Diabetes, Integumentary, Eye, and Hearing Disorders

Vocabulary-style flashcards generated from lecture notes covering Diabetes Mellitus, Integumentary Function, Dermatologic Disorders & Wounds, Eye & Vision Disorders, and Hearing & Balance Disorders.

Diabetes Mellitus

A chronic metabolic disorder of glucose metabolism characterized by persistent hyperglycemia resulting from insulin deficiency, insulin resistance, or both.

Beta Cells → Insulin

Pancreatic islet cells responsible for synthesizing and secreting insulin to lower blood glucose levels.

Alpha Cells → Glucagon

Pancreatic islet cells responsible for producing glucagon to raise blood glucose levels.

Insulin Physiological Actions

Lowers blood glucose by facilitating cellular glucose uptake, promoting glycogen and fat/protein storage, and inhibiting hepatic glucose production.

Glucagon Physiological Actions

Increases blood glucose levels by stimulating glycogenolysis and gluconeogenesis in the liver.

Type 1 Diabetes Mellitus Etiology

An autoimmune disorder characterized by destruction of pancreatic beta cells, resulting in severe or complete endogenous insulin deficiency.

Type 2 Diabetes Mellitus Etiology

A chronic metabolic disorder characterized by peripheral insulin resistance paired with a progressive decline in pancreatic beta-cell insulin secretion.

Acute Complication Predisposition by Diabetes Type

Type 1 diabetes predisposes primarily to Diabetic Ketoacidosis (DKA), whereas Type 2 diabetes predisposes primarily to Hyperglycemic Hyperosmolar State (HHS).

Osmotic Diuresis in Diabetes

Excess serum glucose exceeds the renal threshold, spilling into the urine and osmotically pulling water and electrolytes, leading to severe polyuria and dehydration.

Gestational Diabetes Cause

Placental hormones inducing insulin resistance during pregnancy, typically developing in the second or third trimester.

Gestational Diabetes Complications & Risks

Includes large-for-gestational-age infants, maternal/neonatal birth complications, and an increased future maternal risk of developing Type 2 diabetes.

Classic Triad of Diabetes Symptoms (3 P's of Hyperglycemia)

Polyuria (excessive urination), Polydipsia (excessive thirst), and Polyphagia (excessive hunger).

Polyuria Mechanism in Hyperglycemia

Elevated blood glucose levels exceed renal reabsorption capacity, causing glucosuria and osmotic fluid excretion.

Polydipsia Mechanism in Hyperglycemia

Intracellular dehydration and fluid loss secondary to osmotic diuresis trigger the hypothalamic thirst center.

Polyphagia Mechanism in Diabetes

Cellular starvation caused by the body's inability to transport glucose into cells due to insulin deficiency or resistance.

General Manifestations of Diabetes Mellitus

Fatigue, blurred vision, delayed wound healing, recurrent infections, and unintentional weight loss (most prominent in Type 1 DM).

A1C

A diagnostic blood test measuring average glycemic control over approximately $2–3\,\text{months}$; monitored at least twice yearly when stable.

Ketone Testing Indications

Indicated during acute illness, stress, or persistent hyperglycemia, particularly in patients with Type 1 diabetes.

Insulin Therapy

Type 1 needs insulin for life but Type 2 may require insulin temporarily or long term.

Rapid acting insulin

right before meals (fastest), Lispro (humolog), Aspart (Novolog), or Glulisine (Apidra). Onset is 10-30 minutes. Peak is 30 minutes to 3 hours. Duration is 3-5 hours.

Short acting

Regular ( Humulin R, Novolin R) insulin. Onset is 30-60 minutes, peak is 2-5 hours, and duration is 5-8 hours.

Intermediate acting

insulin, such as NPH (Humulin N, Novolin N). Onset is 1-2 hours, peak is 4-12 hours, and duration is 10-16 hours.

Long-acting insulin

insulin, such as Glargine (Lantus) or Detemir (Levemir). Onset is 1-2 hours, no peak, and duration is up to 24 hours.

Rapid-Acting Insulin Administration Timing

Must be administered within $5–15\,\text{minutes}$ prior to meal consumption due to its rapid onset.

