PATHO FINAL REVIEW
àACUTE/CHRONIC KIDNEY DISEASE & RENAL FAILURE
- calcium & phosphorous imbalance > what does it lead to in the kidneys? impaired phosphate elimination
& hypocalcemia > contributes to bone disease; hypercalcemia > contributes to stones
o struvite stones are made of magnesium & phosphate, they form when the body has an alkaline
environment (attracts bacteria); the presence of bacteria contains the urease enzyme which
splits urea in the urine into ammonia (toxic)
- what are clinical manifestations in acute kidney injury?
o pre-renal: marked by a ¯ in renal blood flow / as blood flow falls gfr falls
§ etiology: hypovolemia (hemorrhage, burn injury & dehydration), ¯ vascular filling
(shock), heart failure, ¯ renal perfusion due to vasoactive mediators, drugs, chemo
§ s/s: decreased urine output (oliguria), peripheral edema (because body wants to retain
as much fluid as possible), shortness of breath
o intrinsic > acute tubular necrosis > characterized by destruction of tubular cells (reversible)
§ prolonged renal ischemia; obstruction resulting from hemoglobinuria & myoglobinuria
§ exposure to nephrotoxic drugs (antibiotics), metals & organic solvents can cause renal
vasoconstriction, direct tubular damage/obstruction
o post-renal: obstruction of urine outflow in the ureter, bladder & urethra; both ureters must be
occluded to produce renal failure
§ etiology: kidneys stones (ureters), bladder tumor,
benign prostatic hyperplasia (most common cause > compress urethra)
§ s/s: oliguria/anuria, dysuria, hematuria, urinary retention (can lead to renal
impairment & UTIs)
- what organ is responsible for eliminating potassium? kidneys excrete approx. 90% of potassium
- what is the function of raa system?
o activated by low bp; renin is released into the bloodstream & combines to angiotensin i, which is
converted to angiotensin ii (vasoconstrictor)by the ace enzyme in the lungs; angiotensin ii
releases aldosterone which stimulates sodium & water reabsorption to regulate bp
o excess activation of raas can lead to htn, chf, stroke, ckd
- inadequate blood prefusion leads to what kidney issue?
o decrease in renal blood flow decreases the
gfr; ischemic changes occur when blood flow
falls to less than 25% of normal > can lead
to renal failure
- chronic kidney disease represents:
o loss of functioning nephrons (80% of
nephrons need to be nonfunctioning for s/s
to manifest)
o progressive deterioration of glomerular
filtration & tubular reabsorptive capacity
o decline in endocrine function
§ albuminuria/proteinuria > measures
nephron injury & repair
o etiology: htn & dm, obstruction in urinary tract, glomerulonephritis, cancers, autoimmune
disorders, diseases of heart & lungs, chronic use of pain meds, polycystic kidney disease
àURINARY TRACT INFECTION
• MOST COMMON BACTERIA IN UTI > E. COLI (gram negative; very difficult to eradicate)
o bacteria normally enter through urethra; through blood in immunocompromised pts
o Host defenses > washout phenomenon, protective mucin layer, immune responses and IgA &
normal bacterial flora (men > prostatic fluid; women > lactobacillus)
• what is acute pyelonephritis? a severe upper UTI (infection reaches kidneys through bladder),
inflammatory process w/ abscess formation & tubular necrosis; affects the kidney parenchyma &
renal pelvis
o s/s: dysuria, urgency, frequency, sudden onset fever/chills, unilateral/bilateral flank pain,
dehydration, vomiting, diarrhea, pyuria, confusion in elderly
o URINE CULTURE USED TO DETECT UTIs
• what is chronic pyelonephritis? a progressive process due to scarring and deformation of the
renal calyces & pelvis; atrophy/thinning of renal cortex; recurrent or persistent infection
o s/s: similar to acute pyelonephritis, may occur gradually
àPROSTATE CANCER
• Risk factors? Age, race, family hx, diet (fatty foods, processed meat, dairy products), obesity
• Etiology: enlargement causes compression in urethra
• What is hyperplasia? Enlargement of an organ/tissue due to increased reproduction of cells;
sometimes indicates cancer but normally during puberty the
prostate grows in size, then continues to grow slowly during
adulthood (normal)
• Enlargement of the prostate leads to? Compression of urethra;
obstructs urinary out flow which can lead to > urinary
retention, renal impairment, UTIs, hematuria, bladder stones
& bladder decompensation
• Renal Colic > why is pain being caused? Stones become lodged
and stretches the tissue trying to pass through (think of
stretch in urethra or ureter)
Prevention/Diagnosis of Prostate Cancer:
§ Perform hx & physical, digital rectal exam, urinalysis; obtain blood
sample for serum creatinine & PSA (if elevated it can indicate cancer or
other abnormality; controversial)
§ How to confirm if it’s prostate cancer > BIOPSY!
àNEURO disorders
ISCHEMIC STROKE > interruption of blood flow in a cerebral vessel (most common)
§ Thrombus: clot in a small/large vessel; may be caused by atherosclerosis
§ Embolic: clot that travels to the brain; most frequent site > middle cerebral artery
o Cardiogenic > due to heart disease & atrial fibrillation which lead to clot formation;
cardioembolic stroke > occlusion of cerebral vessel w/ debris from a cardiac source
HEMORRHAGIC STROKE > bleeding into brain tissue due to blood vessel rupture, caused by htn,
aneurysms, av malformations, head injury or blood dyscrasias (abnormal condition of blood)
§ most frequent fatal stroke
§ Aneurysm > A bulge at the site of a localized weakness in the muscular wall of an arterial
vessel; can lead to rupture
o s/s: sudden onset, can occur when pt is active; one-sided, weakness of face, arm & leg;
unilateral numbness; slurred speech/language disturbance (expressive aphasia);
imbalance
from kaplan > intracerebral hemorrhage: bleeding in the brain caused by
increased htn / epidural hematoma: arterial bleed in middle meningeal artery
Transient Ischemic Attack (TIA/mini stroke) > WARNING SIGN
à ISCHEMIC PENUMBRA > area of ischemic tissue that lies bet. normal
perfused viable brain tissue & area of infarction core (creates occlusion bet.
