Pathophysiology Review: Integumentary, Endocrine, and Fluid & Electrolyte Disorders

Flashcard practice set covering Integumentary Disorders, Endocrine Pathologies, and Fluid, Electrolyte, & Acid-Base Homeostasis.

What are macular stains commonly known as, and where do they typically appear on an infant?

Commonly known as angel's kisses or stork bites, macular stains are flat, light red vascular birthmarks that typically appear around the eyelids, on the forehead, baby's nose, or upper and lower lips.

What are the two types of hemangiomas and their characteristic visual appearances?

Superficial hemangiomas occur on the surface of the skin as bright red patches with a strawberry appearance (rough texture). Deep hemangiomas occur below the surface of the skin and are usually red or bluish.

What is a port-wine stain (nevus flammeus), and what condition is indicated by its presence on the face?

A port-wine stain (nevus flammeus) is a flat purple to dark red capillary malformation that darkens and thickens over time without vanishing. A facial port-wine stain is a sign of Sturge-Weber syndrome.

What number and size threshold of café-au-lait spots suggest neurofibromatosis?

Having several café-au-lait spots larger than a quarter can be an indicator of neurofibromatosis.

Where are Mongolian spots typically located, and what is their clinical progression?

Mongolian spots (congenital dermal melanocytosis) are flat, bluish-gray patches that look like bruises, commonly found on the buttocks and lower back. They require no treatment and usually vanish when the child reaches school age.

What vision changes are associated with albinism?

Vision changes in albinism include nystagmus, strabismus, extreme nearsightedness or farsightedness, photophobia, astigmatism, and functional blindness.

What is vitiligo, and how does it develop on the body?

Vitiligo is an autoimmune disease where melanin-producing cells die, causing slowly enlarging white patches of hypopigmentation with irregular shapes. It usually develops on sun-exposed areas first.

What is the timing and manifestation of allergic contact dermatitis?

Allergic contact dermatitis is a Type IV cell-mediated hypersensitivity reaction where symptoms appear $24 - 48\text{ hours}$ after exposure as pruritus (itching), erythema (redness), edema, and small vesicles (blisters).

Which chronic inflammatory skin condition is characterized by thick red patches covered by flaky, silver-white scales?

Psoriasis.

What are the characteristic sores seen in impetigo, and what organisms cause them?

Impetigo manifests as red sores on the face (especially around the nose and mouth), hands, and feet that burst and develop honey-colored crusts. It is typically caused by Staphylococcus aureus or Streptococcus pyogenes.

What are the late local physical signs of necrotizing fasciitis?

Late local signs include bronze-purple discoloration, blistering, crepitus, drainage, and tracking of erythema or tenderness.

How does Herpes Zoster (shingles) physically present on the body?

Herpes Zoster presents as a painful, red or silvery vesicular rash that develops in a linear course along the path of a sensory nerve (on one side of the head or torso).

According to the Rule of Nines for estimating burn surface area in adults, what percentages are assigned to each body region?

Head and neck: $9\%$, Each upper limb: $9\%$ (total $18\%$), Front of trunk: $18\%$, Back of trunk and buttocks: $18\%$, Front of legs: $18\%$, Back of legs: $18\%$, Perineum: $1\%$.

What distinguishes third-degree (full thickness) burns from lower-degree burns regarding sensation and visual appearance?

Third-degree burns extend through all three skin layers, presenting with a leathery surface colored black, brown, tan, red, or white. Patients feel no pain at the site because pain receptors, sweat glands, hair follicles, and blood vessels are destroyed.

What are the ABCD rules for detecting suspicious skin cancer features?

A = Asymmetry (one side does not match the other), B = Border irregularity (jagged or blurred), C = Color variations (shades of black, brown, tan, white, red, or blue), D = Diameter larger than $6\text{ mm}$.

What are the distinguishing characteristics of Basal Cell Carcinoma, Squamous Cell Carcinoma, and Malignant Melanoma?

Basal Cell Carcinoma arises from the stratum basale as a shiny, pearly bump with a central depression; Squamous Cell Carcinoma arises from stratum spinosum keratinocytes as a raised, scaly, concave ulcer; Malignant Melanoma arises from melanocytes as a rapidly metastasizing, irregular brown/black patch or changing mole.

What is the primary distinction between endocrine and exocrine glands?

Endocrine glands release chemical substances (hormones) directly into the bloodstream or body tissues without ducts. Exocrine glands release enzymes through ducts to another organ or outside the body.

What six major tropic hormones are secreted by the anterior pituitary gland?

