Final Exam 2 Flashcards
Hemotology, Cardio/Pulm, MSK, Endo/Repro, Digestive
<p>total volume of blood ejected by ventricle per minute</p>
<p>cardiac output</p>
<p>increased PVR increases what?</p>
<p>afterload -> more pressure to push blood out of heart if pressure is higher is system</p>
<p>Increased preload is a result of what?</p>
<p>- hypervolemia- renal failure- regurgitation of cardiac valves</p>
<p>Increased afterload is a result of what?</p>
<p>- hypertension- vasoconstriction</p>
<p>Explain how increased preload can lead to decreased SV and heart failure</p>
<p>- increased preload -> stretching of myocardium -> decreased contractility -> decreased SV + increased ventricular end-diastolic pressure -> pressure backs into pulmonary and venous systems (pulmonary and peripheral edema)</p>
<p>Optimal levels for total cholesterol, LDL, and HDL</p>
<p>- total cholesterol: <200 mg/dL- LDL: <100 mg/dL- HDL: >60 mg/dL</p>
<p>Explain the pathophysiology of atherosclerosis</p>
<p>- injury to endothelial cells in artery wall -> inflammation- inflammatory process summons macrophages and produces oxygen free radicals- LDL becomes oxidized (causes additional recruitment)- macrophages engulf oxidized LDL -> foam cells- accumulation of foam cells = fatty streak- fatty streak + collagen from injured vessel = fibrous plaque- plaques may occlude blood flow or rupture (rupture initiates clotting and thrombus formation -> ischemia -> infarction)</p>
<p>What usually causes CAD?</p>
<p>atherosclerosis (plaque formation)</p>
<p>Explain how coronary occlusion leads to myocardial infarction</p>
<p>- myocardial cells become ischemic in 10 seconds of occlusion- cells deprived of glucose needed for aerobic metabolism -> switch to anaerobic (lactic acid accumulation)- heart cells lose ability to contract -> CO decreases</p>
<p>How long can myocardial cells go without O2 before myocardial infarction</p>
<p>about 20 minutes</p>
<p>angina caused by gradual luminal narrowing and hardening of arterial walls; consistent type of pain; relieved by rest and nitrates</p>
<p></p>
<p>stable angina pectoris</p>
<p>clinical manifestation of stable angina pectoris</p>
<p>- transient substernal chest pain (may be mistaken for indigestion)- pallor, diaphoresis, and dyspnea (may all be associated w/ pain)</p>
<p>chest pain attributable to to transient ischemia of myocardium that occurs unpredictably and often at rest; caused by vasospasm of one or more major coronary arteries with or without atherosclerosis</p>
<p>prinzmetal angina (varient angina)</p>
<p>2 things linked to silent ischemia</p>
<p>DM and chronic stress</p>
<p>angina that is increasing in severity or frequency, new-onset, or at rest; result of reversible myocardial ischemia and is a sign of impending infarction; EKG showsST depression and T wave inversion</p>
<p>unstable angina</p>
<p>persistent coronary occlusion leads to infarction of the myocardium closest to the endocardium; EKG showsST depression and T wave inversion without Q waves</p>
<p>non-STEMI</p>
<p>continued coronary occlusion that leads to transmural infarction extending from endocardium to pericardium; EKG showsmarked elevations of ST segments</p>
<p>STEMI</p>
<p>explain how acute mental stress can lead to MI or sudden cardiac death</p>
<p>- stress -> ANS activity -> increased HR, BP and coronary constriction- atherosclerosis or poor LV function -> increased demand and decreased supply- leads to ischemia, plaque rupture, and thrombosis (from platelet activity)- may also cause electrical instability -> VFib/Vtach</p>
<p>classic signs of myocardial infarction</p>
<p>- heavy/crushing chest pain- pain may radiate to neck, jaw, back, shoulder, or left arm- N/V- diaphoresis</p>
<p>4 areas of damage caused by HTN</p>
<p>- retina- renal disease- CAD/CHF- neurologic disease (stroke, dementia, encephalopathy)</p>
<p>How do the factors leading to HTN cause damage</p>
<p>- vasoconstriction -> increased PVR
- renal salt and H2O retention -> increased blood volume
- increased PVR + increased volume -> sustained HTN and vascular remodeling</p>
<p>name 3 acute coronary syndromes (ACS)</p>
<p>- unstable angina- non-STEMI- STEMI</p>
<p>ejection fraction <40% and an inability of the heart to generate adequate CO to perfuse tissues</p>
<p>heart failure w/ reduced ejection fraction (HFrEF) or systolic HF</p>
<p>Explain how increased PVR can lead to heart failure</p>
<p>- increased PVR -> increased afterload (increased resistance to ventricular ejection)- increased workload in LV- increased RAAS and SNS- hypertrophy- increased myocyte demand for O2 (reactive ischemia)- ventricular remodeling- decreased contractility (decreased CO and perfusion of tissues)</p>
symptoms of left heart failure (CHF)
- paroxysmal nocturnal dyspnea- cough (w/ frothy/pink-tinged sputum)- orthopnea- exertion dyspnea- fatigue- decreased urine output- edema
Exam findings of left heart failure (CHF)
- cyanosis- inspiratory crackles- pleural effusions- HTN or hypotension
pulmonary congestion despite a normal stroke volume and CO; results from increased LVEDP which reflects back into pulmonary and venous system
heart failure w/ preserved ejection fraction (HFpEF) or diastolic heart failure
inability of the RV to provide adequate blood flow into pulmonary circulation; usually due to preceding left heart failure
right heart failure
clinical manifestations of right heart failure
- fatigue- distended jugular veins- ascities- edema- anorexia and GI distress
most common valvular abnormality
aortic stenosis
3 causes of aortic stenosis
- congenital bicuspid valve degeneration- changes w/ aging- rheumatic heart disease
cardiovascular and pulmonary outcomes of aortic stenosis
- LV hypertrophy -> left heart failure- pulmonary edema
most common form of rheumatic heart disease
mitral stenosis
valvular abnormalities that cause systolic murmur
- aortic stenosis- mitral regurgitation (heard throughout)- tricuspid regurgitation (heard throughout)
valvular abnormalities that cause diastolic murmur
- mitral stenosis- aortic regurgitation
painful, red, raised lesions found on the hands and feet. They are associated with a number of conditions, including infective endocarditis, and are caused by immune complex deposition
Osler's nodes
non-tender, small erythematous or haemorrhagic macular or nodular lesions on the palms or soles only a few millimeters in diameter that are indicative of infective endocarditis
Janeway lesions
systemic, inflammatory disease caused by delayed exaggerated response to infection by group A B-hemolytic streptococcus (pharyngeal infection only)
rheumatic fever
antibodies directed against M proteins of streptococci cross-react w/ tissues of heart
rheumatic heart disease (RHD)
symptoms of rheumatic fever
- fever- lymphadenopathy- N/V and ABD pain- arthralgia - epistaxis- tachycardia
Risk factors for introduction of bacteria into endocardium
- dental, GU, or cardiac procedures- skin, wound, lung, or GU infections- indwelling catheters- injection drug use
signs and symptoms of infective endocarditis once vegetation forms
- fever, night sweats, malaise, weight loss- heart murmurs and failure- embolization of vegetation -> abscesses, petechiae, splinter hemorrhages, Osler nodules, and Janeway lesions, right-side emboli = PE; left-side emboli = stroke
What is missing from cells in all types of shock? What is a common finding in all types of shock?