both)
o penumbra is located on the side/surrounds the core
(reversible if treated within hours)
o infarction core is located in the center > area most severely damaged by strokes (irreversible)
MENINGITIS
inflammation of the pia mater, arachnoid, and CSF-filled subarachnoid space
• pathogens enter the CNS via:
o bloodstream by crossing the blood-brain barrier
o direction invasion through skull fracture, lumbar
puncture, or surgery
• two types of meningitis > bacterial (purulent) & viral
(acute lymphocytic)
o bacterial: pneumococcus, meningococcus
o viral: epstein-barr, west nile & MUMPS
• s/s: fever & chills, headaches, stiff neck,
photophobia; back, abdominal & extremity pain; n/v, petechial rash
• diagnostic: Blood culture & serum spinal fluid
o lumbar puncture findings must include a cloudy and purulent CSF under increased pressure
MYASTHENIA GRAVIS
o disorder of transmission at the neuromuscular junction that affects communication bet. the motor
neuron and the innervated muscle cell (brain tells the muscle to contract, but muscle can’t >
causes weakness/fatigue)
§ PATHO: Autoimmune disease caused by antibody-mediated loss of Ach receptors in neuromuscular
junction
§ Factors: unknown but related to abnormality of the thymus
§ s/s: diminished motor response, muscle fatigue/weakness in limbs more pronounced in proximal
extremities; ptosis (drooping) & diplopia (double vision); monotone speech; symptoms worsen
throughout the day
PARKINSON’S DISEASE
o degenerative disorder of basal ganglia function resulting in resting tremors, rigidity &
bradykinesia (slow movement); begins after age 50
§ PATHO: depletion of dopamine & relative excess of cholinergic activity (manifested by hypertonia
which causes tremors/rigidity)
§ s/s: tremors, rigidity, bradykinesia/slow movement, cognitive dysfunction, failure to express
emotion, orthostatic hypotension
MULTIPLE SCLEROSIS > impacts myelin sheath
o demyelinating disorder characterized by inflammation & selective destruction of CNS myelin sheath
§ PATHO: Demyelination of nerve fibers in white matter of brain, spinal cord & optic nerve;
oligodendrocytes are decreased in # or absent
• exacerbations and remissions; as disease progresses, there is less improvement between
exacerbation and increasing neurologic dysfunction
GUILLAIN-BARRE SYNDROME > Gradual Block of Sensation - polyneuropathy
• immune mechanism which causes demyelination neuropathy > progressive weakness & loss of reflexes
§ PATHO: demyelination or axonal degeneration of multiple
peripheral nerves that leads to symmetric sensory,
motor, or mixed sensorimotor deficits; longest axons are
involved first w/symptoms beginning in distal extremities
§ etiology: influenza, epstein-barr, cytomegalovirus
(cmv)
§ s/s: progressive ASCENDING muscle weakness of limbs
(starts at distal portion of extremities), symmetrical
flaccid paralysis, acute resp failure
àVISION & HEARING LOSS
CATARACTS (blurry vision)> lens opacity; interferes w/ the
transmission of light to the retina
§ PATHO: as lens ages, new layers of fibers are added, and the lens
nucleus is compressed; becomes harder (yellowing of lens)
o most common cause of blindness / risk factors: aging, hereditary
§ s/s: bilateral/unilateral, increasing blurred vision, visual
distortion, glare or abnormal presence of light
GLAUCOMA > chronic, degenerative optic neuropathy characterized by optic disk cupping and visual field
loss; associated with elevated intraocular pressure
§ PATHO: congenital or acquired lesions of the anterior
segment of the eye that mechanically obstruct aqueous
flow
à intraocular pressure results from rate of aqueous
humor production, resistance to flow & rate of
removal by drainage system
- Open-Angle Glaucoma > progressive damage to the optic nerve due to IOP, visual field loss;
asymptomatic until it becomes chronic
§ PATHO: impaired outflow results from dysfunction of drainage system; iridocorneal angle remains
open, trabecular meshwork abnormality decreases rate of aqueous humor absorption > build up
- Angle-Closure Glaucoma > occlusion of anterior chamber angle by iris
§ PATHO: impaired outflow results from occlusion of iridocorneal angle which impairs access to
drainage system
§ s/s: ocular pain, blurred/iridescent vision, relieved by sleep (promotes pupillary constriction),
unilateral headache, n/v, hazy cornea
à OPHTHALAMIC EMERGENCY > need to reduce intraocular pressure
HEARING LOSS > CONDUCTIVE & SENSORINEURAL
§ Conductive: auditory stimuli are not transmitted through the
auditory canal, tm, or middle/inner ear (temporary or permanent)
o causes: impacted earwax, foreign body, otitis externa/media,
trauma & tumors
§ Sensorineural: occurs with disorders that affect the inner ear,
auditory nerve, or auditory pathways of the brain; soundwaves are
conducted to inner ear, but abnormal cochlear apparatus
distorts/decreases transfer of information to the brain
o causes: noise, cns infections, ototoxic drugs, idiopathic
o damage to both is associated w/ auditory receptive aphasia > Wernicke’s area
àMUSCULOSKELETAL
-OSTEOMYELITIS > inflammation of the bone (marrow) caused by infection
§ PATHO: bacteria proliferates in the bone where injury occurred,
neutrophils & lysosomes appear and spread within the bone shaft & incite
an inflammatory response
o HEMATOGENOUS > infection reaches the bone through the blood stream
o CONTIGUOUS SPREAD > caused by an exogenous source (i.e., surgery)
o CHRONIC > secondary to an open wound
§ hallmark feature of chronic osteomyelitis is the presence of infected dead
bone, a sequestrum, that has separated from the living bone
§ TX: remove infected part of bone, administer antibiotics & clean wound
§ LOOK AT WBC COUNT FOR DIAGNOSTICS!