1. Thyroid-stimulating hormone (TSH), 2. Adrenocorticotropin (ACTH), 3. Prolactin (PRL), 4. Growth hormone (GH), 5. Follicle-stimulating hormone (FSH), 6. Luteinizing hormone (LH).

Where are oxytocin and Antidiuretic Hormone (ADH) produced and stored?

Oxytocin and ADH are produced by the hypothalamus and stored in and released from the posterior pituitary gland.

How does Pituitary Dwarfism differ from Achondroplasia?

Pituitary Dwarfism is a rare condition caused by growth hormone deficiency from the anterior pituitary, producing a small but proportionate body structure. Achondroplasia is a non-pituitary genetic mutation causing disproportionate dwarfism.

What are the key clinical contrasts between Diabetes Insipidus (DI) and Syndrome of Inappropriate Antidiuretic Hormone (SIADH)?

Diabetes Insipidus involves low ADH causing massive polyuria, dehydration, and hypernatremia ('Dry Inside'). SIADH involves excessive ADH causing low urine output ($< 30\text{ cc/hr}$), fluid volume overload, hyponatremia, and cerebral edema ('Soaked Inside').

What clinical manifestations differentiate Hypothyroidism from Hyperthyroidism (Grave's Disease)?

Hypothyroidism presents with a hypometabolic state: bradycardia, hypotension, weight gain, cold intolerance, dry skin, and constipation. Hyperthyroidism presents with a hypermetabolic state: tachycardia, hypertension, weight loss, heat intolerance, diaphoresis, diarrhea, goiter, and exophthalmos (bulging eyes).

What life-threatening complications can occur in severe Hypothyroidism and Hyperthyroidism?

Hypothyroidism can progress to Myxedema Coma (generalized edema, severe hypotension, hypothermia, hyponatremia, bradycardia). Hyperthyroidism can progress to Thyroid Storm / Thyrotoxicosis (fever up to $105^\circ\text{F}$, acute dehydration, extreme tachycardia, heart failure).

How do Parathyroid Hormone (PTH) and Calcitonin regulate serum calcium levels?

When serum calcium is low, Parathyroid Hormone (PTH) is released to draw calcium from bones, increase renal reabsorption, and increase GI absorption. When serum calcium is high, Calcitonin is released by the thyroid to inhibit bone calcium loss and decrease serum calcium levels.

What cluster of risk factors defines Metabolic Syndrome?

Metabolic Syndrome requires a cluster of 3 or more of: 1. Hyperglycemia (insulin resistance), 2. High blood pressure ($> 130/85\text{ mmHg}$), 3. Hypercholesterolemia / high triglycerides, 4. Low HDL cholesterol, 5. Increased waist circumference ($> 40\text{ inches}$ in men, $> 35\text{ inches}$ in women).

What are the classic '3 P's' of Diabetes Mellitus and their underlying causes?

1. Polyuria: increased urine output caused by osmotic diuresis from glucosuria. 2. Polydipsia: excessive thirst caused by intracellular and intravascular dehydration. 3. Polyphagia: excessive hunger triggered by cellular starvation.

How do the etiologies and treatments of Type 1 DM and Type 2 DM differ?

Type 1 DM is an autoimmune destruction of pancreatic beta cells causing absolute insulin deficiency, requiring lifelong exogenous insulin injections. Type 2 DM involves target cell insulin resistance and progressive beta cell dysfunction, managed by lifestyle modifications, oral medications, and sometimes insulin.

What laboratory findings confirm Diabetic Ketoacidosis (DKA)?

Blood glucose $> 250 - 500\text{ mg/dL}$, arterial \t{pH} < 7.30, serum/urine ketones positive, bicarbonate \t{HCO}_3^- < 15\text{ mEq/L}, elevated anion gap, and hyperkalemia.

What are the 'Five Hs' of Pheochromocytoma attacks?

1. Hypertension, 2. Headache, 3. Hyperhidrosis (sweating), 4. Hypermetabolism, 5. Hyperglycemia.

How is total body water divided according to the 'Rule of Thirds' in an average $70\text{ kg}$ adult?

Total body water is $42\text{ L}$ ($2/3$ of body weight). $2/3$ ($28\text{ L}$) is Intracellular Fluid (ICF) and $1/3$ ($14\text{ L}$) is Extracellular Fluid (ECF), which subdivides into Interstitial fluid ($9.5\text{ L}$), Plasma ($3.5\text{ L}$), and Transcellular fluid ($1\text{ L}$).

How do Isotonic, Hypotonic, and Hypertonic solutions affect red blood cell volume?