- oxygen (either not receiving or not able to use it)- decreased CO
Describe the effects of impaired O2 delivery and use in shock
- no O2 -> anaerobic metabolism -> decrease ATP and increase lactic acid- increased lactic acid -> metabolic acidosis- decrease ATP -> decrease Na/K pump -> increased intracellular volume (cellular edema) -> decreased circulatory volume- cellular edema -> lysosomal enzymes -> inflammation and activation of clotting cascade
Describe the effects of impaired glucose delivery and use in shock
- increased serum cortisol, thyroid hormone, and catecholamines -> increased lipolysis, gluconeogenesis, and glycogenolysis- lypolysis = increased serum triglycerides- glycogenolysis = decreased energy stores- gluconeogenesis = proteins used for fuel, decrease albumin and increased urea and ammonia formation- muscle wasting and build up of metabolic products
How does the body compensate for shock
- decrease CO and tissue perfusion -> SNS activation- increased BP, HR, and contractility - RAAS activation (retain Na and H2O to increase preload)- vasoconstriction and activation of ADH -> increase preload- increased volume and CO -> restoration of perfusion
4 types of shock
- hypovolemic- cardiogenic- distributive- obstructive
decreased CO and evidence tissue hypoxia in the presence of adequate intravascular volume (heart cannot contract effectively; fluid volume not affected)
cardiogenic shock
causes of cariogenic shock
direct pump failure- MI, cardiac arrest- ventricular dysrhythmia
signs and symptoms of cardiogenic shock
- confusion- tachycardia- hypotension- tachypnea- venous and pulmonary edema- oliguria (urine output < 30mL/hour)- dusky skin color; skin cold and clammy
caused by loss of whole blood (hemorrhage), plasma (burns), or interstitial fluid (diaphoresis, DM, DI, emesis, diarrhea, or diuresis) in large amounts
hypovolemic shock
signs and symptoms of hypovolemic shock
- hypotension- tachypnea- tachycardia (weak pulse)- hypoxia- decreased/absent urine- thirst, agitation, anxiety, confusion- skeletal muscle weakness- cold, clammy, cyanotic skin
shock due to decreased vascular volume or tone -> vasodilation w/ pooling causes decrease preload, SV, and CO
distributive shock
3 types of distributive shock
- neurogenic shock- anaphylactic shock- septic shock
result of widespread and massive vasodilation due to parasympathetic overstimulation and sympathetic understimulation
neurogenic/vasogenic shock
results from widespread hypersensitivity reaction known as anaphylaxis
anaphylactic shock
signs and symptoms of anaphylactic shock
- vasodilation and increase capillary permeability (due to histamine) -> hypovolemia- decreased contractility and dysrhythmia- bronchial edema and pulmonary obstruction- widespread hypoxia
toxins and endotoxins related into blood cause systemic inflammatory response syndrome (SIRS); metabolism becomes anaerobic due to decreased MAP, clot formation in capillaries, and poor cellular uptake of O2
septic shock
signs of sepsis
- bacteremia + SIRS- SIRS: fever, tachycardia, tachypnea, leukocytosis
septic shock is related to what clotting abnormality
DIC
shock due to indirect pump failure (cardiac tamponade, or PE); cardiac function decreases by non-cardiac factors (total body fluid not affected)
obstructive shock
signs of cardiac tamponade
- JVD- paradoxical pulse- decrease CO- muffled heart sounds
progressive dysfunction of 2 or more organ systems resulting from an uncontrolled inflammatory response to severe illness or injury; most commonly caused by septic shock
multiple organ dysfunction syndrome (MODS)
Explain pathogenesis of MODS
- injury/sepsis/trauma -> neuroendocrine response and release of inflammatory mediators- activation of complement, coagulation, and kinin systems (massive systemic inflammatory response)- hypermetabolism- vasodilation and selective vasoconstriction -> maldistribution of blood flow -> hypoperfusion and decreased CO- hypermetabolism and hypo perfusion -> increased O2 demand -> tissue hypoxia/metabolic failure -> acidosis- organ dysfunction
autoimmune condition characterized by formation of thrombi filled w/ inflammatory and immune cells; strongly associated w/ smoking
Buergers disease
pain w/ ambulation due to gradually increasing obstruction of arterial blood flow to the legs by atherosclerosis in the iliofemoral vessels; seen in arterial PVD
intermittent claudication
3 factors that promote venous thrombosis (triad of Virchow)
- venous stasis (immobility, age, CHF)- venous endothelial damage (trauma, IV meds)- hypercoagulable states (inherited disorders, pregnancy, malignancy, OCP, or HRT)
6 Ps of acute arterial occlusion
- Pain- Paresthesias- Paralysis- Pallor- Pulselessness- Perishingly cold/Poikilothermia
Explain the rhythm of Cheyne-Stokes respirations
- increased levels of CO2 -> tachypnea- CO2 levels decrease -> leads to apnea until CO2 accumulates again
PaCO2 is greater than 44 mmHg
hypercapnia (increased CO2 levels) -> leads to respiratory acidosis
PaCO2 less than 36 mmHg
hypocapnia (decreased CO2 levels) -> leads to respiratory alkalosis
7 causes of hypercapnia
- depression of respiratory center by drugs- diseases of the medulla- abnormalities of spinal conducting pathways (spinal cord disruption)- diseases of NMJ or respiratory muscles (MG or MD)- thoracic cage abnormalities- large airway obstruction (tumors/sleep apnea)- increased work of breathing or physiologic dead space
pathological condition which results when the alveoli of the lungs are perfused (Q) with blood as normal, but ventilation (the supply of air or V) fails to supply the perfused region -> low V/Q
pulmonary shunt
V/Q mismatching results in what?