-TYPES OF FRACTURES?
o COMPOUND > bone breaks through skin into two or more fragments, prone to infection
o COMMINUTED > bone shatters with several fractures; pins + external fixation device used to
stabilize
o COMPRESSION > one or more bones in the spine weaken & crumple
o GREENSTICK > occurs during infancy/childhood when bones are soft; bone bends & breaks
(think green > fresh)
§ fractures can be open/Closed ; location: proximal, midshaft, distal
§ caused by sudden injury (trauma), stress fracture (wear & tear/overuse) & pathologic
fractures
§ complications: loss of skeletal continuity, injury from bone fragments, pressure from
swelling/hemorrhage (compartment syndrome), involvement of nerve fibers & development of
fat emboli (acts like a pulmonary embolism)
-OSTEOPOROSIS > loss of bone mass & deterioration; causes increase in bone fragility (risk for
pathological fractures)
o etiology: can occur due to endocrine disorder/malignancy (inadequate calcium absorption);
most often associated w/ aging > menopausal women are more at risk
o diagnosis: dual-energy x-ray absorptiometry & t score (-2.5 indicates osteoporosis)
-RHEUMATOID ARTHRITIS > systemic inflammatory and autoimmune disease that affects the joints
SYMMETRICALLY; most frequently attacks hands, fingers, wrists, shoulders, elbows, knees & ankles
o PATHO: altered immune response, synovial joint inflammation, joint destruction; irreversible
o S/S: systemic manifestations such as fatigue, anorexia, weight loss, low-grade fever, vasculitis &
generalized aching and stiffness / like joint pain, the stiffness is often worse in the morning or
after a period of inactivity, lasts at least 1 hour for at least 6 weeks, swan neck & ulnar drift;
limited motion related to pain & fibrosis (causes immobility of joints)
Diagnostics: Serum rheumatoid factor > indicates RA if elevated
-OSTEOARTHRITIS > degenerative joint disease relating to overuse of joints
o PATHO: inflammation caused when cartilage tries to repair itself; affects hand, knee, hip, foot &
spine ASYMMETRICALLY
o S/S: joint pain, stiffness (usually lasts no more than 30mins in the morning), limited movement,
joint subluxation (dislocation of joint & misalignment of bone ends), instability & deformities
(occur later as disease progresses)
àDISORDERS OF ENDOCRINE SYSTEM
-ANTERIOR PITUITARY FUNCTION:
§ adrenocorticotropic hormone (ACTH): controls release of cortisol from adrenal cortex
§ thyroid-stimulating hormone (TSH): stimulates thyroid hormone release (t3 & t4)
§ growth hormone (GH): aids in growth & metabolism
§ follicle-stimulating hormone (FSH): stimulates growth of ovarian follicles & sperm production;
acts on gonads
§ luteinizing hormone (LH): stimulates ovulation & development of corpus luteum in women;
stimulates testosterone production in males; acts on gonads
§ prolactin: stimulates milk production from mammary glands
-PITUITARY DISEASE OCCURS DUE TO:
§ pituitary hormone hypersecretion/hyposecretion
§ localized mass effect (benign/malignant tumor)
o most common > pituitary adenoma (adults) & hypothalamic tumors (children)
o diagnosis > serum cortisol, serum tsh, plasma osmolality
DISORDERS OF ANTERIOR PITUITARY:
-HYPERPITUITARISM > hyperfunction & excessive hormone production
o adenoma (tumor)arising from pituitary
o hyperplasia (enlargement of gland)
o carcinoma/hypothalamic lesions
o s/s: female > amenorrhea, galactorrhea, infertility; male > decreased libido, impotence;
increased icp, headache, n/v, seizures, obstructive hydrocephalus, paresthesia on one side
of the face, cranial nerve deficits, visual field abnormalities
-HYPOPITUITARISM > deficiency of one or more pituitary hormones
o etiology: congenital, destruction of gland (surgery/radiation), tumor, infection,
deficiency of hypothalamic hormones
o s/s: gh deficiency > short stature in children; increased rate of bone absorption in adults
(osteoporosis; male > decreased libido, ed; female > amenorrhea
à life threatening > ¯ acth (secondary adrenal insuffiency)& ¯ tsh (hypothyroidism)
DISORDERS OF POSTERIOR PITUITARY:
-SYNDROME OF INAPPROPRIATE ANTIDIURETIC HORMONE (SIADH) > excessive adh secretion
§ etiology: non-endocrine > bronchogenic carcinoma, severe pneumonia, pneumothorax, lung
cancers (paraneoplastic syndrome); cns related > head injury, brain surg/tumor; meds > thiazide
diuretics, nicotine, tca, vincristine
§ s/s: concentrated urine, retention of fluid, sodium deficiency (bc it’s diluted)
§ with adh > urine output decreases & urine concentration increases
-DIABETES INSIPIDUS (DI)> deficiency of adh (vasopressin)
§ etiology: head trauma, brain tumor, radiation/ablation of gland, cns infections & failure of
