Patho Final Exam
Cellular Function
Energy (ATP): d/t glucose/trigly/protein breakdown → protein last resort.
- Stored by building big molecules
- Krebs (citric acid) and aerobic/anaerobic respiration
Cell proliferation: cells divide + reproduce (meiosis/mitosis)
Cell differentiation: cells now specialized
- Stem: less differentiated → can differentiate/fill different roles
Basic Cell Function: Exchanging Materials
Selective Permeability- Ability of cell wall to allow substances through the membrane and block others
- Substances with free passage- enzymes, glucose, electrolytes
Diffusion- movement of solutes toward lower solute
concentration
Facilitated diffusion- movement of solutes toward lower
solute concentrations with the help of a transport molecule
Osmosis- Passive movement of water/solvent across
membrane towards higher concentration
Active Transport- Movement against concentration
gradient
Cellular Adaptation
Atrophy (cell size ↓): lowers functionality
* Less workload = small size + less energy usage
Hypertrophy (cell size ↑): lower functionality
* More workload = bigger organelle size + contractility
Metaplasia: replacement normal → abnormal
Dysplasia: mutation of normal → abnormal
Hyperplasia (cell # ↑): increases functionality
* More workload = bigger tissue size d/t cell proliferation
Common Causes of cell death
↓ Most diseases begin with cell injury (ischemia, necrosis, free radicals)
↓ Causes of cell injury include physical, chemical, or biological agents; radiation; and nutrition imbalances
↓ Apoptosis: programmed cell suicide
↓ Necrotic cell death, Gangrene = necrosis by hypoxic injury
Cancerous Cellular Damage:
Neoplasm: “new growth”, uncontrolled/unregulated → in 1 location and spread to another.
Benign cancers: slow, progressive, localized, defined, differentiated = like host tissue
Malignant cancers: rapid, metastatic, undifferentiated, fatal
Innate vs. Adaptive Immunity
Innate Immunity
1. Barriers
Adaptive Immunity “acquired defenses”
2.
3.
4.
5.
-
Nonspecific but immediate: recognizes nonself but not specific
pathogens
Skin and mucous membranes, chemicals, microbiome
Not impenetrable
Inflammatory response
damage/trauma to tissue (mast cells trigger) = vascular rxn
Nondiscriminatory: same sequence regardless of course, local and
systemic
Acute phase: right after injury → until threat is gone
Vasodilation and vasoconstriction, phagocytosis, fibrinogen
Chronic phase: if acute does not resolve issue, lasts until healing is
complete
Chronic often occurs in presence of resistant organisms
Pyrogens
By bacteria or after exposure
Systemic inflammatory response (fever) → life-threatening = bad
environment 4 bacteria.
Interferons
From virus-infected cells → bind to uninfected (release enzyme
prevents viral replication)
Complement proteins
Plasma proteins enhance Ab + activated by antigens
immune/inflammatory response
Follow those that escape innate defenses =
have memory → distinguishes self from
nonself
1. Cellular Immunity (Destroy the
antigen)
- T cells: regulator cells (helper T and
suppressor T) and effector cells
(cytotoxic killer T cells) are
produced in marrow and mature in
thymus
- 4 types of Th (helper) cells
- Viruses and CA (cancer);
hypersensitivity and transplant
rejection
2. Humoral Immunity (Produce Ab
against antigen)
- B cells: memory
cells/immunoglobulin-secreting cells
= Ab 72 hrs after first exposure
- Memory cells: faster to same
antigen in future
- Active and passive acquired
immunities
Transplant Reactions
Success = best match of tissue antigens from donor
Allogeneic: donor/recipient = related or unrelated, similar tissue
types (common)
Syngeneic: donor/recipient = identical twins
Autologous: donor/recipient = same person (successful)
Xenogenic: donor/recipient = different species
Responses to transplant:
- Hyperacute tissue rejection: immediate bc of complement system → necrosis
- Acute tissue rejection: within 3m, treatable = fever, edema, etc.
- Chronic tissue rejection: 4m+, Ab-mediated bc of ischemia in vessel of transplanted tissue
Autoimmunity
-
Can’t recognize itself = immune response against self
Triggering mechanism = unclear → affects any tissue
Known predictors: genetics, female, abnormal stressors
Frequently progressive relapsing-remitting disorders w/ periods of exacerbation and remission
Dx (diagnosis) tries to eliminate possibilities
-
Ex. Systemic Lupus Erythematosus (Chronic stress-related inflammatory affecting connective tissue; mild →
severe)
Describe and compare fluid imbalance disorders
Tonicity: osmotic pressure of 2 solutions separated by semipermeable membrane
Hypotonic: lower solute → fluids shift out
of intravascular compartment >
intracellular space
Isotonic solutions:
equal solute = no fluid
shifts
Hypertonic solutions: higher solute→ fluids shift
from intracellular compartment > the
intravascular space
Fluid excess
Edema:
-In interstitial space
-Issue w/ distribution, not always fluid overload
-Anasarca: generalized edema
Hypervolemia or fluid volume excess:
-In intravascular space
-Excessive Na+ or H2O intake & insufficient losses
Water intoxication:
-In intracellular space
-May lead to rupture (lysis)
-Most sensitive = cerebral cells
Excessive sodium or water intake:
-Na+ diet
-Psychogenic polydipsia (super thirsty)
-Hypertonic fluid administration (fluid going where?)
-Free H2O
-Enteral feeding
Inadequate Na+ and H2O elimination:
-Hyperaldosteronism
-Cushing’s
-SIADH
-Renal/heart/liver failure
Manifestations:
Peripheral + periorbital + cerebral edema, anasarca, Fast weight gain, Dyspnea (SOB), crackles, Bounding pulse,
tachycardia, HTN, JVD, Polyuria, Bulging fontanelles (babies)
Fluid Deficit
Inadequate fluid intake:
-Poor oral intake
-Inadequate IV fluid replacement
Excessive fluid or sodium losses:
-GI losses
-diaphoresis
-hyperventilation
-Hemorrhage
-Nephrosis
-DM/Diabetes insipidus
-Burns + open wounds
-Ascites
-Effusions
-Diuretics
-Osmotic diuresis
Manifestations:
Thirst, dry mucous membranes, ↓ skin turgor, weight loss, altered LOC, hypotension, tachycardia, weak/thready pulse,
flat jugular veins, oliguria, sunken fontanelles (babies)
Describe and compare electrolyte disorders
Sodium (+)
- Extracellular fluid (ECF): neuro function; regulates fluid volume → kidney reabsorbs
Potassium (+)
- Intracellular fluid (ICF): muscle contraction; cardiac conduction → kidneys eliminate
Calcium (+)
- Bone health; neuromuscular + cardiac function
- Insufficiency → osteoporosis
Magnesium (+)
- ICF; bone; cellular functions
- Alcoholism → low levels
Chloride (-)
- ECF; bound to other ions
- Need for HCl production
Sodium: NA+
- Most significant cation
- Controls serum osmolality + H2O balance
- Role in acid-base balance + muscle and nerve impulses + H2O balance
Hypernatremia
Causes:
Excessive Na+ (diet, hypertonic IV saline, Cushing’s, corticosteroids),
Deficient H2O (not drinking H2O, third spacing, excessive output, prolonged hyperventilation, diuretics, diabetes
insipidus)
Manifestations: SALTED: skin flushed, agitation, low grade fever, thirst, edema, decreased urine output.
Hyponatremia
Causes:
Deficient sodium (diuretics, GI losses, diaphoresis, insufficient aldosterone, adrenal insufficiency, diet Na+ restrictions)
Excessive H2O (hypotonic IV saline, hyperglycemia, H2O intake, renal failure, SIADH, HF)
Manifestations: LOW SODIUM: LOC altered, orthostatic hypotension, weak muscles, seizures, osmolality low, diarrhea,
increased ICP, urine, more bowel sounds.
Potassium: K+
- Primary intracellular cation → excreted thru kidneys/GI.
- Electrolyte conduction, acid-base, metabolism
Hyperkalemia
Causes:
Deficient excretion: renal failure, Addison’s, meds, and Gordon’s syndrome
Excessive intake: oral K+ supplements, salt substitutes, rapid IV administration of diluted K+
Increased release from cells: acidosis, transfusions, burns, other cellular injuries
Manifestations: MURDER: muscle weakness, urinary output (little or non), respiratory distress (d/t muscle weakness),
decreased cardiac contractility (low HR/pulse), early: muscle twitches/cramping, rhythm changes (EKG)
Hypokalemia
Causes:
Excessive loss: V/D (vomiting, diarrhea), NG suctioning, fistulas, laxatives, K+-losing diuretics, Cushing’s,
corticosteroids
Deficient intake: malnutrition, extreme dieting, alcoholism
Increased shift into the cell: alkalosis and insulin excess
Manifestations: 6 L’s: lethargy, low/shallow respirations, limp muscles, lethal dysrhythmias, leg cramps, lots of urine.
Calcium: Ca2+
- Bones and teeth
- Blood clotting, hormone secretion, receptor functions, nerve transmission, muscular contraction
- Inverse = PO3, synergetic = Mg2+
Hypercalcemia
Causes: Increased intake or release: Ca2+ antacids + supplements, CA, immobilization, corticosteroids, vitD deficiency,
↓ PO3
Manifestations: BACK ME: bone pain, arrhythmias, cardiac arrest, kidney stones, muscle weakness, excessive
urination.