hypoxemia
air pressure in the pleural space = barometric pressure; air drawn into pleural space on inspiration is forced out on expiration
open (communicating) pneumothorax
one-way valve that permits air to enter on inspiration but prevents escape during expiration (causes mediastinal shift) -> life threatening
tension pneumothorax
Name 5 types of pleural effusion drainage
- transudative (hydrothorax): watery drainage from intact capillaries- exudative: WBC and protein- empyema: pus-like drainage- hemothorax: bloody drainage- chylothorax: milky lymphatic drainage and fat droplets
diseases characterized by airway obstruction that is worse w/ expiration (more force is required to expire a given volume of air and emptying of the lungs is slowed)
obstructive lung diseases
3 most common obstructive lung diseases
- asthma- emphysema- chronic bronchitis
Describe an acute asthmatic response
- inhaled Ag binds to mast cells covered w/ preformed IgE- mast cells release mediators- mediators induce bronchospasm, edema from increased capillary permeability, and mucous secretion (goblet cells)- dendritic cells process and present Ag to Th2 -> produce ILs- eosinophils activated -> damage respiratory epithelium - neutrophils add to inflammation and airway obstruction
clinical manifestations of asthma attack
- chest constriction- expiratory wheezing- dyspnea- nonproductive cough- prolonged expiration- tachycardia- tachypnea
decrease in systolic BP during inspiration of more than 10 mmHg; may be seen during asthma attack
pulses paradoxus
COPD includes what 2 disorders
chronic bronchitis and emphysema
hyper-secretion of mucus and chronic productive cough for at least 3 months of the year for at least 2 consecutive years
chronic bronchitis
pathogenesis of chronic bronchitis
- chronic irritation from inhaled substances/irritants such as tobacco smoke- inflammation causes bronchial edema, hyper-secretion of mucus (goblet cells), and smooth muscle hypertrophy w/ fibrosis, and bacterial colonization of airways
clinical manifestation of chronic bronchitis
- productive cough (classic)- prolonged expiration- cyanosis- chronic hypoventilation- polycythemia- cor pulmonale
abnormal permanent enlargement of gas-exchange airways accompanied by destruction of alveolar walls without obvious fibrosis
emphysema
primary emphysema is inherited and linked to what deficiency
a1-antitrypsin deficiency
pathogenesis of emphysema
- destruction of alveoli through breakdown of elastin within the septa (increased protease activity)- loss of elastin = loss of recoil of bronchial walls- produces large air spaces within lung parenchyma (bullae)
mucous plugs and narrowed airways cause ____; leads to hyperinflation of alveoli and hyper-expansion of chest
air trapping
clinical manifestations of emphysema
- dyspnea- wheezing- barrel chest (classic)- prolonged expiration
diseases characterized by decreased compliance of lung tissue (takes more effort to expand lungs during inspiration)
restrictive lung disease
autosomal recessive defect on chromosome 7 that causes defective epithelial chloride ion transport and deficient Na in airways, bile ducts, pancreas, and sweat ducts
cystic fibrosis
3 causes of pulmonary edmea
- left heart failure: causes increased pulmonary capillary hydrostatic pressure- injury to capillary endothelium: movement of fluid and protein from capillary to alveoli- blockage of lymphatics: inability to remove excess fluid from interstitial space
Pathogenesis of ARDS
- acute lung injury -> inflammation and neutrophil aggregation w/ release of mediators and complement- platelet activation -> micro thrombi in pulmonary circulation -> decreased flow to lungs -> pulmonary HTN and V/Q mismatch- damage to alveolar and endothelial cells -> disrupts alveolocapillary membrane -> fluid enters interstitial space -> impaired surfactant production and atelectasis
3 phases of ARDS
- exudative phase: pulmonary edema and hemorrhage w/ severe impairment of ventilation- proliferative phase: proliferation of type II pneumocytes; formation of hyaline membrane- fibrotic phase: tissue remodeling (destruction of alveoli and bronchioles)
Final result of ARDS
acute respiratory failure- hypoxemia- hypercapnia- acidosis
pathologic course of pneumonia
- aspiration of bacteria -> adherence to alveolar macrophages- inflammatory response - consolidation of lung parenchyma- leukocyte infiltration (neutrophils and macrophages)- phagocytosis in alveoli- resolution of infection
clinical manifestation of PE
sudden onset of symptoms - pleuritic chest pain - dyspnea - tachypnea - tachycardia - cough/hemoptysis - unexplained anxiety/sense of doom - massive occlusion = pulmonary HTN and shock
mean pulmonary A. pressure greater than 25 mmHg at rest
pulmonary artery HTN (PAH)
PAH is associated w/ what conditions
- COPD- interstitial fibrosis- obesity-hypoventilation syndrome
pathogenesis of PAH
- conditions cause chronic hypoxemia and chronic acidosis - Pulmonary A. vasoconstriction - increased pulmonary A. pressure - intimal fibrosis and hypertrophy of medial smooth muscle layer of pulmonary As.