DKA

• Insulin deficiency

• Ketones + metabolic acidosis

• More common Type 1

HHS

• Severe hyperglycemia + dehydration

• Minimal/absent ketosis

• More common Type 2

Hypoglycemia Diagnostic Threshold

Defined as a blood glucose level $<70\,\text{mg/dL}$.

Adrenergic symptoms

SNS response to low blood glucose, including sweating, shaking, and palpitations.

Neuroglycopenic

Neuro response to low blood glucose leading to confusion, weakness, and dizziness.

Rule of 15 for Conscious Hypoglycemia

Administer $15\,\text{g}$ of fast-acting carbohydrate, wait $15\,\text{minutes}$, recheck blood glucose, repeat if still $<70\,\text{mg/dL}$, and follow with a complex carbohydrate/protein snack or meal.

Emergency Management of Unconscious Hypoglycemia

Administer subcutaneous or intramuscular glucagon in outpatient settings, or intravenous dextrose in hospital settings; never give oral fluids or foods.

Diabetic Ketoacidosis (DKA) Key Features

Type 1, Severe hyperglycemia, profound dehydration/electrolyte loss, fat breakdown yielding serum ketones, and metabolic acidosis. Blood glucose > 200

Clinical Manifestations of DKA

Polyuria, polydipsia, nausea/vomiting, abdominal pain, fruity breath odor, Kussmaul respirations, dehydration, and altered level of consciousness.

Kussmaul Respirations

Deep, rapid respiratory pattern functioning as a metabolic compensatory mechanism to exhale carbon dioxide and alleviate ketoacidosis.

First Priority Intervention for DKA

Intravenous isotonic fluid resuscitation to restore intravascular volume, tissue perfusion, and renal function.

Potassium Management Priority in DKA

Monitor serum potassium closely and replace prior to or during insulin therapy, as regular IV insulin drives potassium into cells, predisposing to dangerous hypokalemia.

Hyperglycemic Hyperosmolar State (HHS) Key Features

Usually type 2. Gradual onset. Extremely high blood glucose, severe dehydration, elevated serum osmolality, and minimal or absent ketosis. Profound dehydration, neurologic changes, weakness, seizures/coma. Blood glucose > 600

Primary Clinical Distinctions Between DKA and HHS

DKA features ketoacidosis, metabolic acidosis, and Kussmaul respirations (mostly Type 1), whereas HHS features marked hyperosmolar dehydration without ketoacidosis (mostly Type 2).

HHS Primary Treatment Priorities

Aggressive IV fluid rehydration, intravenous regular insulin administration, and electrolyte replacement.

Macrovascular Complications of Diabetes

Large blood vessel disease leading to coronary artery disease (CAD/MI), cerebrovascular disease (stroke), and peripheral arterial disease (PAD).

Microvascular Complications of Diabetes

Small blood vessel damage leading to diabetic retinopathy, diabetic nephropathy

Neuropathy complications of diabetes

Peripheral and autonomic

Diabetic Peripheral Neuropathy Presentation

Progressive sensory impairment, numbness, tingling, burning pain, and diminished temperature/pain perception occurring in a stocking-glove distribution.

Diabetic Autonomic Neuropathy Manifestations

Orthostatic hypotension, gastroparesis, neurogenic bladder dysfunction, erectile dysfunction, and hypoglycemia unawareness.

Gastroparesis in Diabetes

Autonomic nerve damage delaying stomach emptying, resulting in nausea, vomiting, bloating, and unpredictable blood glucose fluctuations.

Hypoglycemia Unawareness

Absence of autonomic warning signs (tremors, sweating, tachycardia) prior to the onset of severe neuroglycopenic symptoms, common in long-standing diabetes.

Pathophysiologic Factors in Diabetic Foot Ulceration

Sensory neuropathy (unfelt injury), autonomic neuropathy (dry/cracked skin), motor neuropathy (foot deformities), peripheral arterial disease (ischemia), and hyperglycemia (impaired healing/infection).

High-Risk Factors for Diabetic Foot Ulcers

Peripheral neuropathy, peripheral arterial disease, foot deformities, corns/calluses, history of prior ulcer or amputation, smoking, and poor glycemic control.

Monofilament Test

A diagnostic screening tool using a standard sensory nylon monofilament to detect loss of protective sensation in the diabetic foot.