Hypocalcemia
Causes: Excessive losses: hypoparathyroidism, renal failure, ↑ PO3, alkalosis, pancreatitis, laxatives, diarrhea, meds
Deficient intake: ↓ diet, alcoholism, absorption disorders, low albumin
Manifestations: CRAMPS: convulsions, reflexes hyperreflexia, arrhythmias, muscle spasms, positive signs (trousseau’s,
chvostek’s), sensations of numbness/tingling (paresthesia)
Chloride: Cl- Assists in fluid distribution by attaching to water or sodium
- Plays a role in acid-base balance when bound with hydrogen
- In gastric secretions, pancreatic juices, bile, CSF
Phosphorus PO3:
- Bones; some in blood stream
- Bone + tooth mineralization, metabolism, acid–base balance, cell membrane formation
Describe and compare acid-base disorders
pH (Normal serum pH: 7.35–7.45) → Body fluids, kidneys, lungs maintain balance
pH = H+ concentrations
– H+ = acid; More H+ = ↓ pH
Acids = by-products of metabolism
– Volatile: (carbonic acid)
– Volatile gasses (CO2)
– Nonvolatile acids
3 systems maintain acid–base balance:
Respiratory Regulation:
- Alters CO2 excretion
Renal Regulation:
- Excretion or retention of H+ or bicarbonate
- Compensates by ventilation ↓/↑
- CO2 = acidic so ↑ respirations excretes
CO2 which ↓ acidity in the body
- Effective = permanently removes H+
- Slowest, but lasts the longest
- Compensates by making acidic or alkaline pee → bicarb is basic
Buffers:
- Chemicals that combine with acid or base to change pH
- Immediate rxn to counteract pH variations until compensation is initiated
- 4 buffer mechanisms: bicarbonate–carbonic acid, phosphate, Hgb system, protein system
- K+ and H+ move interchangeably into and out of the cell
- Extracellular excess → H+ goes inside cell, K+ moves out
- K+ imbalances = pH imbalances
Arterial Blood Gas Interpretations
Base excess/deficit
- Indicates serum buffer concentration, particularly bicarbonate
- Positive values indicate an excess of base or a deficit of acid
- Negative values indicate a deficit of base or an excess of acid
● Uncompensated = unpaired result is within nml range;
● Partially compensated = unpaired result is opposite letter of the pairs, but
pH is still abnormal;
● Fully compensated: unpaired result is opposite letter and the pH has
returned to nml
Metabolic Acidosis- Deficiency of bicarb/lots of H+
Causes: Bicarb deficit: intestinal/renal losses; Acid excess:
tissue hypoxia → lactic acid, ketoacidosis, drugs/toxins,
renal retention
Manifestations: HA, malaise/fatigue/lethargy,
weakness,coma, warm and flushed skin, N/V, anorexia,
hypotension, dysrhythmias, shock, Kussmaul’s
respirations, and hyperkalemia
Respiratory Acidosis- CO2 retention = ↑ carbonic
acid
Causes: Hypoventilation or ↓ gas exchange
Include acute asthma exacerbations, COPD,
airway obstructions, pulmonary edema, PNA,
OD, respiratory failure, and CNS depression
Manifestations: HA, blurred vision, tremors,
muscle twitching, vertigo, irritability,
disorientation, lethargy, coma, tachycardia→
bradycardia, BP fluctuations, diaphoresis
Metabolic Alkalosis- Excess bicarb, deficient acid, or
both
Causes: Excess bicarb: Lots of antacids,
bicarb-containing fluids, hypochloremia;
Deficient acid: GI loss, hypokalemia, renal loss,
hypovolemia, hyperaldosteronism
Manifestations: confusion, hyperactive reflexes,
paresthesia, tetany, seizures, respiratory
depression, dysrhythmias, and coma
Respiratory Alkalosis- Excess exhalation of CO2 →carbonic acid
deficits
Causes: Conditions that result in hyperventilation
Include acute anxiety, pain, fever, hypoxia, gram-negative
septicemia, aspirin OD, excessive mechanical ventilation, and
hypermetabolic states
Manifestations: paresthesia, dizziness, vertigo, syncope, muscle
irritability and twitching, tetany, can’t concentrate, seizures,
tachycardia, dysrhythmias, dry mouth, anxiety, excessive
diaphoresis, and coma
Compare and contrast disorders of the pituitary gland
Hypopituitarism
pituitary gland doesn’t make enough of some or all of its
hormones (panhypopituitarism) (e.g., TSH, GH, ACTH,
FSH, LH, prolactin, melanocyte-stimulating hormone,
ADH, & oxytocin)
Causes:
congenital defects, cerebral/pituitary trauma, brain
infections, autoimmune conditions, TB, pit tumors,
hemochromatosis, histiocytosis X, sarcoidosis,
hypothalamic dysfunction
Can Cause:
Dwarfism (GH): being short d/t low levels of GH,
somatotropin, or somatotropin-releasing hormone
Diabetes insipidus (ADH): lots of fluid excretion in kidneys
d/t low ADH
Manifestations:
Fatigue, HA, amenorrhea, infertility (women), low libido,
stress intolerance, weakness, nausea, constipation, weight
change, anorexia, abdominal discomfort, cold sensitivity,
visual disturbances, hair loss, joint stiffness, hoarseness,
facial puffiness, polydipsia, polyuria, hypotension, being
short/delayed growth and development
Hyperpituitarism
Pituitary gland too much of some or all of the pituitary
hormones - caused by tumors secreting hormones
Can cause:
Gigantism: being tall d/t lots of GH b4 puberty
Acromegaly: big bone size d/t lots of GH in adulthood
Syndrome of inappropriate antidiuretic hormone (SIADH):
lots of renal H2O retention d/t lots of ADH
Hyperprolactinemia: lots of prolactin = menstrual
dysfunction and galactorrhea
Cushing’s syndrome: lots of cortisol d/t lots of ACTH
Hyperthyroidism: hypermetabolic state d/t lots of thyroid
hormones from increased TSH
Manifestations:
HA, visual field loss/double vision, lots of sweating,
hoarseness, Galactorrhea, sleep apnea, carpal tunnel
syndrome, joint pain and stiffness, muscle weakness, and
paresthesia
Describe and differentiate the types of diabetes mellitus (Type 1 vs. Type 2)
-
Hyperglycemia d/t defects in insulin production, insulin action, or both
Impaired insulin production or action = abnormal carbs, protein, and fat metabolism d/t glucose transportation
issue
Complications:
hyperglycemia/hypoglycemia, DKA, heart disease, CVA, HTN, diabetic retinopathy, blindness, kidney disease,
neuropathy, amputation, periodontal disease, delayed healing, pregnancy complications, and ED
Manifestations:
Hyperglycemia, glucosuria, polyuria, polydipsia, polyphagia, weight loss, blurred vision, and fatigue
Type 1 Diabetes
Immune system destroys pancreatic β-cells → need
insulin for energy
- Children + young adults
- Cannot be prevented
Type 2 Diabetes
Pancreas gradually loses ability to make insulin
- 1st managed w/ orals that increase insulin
production/action.
Prediabetes
- BGL higher than normal → not high enough 4 dx
- Insulin-resistant cells d/t adipokines by adipose cells
- Lifestyle changes can prevent or delay T2D
Metabolic Syndrome
- Risk factors occurring together: ↑ glucose, ↑ BP, ↑ cholesterol, ↑ waist circumference
- Not a form of DM, but related →increases risk of CVD, DM, CVA
Compare and contrast disorders of the thyroid gland
Goiter: Visible enlargement of thyroid gland
- Painless → can affect respiratory and GI but not malignant.
- Benign causes: cysts, thyroiditis, and thyroid adenomas.
- In hyperthyroidism, hypothyroidism, and normal thyroid states
- Common cause = Iodine deficiency cx
- Leads to low T3 & T4 → more TSH to compensate → thyroid hyperplasia/hypertrophy
Hypothyroidism
Thyroid doesn’t make enough hormones
- 5/10 Americans - common
- May be d/t hypothalamus, pituitary, or thyroid dysfunction
- Hypometabolic state
* Risk factor: getting old.
- Causes: autoimmune thyroiditis (Hashimoto's Thyroiditis) and
iatrogenic (medical tx)
- Manifestations: fatigue, sluggishness, cold sensitivity,
constipation, pale and dry skin, facial edema, hoarseness,
HLD, weight gain, myalgia, arthralgia, muscle weakness,
heavy menses, brittle fingernails, hair loss or thinning,
bradycardia, hypotension, constipation, depression, and goiter
Myxedema
Rare and life-threatening advanced hypothyroidism →
triggered by infection, trauma, illness, CNS suppressants
Hyperthyroidism
Super high level of thyroid hormones =
hypermetabolic state
- Causes: lots of iodine, Graves’ disease
(autoimmune-stimulates thyroid hormone production),
non malignant thyroid tumors, thyroid inflammation,
lots of thyroid hormone replacement
- Manifestations: weight loss, tachycardia, HTN, big
appetite, nervousness, anxiety, irritability, tremor,
diaphoresis, menses changes, heat sensitivity,
diarrhea, goiter, difficulty sleeping, and exophthalmos
Thyrotoxicosis (thyroid storm) = emergency
Sudden worsening of hyperthyroidism sxs d/t infection
or stress
- Fever, ↓ mental alertness, abdominal pain
Compare and contrast disorders of the adrenal glands
Pheochromocytoma
Tumor of the adrenal medulla that secretes EPI and NOREPI - life- threatening,can be single or multiple tumors in 1 or
both adrenal glands
- Manifestations: fight-or-flight response, HTN, tachycardia, forceful heartbeat, profound diaphoresis, abdominal
pain, HA, anxiety, feeling of extreme fright, pallor, weight loss
- Complications: Hypertensive crisis, CVA, renal failure, psychosis, seizures
Cushing’s Syndrome
Lots of glucocorticoids
(hypercortisolism)
- Causes: Iatrogenic d/t taking too
many of glucocorticoid meds,
adrenal tumors that secrete
glucocorticoids, pituitary tumors that
secrete ACTH and cortisol,
paraneoplastic syndrome
- Manifestations: Obesity (especially
around the trunk), “moon” face +
“buffalo hump,” muscle weakness,
delayed growth/development, acne,
purple striae, thin skin that bruises
easily, delayed healing,
osteoporosis, hirsutism, insulin
resistance (hyperglycemia), HTN,
edema, hypokalemia, mood
changes, psychosis
Addison’s Disease
Too little adrenal cortex hormones
(cortisol)
- Causes: Autoimmune, infections,
hemorrhage, tumors, pituitary
dysfunction that results in insufficient
ACTH levels
- Manifestations: Hypotension, HR
changes, hypoglycemia, chronic
diarrhea, hyperpigmentation, pallor,
extreme weakness, fatigue, anorexia,
mouth lesions on the inside of a cheek,
N/V, salt craving, slow and sluggish
movement, weight loss, mood changes,
depression, hyperkalemia
Respiratory Function
Upper respiratory tract:
-Mouth, nasal cavity, sinuses, pharynx, larynx
- Infections here trigger inflammatory response - responsible for multiple symptoms
- Many infections are interrelated due to close proximity
- Viruses cause most primary infections; inflammatory response increases risk of secondary bacterial infection
Laryngotracheobronchitis: ”croup”
- viral in peds
(parainfluenza/adenoviruses)
- Larynx swell → airway narrowing,
obstruction, respiratory failure
- Manifestations: congestion, seal-like
barking cough, hoarseness, inspiratory
stridor, dyspnea, anxiety, central
cyanosis
Laryngitis:
- Larynx inflammation = self-limiting
- Vocal cords irritated/swollen d/t inflammatory process →
occasionally blocked airway
- D/t infection, lots of exudate, irritants (smoke, allergic rxn or
overuse)
- Manifestations: hoarseness, voice loss, tickling raw feeling in the
throat, sore throat, dry cough, difficulty breathing
Epiglottitis:
- Life-threatening; Inflammatory response → epiglottis swelling & block airway
- Causes: Hib vaccine, strep, PNA & staph A, trauma
Clinical Manifestations: fast in peds (hours) vs. adults (days) - Fever + chills, Shaking, Sore Throat, hoarseness,
muffled speech, Dysphagia, Drooling w/mouth open, Mild inspiratory stridor: harsh, hi-pitched sound due to restriction),
Respiratory Distress, Central cyanosis, Anxiety, irritability, restlessness, Pallor, Leaning forward when sitting
(unconscious attempt to help breathe)
Lower respiratory tract infections:
- Trachea, bronchi, bronchioles, & alveoli
- Trigger inflammation & can have similar manifestations / etiology to URI
- Lower tract infections = life threatening
Acute Bronchitis:
- Tracheobronchial inflammation (large bronchi) → follows
upper infection
- Causes: viruses; pathogen rarely identified; not bacterial
often
- Big risk: young, old ppl, smokers & pts w/ chronic
bronchial disorders (asthma, COPD)
- Bronchial lining is irritated & airways narrow from
swelling
- Manifestations: productive/nonproductive cough,
dyspnea, wheezing, low-grade fever, pharyngitis, malaise,
chest discomfort
Bronchiolitis:
- Bronchioles inflammation d/t viral infection (RSV)
- In peds <12mo → common in fall & winter
- Peds get RSV by 2yo.
- Usually from upper → bronchioles = epithelial necrosis &
inflammation
- untreated? atelectasis & respiratory failure
- Manifestations: Nasal + congestion, Cough, Wheezing,
Abnormal lung sounds, Rapid, shallow respirations,
Labored breathing, Prolonged expiration, Dyspnea or
tachypnea, Circumoral cyanosis, Fever, Tachycardia,
Malaise, Lethargy
Pneumonia:
Lung inflammation; Affects gas transfer (alveoli, alveolar ducts, bronchioles)
- Streptococcus PNA = 75% of cases (bacterial)
-
Micro-aspiration (breathing in pathogens from upper respiratory tract) leads to development of bacterial when
in large quantities; sometimes from blood / tissue infection
Viral PNA:
- Nonproductive cough - Low-grade
fever
- Normal (low) WBC count
- Minimal change on X-ray
- Less severe
- No Abx; supportive Tx
Bacterial PNA;
- Productive cough, fever,
- Higher fever
- Elevated WBC count - On XR - severe
- Yes Abx
- From irritating agents (aspiration of gastric content, intubation, suctioning,
smoking) or stasis (no movement) of pulmonary secretion
Aspiration PNA:
frequently occurs when gag reflex is impaired due to brain injury/anesthesia
Classified based on causative agent/event:
- Lobar: confined to single lobe & described based on affected lobe
- Broncho: most frequent type; patchy & spread through several lobes
- Interstitial: AKA atypical; in areas between the alveoli; from viruses (flu A/B)
Manifestations: productive or nonproductive cough, fatigue, pleuritic pain, dyspnea, fever/chills, crackles, pleural rub,
tachypnea, mental status changes (elderly)
Prevention: washing hands ,avoiding crowds, vaccines, turning/coughing/deep breathing, no smoking
Complications: septicemia, pulmonary edema, lung abscess, ARDS
Tuberculosis (TB):
- 2022: Cause of death for ppl w/ HIV.