right ventricular enlargement caused by PAH
cor pulmonale
Explain how PAH causes cor pulmonale
- resistance and pressure in pulmonary A. increases- workload of RV increases- leads to hypertrophy of RV and right heart failure
non-small cell lung cancer that usually originates in the peripheral regions of pulmonary parenchyma; moderate growth rate
adenocarcinoma
neuroendocrine lung cancer that has the highest correlation w/ smoking and arise centrally (hilar/mediastinal); very rapid growing and poor prognosis
small cell carcinoma
3 conditions associated w/ pulmonary shunting/low V/Q
low ventilation of perfused areas- atelectasis- asthma- pulmonary edema
1 condition associated w/ alveolar dead space/high V/Q
pulmonary emboli
2 conditions associated w/ alveolar capillary membrane barrier slowing diffusion of O2
- emphysema: decrease surface area- chronic bronchitis: thickened alveolar capillary membrane w/ edema and fibrosis
Formation of fibrous tissue or nodules in the lungs due to chronic environmental exposure
pneumoconiosis
Types of people at high risk for pneumonia and TB
- nursing home pts- prisoners- COPD- TB = pneumonia + pts w/ HIV
5 types of incomplete fractures
- greenstick- torus- bowing- stress- transchondral
break in one cortex of bone with splintering of inner bone surface; commonly occurs in children and elderly
greenstick fracture
buckling of cortex of a bone
torus fracture
bending of a bone
bowing fracture
diseases that cause pathologic fractures
- osteoporosis- RA- Paget disease- osteomalacia- rickets- hyperparathyroidism- radiation therapy- cancer- infection
healing that occurs when adjacent bone cortices are in contact with one another; usually due to surgical fixation and restriction of movement between fragments
direct/primary healing
healing that involves both intramembranous and endochondral bone formation, development of callus, and bone remodeling; occurs in fractures that are treated with non-rigid or semi-rigid bone fixation (casts, braces, etc.)
indirect/secondary healing
List the 5 steps of callus formation
- hematoma formation- organization of hematoma into fibrous network- invasion of osteoblasts; lengthening of collagen strands and deposition of calcium -callus formation -remodeling: excess callus is reabsorbed and trabecular bone is deposited
lateral epicondylitis
tennis elbow
medial epicondylitis
golfer's elbow
rapid breakdown of muscle that causes release of intracellular contents, including protein pigment myoglobin, into the extracellular space and bloodstream
rhabdomyolysis (myoglobinuria)
Classic triad of rhabdomyolysis
- muscle pain- weakness- dark urine (sometimes only thing present)
Most important lab value for rhabdomyolysis
serum creatinine kinase (CK) level
Normal CK level
- men: 5-25- women: 5-35
causes of rhabdomyolysis
- electrical injury/burns- blunt trauma- drugs (EtOH, PCP, amphetamines, heroin, cocaine)- DKA- heat stroke- status epilepticus - tetanus- strenuous exercise
Goals of treatment for rhabdomyolysis
maintaining adequate urinary flow (IV hydration) and prevention of kidney failure
causes of compartment syndrome
- bleeding after fracture (increases pressure)- decrease compartment volume (tight bandage or cast)- combination both conditions
Explain the pathophysiology of compartment syndrome
- limb compression -> local pressure -> tamponade- muscle/capillary necrosis- edema -> rising compartment pressure -> compartment tamponade- muscle ischemia/infarction- neural injury -> Volkmann ischemic contracture
explain pathophysiology of crush syndrome
- muscle infarction due to compartment syndrome- myoglobinemia -> renal failure- ECF shift -> shock - acidosis/hyperkalemia -> cardiac dysrhythmia
causes of osteoporosis
- decreased levels of estrogen (main hormone) and testosterone - decreased activity level- inadequate levels of vitamin D, C, and Mg
causes of osteomalacia
- deficiency of vitamin D -> lowers absorption of calcium from intestines
clinical manifestations of osteomalacia
- pain- bone fractures- vertebral collapse- bone malformations (bowed legs or "knock-knees")- muscular weakness -> waddling gait
state of increased metabolic activity in bone characterized excessive resorption of spongy bone and accelerated formation of softened bone; usually affects the axial skeleton
Paget disease
bone infection most often caused by staphylococcal infection
osteomyelitis
clinical manifestations of osteomyelitis
- acute/chronic inflammation- fever- pain- necrotic bone
Treatment for osteomyelitis
- antibiotics- debridement- surgery- hyperbaric O2 therapy
manifestation of OA
- pain- stiffness- enlargement of joint- tenderness- limited ROM- deformity
What is activated in RA that develop an exaggerated immune response?
synovial fibroblasts (SFs)
main 2 classes of immunoglobulins that are part of rheumatoid factors (RF)
- IgM and IgG- occasionally IgA
What will be present in joint fluid with RA?
