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93 Cards in this Set
- Front
- Back
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plaque
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elevated, firm and rough lesion with flat top surface like in psoriasis
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papule
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circumscribed firm < 1 cm like with elevated moles
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macule
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flat mole
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vesicle
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chicken pox, herpes; does not extend into dermis and fluid with serous fluid
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pustule
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similar to a vesicle but filled with a purulent fluid – acne, impetigo
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cyst
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encapsulated elevated lesion; in the dermis filled with liquid or semisolid material – sebaceous cyst
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keloid
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irregular shaped elevated progressively enlarging scar that grows beyond the boundaries of the wound; caused by excessive collagen formation during healing
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ulcer
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loss of epidermis and dermis; concave; varies in size i.e. decubitus or stasis ulcers
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What is the most significant cause of pressure ulcer
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Interruption of blood flow to and from the skin or deeper tissue
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Stage 1
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– nonblanchable redness over bony prominence
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Stage 2
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– partial thickness skinloss involving epidermis or dermis shallow open ucler with a red pink wound bed serum filled blister sometimes also
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Stage 3
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– full thickness skin loss with damge or necrosis of subcutaneous tissue that may extend to the fascia may include tunneling
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Stage 4
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– full thickness skin loss with extensive destruction, tissue necrosis, or damage to muscle bone or supporting structures
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• Peripheral itch mediators
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– Neuropeptides
– Serotonin – Prostaglandins – Bradykinin – Histamine |
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itch sensation is carried by
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specific unmyelinated C-nerve fibers
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allergic contact dermatitis
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– T cell mediated or delayed hypersensitivity
– Allergens are the irritant with a response of cytokines, cytotoxins and natural killer cells – Treatment steroids; REMOVE OFFENDING AGENT – Inflammatory Skin Disorders |
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Allergen plus a carrier protein is sent to the skin
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; this forms a hapten-specific sensitizing antigen. Langerhans cells process the antigen and carry it to T cells that then become sensitized to the antigen and release cytokines and chemokines leading to leukocyte infiltration and inflammation
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Seborrheic Dermatitis
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– Chronic inflammation of scalp, eyebrows, eyelids, ear canals, nasolabial folds, axillae, chest and back
YEAST....use topical corticosteriods |
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Psoriasis characteristics
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T cell mediated autoimmune disease
• Dermis/epidermis thickened – with cellular hyperproliferation – Altered keratinocyte differentiation – Expanded vasculature – Infiltration of neutrophils – inflammation |
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epidermis psoriasis characteristics
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• Shedding epidermis q3-4 days
• Not enough time for keratinization or cell maturation – Loose cohesive keratin with a silvery scaly appearance |
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how often is skin normally shed?
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26 days
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Lyme Disease
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spirochete Borrelia
• Localized infection – Soon after bite – Erythema, fever, fatigue, malaise |
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What is the latent stage of lyme disease
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– Arthritis, encephalopathy, polyneuropathy
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Hydrouteter
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– Dilation of ureter and pelvicaliceal system....
blockage below which leads to accumulation above |
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how does obstruction lead to Tubular Fibrosis
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. This increased pressure reaches the glomerulus which decreases filtration. This ongoing dilatation leads to enlargement of tubulointersitial fibrosis…
The deposit of extracellular matrix is countered by its breakdown from metalloproteinases. This imbalance leads to loss of functioning nephrons and kidney damage |
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How long does kidney damage take
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Detectable damage within 7 days in the distal renal tubule; by 14 days both distal and proximal aspects of nephron have been affected; by 28 days glomeruli damage is present
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• Affected kidney unable to conserve
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– Sodium
– Bicarb – Water |
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affected kidney unable to excrete
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– Potassium
– Hydrogen |
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kidney damage from obstruction leads to
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leads to metabolic acidosis and dehydration
How bad the kidney damage is depends on the longevity and severity of the obstruction |
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• Compensatory Hypertrophy and Hyperfunction
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THIS IS WHY WE CAN LIVE WITH ONE kidney
– Kidney can partially counteract the negative results of unilateral obstruction – Via obligatory growth and compensatory growth processes – Processes cause unobstructed kidney to increase glomeruli and tubules but not total number of functioning nephrons |
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Postobstructive diuresis
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follows any resolution of obstruction and is the body’s way of restoring electolyte and fluid balance
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risk factors for kidney stones
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– Age
– Gender – Fluid intake – Diet • Geographic location can also be a risk factor because of specific temperatures, humidity and rain fall |
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What are kidney stones made of
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• Calcium oxalate/phosphate
– 70-80% – Idiopathic calcium urolithiasis • Struvite (magnesium, ammonium) – 15% – In presence of UTI • Uric Acid – 7% – Gouty arthritis Calcium stones = hypercalcuria, mild RTN, crystal growth inhibitor deficiency UTI due to Klebsiella, Pseudomonas most common |
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Most common type of UTI
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cystitis
• 85% cases E. coli; 10% cases Staphylococcus; Less common klebsiella, proteus • Fungal Candida • Depend on 2 factors – Host defense mechanism and virulence of uropathogen |
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Rhabdomyolysis
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• Severe muscle trauma with muscle cell loss
• Excess of myoglobin in urine (myoglobinuria) – Compartment Syndromes – Crush Syndrome • CK released in large amounts Muscle cell damage releases the myoglobin |
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causes of rhabdo
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Other causes can be malignant hyperthermia, infection, snakebite, statins, long distance runners with excessive muscle activity
ETOH and drug |
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• Osteoporosis
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– Porous bone
– Density of bone decreased and therefore structural integrity of bone impaired • Type 1 – Postmenopausal – Senile • Type 2 – from drugs/another disease process |
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IGF helps in
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fracture healing and collagen synthesis; these levels decline by age 60…excessive phosphorus in sodas and junk food also interrupt calcium-phosphorus balance making bones more brittle
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What type of drugs lead to osteoporosis
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in people receiving large doses of heparin (promotes bone resorption), steroids for RA
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– Normal bone density
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>833
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– Osteopenia (decreased bone mass) bone density
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648 – 833 mg/cm2
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– Osteoporosis bone density
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<648
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Risk factors for osteoporosis
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white and asian and female
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Regional osteoporosis
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confined to one area; has a known cause. Associated with limb immobilization with a negative calcium balance that continues as long as immobilization occurs
....broken bone |
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osteoclasts
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differentiated cells that function to resorb bone.