- Mycobacterium tuberculosis (aerobic bacillus) → resistant to immune
- Get it thru infected air droplets → needs to be active to spread
- Risk factors: weak immune system, malnutrition, overcrowded living, substance abuse
- Affect lungs, liver, brain & bone marrow
- Opportunistic = likely to become active in person w/ weak immune system
- 3 stages of pathogenesis: primary, latent & active
- Manifestations of active TB: Productive cough, hemoptysis, Night sweats, Fever/chills, Fatigue, weight loss, Anorexia
Alterations in ventilation
Asthma
- Chronic pulmonary disease → intermittent reversible airway obstruction
- Acute inflammation, bronchoconstriction, bronchospasm, bronchial edema & mucus production
- Cause: Unknown
- Associated w/ early exposure to infections (TB, measles, hep A)
Status Asthmaticus: prolonged asthma attack → no response to tx
- Possible intubation = life-threatening; May develop respiratory alkalosis 2’ to tachypnea
Extrinsic: allergens (food, dust,
medication), presort in childhood /
adolescence
Intrinsic: no allergic rxn, after 35yo; URI + smoking
Nocturnal: b/w 3 & 7am → circadian
rhythm, ↓ cortisol & histamine levels
Exercise Induced: common; 10-15 min after exercise ends; active rxn →
refractory (sxs-free) period
Occupational: Rxn to substances at work
(plastics, etc); worsens w/ more
exposure & relief on weekends
Drug-induced: By aspirin / NSAIDS; prevent conversion of prostaglandins =
IL release
- Clinical manifestations: Wheezing, SOB, Prolonged expiratory phase,
Dyspnea, Chest tightness, Cough, Tachypnea, Hypoxia, Anxiety
Chronic obstructive bronchitis:
Inflammation of the bronchi, a productive
cough, excessive mucus
- Complications: lots of respiratory
infections + respiratory failure
- Manifestations: hypoventilation,
hypoxemia, cyanosis,
hypercapnia, polycythemia,
clubbing, dyspnea at rest,
wheezing, edema, weight gain,
malaise, CP, and fever
Emphysema:
destruction of alveolar walls = large, permanently inflated alveoli
- Enzyme deficiency = genetic predisposition
- Inflammation changes enzyme levels → long term damage
- Limits O2 entering bloodstream
- Alveoli collapse d/t destroyed elastic fibers & trapped air
- Terminal bronchioles narrowed
- Manifestations (usually not coughing): SOB upon exertion, diminished
sounds, Wheezing, tightness, Tachypnea, Hypoxia, Hypercapnia, big AP
thoracic diameter (1:2 to 1:1); barrel chest, Activity intolerance, Anorexia,
malaise
Chronic Obstructive Pulmonary Disease (COPD):
Irreversible, progressive tissue degeneration & airway obstruction
- Biggest contributor: smoking
- Changes in airways, lung functional tissue & pulmonary circulation
- Ex. Chronic inflammation, ↑ inflammatory cell count in lungs, changes from repeated injury & repair
Ventilation is impaired by 1+ of the following:
- Airways & alveoli lose elasticity
- Walls between many alveoli are destroyed
- Walls between the airways become thick & inflamed - Mucus production increases & blocks airways
- Severe hypoxia & hypercapnia can lead to respiratory failure
- Chronic hypercapnia = shifts breathing drive from need to expel CO2 to need to raise oxygen
- Can lead to cor pulmonale: right-sided heart failure due to lung disease
- Often a mixture of chronic obstructive bronchitis & emphysema; sometimes asthma
Cystic Fibrosis:
Life-threatening → severe lung damage + nutrition deficits
- Affects cells that produce mucus, sweat, saliva, digestive secretions (Secretions = thick)
- Causes: autosomal recessive mutation on 7th chromosome → abnormality in Cl- cellular transport protein
- Complications: atelectasis, recurrent infections, cor pulmonale, respiratory failure, malabsorption, malnutrition,
electrolyte imbalances, sterility, and infertility
- Manifestations: meconium ileus, salty skin, steatorrhea, fat-soluble vitamin deficiency, chronic cough, hypoxia,
fatigue, activity intolerance, audible rhonchi, delayed growth/development
Alterations of ventilation and perfusion
Atelectasis
alveoli collapse d/t surfactant deficiencies, bronchus obstruction, lung tissue compression, ↑ surface tension, lung
fibrosis
- Manifestations: low breath sounds, dyspnea, tachypnea, asymmetrical lung movement, anxiety, restlessness,
tracheal deviation, tachycardia
- Prevention: ↑ mobility, cough, deep breathing; effective pain management; incisional splinting
Cardiovascular Function
Conditions resulting in decreased cardiac output
Pericarditis
- Pericardium inflammation d/t viral infection, thoracic
trauma, MI, TB, malignancy, autoimmune
- Pericardial effusion: Fluid In space b/w pericardial sac
and heart → swollen tissue creates friction
Infective Endocarditis (bacterial endocarditis)
Infection of endocardium + heart valves→ by
strep/staph
- Blot clot travels = microemboli and
microhemorrhage
- Osler nodes: more tender
-
Complications: Cardiac tamponade: life-threatening more fluid buildup (pleural effusion)
- Manifestations: narrowing pulse pressure, muffled heart
sounds
Constrictive pericarditis: chronic inflammation → no elasticity
Manifestations: pericardial friction rub (grating sound); severe
CP (worse w/ breathing, better when sitting) dyspnea,
tachycardia, palpitations, edema; flu like sxs
-
-
Janeway lesions: painless
Risk factors: IV drug use, valve disorder,
prosthetic heart valves/implanted devices,
rheumatic heart disease, aortic coarctation,
congenital heart defect, Marfan Syndrome
Life-threatening complications: MI, CVA, PE
Heart Failure
Inadequate pumping = ↓ CO and ↑ preload/afterload
- Causes: congenital defect, MI ,valvular disease, dysrhythmia, thyroid disease Compensatory mechanisms
(sympathetic NS, RAAS, hypertrophy) help at first, but perpetuate HF
- Systolic dysfunction: ↓ contractility (ventricles can’t pump hard enough during systole)
- Diastolic dysfunction: ↓ filling (not enough blood fills ventricles during diastole)
- Mixed dysfunction: ↓ contractility and filling (systolic and diastolic)
Left Sided Failure
CO falls → blood goes to pulmonary circulation =
pulmonary congestion, dyspnea, activity intolerance
Causes: L ventricular infarction, HTN, aortic or mitral valve
stenosis
Right Sided Failure
Blood goes to peripheral circulation = edema/weight gain
Causes: pulmonary disease, left HF, pulmonic or tricuspid
valve stenosis
Depending on underlying cause = acute or chronic.
graded I-IV → appear as compensatory mechanisms fail
Indicate systemic or pulmonary fluid congestion
Cardiomyopathies
Acquired or inherited conditions that weaken + enlarge myocardium
- Disease of muscle → harder for heart to pump blood to body → can lead to HF
Dilated Cardiomyopathy (most common)
cardiomegaly and ventricular dilation damage myocardium muscle fibers = decreased CO and blood stagnation
Heart disease caused by narrowing or blockage in coronary arteries/poorly controlled ↑ BP
- Risk factors: African American men and old ppl.
- Causes: most often no known cause: chemo, ETOH, coke, pregnancy, infection, thyrotoxicosis, DM,
neuromuscular disease, HTN, CAD, med hypersensitivity
- Manifestations: breathing changes and nonproductive cough, Fatigue, dysrhythmia(s), cardiac pain, dizziness,
activity intolerance, abnormal lung sounds, peripheral edema, Ascites, hepatomegaly, weak pedal pulse,
cool/pale extremities, poor capillary refill, JVD
Hypertrophic Cardiomyopathy
Ventricle wall = stiff, unable to relax → affects systolic function in men + sedentary.
- Most often inherited → defects in gene that control heart muscle growth.
- Risk factors: HTN, obstructive valvular disease, thyroid disease, dominant genes
- Manifestations: dyspnea/intolerance on exertion, fatigue, syncope, orthopnea CP, dysrhythmia, L ventricular
failure (HF), MI
Restrictive Cardiomyopathy (least common)
Rigidity of ventricles → diastolic function w/ poor prognosis;
- Causes: idiopathic, amyloidosis, hemochromatosis, radiation, connective tissue diseases, MI, sarcoidosis,
cardiac neoplasms
- Manifestations: fatigue, breathing/lung changes, HTN, big liver+ascites, JVD, murmurs, peripheral cyanosis,
pallor
Conditions that Result in Ineffective Tissue Perfusion
Dyslipidemia
Lots of lipids in blood = risk for chronic disease
- lipids from diet → made by liver
Classified based on density, triglycerides (low density) and protein (high density)
- very-low-density lipoproteins
- LDLs: “bad” most-serum cholesterol → invasive
- HLDLs: “good” → removes LDL from blood.
Manifestations: asymptomatic until it causes other diseases & complications
Atherosclerosis
Chronic inflammatory disease triggered by a vessel wall injury → thickening/hardening lesions calcifying on arterial wall
- Obstructs vessel → platelet aggregation + vasoconstriction
- Complications: PVD, CAD, thrombi, HTN, CVA
- Manifestations: asymptomatic until complications develop
Coronary Artery Disease
Narrowing/blockage of arteries in myocardium
- Causes: atherosclerosis, vasospasm, cardiomyopathy, and thrombi occlusion
- Most common type of heart disease in US & leading cause of MI
- Nonmodifiable risk factors: age, FHx
- Modifiable risk factors: tobacco, obesity, physical inactivity, stress, DM, HLD, HTN
Clinical Manifestations: CP radiates (neck, jaw, arm, back), Indigestion sensation, N/V, cold/clammy extremities,
Diaphoresis, Dyspnea, Fatigue, Weakness, Sleep disturbances
Obstructive- Plaque accumulates in large arteries → narrowing
and low blood supply to myocardium
- Occluded 50%+ - may become completely occluded.
Nonobstructive - Damage or injury to lining of
coronary arteries → can’t vasodilate in when we
need more myocardial O2
Coronary microvascular disease- Affects smallest arteries of the myocardium
Virchow’s Triad: Hypercoagulability, vascular damage, circulatory stasis.
-increases risk for developing thrombi.
Peripheral Vascular Disease (PVD)
- Narrowing of the peripheral vessels, arteries and/or veins
- Causes: atherosclerosis in arteries, clot, inflammation, or vasospasm
Thromboangitis Obliterans (Buerger’s Disease)
inflammatory condition of arteries
- May lead to clot → complete occlusion of small/medium
arteries in extremities
- Males smokers 20-40yrs
- Cause: unknown
Raynaud's Phenomenon
- Vasospasms of the arteries r/t sympathetic stimulation
- Autoimmune (i.e., lupus and scleroderma)
- Females 18-30yrs
-↑ vessel occlusion = ischemia of affected tissue
Stable Angina
CP by ischemia d/t more O2 demand
- feels better at rest.
- low blood flow may/may not cause permanent ischemia
Unstable Angina
Unpredictable CP
- at rest
- worse w/ frequency + intensity
- “preinfarction” state
Myocardial Infarction “heart attack” “acute coronary syndrome”
- Death of the myocardium from sudden blockage of coronary blood flow
- Bad tissue perfusion r/t atherosclerosis, clot, vasospasm
- Myocardial O2 supply can’t meet body’s O2 needs
- Cells die as O2 dwindles → tissue necrosis.
- Risk factors: dyslipidemia, DM, HTN, stress, tobacco
- Manifestations: Unstable CP, Fatigue, N/V, Coughing, SOB, Diaphoresis, Indigestion, Elevation in cardiac
biomarkers, Dysrhythmias, Anxiety, Syncope+dizziness, Sleep disturbance
Conditions that Result in Decreased Cardiac Output and Ineffective Tissue Perfusion
Hypertension
Prolonged elevation in BP = excessive cardiac workload d/t vasoconstriction → more afterload
- ↓ renal blood flow inappropriately activates (RAAS)
- Prevalent chronic health conditions in U.S.
- Risk factors: age, ethnicity, hx, weight, inactivity, smoking, EtOH, stress, high vit D intake
Primary (essential) HTN:
common (95%), gradual →
no identifiable cause;
Secondary HTN: more sudden/severe
- Renal disease, DM, adrenal gland tumors,
meds, drug use (coke & amphetamines)
Malignant HTN (hypertensive crisis):
nonresponsive to interventions →
180/120+symptoms.