inflammatory exudate
Explain the pathogenesis of RA
- CD4 T helper cells and others in synovial fluid activated -> release cytokines- activation of B lymphocytes -> formation of RF -> formation of autoimmune complexes and probable deposition in joint tissue- inflammatory cytokine release- RANKL release and osteoclast activation- angiogenesis in the synovium
Pt is said to have RA if the have 4 or more of the following:
- morning joint stiffness- arthritis in 3 or more joints- arthritis in hand joints- symmetric arthritis- rheumatoid nodules- abnormal amounts of serum RF- radiographic changes
explain the pathophysiology of ankylosing spondylitis
- inflammation of fibrocartilage (mainly in vertebrae and sacroiliac joint)- inflammatory cells infiltrate and erode fibrocartilage - repair begins -> scar tissue ossifies and calcifies - joint eventually fuses
when uric acid crystals occur in synovial fluid
gouty arthritis
type of metabolism gout is related to
purine (adenine and guanine) metabolism -> uric acid is end product
3 stages of gout
- asymptomatic hyperuricemia- acute gouty arthritis- tophaceous gout
stage of gout; serum urate level is elevated but arthritic symptoms, tophi, and renal stones not present
asymptomatic hyperuricemia
stage of gout; attacks develop w/ increased serum urate concentrations; tends to occur w/ sudden/sustained increases in hyperuricemia but can be triggered by trauma, drugs, and alcohol
acute gouty arthritis
stage of gout; progressive inability to excrete uric acid expands to curate pool until monosodium rate crystal deposits (tophi) appear in cartilage, synovial membrane, tendons, and soft tissue
tophaceous gout
associated w/ chronic anxiety
stress induced muscle tension
chronic widespread joint and muscle pain with associated increased sensitivity to touch, absence of inflammation, fatigue, and sleep disturbances
fibromyalgia (FM)
Where are majority of osteosarcomas found?
located in the metaphyses of long bones; about half occur around the knees
malignant tumor of striated muscle; highly malignant w/ rapid metastasis
rhabdomyosarcoma
What muscles most commonly develop rhabdomyosarcoma?
- tongue, neck, larynx, nasal cavity, axilla, vulva, and heart
List the 7 hormones released from the anterior pituitary and their target tissues
- Prolactin (mammary gland)- ACTH (adrenal cortex)- GH (bone/muscle/tissues)- TSH (thyroid gland)- LH + FSH (ovaries and testes)- MSH (melanin in skin)
Acromegaly vs gigantism
- acromegaly: occurs in adults (after growth plates have close)- gigantism: occurs in childhood (before growth plates close)
form of thyrotoxicosis in which excess amounts of TH are secreted from the thyroid gland
hyperthyroidism
clinical manifestations of hyperthyroidism
- thin hair- tachycardia- weight loss (elevated metabolism)- exophthalmos (protruding eyes)- hyperreflexia - enlarged thyroid
over secretion of T3/T4 due to abnormal antibodies (TSIs) that stimulate TSH receptors (type II hypersensitivity)
Grave's disease
What causes goiters?
thyroid enlargement due to iodine deficiency - follicles make thyroglobulin but cannot make TH
dangerous worsening of thyrotoxic state in which death can occur within 48 hours without treatment; sxs caused by increased action of T4 and T3 exceeding metabolic demands
thyrotoxic crisis (thyroid storm)
Sxs of thyrotoxic crisis
- hyperthermia- tachycardia- high output heart failure- agitation/delirium- N/V/D
clinical manifestation of cretinism
- difficulty eating- protruding tongue- hypotonia- lethargy- bradycardia- cognitive disability varies
most common form of primary hypothyroidism; gradual inflammatory destruction of thyroid tissue by infiltration of auto reactive T lymphocytes and circulating thyroid antibodies
autoimmune thyroiditis (Hashimoto's thyroiditis)
clinical manifestations of hypothyroidism
- loss of hair- bradycardia- decreased metabolism- lethargy- cold intolerance- muscle weakness- LE edema
characteristic sign of severe or long-standing hypothyroidism; will see non pitting, boggy edema (around eyes, hands, feet, and supraclavicular fossa), slurred speech, and hoarseness
myxedema
clinical manifestation of myxedema coma (medical emergency)
- hypothermia w/o shivering- hypoventilation- hypotension- hypoglycemia - lactic acidosis
high levels of ADH in the absence of normal physiologic stimuli for release
syndrome of inappropriate ADH secretion (SIADH)
How does SIADH affect the following:- urine output- urine osmolality- serum Na- serum osmolality
- urine output: low- urine osmolality: high- serum Na: low (hyponatremia)- serum osmolality: low (hypoosmolar)
symptoms of SIADH
- water retention - low urine output- N/V- mental changes
failure of hypothalamus to produce ADH or release it from posterior pituitary; decrease in ADH plasma levels
neurogenic/central diabetes insipidus (DI)
kidneys unable to respond to ADH; increase plasma ADH
nephrogenic diabetes insipidus (DI)
How does DI affect the following:- urine output- urine osmolality- serum Na- serum osmolality
- urine output: high- urine osmolality: low- serum Na: high (hypernatremia)- serum osmolality: high (hyperosmolar)
symptoms of DI
- polyuria- thirst- high urine output- signs of dehydration
treatment of SIADH
- fluid restriction- treat the cause
characterized by greater than normal secretion of PTH and hypercalcemia
hyperparathyroidism
How does hyperparathyroidism affect Ca and Pi
- increased Ca levels (hypercalcemia) -> increases bone resorption to release Ca and GI reabsorption- decreased Pi levels (hypophosphatemia) -> PTH causes Pi to be excreted in urine
clinical manifestations of primary hyperparathyroidism
- fatigue- headache- depression- anorexia- N/V- pathologic fractures
How does hypoparathyroidism affect Ca and Pi
- decreased Ca levels (hypocalcemia)- increased Pi levels (hyperphosphatemia)
clinical manifestations of hypoparathyroidism
- symptoms of hypocalcemia (ex. tetany and muscle spasms)- dry skin- loss of body and scalp hair- hypoplasia of developing teeth- bone deformities
refers to clinical manifestations resulting from chronic exposure to excess cortisol regardless of cause
Cushing syndrome
clinical manifestations of Cushing's syndrome