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• Glucocorticoid induced osteoporosis
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– Steroids increase RANKL expression and inhibit OPG production by osteoblasts
– Immunosuppressive drugs (antirejection) also alter RANKL/OPG system |
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age related osteoporosis
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– Begins in 4th decade
– Decreased serum GH and IGF with increased binding of RANKL and decreased OPG affect osteoblast/osteoclast function |
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• Endogenous osteomylitis
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blood to bone. bacteremic to blood i.e. sinus, ear and dental infections which are the primary source; in adults spine and pelvis common
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exogenous osteomylitis
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outside to bone. surgical procedures, open wounds – human and animal bites, fists to the mouth
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treatment for osteomyelitis
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antibiotics and debridement; hyperbaric oxygen also used to treat osteomyelitis
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osteoarthritis
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• Age related disorder of synovial joints
• Local area of loss and damage of articular cartilage |
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Osteophytosis
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new bone formation of joint margins
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Hallmark finding of OA
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loss of articular cartilage – likely through enzymatic breakdown of the cartilage matrix where it begins with destruction of proteoglycans and collagen fibers.
– EARLY – loses its glistening appearance – PROGRESSION – loss of surface area and fissures called fibrillations develop; thin or absent leaving subchrondral bone unprotected – Cysts may develop – Cartilage coated osteophytes alter bone contours and joint anatomy = synovitis and effusion |
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Ankylosing Spondylitis
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• Chronic inflammatory joint disease
– Stiffening and fusion of the spine and SI joints – Inflammation primary process – Enthesis point of destruction – Fibrosis, ossification, joint fusion |
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Enthesis
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point at which ligaments, tendons and the joint capsule are inserted into the bone
With this HLA-B27 there is a suggestive genetic component and can also be measured in the blood and used as diagnosis |
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most common thyroid problem
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hypothyroidism
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primary hypothyroid
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Defective hormone synthesis from autoimmune thyroiditis, endemic iodine deficiency or loss of thyroid tissue after txt for hyperthyroidism
Congential defects |
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secondary hypothyroid
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Pituitary or hypothalamic failure with failure to stimulate normal thyroid function
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Myxedema is
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characteristic sign of long standing hypothyroidism – edema around eyes and facial puffiness
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primary Hyperparathyroidism
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Primary is a common endocrine disorder caused by parathryoid adenomas,
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SECONDARY HYPERPARATHYROIDISM
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Increase in PTH secondary to a chronic disease state which causes hypocalcemia
CRF results in hyperphosphatemia, reduced levels of activated vitamin D and hypocalcemia which stimulates PTH Decreased sensitivity of activation of the parathyroid calcium-sensing receptor leading to increases in PTH secretion |
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Autoimmune Type 1 DM
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Environmental genetic factors trigger cell mediated destruction of pancreatic cells
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Non autoimmune Type 1 DM
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Secondary to another disorder
Idiopathic diabetes (Type IB) Type Ib occurs in asian and african descent with varying degrees of insulin deficiency |
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Lymphocyte and macrophage infiltration of islets causing inflammation and islet beta cell death
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● through cytotoxic T cells and autoantigen processes more islet beta cell apoptosis occurs and therefore lower insulin levels
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Production of autoantibodies against islet cells, insulin, GAD and cyotplasmic proteins
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These autoantibodies can be detected in finding out the etiology of DM in an individual; made during islet cell death –when a beta cell dies
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Need glucagon for
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gluconeogenesis
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Insulin sensitive tissue
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liver, muscle, adipose tissue
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Amylin co secreted with
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with insulin so a insulin deficiency results in an amylin deficiency
Normally, amylin inhibits glucagon secretion so if deficient then another mechanism for increased glucagon |
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glucagon
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Pancreatic alpha cells are less responsive to glucose inhibition resulting in increased glucagon secretion which causes increased hepatic production of glucose and resultant hyperglycemia
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Somogyi effect
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hypoglycemia followed by hyperglycemia
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Polyoi pathway
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– accumulation of shunted saccarides (which were originally glucose) to eyes, kidney, nerves; depositio of these into these areas cause comps of DM that we know – visual changes, nerve changes
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Chronic complications of DM