renal tubules to respond to adh
§ s/s: dilute, waterlike urine & intense thirst
o renal tubules can’t retain fluid due to lack of adh so the body tries to excrete as much
fluid as it can, causing dehydration
DISORDERS OF THYROID GLAND:
o thyroid releases t3 & t4; t3 stimulates metabolism, t4 is inactive until converted into t3
o both exert the negative feedback on the hypothalamus
o thyroid hormone regulates metabolic rate & forms part of cardiac function
o t3 & t4 are both decreased in hypothyroidism; tsh differentiates bet. primary/secondary disorders
-HYPERTHYROIDISM > excessively high levels of circulating thyroid hormone
o etiology: grave’s disease, adenoma, thyroid storm & iodine-containing agents
o s/s: ­ hr & palpitations, sob, fine muscle tremors, heat intolerance, excessive sweating, muscle
cramps, thin hair/skin, anxiety & nervousness, ­ appetite & gi motility (diarrhea), weight loss
due to ­ metabolism & burning of fat, glucose, etc
§ GRAVE’S DISEASE > autoimmune disorder; abnormal stimulation of thyroid antibodies
o s/s: exophthalmos (bulging eyes), goiter (enlargement of thyroid), weight loss &
anxiety are caused by cytokine-mediated responses
§ THYROID STORM > thyroid crisis, causes ­ bp that leads to cardiac collapse (life threatening)
o precipitated by stress (due infection, dka,physical/emotional trauma, thyroidectomy)
o s/s: very high fever, tachycardia, chf, angina, agitation, restlessness & delirium
-HYPOTHYROIDISM > low production of t3 & t4; tsh will be high bc it’s trying to stimulate the
production thyroid hormones
o etiology: congenital or acquired (primary/secondary disease); thyroidectomy, radiation, iodine,
hashimoto thyroiditis (increased in women)
o s/s: hypometabolic state > weakness, fatigue, weight gain, cold intolerance/dry skin, mental
sluggishness & dullness (lethargy), puffy face/edema, ¯ gi motility (constipation), hoarse
voice, coarse/dry & brittle hair, enlarged heart > slow pulse & ¯ cardiac output
• MYXEDEMA > CO2 retention, fluid & electrolyte imbalance, hypothermia
o s/s: coma, cardiovascular collapse, hypoventilation/hyponatremia, hypoglycemia, lactic
acidosis, unable to metabolize sedatives, hypothermia
o MYXEDEMA COMA (LIFE THREATINING) > BODY GOES INTO HYPOTHRYOIDISM CRISIS
DISORDERS OF THE PARATHYROID:
-HYPERPARATHYROIDISM > increased secretion of calcium by parathyroid hormone
o etiology: hyperplasia, adenoma, chronic renal failure, excessive calcium intake
o s/s: kidney stones, pathologic fractures, constipation, fatigue/weakness, increased phosphorus
-HYPOPARATHYROIDISM > deficient secretion of calcium by parathyroid hormone
o etiology: surgery (neck), radiation, digeorge syndrome, inadequate calcium intake
o s/s: tetany, muscle cramps, hypotension, convulsions, diarrhea, decreased phosphorus
DISORDERS OF ADRENAL GLAND
-ADDISON’S DISEASE > adrenal cortical hormones are deficient; acth levels will be elevated (lack of
feedback inhibition)
o Etiology: hemorrhage, aids, drugs & cancer
o s/s: mineralocorticoid deficiency (aldosterone)> ¯ na & cardiac output, ­ k+, dehydration,
weakness, fatigue, cardiovascular collapse & orthostasis (orthostatic hypotension)
o s/s: glucocorticoid deficiency (cortisol)> hypoglycemia, lethargy & weakness, fever, gi
symptoms(n/v, decreased appetite & weight loss)& acth elevation (bronze pigment)
o secondary adrenal cortex insuffiency > abrupt withdrawal of glucocorticoids
o acute adrenal crisis > cardiovascular collapse (life threatening)
-CUSHING’S SYNDROME (HYPERCORTISOLISM)
o etiology: pituitary form results from excessive production of acth by a tumor; adrenal form
caused by benign/malignant adrenal tumor; ectopic form, nonpituitary secretion tumor > small
cell lung cancer; excess cortisol-like medication such as prednisone
o s/s: altered fat metabolism > truncal obesity, buffalo hump & moon face;
muscle weakness/wasting in extremities, abdominal fat, purple striae, osteoporosis, hirsutism
§ increased glucogenesis & hyperglycemia; hypokalemia, hypernatremia. hypervolemia
àHEART FAILURE
- RIGHT VENTRICULAR DYSFUNCTION > RIGHT HEART FAILURE
o patho: increased pulmonary blood volume produces right heart strain
o etiology: consequence of left-sided heart failure
o s/s: impaired liver function (ascites), increased swelling/edema & pressure, jugular vein
distention, splenomegaly, weight loss & anorexia bc they’re so full of fluids that they don’t
eat (important to monitor daily weight)
à COR PULMONALE > WHEN RIGHT SIDE FAILURE OCCURS IN RESPONSE TO COPD
- LEFT VENTRICULAR DYSFUNCTION > LEFT HEART FAILURE