- fat deposition on neck/back (buffalo hump)- fat deposition on the face (moon face)- ABD fat deposition- bruising (breakdown of collagen)- stretch marks- muscle weakness/wasting- osteoporosis- adrenal hyperplasia
How would Cushing disease affect the following values:- K- Na- glucose
- K: hypokalemia (aldosterone -> K excretion)- Na: hypernatremia (aldosterone -> Na reabsorption)- glucose: hyperglycemia (high cortisol)
primary adrenal insufficiency (hyposecretion of all adrenal steroids) usually due to autoimmune restriction of adrenal gland
Addison's disease
How would Addison's disease affect the following values:- K- Na- glucose
- K: hyperkalemia (no aldosterone for K excretion)- Na: hyponatremia (no aldosterone for Na reabsorption)- glucose: hypoglycemia (low cortisol)
clinical manifestations of Addison's diseases
- weakness/fatigue- skin hyperpigmentation (due to high MSH associated w/ high ACTH)- hypotension - tachycardia- N/V/D- adrenal atrophy
hyper-secretion of aldosterone due to adrenal neoplasm
primary hyperaldosteronism (Conn syndrome)
Symptoms of pheochromocytoma
- persistant HTN- headache- pallor- diaphoresis- tachycardia/palpitations- anxiety
lab value diagnosis criteria for DM
- HbA1c > 6.5%- fasting plasma glucose (FPG) > 126 mg/dl (fasting = at least 8 hours)- 2 hour plasma glucose > 200 mg/dl during oral glucose tolerance test (OGTT)- symptoms of hyperglycemia w/ random plasma glucose > 200 mg/dl
Describe pathophysiology of IDDM
- autoantigens form on B-cells and circulate in bloodstream/lymphatics- activation of cellular immunity (T cells) and humoral immunity (autoantibodies) towards B-cells- destruction of B-cells with decreased insulin secretion
clinical manifestations of IDDM
- polydipsia (water attracted to glucose -> intracellular dehydration)- polyuria (hyperglycemia = osmotic diuretic)- polyphagia (depletion of cellular stores due to lack of glucose -> starvation)- weight loss- fatigue- visual changes- paresthesias
What is one of the most important contributors to insulin resistance and NIDDM
obesity
clinical manifestations of NIDDM
- some classic sxs (polyuria/polydipsia)- fatigue- pruritus- recurrent infections- visual changes- neuropathy- individual is usually overweight w/ dyslipidemia and HTN
low blood glucose during the night that may lead to rise in morning blood glucose; tx is a nighttime snack to prevent hypoglycemia
Somogyi effect
early morning rise in blood glucose level related to release of GH, cortisol, and catecholamines w/o preceding hypoglycemia; tx is insulin to counter hyperglycemia
dawn phenomenon
symptoms of hypoglycemia
- pallor- tremor- tachycardia/palpitations- diaphoresis - headache- irritability/anxiety- confusion- seizures- coma
serious complication related to deficiency of insulin and increase in levels of insulin couter-regulatory hormones (catecholamines, GH, cortisol, and glucagon)
diabetic ketoacidosis (DKA)
3 main characteristics of DKA
- hyperglycemia- acidosis- ketonuria
Why is DKA more common in IDDM?
insulin is more deficient
Pathophysiology of DKA
- w/ insulin deficiency -> lipolysis is enhanced (increased fatty acid delivery to liver)- increased glyconeogenesis (contribute to hyperglycemia and production of ketone bodies)- increased ketones -> decreased pH -> metabolic acidosis
clinical manifestations of DKA
- Kussmaul respirations- fruity/acetone odor in breath- CNS depression- ketonuria- anorexia- N/V and ABD pain- postural dizziness
more common complication of NIDDM that differs from DKA w/ higher degree of fluid deficiency rather than insulin deficiency
hyperosmolar hyperglycemic nonketoic syndrome (HHNKS)
In which disease are glucose levels higher: DKA or HHNKS?
HHNKS -> due to volume depletion
clinical manifestations of HHNKS
- severe dehydration (from polyuria)- loss of electrolytes (ex. potassium)- neurologic changes (stupor, coma, seizures)- hypotension/hypoperfusion/tachycardia- N/V and ABD pain
clinical manifestation of diabetic neuropathy
- glove and stocking loss of sensation- loss of motor nerve function w/ clawed toes and small muscle wasting in hands- Charcot joints (joint and ligament degeneration; mainly in feet)
How does diabetic neuropathy lead to amputation?
- decrease in sensation -> painless trauma -> ulceration -> infection- muscle atrophy -> changes in gait -> new pressure points -> ulceration -> infection- autonomic neuropathy -> decreased perspiration -> dry skin/cracks/fissures -> infection- All lead to soft tissue infection and osteomyelitis
5 main reasons diabetics have increased risk for infection throughout the body
- impaired senses (neuropathy and retinopathy)- hypoxia (glycosylated Hgb impaired O2 delivery to tissues)- pathogens (some proliferate rapidly due to high glucose levels)- blood supply (vascular changes and reduced supply of WBCs)- suppressed immune response (impaired innate and adaptive immune system)
rare form of dysphagia related to loss of inhibitory neurons in the myenteric plexus w/ smooth muscle atrophy in the middle/lower parts of esophagus
achalasia
What does achalasia lead to?
altered esophageal peristalsis and failure of lower esophageal sphincter (LES) to relax -> can cause distention/obstruction in esophagus
type of diaphragmatic hernia w/ protrusion of the upper part of the stomach through the diaphragm into the thorax
hiatal hernia
proximal portion of stomach moves into the thoracic cavity through the esophageal hiatus
sliding hiatal hernia (type 1; most common)
herniation of the greater curvature of the stomach through a secondary opening in the diaphragm alongside the esophagus
paraesophageal hiatal hernia (type 2)
narrowing or blocking of the opening between the stomach and the duodenum (can be congenital or acquired)
pyloric obstruction (gastric outlet obstruction)
most common acquired cause of pyloric obstruction
- peptic ulcer disease or carcinoma near pylorus- duodenal ulcers more likely to cause obstruction
7 common causes of intestinal obstruction
- hernia- intussusception - torsion (volvulus)- diverticulosis- tumors- paralytic ileus- fibrous adhesions (post-op; Crohn's)
most common type of bowel obstruction
small bowel obstruction (SBO)
How would a bowel obstruction lead to pneumonia?