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Polyoi Pathway
Protein kinase C Oxidative Stress Hexosamine pathway Microvascular Disease Macrovascular Disease |
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Acute complications of DM
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Hypoglycemia
Diabetic Ketoacidosis Hyperosmolar hyperglycemic nonketotic syndrome (HHNKS) Somogyi Effect Dawn Phenomenon |
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DKA
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Absolute or relative deficiency of insulin
Most common in Type 1 Increase in catecholamines, cortisol, glucagon, GH Decreased glucose uptake, increased release of fatty acids, acc gluconeogenesis and ketogenesis Hepatic overproduction of ketones When ketones formed, loss of bicarb occurs |
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HHNKS
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Precipitated by infection, meds, nonadherence to DM meds or other disease
Most common in Type 2 Less of an insulin deficiency and more of a fluid deficiency Lack of ketosis Can stop lipolysis but can’t use glucose properly Glucose levels are higher due to volume depletion |
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Normal lung contains little fluid and is kept balanced by
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lymphatic drainage and capillary hydrostatic pressure, capillary oncotic pressure and capillary permeability; surfactant also repels water keeping the lining dry
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the most common cause of pulmonary edema is
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– Most common cause is heart disease, capillary injury, lymphatic obstruction
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• Capillary injury increases capillary permeability and causes
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water and plasma proteins to leak out of the capillary and move into the intersitium
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– Pulmonary edema will typically begin to develop at a wedge pressure of
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20 mm Hg
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– Increased hydrostatic pressure; when exceeds oncotic pressure
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fluids moves out into the intersitium
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– Fluid picked up by lymphatics but when flow out of capillaries exceeds
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lymphs ability to remove it =PULMONARY EDEMA. Hydrostatic pressure > interstitial pressure = fluid movemen = pulm edema.
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ARDS=
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noncardiogenic pulmonary edema)
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– Initial lung injury damages
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pulmonary endothelium and activates complement and platelet aggregation and intravascular thrombus formation,( surfactant inactivated, protein rich edema fluid)
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what is central to ARDS
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– Neutrophil activation... platelets release neurophils
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– Activated neutrophils release inflammatory mediators including
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protease enzymes, oxygen free radicals and platelet activating factor. Mediators also cause pulmonary vasoconstriction
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• Increased capillary membrane permeability is a hallmark of
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ARDS. This allows fluids, proteins and blood cells to leak from the capillary into the pulmonary interstitium and alveoli.
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– Know: lung injury, response includes neutrophils to site. Netrophil activation happens: inc cap perm. And pulm vasoconstriction.
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Two combined give you ARDS: EDEMA AND PULM HTN AND LACK OF PROPER OXYGENATION
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asthma
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– Inflammation resulting in hyperresponsiveness of the airways
– Airway epithelial cell irritation combined with exposure to antigens initiates both an innate and an adaptive immune response – Allergen exposure leads to activation of T helper cells and release interleukins that stimulate production of IgE (mast cells, histamine, lung problems) – Airway obstruction worse with expiration; either more force or more time is required to meet adequate oxygenation needs |
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mechanism of asthma
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• Activation of IgE causes mast cell degranulation and release of histamine, prostaglandins and leukotrienes
• IL-5 stimulates eosinophils which cause direct tissue injury and release toxins that contribute to hyperresponsiveness, fibroblast proliferation and airway scarring • IL-8 causes a more exaggerated inflammatory response • IL-13 impairs mucus clearance and contributes to bronchoconstriction • Inflammatory process = • Bronchial smooth muscle spasm, Vascular congestion, Increased vascular permeability, Edema formation, Production of thick mucus, Impaired mucociliary function, Thickening of airway walls, Increased contractile response of bronchial smooth muscle |
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– Centrilobular
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• Septal destruction occurring in respiratory bronchioles and alveolar ducts; usually in upper lobes of the lung
• Occurs in smokers and those with chronic bronchitis |
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– Panlobular
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• Entire acinus is involved with damage more randomly distributed
• Occurs in older adults and those with genetic mutation |
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SBO
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• Distension occurs from increased gas and water balance
• Distension decreases intestinal absorption of water and electrolytes • Water sequestered in intestinal lumen causing dehydration = hypovolemic shock • If obstruction at pylorus, metabolic alkalosis from decrease absorption of H+ ions occurs initially then metabolic acidosis from decreased bicarb absorption |
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LBO
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• Depends on the competence of the ileocecal valve
• When incompetent, the intraluminal pressure within the intestinal lumen exceeds capillary pressure distension occurs causing ischemia |