Neural Function
Cerebral Palsy
Nonprogressive disorders in infancy/early childhood → affect motor movement + muscle coordination
- Cerebellum damage during prenatal period (childbirth) → at any time 1st 3yrs (brain developing)
- Males, African Americans, low SES
- Contributing Factors: Prematurity, Low birth weight, Breech, Multiple fetuses, Hypoxia, hemorrhage, Neuro
infections, Head injury, Maternal infections + exposure to toxins during pregnancy (rubella/varicella)
- Complications: Balance/coordination issues, Atrophy below waist, Scoliosis, Malnutrition,
Communication/speech delays, Learning/cognition difficulties, Seizures, Vision/hearing issues, Incontinence,
Constipation, Chronic pain
- Manifestations: May affect entire body or one area → Still has early reflexes, development delays, ataxia,
spasticity, flaccidity, hyperreflexia, asymmetrical walking, unusual positioning of limbs when resting or when
held up, excessive drooling, dysphagia, impaired sucking, speech issues, facial grimaces, tremors
Meningitis
Inflammation of the meninges and subarachnoid space → CSF may also be affected.
- Causes: Bacteria (life threatening), Viruses (most common + self limiting)
- Infection/irritant→inflammatory process→ swelling of meninges and increased ICP
- Risk factors: <25yrs, Community setting, Pregnancy (risk of listeria), Working w/ animals, Immunodeficiency
- Manifestations: Fever/chills, LOC changes, N/V, photophobia, HA, stiff neck/neck pain, agitation, bulging
fontanelle(s), poor feeding + irritability in children, tachypnea, tachycardia, rash
- Complications: neuro damage, seizures, hearing loss, blindness, speech+learning difficulties, behavior issues,
paralysis, acute renal failure, adrenal gland failure, cerebral edema, shock, death
Encephalitis
Brain/spinal cord inflammation d/t infection
Causes:
- Viral (most common = herpes) and bacterial
- Infection → inflammatory response = vasodilation, ↑ capillary permeability, leukocyte infiltration
- Primary: direct viral infection of brain/spinal cord) or secondary (from elsewhere in body)
- Most mild/self-limiting/go undetected → can be severe + life-threatening
Can progress in: Immunocompromised, peds, older adults, In high-incidence areas
Complications: nerve cell degeneration, cerebral edema/hemorrhage, brain damage
Manifestations: sxs similar to meningitis, but w/ more gradual onset: Flu-like sxs, HA, stiff neck, confusion,
hallucinations, personality changes, diplopia and photophobia, seizures, muscle weakness, ataxia, paresthesia or
paralysis, LOC, tremors, abnormal deep tendon reflexes, rash, and bulging fontanelle(s)
Increased Intracranial Pressure
↑ volume in cranial cavity → brain tissue, CSF, blood
- Causes: TBI, tumor, hydrocephalus, cerebral edema/hemorrhage
- Monro-Kellie hypothesis: ↑ in volume of one component must be compensated for by decrease in volume of
another
- mostly by shifts in CSF and blood volume
Autoregulation: BV dilate to increase blood flow and
constrict if ICP ↑
Cushing’s reflex: hypothalamus = ↑ sympathetic
stimulation when MAP is below ICP
Cushing’s triad: ↑ BP, bradycardia, Cheyne-Stokes respirations
● Manifestations: ↓ LOC, vomiting (projectile), Cushing’s triad, fixed/dilated pupils, posturing
Spinal Cord Injury
Direct injury to spinal cord or indirectly from damage to surrounding bones, tissues, BV
- Direct: spinal cord is pulled, pressed sideways, or compressed
- Causes: MVA, falls, violence, sports, weakening vertebral structures (RA/osteoporosis)
- Hemorrhage, fluid, edema can occur inside or outside spinal cord (within spinal canal)
- Lots of blood or fluid compresses spinal cord → damage (secondary injury)
- Spinal shock: Temporary suppression of neurologic function because of spinal cord compression; neurologic
function gradually returns
- Most common in Caucasians and males; average age has increased from 29 years to 43 years
- Complications: paralysis, neurological loss, Bladder dysfunction, bowel dysfunction, pain and/or altered
sensation in the legs, loss of sexual sensation, and saddle numbness,
- Autonomic Hyperreflexia (Massive sympathetic response that can cause HA, HTN, tachycardia - associated w/
above T6 ),
- neurogenic shock (sympathetic impulses disrupted → abnormal vasomotor response - decreased HR and BP),
respiratory failure, chronic pain, death
Manifestations:
- Cervical injuries: Most significant at + above C4, Upper and lower extremities are impacted; breathing
difficulties; loss of normal bowel and bladder control; paresthesia; sensory changes; spasticity; pain; weakness;
paralysis; blood pressure instability; temperature fluctuations; and diaphoresis
- Thoracic injuries: Trunk & lower extremities impacted;many manifestations can be the same as cervical injuries,
with the exception of breathing difficulties
- Lumbar sacral injuries: Lower extremities impacted in varying degree
Transient Ischemic Attack “mini stroke”
Temporary cerebral ischemia → neuro deficits sxs
- Causes: cerebral artery occlusion (e.g., thrombus, embolus, or plaque);
cerebral artery narrowing(e.g., atherosclerosis or spasms), or cerebral artery
injury (e.g.,inflammation or hypertension)
- Neuro deficits mimic CVA → but these deficits resolve within 24hrs (1–2
hours mostly)
- Warning sign CVA → not all CVAs come after TIA
- 1/3 with TIA will eventually have CVA → Half of these CVAs occur within 1
year of TIA
- Reflect the location of the ischemia
- Complications: permanent brain damage, falls/injury, CVA
- Manifestations begin suddenly → only for short time.
Cerebrovascular Accident “stroke”
“brain attack”
Interruption of cerebral blood supply =
ischemic damage permanent
- Causes: Total vessel occlusion (clot
or plaque) or cerebral vessel rupture
(aneurysm, malformation, or HTN)
- Two major types of CVA: Ischemic
strokes = common; Hemorrhagic
strokes = fatal
- Complications: neurologic deficits
and death
Manifestations: Muscle weakness or paralysis of the face, arm, or leg (usually unilateral), Ataxia, Changes in sensation
Agnosia (can’t identify sensory stimuli), Unilateral paresthesia, Aphasia or receptive aphasia, Dysphagia, Dysgraphia,
Vision issues, difficulty reading, LOC changes; confusion, Personality/mood/emotional changes, Vertigo or dizziness,
Incontinence of bowel or bladder
Risk factors: Physical inactivity, stress, obesity, HTN, smoking, HLD, DM, atherosclerosis, birth control pills, EtOH +
drugs, being old.
Epilepsy
Seizure disorder d/t spontaneous firing of abnormal neurons → recurrent seizures w/ no underlying cause
- Complications: Brain damage, TBI, Aspiration, Mood disorders,
- Status epilepticus: seizure activity longer than 5min or subsequent seizure(s) that occur b4 they regained
consciousness within time frame
Multiple Sclerosis
Autoimmune: progressive, irreversible demyelination of brain, spinal cord and CN
- Damage in diffuse patches throughout NS → slows/stops nerve impulses; Progression varies
- Complications: epilepsy, paralysis (legs), depression
- Remissions + exacerbations (days→months)
- Manifestations: Sensory: Vision issues, Slurred speech; Paresthesia; Hearing loss, Fatigue; Dizziness, low
attention span, poor judgment/memory loss, Difficulty reasoning and solving problems, Dysphagia, Problems
moving arms or legs, Weakness and/or tremor in one or more arms or legs, Ataxia; Unsteady gait; Muscle
spasms, Constipation and stool leakage, Urinary frequency, urgency, hesitancy, or incontinence, Sexual
dysfunction
Parkinson’s Disease
Progressive → destruction of the substantia nigra d/t lack of dopamine
- 80% of dopamine-producing cells destroyed → movement issues (tremors of hands/head)
- Can disappear/decrease when body part moved intentionally.
- “Pill rolling”
- Cause: unknown
-
Manifestations: Slowing/stopping of automatic movements (blinking), Constipation, Urinary hesitancy and/or
urgency, Dysphagia, Drooling, Anosmia (no smell), Mask Like appearance, Myalgia, Muscle cramps/dystonia,
shuffling gait, tremors
Amyotrophic Lateral Sclerosis “Lou Gehrig”
Damage of upper motor neurons of cerebral cortex + lower motor neurons of brainstem/spinal cord
- Sensory neurons, cognitive function, CN 3/4/6 = not affected
- Nerves can’t trigger muscle movement = muscle weakness, disability, paralysis, death (3yrs) → big risk of
dementia.
- No definitive cause
Manifestations: worse as more motor neurons are damaged
- Loss of upper motor neurons → spastic paralysis + hyperreflexia
- Loss of lower motor neurons → flaccid paralysis
- Early manifestations: Footdrop, LE weakness, Hand weakness, Slurred speech, Dysphagia, Muscle cramps
UE and tongue
- Begins in UE/LE → spreads to other parts → muscles become weaker until paralysis → will affect
chewing/swallowing/speaking/breathing
Huntington’s Disease
Autosomal dominant → Chromosome 4 defect
- Degeneration of neurons → progressive atrophy (basal ganglia/frontal cortex)
- Ventricles dilate, gamma-aminobutyric acid levels diminish → Ach levels fall
- Gene transmitted to next generation → more chance of developing sxs at earlier age
- Appear b/w 30-40yrs → may appear in childhood or adolescence
- Duration: 10-30yrs
- Causes of death: infection (PNA), fall injuries, or other complications (suicide)
Manifestations:
- Initially insidious → Varies.
- Unusual behaviors: Mood swings, irritable, apathetic, passive, depressed, angry → Antisocial behavior:
hallucinations, paranoia, psychosis
- Mistaken for psychiatric disorders
- Early signs: Trouble driving, learning new things, remembering facts, answering Qs, making decisions →
changes in handwriting
- Uncontrolled, rapid, jerky movements (chorea) (tremors, grimaces, twitching) in fingers, feet, face, or trunk: →
intense when anxious, clumsiness, unsteady gait → more falls
- Disease progressed if: difficult concentrating on intellectual tasks, slurred speech, and other functions
(e.g.,swallowing, eating, speaking, and walking) decline → some can’t recognize family.
Dementia
Cortical function decreased = impairing cognitive skills + motor coordination
- Common: memory issues → short-term memory losses + confusion about historical events
- Behavioral + personality changes interfere w/ relationships, work, and ADLs.
- Alzheimer’s disease: Most common form → Brain tissue degenerates/atrophies → decline in memory + mental
abilities
-
Manifestations: Memory loss, abstract thinking issues, issues w/ following convos, reading/writing
issues, disorientation, loss of judgment, difficulty performing familiar tasks, personality changes,
hallucinations, incontinence of bowel or bladder
Gastrointestinal Function
Congenital defects of gastrointestinal system
Cleft Lip and Palate
Cleft lip: failure of the maxillary
processes and nasal elevations or
upper lip to fuse during development
Cleft palate: failure of the hard and
soft palate to fuse in development,
creating an opening between the oral
and nasal cavity
- feeding/speech/hearing
issues + ear infections
Esophageal atresia
- Incomplete formation of the esophagus
- Common: type C,
- Most severe: type D
- Cause: unknown
- Associated with VACTERL (vertebral anomalies, anal atresia, cardiac
malformations, tracheoesophageal fistula, renal anomalies, and limb anomalies),
heart defects, mental and/or physical development delays, genital hypoplasia,
and ear abnormalities.
- Risk factors: old dad + mom uses IVF
- Manifestations: Secretions, coughing, vomiting, cyanosis after feeding
- Complication: aspiration PNA
Pyloric Stenosis
Narrowing/obstruction of pyloric sphincter
- Muscle fibers = thick and stiff → stomach can’t empty food into SI
- At birth or later → 3 weeks of life.
- Cause: unknown → multifactorial
- Exposure to macrolides (Abx) = increased risk
- Manifestations appear within several weeks after birth and include:
￭ Hard mass in the abdomen + Regurgitation + projectile vomiting, Wavelike stomach contractions, Small poops + can’t
gain weight, Dehydration, Irritability
Compare and contrast disorders of the upper GI system
Hiatal Hernia
A section of the stomach protrudes upward through an
opening in the diaphragm
- Causes: Weakening of the diaphragm muscle; Increased
intrathoracic pressure (straining during BM) or ↑
intra-abdominal pressure (pregnancy/obesity); Trauma;
Congenital.
- Risk factors: being old and smoking.