- distention -> pressure on diaphragm -> decreased respiratory volume -> atelectasis -> pneumonia
How would a bowel obstruction lead to peritonitis?
- distention and prolonged increased of wall tension -> decreased venous return -> bowel edema -> increased capillary permeability (fluid loss into peritoneum) -> bacterial translocation to peritoneum
How would a bowel obstruction lead to loss of water/electrolytes and dehydration?
- ABD pain leads to N/V, decreased intake, decreased nutrient absorption, and decreased carb reserves (ketosis)
What 2 electrolytes are affected most by a bowel obstruction?
- K (hypokalemia)- Cl (hypochloremia)
How would a bowel obstruction lead to shock?
- distention -> increased capillary permeability - dehydration from loss of water/electrolytes- both lead to hypovolemia -> shock
2 most common causes of ulcers
NSAIDs and H. Pylori infection (both are erosive factors)
most common type of peptic ulcer
duodenal ulcer (also caused by NSAIDs and H. Pylori)
How do gastric ulcers form?
- caused H. Pylori, NSAIDS, bile salts, alcohol, or ischemia- damage to mucosal barrier -> decreased function of mucosal cells -> diffusion of acid into gastric mucosa- formation of histamine -> increased acid production, increased capillary permeability and mucosal edema- conversion of pepsinogen to pepsin causes further erosion and bleeding -> ulcer
Consequences of upper and lower GI bleeding
- blood volume depletion -> decreased CO -> compensatory constriction of peripheral arteries- decreased blood flow to kidneys (renal failure)- decreased blood flow to GI structures -> bowel/liver infarction/necrosis- decreased blood flow to brain and heart- metabolic acidosis -> lactic acidosis -> death
Chief problem of pancreatic insufficiency
fat malabsorption -> steatorrhea
chronic inflammatory disease that causes ulceration of the colonic mucosa (most common in rectum and sigmoid colon)
ulcerative colitis (UC)
idiopathic inflammatory disorder that affects any part of the GI tract from the mouth to the anus; spreads with discontinuous transmural involvement (skip lesions)
Crohn's disease (CD)
most common sites of CD
ascending colon and transverse colon
common complications of obesity
- cardiovascular problems (HTN, CAD, stroke, MI)- pulmonary (sleep apnea, asthma)- endocrine (NIDDM, infertility)- MSK (OA, low back pain, plantar fasciitis)- GI (GERD, gallstones, fatty liver)
portal HTN commonly causes what?
- esophageal varices- splenomegaly - caput medusae (ABD varices)- hemorrhoidal varices (internal hemorrhoids)
Mechanisms that cause ascites
- portal HTN -> increased lymph production -> leakage into peritoneal space and decreased plasma volume- hepatocyte failure -> decreased albumin synthesis -> decreased oncotic pressure in capillaries - altered metabolism + decreased renal flow -> increased RAAS
most hazardous toxin not removed from liver during hepatic ecephalopathy
- ammonia (end product to protein digestion) -> usually converted to urea
causes of hyperbilirubinemia
- post hepatic obstruction to bile flow- intrahepatic obstruction- prehepatic excessive production of unconjugated biluribn (hemolysis of RBC)
clinical manifestations of cirrhosis
- portal HTN (ascites, varices, splenomegaly)- decreased bilirubin metabolism (jaundice)- decreased bile in GI tract (light colored stools)- decreased vitamin K absorption (bleeding)- decreased hormone metabolism and increased androgens/estrogens- decreased protein, fat, and carb metabolism- toxin accumulation (hepatic encephalopathy)
lab changes seen with cirrhosis
- increased AST and ALT- increased bilirubin- low serum albumin- prolonged PT- elevated alkaline phosphatase
5 types of hepatitis and their routes
- Hep A (fecal-oral; most common), parenteral, sexual- Hep B (parenteral, sexual, transplacental)- Hep C (parenteral, sexual, transplacental)- Hep D (Hep B coinfection, fecal-oral, sexual)- Hep E (fecal-oral)
types of hepatitis that cause chronic active hepatitis
- Hep B- Hep B/Hep D coinfeciton- Hep C
cardinal manifestations of cholelithiasis
- epigastric and right hypochrondrium pain- intolerance of fatty foods
pathophysiology of acute pancreatitis
- duct obstruction -> acing cell injury- intracellular and extracellular activation of enzymes- lipase -> fat necrosis - trypsin, chymotrypsin, phospholipase, and elastase along w/ inflammation (complement and cytokines) cause cell injury, edema, thrombosis, hemorrhage, and necrosis
What can acute pancreatitis lead to?
- shock- SIRS- ARDS- acute tubular necrosis (ATN)- coagulation disorders- translocation of intestinal bacteria -> sepsis- pancreatic abscess
closely associated w/ development of colorectal cancer
colorectal polyps
signs and symptoms of colorectal cancer
- pain- mass- change in bowel habits- blood in stool- anemia
3 criteria for PCOS
- few or anovulatory menstrual cycles- elevated levels of androgens- polycystic ovaries (do not have to be present)
leading cause of infertility in the US
PCOS
syndrome directly related to genetic predisposition, insulin resistance, and excess of insulin and androgens
PCOS
how does insulin resistance and hyperinsulinemia lead to PCOS
- insulin resistance overstimulates androgen secretion and reduces hepatic secretion of sex hormone binding globulin- increased free testosterone levels- leads to disordered LH/FSH release- anovulation and hyperandrogenism -> PCOS
Why are HTN, dyslipidemia, and hyperinsulinemia commonly present w/ PCOS?