Daily Diabetic Foot Inspection Teaching

Inspect all surfaces of both feet daily (including soles and between toes, using a mirror if necessary) for cuts, blisters, redness, or swelling.

Daily Diabetic Foot Hygiene Guidelines

Wash feet daily in warm water, dry thoroughly between toes, apply lotion to tops and bottoms of feet (never between toes), and trim nails straight across.

Footwear Guidelines for Diabetic Patients

Never walk barefoot, wear properly fitted shoes and seamless socks, inspect inside shoes before putting them on, and avoid heating pads or hot water bottles.

Surgical Stress Response Effect on Blood Glucose

Surgical stress elevates counter-regulatory hormones (epinephrine, cortisol, glucagon, growth hormone), leading to significant hyperglycemia and potential DKA in Type 1 DM.

Perioperative Blood Glucose Target Range

Target glucose range maintained between $100–180\,\text{mg/dL}$ for hospitalized surgical patients.

Basal Insulin Management in NPO Surgical Patients

Basal insulin must never be completely eliminated in Type 1 DM patients while NPO, as withholding basal insulin precipitates DKA.

Management of Diabetic Patients on Enteral Tube Feedings

Continue basal insulin and administer short-acting insulin as ordered; if tube feedings are abruptly held, immediately monitor glucose and administer IV dextrose to prevent severe hypoglycemia.

Diabetic Retinopathy Clinical Signs

Retinal microvascular damage presenting with blurred vision, floaters, cobwebs, spotty vision loss, or sudden painless visual impairment.

Diabetic Retinopathy Prevention Measures

Strict glycemic control, blood pressure and lipid control, and routine annual dilated ophthalmologic examinations.

Diabetic Dermopathy ('Shin Spots')

Small-vessel cutaneous disorder appearing as hyperpigmented, dull red papules that progress to brown patches on the lower anterior legs.

Mechanisms Increasing Skin Infection Risk in Diabetes

Impaired tissue perfusion, reduced immune response, sensory loss leading to unrecognized skin breakdown, and elevated tissue glucose levels favoring pathogen growth.

Skin functions

• Protection/barrier

• Sensation

• Fluid balance

• Temperature regulation

• Vitamin D production

• Immune response

Epidermis

The thin, avascular outermost skin layer containing keratinocytes and melanocytes, functioning as a protective physical barrier.

Dermis

The vascular middle skin layer containing collagen, elastic fibers, blood and lymph vessels, nerves, hair follicles, and sweat/sebaceous glands.

Subcutaneous Tissue (Hypodermis)

The innermost skin layer composed of adipose and connective tissue providing thermal insulation, shock absorption, and structural protection.

Cyanosis Assessment

Evaluated at oral mucosa and conjunctiva; presents as bluish discoloration in light skin and gray/dull appearance in dark skin due to reduced oxygenation.

Erythema Assessment

Red, pink, or purple-gray skin discoloration caused by capillary dilation and inflammation, evaluated by inspecting color changes and localized warmth.

Macule vs. Patch

Flat, nonpalpable skin color changes differentiated by size: a macule is $<1\,\text{cm}$ and a patch is $>1\,\text{cm}$.

Papule vs. Plaque

Solid raised skin lesions differentiated by size: a papule is $<0.5\,\text{cm}$ and a plaque is $>0.5\,\text{cm}$.

Vesicle vs. Bulla

Elevated, fluid-filled skin lesions differentiated by size: a vesicle is $<0.5\,\text{cm}$ and a bulla is $>0.5\,\text{cm}$.

Erosion

Superficial loss of epidermis, often resulting from friction or injury, that does not penetrate into the dermis.

Ulcer

Deeper loss of skin layers, extending into the dermis or beyond, often resulting from pressure, infection, or poor circulation.

Fissure

A narrow slit or crack in the skin that can be painful and may bleed, often caused by dryness or inflammation.

Skin turgor

A measure of skin's elasticity and hydration, often assessed by pinching the skin and observing how quickly it returns to its normal position. Naturally decreases with age.

Edema

swelling caused by excess fluid accumulation in the tissues, often associated with injury, inflammation, or medical conditions.

Clubbing of Nails

Nail plate distortion characterized by a nail angle $\ge 180^\circ$ and a spongy nail base, indicative of chronic hypoxia or pulmonary disease.