Isotonic solutions ($0.9\%\text{ NaCl}$, Lactated Ringer's) cause no fluid shifts. Hypotonic solutions ($0.45\%\text{ NaCl}$, $D_5W$) shift fluid into cells causing them to swell and lyse. Hypertonic solutions ($5\%\text{ Dextrose in Normal Saline}$, $3\%$ or $5\%\text{ NaCl}$) draw fluid out of cells causing them to shrink.

What is the distinction between sensible and insensible fluid losses?

Sensible losses can be seen and measured (urination, defecation, wound drainage, emesis). Insensible losses cannot be directly measured (evaporation from skin/sweating, respiratory loss from lungs).

How does the Renin-Angiotensin-Aldosterone System (RAAS) increase blood volume and pressure?

A drop in renal perfusion causes kidneys to release renin, converting angiotensinogen to Angiotensin I. ACE in lungs converts Angiotensin I to Angiotensin II, causing systemic vasoconstriction and stimulating the adrenal cortex to secrete Aldosterone. Aldosterone causes the kidneys to retain \t{Na}^+ and water while excreting \t{K}^+.

What are the primary intracellular and extracellular cations and anions?

Chief intracellular cation: Potassium ($\text{K}^+$); Chief intracellular anion: Phosphate ($\text{PO}_4^{2-}$). Chief extracellular cation: Sodium ($\text{Na}^+$); Chief extracellular anion: Chloride ($\text{Cl}^-$).

What are the normal serum ranges for Sodium, Potassium, Calcium, and Magnesium?

Sodium ($\text{Na}^+$): $135 - 145\text{ mEq/L}$. Potassium ($\text{K}^+$): $3.5 - 5.0\text{ mEq/L}$ (or $3.5 - 5.5\text{ mEq/L}$). Total Calcium ($\text{Ca}^{2+}$): $9.0 - 11.0\text{ mg/dL}$. Magnesium ($\text{Mg}^{2+}$): $1.5 - 2.5\text{ mEq/L}$ (or $1.8 - 3.0\text{ mEq/L}$).

What EKG changes distinguish Hyperkalemia from Hypokalemia?

Hyperkalemia features tall, peaked T waves, widened QRS complexes, prolonged PQ intervals, and flat P waves. Hypokalemia features flattened T waves, ST-segment depression, prolonged PR intervals, and prominent U waves.

What are Chvostek's sign and Trousseau's sign, and what electrolyte deficits do they indicate?

Chvostek's sign is facial twitching when tapping the facial nerve; Trousseau's sign is carpopedal spasm induced by blood pressure cuff inflation. Both indicate Hypocalcemia and Hypomagnesemia.

What are the normal arterial blood gas (ABG) values for pH, PaCO2, and HCO3-?

\t{pH}: $7.35 - 7.45$ (perfect $7.4$); \t{PaCO}_2: $35 - 45\text{ mmHg}$; \t{HCO}_3^-: $22 - 26\text{ mEq/L}$.

How do the respiratory and renal systems regulate arterial pH?

The respiratory system regulates \t{CO}_2 (an acid) by altering ventilation rate/depth (fast response, temporary). The renal system regulates \t{H}^+ (acid) and \t{HCO}_3^- (base) excretion or retention (slow response, long-lasting).

How do Hydrogen (H+) and Potassium (K+) ions interact across cell membranes during Acidosis and Alkalosis?

In Acidosis, excess extracellular \t{H}^+ ions move into cells, forcing \t{K}^+ out into the bloodstream, resulting in hyperkalemia. In Alkalosis, \t{H}^+ moves out of cells, forcing \t{K}^+ into cells, resulting in hypokalemia.

What criteria distinguish uncompensated from compensated acid-base disorders on an ABG?

Uncompensated disorders have an abnormal \t{pH} and only ONE abnormal component (\t{PaCO}_2 OR \t{HCO}_3^-). Compensated disorders have both \t{PaCO}_2 AND \t{HCO}_3^- out of range as the opposing organ adjusts to bring \t{pH} back toward normal.

What ABG profile indicates uncompensated Respiratory Acidosis?

\t{pH} < 7.35, \t{PaCO}_2 > 45\text{ mmHg}, and normal \t{HCO}_3^- ($22 - 26\text{ mEq/L}$).

What ABG profile indicates uncompensated Metabolic Acidosis, and how does the body compensate?

Uncompensated Metabolic Acidosis: \t{pH} < 7.35, normal \t{PaCO}_2 ($35 - 45\text{ mmHg}$), and \t{HCO}_3^- < 22\text{ mEq/L}. The body compensates by hyperventilating (Kussmaul respirations) to blow off excess \t{CO}_2 acid.