o patho: diminished cardiac output & decreased peripheral blood flow, accumulation
of blood in pulmonary circulation
o etiology: acute mi, hypertension
o s/s: fluid goes into lungs > pulmonary congestion, dyspnea, shortness of breath, impaired gas
exchange > hypoxia, orthopnea
àDIABETES MELLITUS
TYPE 1 > INSULIN DEFICIENCY > BETA CELL DESTRUCTION
o type 1a: immune-mediated diabetes > immune system mistakenly attacks the body’s beta cells
o type 1b: ideopathic diabetes > no cause of disease
*ALL PTS REQUIRE INSULIN REPLACEMENT*
-DEVELOPMENT OF DIABETIC KETOACIDOSIS
§ lack of insulin enables glucose to bind & be used as energy, this increases fatty acids from adipose
tissue > ketone production
o can lead to metabolic acidosis (low serum bicarb + low ph)
o pts present with a fruity acetone breath
TYPE 2 > INSULIN RESISTANCE > impaired secretion of insulin from beta cells
§ risk factors (acquired): older adults, obesity, strong genetics, sedentary lifestyle
-HYPEROSMOLAR HYPERGLYCEMIA STATE (HHS)
o hyperglycemia/hyperosmolarity > excess glucose pulls water out of the cells & causes dehydration
o absence of ketoacidosis
CLINCAL MANIFESTATIONS > 3 POLYS
o polyuria: excessive urination
o polydipsia: excessive thirst
o polyphagia: excessive hunger
DIAGNOSTIC TESTS:
o fasting/non-fasting blood glucose
o normal = fpg 100 mg/dl or less
o pre-diabetes = fpg 100-125 mg/dl
o diabetes = fpg 126 mg/dl or higher
o GLYCOSYLATED HEMOGLOBIN (HBA1C) > reflects glucose
over the last 120 days (lifespan of rbcs)
o normal = 3.9%-5.6%
o increased risk = 5.7%-6.4%
o dm = 6.5% or greater
o CHRONIC COMPLICATIONS OF DIABETES:
MICROVASCULAR CHANGES (SMALL VESSELS)
o retinopathy > prone to cataracts, glaucoma
o neuropathy > decreased sensation in feet
o nephropathy > ckd > dialysis
MACROVASCULAR CHANGES (LARGE VESSELS)
o coronary heart disease
o stroke
o peripheral vascular disease
àPERIPHERAL VASCULAR DISEASE
o disorder of circulation in extremities
s/s: ischemia, pain, impaired function, infarction, tissue necrosis
-PERIPHERAL ARTERIAL DISEASE > narrowed blood vessels reduce blood flow to
the limbs
o s/s: intermittent claudication (pain w/ walking, relieved by rest), calf
pain, vague aching, numbness, thinning of skin, cool weak pulses, stasis
ulcers
§ RAYNAUD’S > vasospasm of arteries & arterioles of extremities
o s/s: change in skin color (pallor, blue, red), sensation of cold,
numbness
§ BUERGER’S (THROMBOANGITIS)> diminished blood flow causes damage &
death of tissue
o s/s: skin thin & shiny, cyanosis, thick/malformed nails, pain,
intermittent claudication
-PERIPHERAL VENOUS DISEASE > proper function depends on competence of valves
§ if not functioning properly > venous distention
ALTERATIONS OF VENOUS BLOOD FLOW:
§ VARICOSE VEINS: dilated tortuous veins that result from increase in pressure & incompetent valves
o s/s: peripheral edema in the veins
§ CHRONIC VENOUS INSUFFICIENCY: impaired blood flow leading to tissue congestion, edema & poor
tissue nutrition
o risk factors: prolonged standing / causes: valvular incompetence & dvt
o s/s: peripheral edema, warmth/redness, brown pigmentation, venous stasis & ulcers
§ THROMBOPHLEBITIS: thrombus formation & inflammatory response occurring in veins
DEEP VEIN THROMBOSIS (DVT) > presence of thrombus in deep/superficial vein can lead to pulmonary
embolism; most common in lower extremities
àCARDIAC DISORDERS
§ ATHEROSCLEROSIS > accumulation of cholesterol (ldl)in vessels
o stable plaque > fixed, firm & not ruptured; obstructs blood flow (tx: nitric oxide)
o unstable plaque > can rupture & lead to platelet adhesion & thrombus formation
(implicated w/ unstable angina & mi)
§ STABLE ANGINA > fixed coronary obstruction; precipitated by situations which increase demand of the
heart; provoked by exertion
o
S/S: CHEST PAIN WITH EXERCISE & MOVEMENT; RELIEVED WITH REST OR NITROGLYCERIN (VASODILATOR)
§ UNSTABLE ANGINA > unstable plaque ruptures causing thrombosis & obstruction in the vessel; leads
to narrowing of coronary lumen > ischemia
o s/s: pain is persistent & severe, occurs at rest with minimal exertion
§ MYOCARDIAL INFARCTION (HEART ATTACK)> occurs due to ischemic death of myocardial tissue;
irreversible myocardial cell death (necrosis)occurs after 20-40 mins of severe ischemia
o STEMI > st-segment elevation + q-wave
§ HYPERTENSION > elevated blood pressure
o modifiers: diet, smoking, physical activity, cholesterol
o non-modifiers: family hx, race/genetics, gender (male > women)
primary hypertension > elevated bp w/o a cause or evidence of disease
secondary hypertension > elevated bp resulting from another disorder (kidney disease, birth
control, etc.)