- Manifestations: Indigestion, heartburn, burping, nausea,
CP, strictures, dysphagia, soft upper abdominal mass
(protruding stomach pouch)
- Worsen with recumbent positioning, eating (after big
meals), bending over, coughing
Cholelithiasis
(gallstones): common - varies based on size of stone →
affects everyone equally
Cholecystitis: inflammation/ infection in biliary system
caused by calculi
- Risk factors: old ppl, obesity, diet, weight loss, pregnancy,
hormone replacement, long-term parenteral nutrition
- Obstruct bile flow = gallbladder rupture, fistulas,
gangrene, hepatitis, pancreatitis, carcinoma
- Manifestations: Biliary colic, abdominal distension, N/V,
jaundice, fever, leukocytosis
GERD
Chyme or bile backs up from stomach to esophagus → irritating esophageal mucosa
- Causes: foods (chocolate, caffeine, citrus, tomatoes, spicy/fatty foods); EtOH/nicotine; hx of hiatal hernia;
Obesity; Pregnancy; meds (corticosteroids, β-blockers, Ca2+- channel blockers, anticholinergics); Delayed
gastric emptying
- Manifestations: Heartburn, epigastric pain (after eating), dysphagia, dry cough, laryngitis pharyngitis,
regurgitation, sensation of a lump in the throat
- Confused with CP → rule out cardiac disease
- Complications: Esophagitis, strictures, ulcerations, esophageal CA, and chronic pulmonary disease
Disorders of the Liver
Hepatitis
Inflammation of the liver → can be acute, chronic, fulminant.
- Causes: Infections (usually viral), EtOH, meds (acetaminophen, antiseizure, Abx), autoimmune.
- Can result in hepatic cell destruction, necrosis, autolysis, hyperplasia, scarring
- Non Viral hepatitis: non contagious and most recover (toxicity related to meds) → can get liver failure/CA, cirrhosis
(being old + comorbidity increases risk)
- Viral hepatitis: contagious → most will recover w/ time
- Acute hepatitis: 4 phases: asymptomatic, incubation, 3 symptomatic.
- Chronic hepatitis: Continued hepatic disease (6m+) → Can quickly deteriorate
Cirrhosis
Chronic, progressive, irreversible, diffuse damage to liver → low liver function
- Leads to fibrosis, nodule formation, impaired blood flow, bile obstruction → liver failure
- Causes: Hep C + EtOH (most frequent in US)
- Manifestations: Portal HTN; Ascites; Jaundice; Varicosities; Enlarged organs; Slow or severe bleeding; Clotting;
Muscle wasting; HLD; Hyper- or hypoglycemia; Toxin and bile accumulation; Clay poops/dark pee; itchy, ↓ estrogen
absorption
Complications of Liver Disease:
Portal hypertension: portal veins increase pressure.
Ascites: fluid in abdomen → albumin decreases w/ cirrhosis.
jaundice; hepatic encephalopathy; esophageal varices
Disorders of the Pancreas
Pancreatitis
Inflammation of the pancreas → acute or chronic
- Causes: Cholelithiasis, EtOH, biliary dysfunction, hepatotoxic drugs, metabolic/endocrine disorders, trauma, renal
failure, pancreatic tumors, penetrating peptic ulcer
- Pancreatic injury → enzymes leak into pancreatic tissue → autodigestion → in edema/vascular damage, hemorrhage,
necrosis
- Pancreatic tissue replaced by fibrosis→ exocrine/endocrine changes + dysfunction of islets of langerhans
- Acute pancreatitis: emergency → Mortality increases with being old + comorbidity.
- Complications: ARDS, DM, infection, shock, disseminated intravascular coagulation, renal failure, malnutrition,
pancreatic CA, pseudocyst, abscess
- Manifestations of acute pancreatitis: sudden/severe: Upper abdominal pain→radiates to back (worse after eating,
better leaning forward), N/V, jaundice; Low-grade fever; Blood pressure and pulse
- Manifestations of chronic pancreatitis: insidious: Upper abdominal pain; Indigestion; Losing weight; Steatorrhea;
Constipation; Flatulence
Disorders of the lower GI tract
Intestinal Obstruction
Sudden/gradual and partial/complete blockage of contents in intestines
- Mechanical obstructions: Foreign bodies, tumors, adhesions, hernias, intussusception, volvulus, strictures, IBD, and
fecal impaction
- Functional obstructions (paralytic ileus): Neuro impairment; intra- abdominal sx complications; chemical, electrolyte,
mineral disturbances; infections; abd. Blood supply impairment; meds(narcotics)
- Chyme/gas accumulate at blockage → saliva, gastric juices, bile collect → abdominal distension/pain
- Blood flow impairment: strangulation, necrosis, contents seep into abdomen
- Complications: perforation, pH imbalances, fluid disturbances, shock, death
- Manifestations: Abdominal distension/cramping/colicky pain, N/V/D, Constipation; Intestinal rushes; Absent bowel
sounds; Restlessness; Diaphoresis; Tachycardia→weakness; Confusion, shock
Celiac Disease
Gluten-sensitivity → inherited, autoimmune, malabsorption disorder
- combo of environmental factor (gliadin) + genetics
- White/female → in childhood but can show up at any time.
- Results from a defect in the intestinal enzymes that prevents further digestion of gliadin (a product of gluten digestion)
- Intestinal villi atrophy and flatten, resulting in decreased enzyme production, decreasing surface area available for
nutrient absorption
- Manifestations: In infants, generally appear as cereals are added to their diet (usually around 4–6 months of age)
Include abdominal pain or distension, bloating, gas, indigestion, constipation, diarrhea, lactose intolerance, nausea,
steatorrhea, weight loss, irritability, lethargy, malaise, behavioral changes
- Complications: Anemia, arthralgia, myalgia, bone disease, enamel defects, intestinal CA, depression,
growth.development delays, hair loss, hypoglycemia, mouth ulcers, bleeding tendencies, neuro/skin/endocrine
disorders, vitamin/mineral deficiency
Inflammatory Bowel Disease
Chronic inflammation of the GI tract, usually the intestines
- Chiefly seen in women, Caucasians, persons of Jewish descent, and smokers
- Characterized by periods of exacerbations and remissions
- Thought to be caused by a genetically associated autoimmune state that has been activated by an infection
- Immune cells located in the intestinal mucosa are stimulated to release inflammatory mediators that alter the
function and neural activity of the secretory and smooth muscle cells
-
Fluid, electrolyte, and pH imbalances develop
Can be painful, debilitating, and life-threatening
Crohn’s Disease: Insidious, slow-developing, progressive
condition often develops in adolescence
- Characterized by patchy areas of inflammation
involving the full thickness of the intestinal wall and
ulcerations (skip lesions); wall is thick/rigid and
lumen is narrowed
- Form fissures divided by nodules, giving the
intestinal wall a cobblestone appearance
- Granulomas develop on the intestinal wall and
nearby lymph nodes
- The damaged intestinal wall loses the ability to
digest and absorb
- The inflammation also stimulates intestinal motility,
decreasing digestion and absorption
- Manifestations: Abdominal cramping and pain;
Diarrhea; Steatorrhea; constipation; Palpable
abdominal mass; Melena; Anorexia; Weight loss;
Indications of inflammation (e.g., fever, fatigue,
arthralgia, and malaise)
- Complications: Malnutrition; anemia (especially iron
deficiency); fistulas; adhesions; abscesses;
intestinal obstruction; perforation; anal fissure;
delayed growth and development; and fluid,
electrolyte, and pH imbalances
Ulcerative Colitis: Progressive condition of the rectum
and colon mucosa - usually develops in 20s–30s
- Inflammation triggered by T-cell accumulation in
the colon mucosa causes epithelium loss,
surface erosion, and ulceration that begins in the
rectum and extends to the entire colon
- The mucosa becomes inflamed, edematous,
and frail
- Necrosis of the epithelial tissue can result in
abscesses; granulation tissue formed is fragile
- Ulcers merge = inadequate surface area for
absorption
- Manifestations: Diarrhea (usually frequent [as
many as 20x daily]; Watery stools (with blood
and mucus); Proctitis; Abdominal cramping;
Nausea and/or vomiting; Weight loss; Indications
of inflammation (e.g., fever, fatigue, arthralgia,
and malaise)
- Complications: Malnutrition; Anemia;
Hemorrhage; Perforation; Strictures; Fistulas;
Toxic megacolon; Colorectal carcinoma; Liver
disease; Fluid, electrolyte, and pH imbalances
Irritable Bowel Syndrome
Chronic, noninflammatory → exacerbations d/t stress
- Less serious than IBD → noninflammatory = no permanent intestinal damage
- Common: more women than men.
- Complications: hemorrhoids, nutritional deficits, social issues, sexual discomfort
- Manifestations: Stress, mood disorders, food/hormone worsen sxs; Abdominal distension,
fullness/flatus/bloating; abdominal pain (worse by eating, better w/ defecation)
- Manifestations: Chronic constipation or diarrhea, usually accompanied by pain; Non bloody stool w/ mucus;
Bowel urgency; Intolerance to certain foods (gas-forming foods + sorbitol, lactose, and gluten); Emotional
distress; Anorexia
Diverticulosis vs. diverticulitis
- Conditions related to diverticula = outwardly bulging pouches of intestinal wall d/t mucosa sections/large
intestine submucosa layers herniate through weakened muscular layer
Diverticulosis: multiple diverticula → asymptomatic
Diverticulitis: diverticula inflamed d/t retained fecal matter
(asymptomatic → serious)
GI Cancers
Esophageal Cancer
SCC in distal esophagus (usually men)
- Chronic irritation
- Tumors grow the circumference of the esophagus =
stricture, or grow out into lumen = obstruction
- Complications: esophageal obstruction, respiratory
compromise, esophageal bleeding
- Usually asymptomatic early, delaying tx
- Manifestations: dysphagia, CP, weight loss, hematemesis
Colorectal Cancer
- common/fatal → asymptomatic until advanced.
– Associated with fatty, caloric, low-fiber diets with red
meat, processed meat, and alcohol
- Risk factors: male,, African American, FHx, old ppl,
obesity, tobacco, physical inactivity, IBD
- Manifestations: lower abdominal pain, blood in the
stool, diarrhea, constipation, intestinal obstruction,
narrow stools, anemia (iron deficiency), weight loss
Urinary and Reproductive Function
Conditions resulting in altered urinary elimination
Interstitial Cystitis/ Bladder Pain Syndrome
Chronic → women + old ppl → pain/pressure in suprapubic, pelvic + abdominal area
-Cause: unknown
-5% have sxs 2+ years, 5% get end-stage disease where bladder hardens + capacity is low + pain worsens
-Manifestations: Pain in urinary tract (worse w/ pressure), frequency, nocturia, urgency (constant, worse w/ stress),
sexual dysfunction
Urinary Tract Infections
Common bacterial infections → usually ascending.
- Risk factors: Female; Sexually active (multiple partners); Use
of diaphragm with spermicide; hx of DM, Recent
instrumentation (catheters); Structural abnormalities; bad
hygiene; Immobility
- Upper UTI: Pyelonephritis > Acute or Chronic
- Lower UTI: Cystitis > Urethritis
Symptoms of UTIs
-Lower UTIs: dysuria; Urgency; Frequency; Low back
pain; Foul smelling urine; Cloudy urine (pyuria);
Hematuria; Fever
-Upper UTIs (kidneys): Flank pain; Fever; N/V, ↑ BP,
sxs of cystitis
Urinary Tract Infections: Cystitis
Bladder infection → bladder/urethra walls are red/swollen.
