ outward) and hypercalcemia. Alkalosis causes hypokalemia (cell efflux of $\text{H}^+$ draws $\text{K}^+$ inward) and hypocalcemia (increased binding of $\text{Ca}^{2+}$ to albumin).

What essential functions does von Willebrand Factor (vWF) perform during primary hemostasis and factor transport?

vWF mediates platelet adhesion (binding platelets to subendothelial collagen), platelet aggregation (binding platelets to platelets), and serves as the circulating carrier protein for Factor VIII.

How do clinical presentation and lab findings distinguish platelet-type bleeding from factor-type bleeding?

Platelet-type bleeding presents with superficial mucocutaneous bleeding (petechiae, purpura, epistaxis, gum bleeding) and prolonged Bleeding Time (BT). Factor-type bleeding presents with deep tissue hematomas, ecchymosis, hemarthrosis, and prolonged PT or aPTT with normal BT.

What are the inheritance patterns, deficient factors, and laboratory findings in Hemophilia A and Hemophilia B?

Hemophilia A (deficiency of Factor VIII) and Hemophilia B (Christmas Disease, deficiency of Factor IX) are both X-linked recessive disorders. Both feature an increased aPTT with normal PT, normal Bleeding Time (BT), and normal platelet count.

What diagnostic assay serves as the most accurate test for von Willebrand Disease (vWD)?

The Ristocetin cofactor assay.

What enzyme breaks down fibrin clots during fibrinolysis, and what pharmacological agent activates its precursor?

Plasmin digests fibrin strands; tissue Plasminogen Activator (tPA) converts the inactive precursor Plasminogen into active Plasmin.

What underlying mechanism initiates Disseminated Intravascular Coagulation (DIC), and what is its most common underlying cause?

DIC is initiated by the massive systemic release of Tissue Factor (TF / Factor III) into circulation following endothelial or tissue damage, leading to simultaneous widespread microvascular thrombosis and hemorrhage. Sepsis is the most common cause.

What normal reference ranges define Hematocrit (Hct) in adult males and females?

Adult males: $41\%\,-\,53\%$; Adult females: $36\%\,-\,46\%$.

How do Mean Cell Volume (MCV) and Mean Cell Hemoglobin Concentration (MCHC) categorize anemia subtypes?

MCV categorizes red blood cell size (microcytic <$80\,\text{fl}$, normocytic $80\,-\,100\,\text{fl}$, macrocytic >$100\,\text{fl}$). MCHC categorizes hemoglobin concentration (hypochromic, normochromic, hyperchromic).

What laboratory RBC indices and physical signs are characteristic of Iron Deficiency Anemia?

Iron Deficiency Anemia is a microcytic hypochromic anemia (↓MCV, ↓MCH, ↓MCHC); physical signs include pallor, koilonychia (spoon-shaped nails), angular cheilitis/stomatitis, a smooth shiny tongue, and pica.

What key clinical feature distinguishes Vitamin B12 deficiency anemia from Folate (Vitamin B9) deficiency anemia?

Vitamin B12 deficiency anemia presents with distinct neurological symptoms (paresthesias, difficulty walking, memory impairment, altered mental status) due to nerve demyelination, whereas Folate deficiency anemia causes no neurological deficits.

What is Pernicious Anemia, and what etiology leads to its development?

Pernicious Anemia is a severe macrocytic normochromic anemia caused by Intrinsic Factor (IF) deficiency—most commonly due to autoimmune Type A chronic atrophic gastritis with antibodies against parietal cells and IF—preventing Vitamin B12 absorption in the ileum.

What genetic mutation causes Sickle Cell Anemia, and what characteristic inclusions are seen on peripheral blood smear?

An autosomal recessive point mutation producing Hemoglobin S (HbS) instead of HbA. Peripheral blood smears demonstrate sickled erythrocytes and Howell-Jolly bodies.

What cellular inclusion is pathognomonic for Acute Myelogenous Leukemia (AML) on bone marrow biopsy?

Auer Rods (abnormal, red-staining, rod-like granule inclusions inside immature myeloblasts).

What is the most common cancer in children aged 2–4 years, and what cell type predominates?

Acute Lymphocytic Leukemia (ALL), characterized by malignant proliferation and accumulation of immature lymphoblasts.

What characteristic cell finding on peripheral blood smear is associated with Chronic Lymphocytic Leukemia (CLL)?

Smudge cells (fragile leukemic lymphocytes that disintegrate during slide preparation).

What genetic translocation defines Chronic Myelogenous Leukemia (CML), and what targeted therapy is prescribed?

The Philadelphia chromosome, a $t(9;22)$ reciprocal translocation creating the BCR-ABL1 fusion gene; treated with Imatinib (Gleevec) to inhibit BCR-ABL kinase activity.

What specific cell type undergoes malignant proliferation in Multiple Myeloma, and what bone abnormalities result?

Malignant plasma cells proliferate in the bone marrow, secreting IL-6 which activates RANKL and osteoclasts, producing osteolytic "punched-out" bone lesions and severe hypercalcemia.

What distinct giant cell type is required on lymph node biopsy to diagnose Hodgkin Lymphoma?

Reed-Sternberg cells (large multinucleated B-lineage cells, frequently infected with latent Epstein-Barr Virus).

What genetic mutation, viral association, and classic biopsy pattern characterize Burkitt Lymphoma?

Translocation of the myc gene, association with latent Epstein-Barr Virus (EBV) infection, and a pathognomonic "starry sky" appearance on biopsy.