§ kidneys are the main regulators of blood pressure
§ raas mechanism responds to low bp by retaining sodium & water to increase bp
§ vasopressin (adh) responds to low bp by retaining water to increase bp
àRESPIRTORY DISORDERS
§ COPD > inflammation/fibrosis of bronchial wall; loss of elastic fibers impairs expiration &
increase airway collapse and air trapping causing barrel chest (1:1 diameter)
o obstruction of airflow cause V/Q mismatch
o etiology: alpha 1-antitrypsin (hereditary), smoking, asthma & airway hyperresponsiveness
• EMPHYSEMA > enlargement of alveolar sacs & loss of lung elasticity
o etiology: same as copd
o s/s: pink puffer, lack of cyanosis, pursed-lip breathing, barrel chest, use of accessory muscles
• CHRONIC BRONCHITIS > airway obstruction of major/small airways
o marked by increase in goblet cells (detected in sputum culture)which produce excess mucous to
protect from irritants
o causes: smoking & air pollution
o s/s: blue bloaters, cyanosis, fluid retention (edema due to inflammation)
§ ASTHMA > airway inflammation manifested by inflammatory cells (eosinophils & mast cells)
o characterized by bronchoconstriction, edema of bronchial mucosa & increased mucous secretion;
narrowing of bronchioles > wheezing (air goes in but can’t come out)
o s/s: wheezing, sob or dyspnea, chest pain, cough, asthma induced exercise
o mediators: cytokines, interleukins, histamine & leukotrienes
o t helper 2 cells respond to pathogens > stimulate b cells (antibodies) > ige releases histamine
§ PNEUMONIA > inflammation of parenchymal structures in the
lower respiratory tract due to infectious bacteria/virus (s.
pneumonia & legionella) or non-infectious agents (smoking,
aspiration)
o s/s: fever, cough with sputum, chills & dyspnea
à setting > community acquired (48 hrs within admission)
hospital acquired (48 hrs after admission)
à agent > typical (bacteria/exudate, debris on x-ray)
atypical (no bacteria/exudate shown on x-ray)
§ atypical pneumonia > common in immunocompromised
pts (hiv/aids, transplant, cancer)
à distribution > lobar (consolidation in one lobe of the lung, i.e. middle lobe)
bronchopneumonia (patchy consolidation over all of the lung)
§ small cell lung cancer (carcinoma)– most malignant; metastasizes to brain
o paraneoplastic syndrome > mimics the endocrine system by abnormally excreting hormones
§ siadh > abnormal retention of fluid causing decreased urinary output
§ hypercalcemia > kidney stones, cardiac arrythmias, confusion, muscle
twitching/cramps
àHEPATOBILIARY & PANCREATIC DISORDERS
§ PANCREATITIS > reversible inflammation of pancreatic acini cells
o patho: premature activation of pancreatic enzymes (autodigestion)
o etiology: gallstones, alcoholism, hyperlipidemia, hyperparathyroidism, trauma,
steroids/diuretics
o s/s: abdominal epigastric pain radiating to back/chest
§ CHOLECYSTITIS > inflammation of the gallbladder
o patho: obstruction of gallbladder outlet
o etiology: gallstones (calculous) or sepsis, trauma (acalculous)
o s/s: ruq or epigastric pain, n/v, fever (sudden onset)
§ LIVER FAILURE > complication of liver disease
o etiology: alcoholism, non-alcoholic fatty liver disease, hepatitis
o liver failure can affect all the systems of the body
§ anemia > impaired formation of rbc; blood loss
§ fetor hepaticus > musty, sweet breath odor
§ coagulopathy > malabsorption of vitamin k, impaired clotting factors, thrombocytopenia
§ endocrine disorders > alteration in gonadal function – amenorrhea & low testosterone
§ skin disorders > vascular spiders, telangiectasis, spider nevi
§ neuro > ammonia accumulation (detoxified by liver)– confusion, decreased loc
§ renal failure > decreased renal blood flow – oliguria, increased creatinine & azotemia
§ LIVER CIRRHOSIS > functional liver tissue replaced by fibrous tissue; constrictive bands disrupt
blood flow
o can lead to portal hypertension
o s/s: anorexia, weakness, hepatomegaly
& splenomegaly, weight loss;
JAUNDICE – yellow skin color
(abnormally high bilirubin)
§ ESOPHAGEAL VARICES > dilated tortuous veins
found in the submucosa of lower esophagus
(test question had to do w/ ascites)
§ ascites > fluid accumulation in abdomen due
to liver disease/failure
§ HEPATITIS > acute/chronic inflammation of
the liver; autoimmune disorder
o HEP A & E > FECAL/ORAL
o HEP B, C & D > BLOOD/SERUM
àGI DISORDERS
PEPTIC ULCER DISEASE > ulcerative disorder that occur in areas exposed to acid-pepsin secretions
§ most common forms > duodenal & gastric
§ causes: h. pylori, aspirin/warfarin, smoking
§ s/s: burning, gnawing, cramp-like pain over a small area near midline in epigastrium; occurs when
stomach is empty
§ tx: eradicate h. pylori & relieve ulcer symptoms