- Causes: infection and irritants
- Bacteria goes to bladder by urethra → up to kidneys
- E. coli accounts for 75-95% of UTIs
Pyelonephritis
A bacterial infection that causes inflammation in the kidneys
Urinary Tract Obstructions: Nephrolithiasis
Having renal calculi, hard crystals made of minerals that the
kidneys excrete, in renal pelvis, ureters, or bladder
-Men and Caucasians
-common type: Ca2+ w/ oxalate or phosphate
-also include struvite or infection stones, uric acid, cystine
Urinary Tract Obstructions: Hydronephrosis
Abnormal dilation of renal pelvis + calyces of 1+ kidneys
- Unilateral = 1+ ureters obstruction
- Bilateral = urethra obstruction
- Causes: urolithiasis, tumors, BPH, strictures, stenosis,
congenital urologic
- Risk factors: pH changes, lots of salts in pee, urinary
stasis, FHx, obesity, HTN, diet
- Manifestations: Colicky pain in flank that radiates to
abdomen and groin; bloody, cloudy, or stinky pee; dysuria;
frequency; genital discharge; N/V, fever/chills
- Complications: atrophy, necrosis, no glomerular
filtration
- Manifestations: colicky, flank painp; bloody, cloudy, or
stinky urine; dysuria; low urine output; frequency;
urgency; N/V; abdominal distension; UTIs
Benign Prostatic Hyperplasia
Enlargement of prostate as men age → common/nonmalignant → unknown cause → may lead to urinary stasis + UTIs
- ↓ testosterone and ↑ estrogen levels = prostatic stromal cell proliferation → big prostate
- Or stem cells in prostate don’t mature/die → big prostate
- Presses against urethra = obstructs urine
- Manifestations: frequency; urgency; retention; difficulty initiating urination; weak stream; dribbling, nocturia;
bladder distension; overflow incontinence; ED
Describe and compare renal alterations that result in impaired renal function
Glomerulonephritis
bilateral inflammatory disorder of glomeruli d/t strep → renal failure
- men more than women
- Inflammation impairs ability to excrete waste and excess fluid
Nephrotic Syndrome
From Ab–antigen complexes in glomerular membrane →
complement system
- Glomeruli can’t filter albumin
- Causes: systemic diseases, gold therapy, idiopathic
- Results in ↑ glomerular capillary permeability → marked
proteinuria, lipiduria, low albumin, anasarca
- Other manifestations: dark and cloudy urine,
immunoglobulins in urine
Nephritic Syndrome
Inflammatory injury to glomeruli d/t Ab interacting w/
normal antigens in glomeruli
- Glomeruli can’t filter RBCs
- Causes: diseases that initiate the inflammatory response
- Manifestations: gross hematuria, urinary casts and
leukocytes, low GFR, azotemia (increased BUN & Cr),
oliguria, ↑ BP
Complications: impaired renal function
Acute Kidney Injury
Sudden loss of renal function (critically ill hospitalized) → reversible
- Prerenal: extremely low BP or blood volume; cardiac dysfunction
- Intrarenal: reduced blood supply in kidneys, hemolytic uremic syndrome, renal inflammation, toxic injury (meds)
- Postrenal: ureter obstruction, bladder obstruction/dysfunction
- Risk factors: old ppl, autoimmune, and liver disease
Phases:
- Asymptomatic
- Oliguric (daily urine output <400 mL): electrolyte disturbances, fluid volume excess, azotemia, metabolic
acidosis
- Diuretic (daily urine output >5 L): electrolyte disturbances, dehydration, hypotension
- Recovery: glomerular function gradually returns to normal
Chronic Kidney Disease
Gradual loss of renal function = irreversible
- Causes: DM, HTN, urine obstructions, renal diseases, renal artery stenosis, exposure to toxins + nephrotoxic
meds, sickle cell, lupus, smoking, old ppl.
- GFR: measure of how well kidneys filter blood → determines stage; 5 stages of kidney disease
- GFR >90, but has some damage = stage 1
- Less than 15 = stage 5. BAD.
- Manifestations: HTN, polyuria, edema, azotemia (BUN/creatinine accumulation), flank pain, jaundice, anemia,
oliguria
Disorders of the scrotum/testes
Cryptorchidism
One or both testes do not descend from abdomen → scrotum
- Risk factors: Prematurity, low birth weight, small size for age, FHx of genital development issues, multiple
fetuses, maternal estrogen exposure during 1st trimester, maternal EtOH + smoking/ secondhand smoke,
maternal DM, parental exposure to pesticides
- Retractile testicle: moves back and forth b/w scrotum + lower abdomen
- Ascending testicle: testicle returns to lower abdomen → cant easily be returned to scrotum
Torsion of the Testes
Abnormal rotation of testes on the spermatic cord → ischemia + necrosis = EMERGENCY.
- Causes: trauma → also spontaneously
- Manifestations: sudden scrotal edema + pain, n/v, dizziness, absent cremasteric reflex
Menstrual Disorders
Pelvic Organ Prolapse
Muscles, ligaments, and fascia normally support the bladder, uterus, and rectum in female pelvis
- Can weaken w/ age, childbirth, trauma, hormonal changes during menopause → organs shift out of normal
position
-
Examples: cystocele, rectocele, uterine prolapse
Disorders of the Uterus
Endometriosis
Endometrium grows in areas outside uterus
- Common in fallopian tubes, ovaries, peritoneum → tissue can grow anywhere.
- abnormal endometrial tissue acts the same as it would during menses.
- Blood gets trapped → irritates surrounding tissue
- Cause: unknown
- Complications: pain, cysts, scarring, adhesions, infertility
- Manifestations: dysmenorrhea, menorrhagia, pelvic pain, dyschezia (difficulty defecating), infertility,
intermenstrual bleeding, and pain after sex.
Disorders of the Ovaries
Ovarian Cysts
Benign, fluid-filled sacs on ovary → formed in ovulation process
- May rupture = discomfort
- Complications (rare): hemorrhage, peritonitis, infertility, amenorrhea
- Manifestations: may be asymptomatic OR abd pain or discomfort, abnormal menses, abd distension
Polycystic ovary syndrome (PCOS)
Ovary enlarges and contains numerous cysts
- Cause: unknown → linked to hormone and endocrine abnormalities
- Manifestations: infertility (anovulation), amenorrhea, hirsutism, acne, male-pattern baldness
- Increases the risk for obesity, DM, CVD, CA
Misc. Infectious and Inflammatory Disorders
Candidiasis
Yeast infection d/t Candida albicans → opportunistic infection that can appear anywhere.
- Candidiasis usually in vagina → common cause of vaginitis (inflammation of the vagina)
- Candida + other microorganisms part of normal flora → balance each other
- Imbalance d/t vaginal pH changes
- Causes: Abx therapy, bubble baths, feminine products, low immune response, increased glucose in vaginal
secretions
- Not sexually transmitted → men may develop mild sxs after sex with infected partner
- In males → resolve w/o tx.
- Manifestations: Thick, white vaginal discharge (cottage cheese); vulvar erythema and edema; vaginal and
labial itching + burning; white patches on wall; dysuria; painful sex
Pelvic Inflammatory Disease
Infection of the female reproductive system → bacteria ascend from vagina
- Acute or chronic
- Causes: STI; bacteria during childbirth, endometrial/abortions; and bacteria from blood.
- Complications: Reproductive obstructions, peritonitis, abscesses, septicemia, adhesions, strictures, chronic
pelvic pain, ectopic pregnancies, infertility
- Manifestations: Indications of infection; pelvis/lower abd/lower back pain/tenderness, abnormal vaginal +
cervical discharge; bleeding after sex; painful sex; frequency; dysuria; dysmenorrhea; amenorrhea; AUB;
anorexia; N/V.
Epididymitis
Ascending bacterial infections or STIs (common)
- Risk factors: uncircumcised, recent Sx, structural problems in urinary tract, urinary catheterization, unprotected
sex
- Complications: abscesses, fistulas, infertility, testicular necrosis, chronic epididymitis
- Manifestations: indicators of infection (fever, chills, myalgia); scrotal tenderness, erythema, and edema; penile
discharge; bloody semen; painful ejaculation; dysuria; groin pain
Prostatitis
Prostate inflammation → acute or chronic
- Causes: conditions that trigger inflammatory process
- Common: young/middle-aged men, immunocompromised, Hx of STIs
- Manifestations: Dysuria; difficulty urinating; frequency; urgency; nocturia; pain in the abdomen, groin, lower
back, perineum, or genitals; painful ejaculations; indications of infection; UTIs.
Reproductive Cancers
Breast Cancer
Common malignancy in women → 2nd leading cause of CA
- Rates high: Caucasian women, Mortality rate higher in African American women.
- Rare in men.
- Contributing factors: age, early onset of menstruation, FHx, genetics (BRCA1/BRCA2 genes), obesity, chest
wall radiation, EtOH, exogenous estrogen exposure
- Most estrogen-dependent → originate in duct system → may arise in lobules
- Freely movable when early → Fixed as it progresses.
- Metastasis to nearby lymph nodes, lungs, brain, bone, and liver
- Manifestations: Asymptomatic OR painless hard mass w/ uneven edges in the breast or axillary change in the
size + shape of breast or nipple; bloody/clear/purulent nipple drainage
Cervical Cancer
Almost all caused by HPV, detected w/ pap smear → prevention = HPV vaccine.
- Manifestations: asymptomatic OR continuous vaginal discharge; abnormal bleeding b/w menses, after sex, or
after menopause
Hematopoietic Function
Disorders of the WBC’s
Leukocyte disorders
Leukocytes (WBCs) = key players in inflammatory response + fighting infection
- Normal range = 5k - 10k cells/mL in blood
- Leukocytosis: lots of leukocytes → ongoing infectious process
- Leukocytopenia/Leukopenia: low leukocytes → immunosuppression or deficiency
Neutrophils: 1st leukocyte to get to infection site (2k - 7500k cells/mL)
- Neutropenia: neutrophils <1,500 cells/mL → d/t congenital, disease, environment.
- Manifestations depend on severity/cause → include infections and ulcerations (especially mucous
membranes) signs of infection (like fever) (all signs of immunodeficiency)
- Neutrophilia: Lots of granulocytes → in 1st stages of infection. If need immature neutrophils → “Shift to the left”
(shift to immaturity)
Infectious Mononucleosis: “kissing disease’ → spread by oral transmission → by EBV in herpes family.
- Self limiting; prevalent in young adults
- Infects B cells by killing cell or incorporating into its genome
- Manifestations: leukocytosis, fever, sore throat, lymphadenopathy, risk for splenic rupture
Lymphoma
CANCERS AFFECTING THE LYMPHATIC SYSTEM
HODGKIN LYMPHOMA
- Less common; tumors have Reed-Sternberg cells starting in
lymph nodes of upper body (neck, chest, upper arms)
- Spreads from lymph nodes via lymphatic vessels
- Several subtypes, Curable w/ chemo/radiation, Sx
- Adults 20-30yrs →, then peak around 70yrs.
- Physical findings: Enlarged painless lymph nodes- begin in
upper body, mediastinal mass, splenomegaly
- Symptoms: Fever, weight loss, night sweats, pruritus
NON-HODGKIN LYMPHOMA
- Common: (90% of all lymphomas)
- 5YR survival rate = 68%
- Like Hodgkins in manifestation, staging,
tx.
- Spreads + diagnosed differently (no
Reed-Sternberg cells)
- Involves nodes throughout the body
May originate in T or B cells
Leukemia
CANCER OF THE LEUKOCYTES → 2ND MOST COMMON BLOOD CA AFTER LYMPHOMAS
- Leukemia cells abnormally proliferate → crowd nml blood cells (limits functioning)
- Risk factors include mutagens (chemical, viral, radiation), smoking, chemo, diseases (Down syndrome),
immunodeficiencies
- Common: most among peds.
- Acute (less differentiated) or chronic (more differentiated), lymphoid or myeloid (cell line)
- Manifestations: Leukopenia = frequent infections; Anemia = fatigue, activity intolerance; Thrombocytopenia =
increased bleeding risk; Lymphadenopathy; Joint swelling/bone pain, weight loss, anorexia; Hepatomegaly,
splenomegaly; CNS dysfunction
Disorders of the RBC’s
Anemias
Low # of RBCs, low Hgb or abnormal Hgb
- Decreases O2-carrying capacity → tissue hypoxia
- Acquired or inherited
- Manifestations: weakness, fatigue, pallor, syncope, dyspnea, tachycardia
- Size: -cytic (Macrocytic, microcytic, normocytic)
- Hgb: -chromic (Normochromic, hypochromic)
Types of Anemia
RBC Size
Color of RBC
Normocytic Normochromic
Normal
Normal
Normocytic Hypochromic
Normal
Less
Macrocytic Hypochromic
Large
Less
Microcytic Hypochromic
Small
Less
Types of Anemia
PERNICIOUS ANEMIA
- Vitamin B₁₂ deficiency → by an autoimmune lack of intrinsic factor
- Macrocytic, normochromic
- Leads to low maturation, cell division, and neuro complications d/t myelin breakdown
- Manifestations: bleeding gums, diarrhea, impaired smell, loss of DTR, anorexia, personality/memory changes,
positive Babinski’s sign, stomatitis, paresthesia, unsteady gait
IRON-DEFICIENCY ANEMIA
- Hypochromic, microcytic anemia
- Causes: low iron intake in diet/absorption issues, increased bleeding
- GI disorders affecting iron absorption (celiac disease, gastritis, bariatric sx)
- Common: women of childbearing age, peds under 2yrs, old ppl.