Spoon Nails (Koilonychia)

Concave deformity of the nail bed associated with severe, chronic iron-deficiency anemia.

Pitting

of Nails is the presence of small depressions or indentations on the surface of the nails, often associated with psoriasis or other dermatologic conditions.

Beau Lines

Transverse ridges or depressions across the nail plate resulting from temporary arrest of nail matrix growth during severe systemic illness or trauma.

Paronychia

Redness/tenderness around nail

Age-Related Structural Changes of Skin

Thinning of epidermis and dermis, loss of collagen and subcutaneous fat, decreased sweat/sebaceous gland activity, leading to dry, fragile skin prone to tears and bruising.

Common Benign Skin Changes With Aging

• Xerosis → dry skin

• Wrinkles

• Solar lentigines → “liver spots”

• Cherry angiomas

• Seborrheic keratoses

• Telangiectasias

• Uneven pigmentation

• ↓ hair growth

Stasis Dermatitis

Erythematous, scaly, itchy, hyperpigmented skin changes on the lower legs caused by chronic venous insufficiency, predisposing to venous leg ulcers.

Folliculitis

caused by bacteria, leading to symptoms such as redness, swelling, pain, and sometimes pus formation. Common types include cellulitis and impetigo.

Furuncles

Painful nodules resulting from infected hair follicles, commonly known as boils. They can cause redness, swelling, and sometimes drainage of pus.

Carbuncles

A cluster of furuncles that are interconnected, resulting in a larger, painful area of infection. Carbuncles typically involve deeper layers of skin and can cause systemic symptoms such as fever.

Candida

A fungal infection caused by the Candida species, often affecting moist areas of the skin and mucous membranes. It can lead to thrush, vaginitis, and skin rashes.

Infection prevention with skin infections

• Gloves for draining/open lesions

• Standard precautions

• Proper dressing disposal

• Handwashing before and after care

• Patient education on hygiene

Debridement

A medical procedure that involves the removal of dead, damaged, or infected tissue from a wound to promote healing and prevent infection.

Autolytic Debridement

Removal of necrotic wound tissue using the body's own enzymes beneath a moist, occlusive dressing.

Enzymatic Debridement

Removal of devitalized tissue through topical application of prescribed chemical proteolytic agents such as collagenase.

Pressure injury risk factors

• Immobility

• ↓ sensation/LOC

• Poor nutrition

• Moisture/incontinence

• Friction/shear

• Poor perfusion

• Advanced age

• Diabetes/PVD

• Medical devices

Assess with Braden Scale

Stage 1 Pressure Injury

Localized area of intact skin with nonblanchable erythema, potentially presenting with changes in temperature, firmness, or localized pain.

Stage 2 Pressure Injury

Partial-thickness loss of skin with exposed dermis, presenting as a pink/red moist wound bed or an intact/ruptured serum-filled blister.

Stage 3 Pressure Injury

Full-thickness loss of skin with visible adipose tissue, granulation tissue, and potential epibole, undermining, or tunneling.

Stage 4 Pressure Injury

Full-thickness skin and tissue loss with directly visible or palpable fascia, muscle, tendon, ligament, cartilage, or bone.

Unstageable Pressure Injury

Full-thickness tissue loss where the true depth of tissue damage within the wound bed is completely obscured by slough or eschar.

Deep Tissue Pressure Injury (DTPI)

Intact or non-intact skin with persistent, nonblanchable deep red, maroon, or purple discoloration, or a blood-filled blister resulting from severe pressure and shear.

Positioning Measures for Pressure Injury Prevention

Reposition bedbound patients at least every $2\,\text{hours}$, position at a $30^\circ$ side-lying angle, off-load heels completely, and limit head-of-bed elevation to $30^\circ$. Keep skin clean/dry. Manage incontinence. Inspect skin frequently. Avoid prolonged pressure on bony prominences.

Seborrheic dermatitis

A common skin condition causing scaly patches, red skin, and stubborn dandruff, usually occurring on the scalp, face, and upper body.

Impetigo Presentation & Etiology

Highly contagious superficial bacterial skin infection (Staphylococcus or Streptococcus) featuring thin-walled vesicles that rupture to form honey-yellow crusts.