§ complications: hemorrhage, obstruction & perforation of stomach/duodenum wall
GERD > GASTRIC REFLUX DUE TO WEAK/INCOMPETENT LOWER ESOPHAGEAL SPHINCTER
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§
§
ETIOLOGY: H. PYLORI > MOVES THROUGH MUCOUS LAYER OF STOMACH > SECRETES UREASE > PRODUCES AMMONIA
TO BUFFER ACIDITY; H. PYLORI PRODUCES ENZYMES & TOXINS THAT INTERFERE W/ LOCAL PROTECTION OF GASTRIC
MUCOSA AGAINST ACID > RELEASES HISTAMINE > STIMULATES MORE ACID
S/S: HEARTBURN, PAIN IN EPIGASTRIC AREA THAT RADIATES TO THROAT, SHOULDER, OR BACK
COMPLICATION > BARRET ESOPHAGUS
-IRRITABLE BOWEL SYNDROME (IBS) > DISORDER OF THE LARGE INTESTINE
§
§
§
ALTERED BOWEL FUNCTION (CONSTIPATION & DIARRHEA)
PERSISTENT OR RECURRENT SYMPTOMS OF ABDOMINAL PAIN, RELIEVED W/ DEFECATION
S/S: CONSTIPATION/DIARRHEA, N/V, ANXIETY OR DEPRESSION, FLATULENCE & BLOATING
-INFLAMMATORY BOWEL DISEASE (IBD) > crohn’s disease & ulcerative colitis
Etiology: uncertain, genetic factors, antibiotics that damage the microbiome
§ CROHN’S DISEASE > recurrent inflammatory response that can affect any area of the gi tract
from mouth to anus; most commonly affects distal small intestine & proximal colon
o patho: sharply demarcated skip lesions through gi tract; bowel wall thickens & becomes
inflexible; age: 20-30 years
o s/s: exacerbation/remission, intermittent
diarrhea & colicky pain, weight loss, fluid &
electrolyte imbalance, low grade fever &
nutritional deficiencies
o complications > fistula formation, abdominal
access & obstruction
§ ULCERATIVE COLITIS > nonspecific inflammatory
condition of the colon; affects colon & rectum
o patho: begins in the rectum & spreads
proximally affecting primarily the mucosal
layer; continuous inflammatory process can
lead to formation of crypt abscess (necrosis)
> pseudopolyps may develop
o s/s: recurrent diarrhea > stool contains blood & mucous; mild abdominal cramping, fecal
incontinence (no control over anal sphincter), anorexia, weakness & fatigue
o complications: toxic megacolon, colon cancer, anemia due to increased bleeding
àHEMATOLOGIC DISORDERS
ANEMIA > abnormally low # of circulating RBCs or level of hemoglobin (or both)
o etiology: excessive blood loss (trauma), destruction of RBCs, deficient RBC production
(lack of nutritional elements & bone marrow failure)
o s/s: impaired o2 transport, sob, increased hr, lightheadedness, fatigue, pallor
§ blood loss anemia > leads to iron deficiency anemia
o causes: loss of iron through bleeding, dietary deficiency
o asymptomatic until hgb < 8 g/dl
§ hemolytic anemia > premature destruction of rbc (sickle cell disease )
o inherited disorder - abnormal hgb > hbs (causes sickling of cell)
o complications: chronic hemolytic anemia, blood vessel occlusion
§ symptoms can be triggered by cold temps, physical exertion, stress, hypoxia,
dehydration; sickle cell affects the spleen which helps w/ immune system > pt’s
with scd have a weakened immune system & are more likely to get sick
§ megaloblastic anemia > impaired dna synthesis resulting in enlarged rbc due to impaired
maturation & division
o causes: vitamin b12 deficiency & folic acid deficiency
o complications: pernicious anemia (lack of intrinsic factor/inability to absorb b12)
§ aplastic anemia > disorder of pluripotential bone marrow stem cells; reduction of rbc, wbc &
platelets due to radiation, chemo, aids, hepatitis, chemicals/toxins
MALIGNANT LYMPHOMAS > non-hodgkin lymphoma & hodgkin lymphoma
§ causes: unknown, hereditary, immune system impairment (i.e. hiv)
§ non-hodgkin lymphoma > arise from malignant transformation of b or t cells; spreads
randomly to multiple nodal sites
o no presence of reed-sternberg cells; most severe/uncurable
hodgkin
lymphoma > arises from abnormal b cells in a single node or chain of nodes; spreads in
§
orderly fashion
o identified by presence of reed-sternberg cells; less severe/treatable
o s/s: painless lymphadenopathy (swollen lymph nodes), fever, night sweats, weight loss,
increased infection / tx: chemo & radiation
LEUKEMIA > malignant neoplasms of cells originally derived from myeloid/lymphoid tissue
o most common cancer in children & adolescents
o etiology: aggressive radiation/chemo from other cancers, exposure to benzene, antitumor drugs
& genetic predisposition
à acute lymphocytic leukemia (all)
o increased in children, ages 4-12 years old; neoplasm from b or t lymphocytes
à acute myeloid leukemia (aml)
o disease of older adults; neoplasms affect myeloid tissue in bone marrow
à chronic lymphocytic leukemia (cll)
o malignancy of b lymphocytes; most common form; isolated increase in lymphocytes & WBCs
à chronic myeloid leukemia (cml)
o disorder of pluripotent hematopoietic cells; philadelphia chromosome!