- Manifestations: cyanotic sclera, brittle nails, low appetite, HA, irritability, stomatitis, pica, delayed healing
APLASTIC ANEMIA
- Bone marrow depression of all blood cells = pancytopenia
- Idiopathic, autoimmune, medical, viral, or genetic in origin
- Potentially insidious, sudden, and severe onset
- Manifestations: anemia, leukocytopenia, thrombocytopenia sxs.
HEMOLYTIC ANEMIA
- Lots of erythrocyte destruction, or hemolysis
- Causes: idiopathic, autoimmune, genetics, infections, blood transfusion, blood incompatibility in neonate
Thalassemia
Abnormal Hgb; alpha thalassemia = four genes; beta thalassemia= two genes (more severe)
- Manifestations: growth/developmental delays, fatigue, dyspnea, HF, big spleen, bone deformity.
Sickle Cell Anemia
Hgb S → RBCs carry less O2 and clog vessels → hypoxia + tissue ischemia
- Common: African/Mediterranean descent, South/Central America, Caribbean, Middle East
- Heterozygous = less than half RBC are sickle.
- Homozygous = disease → all RBCs are sickle → occlude BV and block blood flow
- Manifestations: 4 months → sickle cell crises: painful episodes of tissue ischemia and necrosis (hours→days)
triggered by dehydration, stress, altitude, or fever
Polycythemia Vera
Rare neoplastic disease of abnormally high RBCs = increase blood volume/viscosity → tissue ischemia/necrosis
- Bone marrow makes too much RBC (sometimes too many leukocytes & platelets)
- Primary = mutation in JAK2 gene → uncontrolled hematopoietic stem cell growth
- Secondary = long term low O2 (severe heart/lung disease, smoking, high altitudes, high levels of carbon monoxide)
- Relative = appearance of increased RBCs because of reduction in plasma (dehydration)
- Hypercoagulable state = clogging + occlusion of BV
- Complications: tissue ischemia/necrosis, clot, HTN, HF, hemorrhage, big spleen/liver, acute myeloblastic leukemia
- Manifestations: cyanotic/plethoric skin, hypertension, tachycardia, dyspnea, headaches, vision impairment
- A unique feature is intense, painful itching that appears to be intensified by heat or exposure to water
(aquagenic pruritus) so individuals avoid exposure to warm water when bathing or showering
Disorders of the Platelets
Normal platelet: 150K - 300K
Thrombocytosis: high platelets (clots risk)
Thrombocytopenia: low platelets (bleeding risk)
Thrombocytopenia
platelet count less than 150K.
Causes:
- Low platelet production: Viral infections; Drugs/radiation; chronic renal failure; Bone marrow hypoplasia or CA
- High platelet consumption: Heparin-induced thrombocytopenia (HIT); Idiopathic (immune) thrombocytopenia
purpura (ITP); Thrombotic thrombocytopenia purpura; Disseminated intravascular coagulation (DIC)
Hemophilia
Inherited bleeding disorder → decreased coagulation (gene mutation that says how to make clotting factors) →
Inherited x-linked recessive.
- Inherited or spontaneous mutation of the factor gene (30%)
- Manifestations: bleeding or signs of bleeding (bruising, petechiae)
- May see s/s during infant circumcision or when infant starts crawling/walking
- Hemarthrosis = bleeding into the joints
Musculoskeletal Function
Traumatic Musculoskeletal Disorders
Fractures
- Breaks in structure of the bone → most common traumatic MSK
- Primary causes: falls, MVA, sports injuries
- Secondary causes: Conditions that weaken bone
- Classification: direction of fx line, # of fx lines, other characteristics
- Manifestations: Deformity (angulation, shortening, androtation), Swelling/tenderness, can’t move limb, crepitus,
pain, Paresthesia, Muscle flaccidity → spasms
Simple: single break w/ bone ends maintaining
alignment + position
Transverse: straight across the bone shaft
Oblique: at an angle to bone shaft
Spiral: twists around the bone shaft
Comminuted: multiple fx lines+ bone pieces
Greenstick: incomplete break = bone bent and outer curve of
bend is broken
*In peds d/t minimal calcification → heals quickly.
Compression: bone crushed into small pieces
Complete: broken into 2+ separate pieces
Incomplete: partially broken
Open/compound: skin is broken, bone fragments may be angled
and protrude out of skin
-Causes more damage to soft tissue and ↑ infection risk.
Closed: skin intact
Impacted: 1 end of bone is forced into adjacent bone
Pathologic: d/t weakness in bone structure
secondary to conditions (tumors or osteoporosis)
Stress/fatigue: From repeated stress (tibia, femur, and
metatarsals)
Depressed: occurs in the skull when the broken piece is forced inward on the brain
Fracture Healing
- Hematoma (aka blood clot) forms
- Necrosis of the broken bone ends occurs from blood vessel damage
- Fibroblasts invade the clot within a few days
- Fibroblasts secrete collagen fibers, which form a mass of cells and fibers called a callus
- Callus bridges the broken bone ends together inside and outside over 2-6 weeks
- Osteoblasts invade the callus and slowly convert it to bone in from 3 weeks to several months (usually 4-6
weeks)
Complications
Delayed union, malunion, nonunion: may occur due to poor nutrition, inadequate blood supply, malalignment, and
premature weight bearing
Compartment syndrome: a serious condition that results from increased pressure in a compartment, usually the muscle
fascia in the case of fractures; excruciating pain; The classic signs of acute compartment syndrome include the 6 'P's':
pain, paresthesia,poikilothermia (inability to regulate temp), pallor, paralysis, and pulselessness
Fat embolism: fat enters the bloodstream, usually after a long bone fracture; Clinical manifestations: hypoxemia,
neurologic dysfunction, petechiae on head or trunk; Prevention: early immobilization of fracture
Osteomyelitis
Osteonecrosis, or Avascular Necrosis: Death of bone tissue due to a loss of blood supply; can result from displaced
fractures or dislocations
Osteomyelitis
Infection of bone tissue → months to resolve = bone or tissue necrosis
Routes of Infection to the Joint
1. Hematogenous Route
2. Dissemination from osteomyelitis
3. Spread from adjacent soft tissue damage
4. Diagnostic or therapeutic measures
5. Penetrating damage by puncture or cutting
Dislocations
-Separation of 2 bones at joint; May be complete or partial (subluxation)
- Causes deformity, immobility, and damage to ligaments + nerves
- Causes: Impact to joint, congenital, pathologic (arthritis,injuries, paralysis, neuromuscular)
- Common: shoulder + clavicle
- Manifestations: Out-of-place, deformed joint; Limited movement; Swelling/ bruising; Intense pain, especially w/
movement; Paresthesia
Sprains
Ligament injury → involves stretching or tearing.
- Causes: forcing joint into weird position
- Severity: grading scale
- Common: ankle + knee
- Manifestations: edema, pain, bleeding, stiffness, limited function, disability, discoloration (bruising)
Strains
- Muscle/Tendon injury → involves stretching or tearing
- Suddenly or over time
- D/t awkward muscle movement or excess force (accident, improper use/overuse of muscle)
- Risk factors: excessive activity, improper stretching b4 activity, poor flexibility
- Common: lower back
- Severity: grading scale
- Manifestations: pain, stiffness, difficulty moving, skin discoloration (bruising), edema
Herniated Intervertebral Disc
Protrusion of nucleus pulposus through annulus fibrosus → Suddenly or gradually
- Can exert pressure on the spinal cord
- Sensory, motor, autonomic function may be impaired depending on location
-
Involves: lumbosacral region → some w/ cervical discs
- Permanent neuro damage if pressure on nerve/blood supply is prolonged.
Causes: improper body mechanics, lifting heavy shit, repetitive use, trauma, vertebral stress d/t obesity,
degenerative (aging/demineralization)
Manifestations: May be asymptomatic, Sciatica, Pain, paresthesia, weakness in lower back/one
leg/neck/shoulder/chest/arm, Low back/leg pain -worse w/ sitting, coughing, sneezing, laughing, bending,
walking, Limited mobility
Metabolic Bone Disorders
Osteoporosis
Progressive loss of bone Ca2+ = brittle bones.
- D/t pathogenetic mechanisms → decrease in osteoblast activity or increase in osteoclast activity
- Spongy bone → porous (in vertebrae and wrist)
- Compact bone → thin
- Causes: genetics, diet (low Ca2+, protein, vit C and D, high phosphorus), hormones (menopause LOW
ESTROGEN & TESTOSTERONE), physical inactivity
- Risk factors: old ppl, female, underweight, undergoing GI procedures (gastrectomy or bypass), Caucasian,
Asian, smoking, EtOH or caffeine, meds (corticosteroids, chemo, thyroid, heparin, antacids), and certain health
conditions (cushing's, thyroid dysfunction, bone tumors, malabsorption, anorexia)
- Complications: pathologic fx (wrist, hip, and spine)
- Manifestations: Asymptomatic in early stages → osteopenia (bone mass less than expected forage, ethnicity,
gender), bone pain, fx w/ little or no trauma, low back/neck pain, kyphosis, height reduction (6 inch) over time
Rickets and Osteomalacia
Rickets: soft, weak bones in peds d/t extreme/prolonged vitD, Ca2+, or phosphate deficiency
Osteomalacia: adult form
- Blood levels low → Ca2+ and phosphate shift out of bone → weak/soft bones
- Risk factors: vitD deficiency (bed bound, institutionalized ppl, working indoors, darker skin tones, strong
sunscreen, celiac disease, CF, gastrectomy, diet imbalances, genetics, renal disease, and liver disease (peds)
- Manifestations: slow as bones weaken → obvious in peds as soft bones can’t support growing child, fx, walking
difficulty, Skeletal deformities (bowed legs, asymmetrical skull, scoliosis, kyphosis, pelvic deformities, sternum
projection), Delayed growth, Dental problems, Bone pain, Muscle cramps/weakness
Paget’s Disease
Progressive metabolic condition→ excessive bone destruction + replacement of bone by fibrous tissue and abnormal
bone
- New bone = bigger but weaker + w/ new BV = fragile, misshapen bones.
- In 1+ areas or throughout body (long bones, skull, pelvis, vertebrae)
- Cause: unknown → by a virus that increase osteoclast activity or genetics (increase in IF-6)
- Onset: insidious.
- Common: men, central European descent, FHx
- Manifestations: Depends on area affected → asymptomatic early, Bone pain, deformities (bowing of the legs,
asymmetrical skull, + big head), Fx, HA, Hearing/vision loss, Joint + neck pain, Short height, Warmth over
affected bone, Paresthesia/radiating pain in the affected region, Hypercalcemia
Inflammatory Joint Disorders
Osteoarthritis vs Rheumatoid Arthritis
Osteoarthritis
Subchondral bone exposed + damaged → cysts and
osteophytes (bone spurs) form as bone remolds itself
● Osteophytes/cartilage break off into synovial
cavity→ more irritation
Not inflammatory in origin, but inflammation d/t tissue
irritation
Causes: idiopathic or mechanical stress (obesity,
overuse, injury, congenital MSK conditions)
Manifestations: (over 40yrs) Gradual, slow →
worsens,
Joint pain = worse w/ movement/weight, tenderness
w/ light pressure, Joint stiffness (morning, after
inactivity) Big+hard joints, swelling, Limited joint ROM,
Crepitus, Hard nodules around joint (bone spurs)
Rheumatoid Arthritis
Systemic, autoimmune → multiple joints
● Inflammatory → affects synovial membrane (other
organs too)
● Affects joints bilaterally (wrists, fingers, knees, feet,
ankles)
● Cause: unknown → genetic vulnerability, allows viirus
or bacterium to trigger disease
Risk factors: female, FHx, old ppl, smoking
Manifestations: Insidious onset → Progressively worsens,
Initially seems to mimic acute viral syndrome,
Fatigue, Anorexia, fever, Lymphadenopathy, Malaise, Muscle
spasms, Morning stiffness 1+ hrs, Warmth, tenderness, and
stiffness in the joints when not used for as little as 1 hour,
Bilateral joint pain, Swollen and boggy joints, Limited joint
ROM, Contractures and joint deformity (boutonniere deformity
and swan neck deformity), Unsteady gait, Depression, Anemia
Gout
Inflammatory disease d/t deposits of uric acid crystals in tissues and fluids
● Uric acid: by-product of breaking down purines (found in body + foods-organ meats, shellfish, anchovies,
herring, asparagus, mushrooms)
● From hyperuricemia d/t a lot of or not enough (most common) uric acid → Not everyone w/ hyperuricemia have
gout
● Causes/risk factors: inborn error in metabolism, obese, diseases (HTN, DM, renal disease, sickle cell), EtOH
(beer more than wine), meds (diuretics), diet rich in meat/seafood
● Manifestations: Depends on phase, Intense pain at affected joint (at night - throbbing, crushing, burning, or
excruciating) Warmth, redness, swelling, tenderness (light touch), Fever, deformities, Limited joint mobility
Phases of Gout
- Asymptomatic, Acute flares or attack, Intercritical period, Chronic gouty arthritis
Ankylosing Spondylitis
Progressive inflammatory disorder affecting the sacroiliac joints, intervertebral spaces, costovertebral joints
- Vertebral joints of lower back at sacroiliac joints inflammation → spine
- NEW BONE FORMS IN AN ATTEMPT TO REMODEL THE INFLAMMATORY DAMAGE → joint fibrosis and
calcification = JOINTS BECOME ANKYLOSED
- Vertebrae appear square → vertebral column becomes rigid + loses curvature
- Genetics seem to play a role in development (HLA-B27 gene is present in most cases)
- Complications: kyphosis, osteoporosis, respiratory + endocarditis
- Remission and exacerbation
- Manifestations: Intermittent lower back pain (early), Pain/stiffness - worse w/ inactivity, better after activity,
Lower back pain → entire back, Pain in other joints (shoulders, hips, lower extremities), Muscle spasms,
Fatigue, fever, Weight loss, Kyphosis
Chronic Muscle Disorders
Muscular Dystrophy
Inherited, noninflammatory disorders → degeneration of skeletal muscle
- 9 forms (Becker, Duchenne, myotonic, and limb-girdle) → varying inheritance patterns/ pathogenesis
- Common across all: muscle protein abnormality (dystrophin) = muscle dysfunction, weakness, muscle fiber loss,
inflammation → involve tissues (cardiac and smooth muscle)
- Fat and fibrous connective tissues → replace skeletal muscle fibers → weakening the muscles
- Some rare, some common
- Most inherited, some d/t mutation (spontaneous)
- Some = disability + rapid decline, others = low sxs, no progression.