o splenomegaly & elevated WBCs; tx > stem cell or bone marrow transplant
àIMMUNE DISORDERS
HYPERSENSITIVITY > excessive/inappropriate activation of
the immune system
§ TYPE I HYPERSENSITIVITY > IGE-MEDIATED DISORDERS
o rapid response > medication allergy/anaphylactic
shock
o initial phase response: vasodilation, vascular
leakage of histamine (edema),
smooth muscle contraction (bronchoconstriction)
§ TYPE II HYPERSENSITIVITY > ANTIBODY-MEDIATED
DISORDERS (IGG & IGM ANTIBODIES)
o delayed response > mismatched blood transfusion, hemolytic disease of the newborn
(erythroblastosis fetalis)
§ TYPE III HYPERSENSITIVITY > COMPLEMENT-MEDIATED IMMUNE DISORDERS
o delayed response > autoimmune disease (lupus, rheumatoid arthritis)
o Activation of complement pathway generates chemotactic & vasoactive mediators that cause tissue
damage by > alterations in blood, increased vascular permeability, destruction of inflammatory
cells; vasculitis is seen in autoimmune diseases
o SYSTEMIC LUPUS ERYTHEMATOSUS > FORMATION OF AUTOANTIBODIES & IMMUNE COMPLEX
§ S/S: REMISSION & EXACERBATION, ARTHRALGIA & ARTHRITIS, MALAR BUTTERFLY RASH,
PHOTOSENSITIVITY, NEPHRITIS, RENAL FAILURE, BRONCHITIS, SECONDARY HTN
§ TYPE IV HYPERSENSITIVITY > T-CELL MEDIATED DISORDERS
o delayed response; immunodeficiency > tuberculosis test, contact dermatitis
HIV/AIDs
§ HIV > disorder that attacks the immune system
o Stage 1: >500 cd4+ cells
o Stage 2: 200-499 cd4+ cells (hiv)
o Stage 3: <200 cd4+ cells (aids)
§ AIDs > develops when hiv has caused serious damage to
immune system; most serious stage of hiv with an
abnormally low cd4+ count
o profound immunosuppression, pt is prone to
opportunistic infections, wasting syndrome
§ transmitted through blood, semen, vaginal fluids, and
breast milk; infectious even if carrier is asymptomatic
§ CELLS AFFECTED BY HIV > lymphocytes called cd4+ t
lymphocytes / t-helper cells, macrophages & dendritic
cells
o pts can acquire kaposi’s sarcoma > purple brown lesions/blotches seen externally (face,
back & trunk) or internally (liver, gi & respiratory tract)
àCELLULAR ADAPTATION
§ Atrophy > decrease in cell size
o ex: muscle disuse, denervation, ischemia, inadequate nutrition
§ Hypertrophy > increase in cell size/functioning tissue mass
o ex: increased muscle workload
§ Hyperplasia > increase in the number of cells in an organ or tissue
o ex: enlarged prostate
§ Metaplasia > reversible change where cell type is replaced by another adult cell type
o ex: chronic irritation/inflammation (seen in smoking)
§ Dysplasia > deranged cell growth; cells vary in size, shape, and organized
o ex: abnormal chronic irritation/inflammation of respiratory tract, reproductive system; can
lead to cancer if not treated
§ intracellular accumulations > buildup of substances which cells can’t eliminate or use immediately
o liver > bilirubin (jaundice)
o heart > cholesterol (atherosclerosis)
o kidneys > protein in urine (proteinuria)
§ cell death > occurs via necrosis & apoptosis
o eliminates cell that are worn out, have been produced in excess, have developed improperly &
have genetic damage
apoptosis > programmed cell death; associated w/ cancer cells (these skip apoptosis)
necrosis > refers to cell death in an organ or tissues that is still part of a living person
Gangrene > is applied when a considerable mass of tissue undergoes necrosis
-WET GANGRENE (venous)> affected area is cold, swollen, pulseless; skin is moist,
black, and under tension. blebs form on the surface, liquefaction occurs, and a foul
odor is caused by bacterial action
• spread of tissue damage is rapid; viable tissue can be saved
-DRY GANGRENE (arterial)> affected tissue dry and shrinks, skin wrinkles and its
color changes to dark brown or black
• spread is dry and slow; can lead to amputation
àSTRESS & ADAPTATION
homeostasis > operated by negative feedback system
§ NEGATIVE FEEDBACK MECHANISM
o when values decrease below set point = negative feedback causes
value to increase
o when values increase above set point = negative feedback causes
value to decrease
§ SYMPATHETIC SYSTEM = FIGHT OR FLIGHT RESPONSE
o increase hr/rr
o dilated pupils
o decreased gi activity + urinary output/kidney function
o pale, cool skin
à CORTISOL = “stress hormone”
o small peptide hormone that regulates pituitary and adrenal
activity
§ angiotensin ii > renal retention of sodium & water
§ adh (vasopressin) > increases water retention
§ stress is known to suppress the immune system
o physiologic stress > controlled on a moment-to-moment basis
by feedback mechanisms
• stress-induced changes in body functions
• detected by body’s normal regulatory sensors
• the body alters function to restore normal balance > when
normal balance is restored, negative feedback stops the reaction!
o psychological stress > not regulated with the same degree of specificity and feedback control;
effect may be inappropriate & sustained
§ directly affects cns > turns on the stress responses, even when body’s internal sensors
have not detected an imbalance
àINTEGUMENTARY DISORDERS
§ nevi (moles) > benign tumors of the skin that predispose individual to cancer
o abnormalities in color, border & shape can indicate cancer
§ malignant melanoma > rapidly progressing malignant tumor of the melanocytes
o brown/black in color, raised edges, irregular borders; arise from pre-existing nevi
§ basal cell carcinoma > neoplasm of the nonkeratinizing cells of the basal layer of the epidermis;
most common skin cancer in white-skinned people
o invades & grows wide & deep; increase in size over time
§ squamous cell carcinoma > second most frequently occurring malignant tumor of the outer
epidermis
o risk of metastasis to lymph nodes
§ types of melanomas:
o superficial spreading (most are this type)
• raised edges, grow horizontally & vertically
• ulcerate & bleed; similar to blood blisters
• brown/black in color
o nodular
• dome-shaped; blue black color
• common in trunk, head & neck
o lentigo maligna
• slow growing; flat
o acral lentiginous
• seen as flat spots on palm, soles of feet, nail beds, mucous membranes
• poor prognosis bc pts ignore the spot
§ PRESSURE ULCERS > ischemic lesions of skin caused by
unrelieved pressure
o occur due to pressure, shear forces, friction, and moisture
à STAGE 1 > NON-BLANCHABLE ERYTHEMA OF INTACT SKIN
à STAGE 2 > PARTIAL-THICKNESS SKIN LOSS (EPIDERMIS AND/OR DERMIS)
à STAGE 3 > FULL-THICKNESS SKIN LOSS INVOLVING DAMAGE OR NECROSIS
OF SUBCUTANEOUS TISSUE
à STAGE 4 > FULL-THICKNESS SKIN LOSS W/ EXTENSIVE DESTRUCTION,
TISSUE NECROSIS, DAMAGE TO MUSCLE/BONE
àNEOPLASIA
neoplasia > malignant growth
§ malignant cells skip apoptosis (programed cell death)
By Thalia Fortun