- Some = in childhood, others = late adulthood.
- Most common/severe: Duchenne MD → males (X-linked recessive)
- Complications: cardiomyopathy, respiratory infections, respiratory compromise, and death
- Manifestations: Depends on type → all muscles or some may be affected, Intellectual disability ( some), Muscle
weakness → worsens to hypotonia, Muscle spasms, delayed muscle motor skills, Difficulty using one or more
muscle groups, Poor coordination, Drooling, Ptosis, Frequent falls, Problems walking, Gowers maneuver,
Unilateral calf hypertrophy, Scoliosis or lordosis, Progressive loss of joint mobility and contractures (e.g.,clubfoot
and foot drop)
Musculoskeletal Tumors
Bone Tumors
Majority = malignant → secondary tumors from other CA (breast, lung, prostate)
- Primary tumors = rare → risk factor = Paget’s disease.
- Cause: unknown.
- Common: men + Caucasians
- Manifestations: Asymptomatic when early→ pathologic fx, bone pain, palpable mass, fatigue, weight loss
Bone Tumor Types
OSTEOCHONDROMA (BENIGN): develops adjacent to
growth plates; MOST COMMON BENIGN;
-b/w 10 - 20yrs
OSTEOSARCOMA (MALIGNANT): Aggressive → begins
in bone cells (femur, tibia, or fibula)
-Children and young adults
CHONDROSARCOMA (MALIGNANT): Slow-growing
tumor - begins in cartilage cells → ends of bone;
-Older adults
EWING SARCOMA (MALIGNANT): Aggressive w/
unknown origin;
May begin in nerve tissue within bone;
-Children and young adults
Integumentary Function
Inflammatory Integumentary Disorders
Atopic Dermatitis “eczema”
- Chronic inflammatory condition → inherited tendency.
- Have d/t asthma or allergic rhinitis
-
-
Common: infants → goes away by early adulthood
Remissions and exacerbations
Cause: unknown → immune system malfunction (similar to hypersensitivity rxn -IgE)
Complications: secondary bacterial skin infections, neurodermatitis (permanent scarring and discoloration from
chronic scratching), and eye problems (e.g., conjunctivitis)
May affect any area, but the pattern exhibited tends to be age-specific
￭ Peds: face, scalp, hands, or feet
￭ Older children and adults: knees and elbows
Manifestations: Worse w/ environmental factors (food+airborne allergens, Staphylococcus Aureus, topical
products, sweating, rough fabrics,
Red to brownish-gray skin patches, Pruritus, which may be severe,especially at night, Vesicles, Thickened
(lichenified),cracked, or scaly skin, Irritated, sensitive skin from scratching
Psoriasis
- Common chronic inflammatory→ effects skin life cycle (keratinocytes) → FORM PLAQUES (most common
type)
- Cellular proliferation increased = cells build up too fast on skin.
- Days-weeks for sxs to show during flare ups.
- Thickening of dermis/epidermis d/t dead cells not shedding fast.
- Cause: unknown → multifactorial:
- environmental, trauma, infections, obesity, EtOH, meds, genetics, immune.
- autoimmune process → T lymphocytes mistake skin cells as foreign
- Onset: 15 - 35yrs → sudden or gradual
- Remissions and exacerbations
- Exacerbations d/t: bacteria or viral infections, dry air/dry skin, skin injuries, meds, stress, too little/too much
sunlight, EtOH
- Can have arthritis = psoriatic arthritis
- Severe in someone w/ weak immune system.
- Begins as a small, red papule → occurs on elbows, knees, trunk → can be anywhere.
Infectious Integumentary Disorders
Cellulitis
- Deep in dermis + subcutaneous tissue
- D/t direct invasion of pathogens through skin break → contamination likely, or spreads from existing infection
- Swollen, warm, tender area of erythema
- Systemic manifestations: indicators of infection (fever, leukocytosis, malaise, arthralgia)
- Complications: necrotizing fasciitis, septicemia, septic shock
- Necrotizing fasciitis: rare, serious infection → destroy skin, fat, muscle.
- d/t high virulent strain of gram+ → minor cut → bacteria release toxins that destroy
tissue/disrupt blood flow/break down tissue.
- Start small, red, painful → painful bronze/purple patch → center = black/necrotic w/ exudate.
- Systemic manifestations: fever, tachy, hypotension, confusion.
- Complications: gangrene, organ failure, shock
Herpes Zoster “shingles”
By varicella-zoster virus → in adulthood after primary infection of varicella as peds.
- Virus is dormant on CN or spinal nerve dermatome → activated years later.
- Affects this nerve only → typical unilateral manifestations
- Weeks → months.
- Manifestations: pain, paresthesia, red/silvery vesicular rash that develops in a line over the area innervated by
affected nerve (one side of the head/torso), sensitive skin, pruritus
- Complications: neuralgia and blindness
- Vaccines available to prevent both varicella + herpes zoster.
Rubella “German measles” “3-day measles”
RNA virus enters bloodstream thru respiratory route → mild in most peds.
- Manifestations: Enlarged cervical + post auricular lymph nodes, fever, HA, sore throat, runny nose, cough, pink
to red maculopapular rash d/t virus dissemination to skin
Roseola
- Herpesvirus 6 or 7 infection
- 6m - 2yrs.
- Incubation of 5-15 days → sudden onset of fever (3-5 days) → then erythematous macular rash (24hrs) = does
not require tx.
Rubeola “red measles”
- Highly contagious → acute viral disease of childhood (direct contact w/ droplets)
- No sxs in incubation period (7-12 days)
- Sxs: High fever, malaise, enlarged lymph nodes, runny nose, conjunctivitis, barking cough, head rash that
spreads distally over trunk, extremities, hands, feet
- Characteristic pinpoint: white spots (Koplik spots) found over buccal mucosa
Tinea “ringworm” “athlete’s foot”
- Superficial fungal infections → fungi grow in warm, moist places (showers)
- Circular, erythematous rash → pruritus and burning
Tinea capitis: scalp → school aged kids → hair loss at
site is common.
Tinea corporis: body
Tinea pedis: feet, especially toes
Tinea unguium: nails, usually toenails
-Begins at tip of 1 or 2 nails → spreads
-Nails white → brown = thicken and crack
Sensory Function
Infectious and Inflammatory Sensory Disorders
Conjunctivitis
Conjunctiva infection/inflammation.
- Causes: viruses (common), bacteria (Staphylococcus, Chlamydia, gonorrhea), allergens (pollen/dust), chemical
irritants, trauma → edema, pain, blurry vision, photophobia
- Viral: watery/mucus-like exudate
- Bacterial: yellow-green exudate
- Allergens/irritants produce redness, itching, excessive tearing
- Risk factors: contact lenses + contaminated makeup + ophthalmic medication
- Bacterial + viral conjunctivitis = contagious through direct contact
Acute Otitis Media
Middle ear infection/inflammation.
- Common: peds → Eustachian tubes narrower, straighter, shorter + immature immune system
- Additional cause: Fluid in middle ear d/t large adenoids d/t inflammation
- Fluid from viral infection = medium for secondary bacteria (Streptococcus pneumoniae + Haemophilus
influenzae)
- Begins as viral URI → common in winter.
- Risk factors: Childcare in group settings, feeding infants in supine position, environmental smoke exposure,
pacifier use, orofacial deformities, Hx of allergic rhinitis
- Complications: Effusions, tympanic membrane rupture, scar tissue, conductive hearing loss, mastoiditis,
cholesteatoma, meningitis, osteomyelitis
- Manifestations: Ear pain, crying or irritability, rubbing/pulling at the ear, mild hearing deficits, sleep disturbances,
red/bulging tympanic membrane, indications of infection, purulent or clear exudate from external ear canal (if
tympanic membrane ruptures), N/V/D, HA.
Chronic Sensory Disorders
Glaucoma
eye conditions→ damage to optic nerve
- Causes: ↑ intraocular pressure + ↓ blood flow to optic nerve
- Pressures inside eye can climb when outflow of aqueous humor is blocked or production of aqueous humor
goes to abnormal level = ischemia/degeneration of optic nerve
- 2nd leading cause of blindness (diabetic retinopathy is #1)
Open-angle:
Closed-angle:
Intraocular pressure may increase gradually over an
extended period
- Most common.
- Manifestations: painless, insidious, bilateral
changes invision (tunnel vision, blurred vision,
halos around lights, low color discrimination)
Sudden blockage of aqueous humor outflow
- acute, subacute, and chronic
- Causes: trauma, sudden pupil dilation (bright light
after in darkness), prolonged pupil dilation (eye
exam meds), emotional stress
- Unilateral → may affect both
- Manifestations: sudden, worsens fast. Sudden
and severe eye pain, HA, N/V, nonreactive pupil,
redness, cornea haziness, vision changes ( halos
around lights)
Cataracts
Opacity or clouding of the lens
- Congenital condition or develop later.
- Risk factors for adult-onset cataracts: FHx, old ppl, smoking, (UV) light exposure, metabolic (DM), meds
(corticosteroids), eye injury (e.g., trauma and infection)
- One or both eyes → not symmetrically
- Manifestations: Cloudy, fuzzy, foggy, or filmy vision, Color intensity loss, Diplopia, Impaired night vision, gradually
progressing to impaired day vision, Halos around lights, Photosensitivity, Frequent changes in eye prescription
Macular Degeneration
Deterioration of macular area of retina d/t impaired blood supply to macula → cellular waste accumulation/ischemia
- Risk factors: getting old! FHx, female, Caucasian, smoking, ↑ UV light exposure, ↓ carotenoid intake, high-fat diet,
CVD, HTN, obesity
- Manifestation: Dry form: blurry vision w/ loss of central vision; Wet form: distortion of straight lines, dark spots in
central vision, sudden loss of central vision
Meniere’s Disease
Disorder of inner ear d/t endolymph swelling
- Stretches membranes → interferes with hair receptors in cochlea+vestibule
- Cause: unknown→ metabolic disturbances, hormonal imbalances, autoimmune, head injuries, otitis media, syphilis
- Risk factors: allergic rhinitis, EtOH ,stress, fatigue, meds (aspirin), respiratory infections
- B/w 20 - 50yrs.
- Manifestations: Occur in waves of acute episodes (months) →small periods of relief; Triggered by changes in
barometric pressure, Include episodes of vertigo, tinnitus, unilateral hearing loss, sensation of fullness
- Other manifestations include N/V/D, HA, uncontrollable eye movement
- Complications: permanent hearing loss