- insulin resistance -> more insulin production- high insulin levels -> increased triglycerides and BP
clinical manifestations of PCOS
- amenorrhea or dysfunctional uterine bleeding- infertility- hirsutism (abnormal hairiness)- acne- HTN- dyslipidemia
Most common causes of PID?
- gonorrhea- chlamydia
complications associated w/ PID
- infertility- ectopic pregnancy- pelvic pain and dyspareunia- pelvic adhesions- perihepatitis- ovary and fallopian tube abscess
Risk factors for pelvic organ prolapse?
- direct trauma (ex. childbirth)- heavy lifting- aging- obesity- hysterectomy
descent of a portion of the posterior bladder wall and trigone into the vaginal canal; usually caused by childbirth
cystocele
bulging of the rectum and posterior vaginal wall into the vaginal canal
rectocele
Treatment for pelvic relaxation disorders
- pessary (for uterine prolapse)- Kegel exercies- surgery
benign tumors that develop from smooth muscle cells in the myometrium (often in the fundus); can cause ABD pressure and cramping
leiomyoma (aka myoma or uterine fibroids)
presence of functioning endometrial tissue or implants outside the uterus (usually ABD and pelvic area); will still respond to hormone fluctuations and can bleed
endometriosis
clinical manifestations of endometriosis
- dysmenorrhea- ABD/pelvic pain- dyspareunia- constipation- infertility
list 9 risk factors for breast cancer
- increasing age- family hx- genetic predisposition (BRCA 1/2)- early menarche/late menopause- no full-term pregnancies- obesity- sedentary lifestyle- smoking/alcohol- oral contraceptive use or HRT
breast cancer manifestations
- painless lump on breast- dimpling of skin- edema- orange peel appearance- nipple discharge
group of proliferations limited to breast ducts and lobules without invasion of the basement membrane
ductal carcinoma in situ (DCIS)
Risk factors for male breast cancer
- gynecomastia- chest wall irradiation- FHx of Kleinfelters Syndrome- presence of BRCA1 and BRCA 2 mutation- Obesity- Hx of testicular cancer
clinical manifestations of ovarian cancer
GI symptoms usually first: bloating, flatulence, discomfort
most significant risk factor for ovarian cancer
family history of ovarian or breast cancer
cell surface antigen used to monitor effectiveness of therapy in ovarian cancer if pre-op levels are high; not a good screening tool
CA-125
diagnostic test for ovarian cancer
transvaginal US
risk factors for endometrial cancer
- obesity- nulliparity- late menopause- HTN- high fat diet
most common symptom of endometrial cancer
unusual vaginal bleeding
clinical manifestations of cervical cancer
- may be asymptomatic- vaginal bleeding or discharge
clinical manifestations of prostate cancer
- signs of bladder outlet obstruction (slow urinary stream, hesitancy, incomplete emptying, frequency, nocturia, and dysuria)- progressive and don't remit (unlike BPH)
screening for prostate cancer
- digital rectal exam (DRE)- prostate specific antigen (PSA) -> many false positives
4 risk factors for testicular cancer
- abnormal testicle development- family or personal hx of testicular cancer- hx of undescended testicles- Klinefelter syndrome
clinical manifestations of testicular cancer
- discomfort or pain in the testicle- feeling of scrotal heaviness- dull ache in lower back or ABD- enlargement of a testicle or change in how it feels- lump or swelling in either testicle
condition in which the foreskin cannot be retracted back over the glans
phimosis
condition in which the foreskin cannot be moved forward (reduced) to cover the glans
paraphimosis
inflammation of the glans penis; associated w/ poor hygiene and phimosis
balanitis
abnormal dilation of the testicular vein and pampinoform plexus within the scrotum; described as a "bag of worms"
varicocele
group of abnormalities in which the testis fails to descend completely
cryptorchidism
clinical manifestations of BPH
- urgency- delay in starting urination- decreased force of stream- long-term urinary retention
overdevelopment of breast tissue in males
gynecomastia
causes of gynecomastia
imbalance of estrogen/testosterone due to- hypogonadism- Klinefelter syndrome- testicular neoplasms- drugs
3 bacterial STIs
- gonorrhea- chlamydia- syphilis
2 parasite STIs
- scabies/crabs
1 fungal STI
candida albicans
2 viral STIs
- HPV- genital herpes
2 protozoan STIs
- trichamonisasis (trich)- giardia lamblia (giardiasis)
common causes of anemia
- impaired erythrocyte production - blood loss (acute or chronic) - increased erythrocyte destruction - combo of these 3 factors
4 common symptoms of anemia (due to tissue hypoxia)
- weakness/fatigue- pallor (skin and mucous membranes)- dyspnea on exertion and increased RR- dizziness and syncope
cardiac and renal compensatory mechanisms for anemia
Cardiac:
- tachycardia - increased stroke volume - capillary dilation
Renal
- RAAS - increased salt and H2O retention - increased extracellular fluid
anemias characterized by erythrocytes that are unusually large in size, thickness, and volume; normal Hgb (normocrhomic)
macrocytic (megaloblastic) anemia
anemias that result due to ineffective erythrocyte DNA synthesis -> due to vitamin B12 or folate deficiencies
macrocytic (megaloblastic) anemia
most common type of macrocytic anemia and is caused by vitamin B12 deficiency
pernicious anemia (PA)
symptoms of pernicious anemia
- weakness/fatigue- paresthesias in feet and fingers (neuro manifestations from B12 deficiency)- difficulty walking- loss of appetite/weight loss- sore tongue that is smooth and beefy red
manifestations specific to folate deficiency anemia
- cheilosis (scales/fissures in mouth)- stomatitis (inflammation of mouth)- burning mouth syndrome (painful ulcers in buccal mucosa and tongue)- GI problems: dysphagia, flatulence, and watery diarrhea
anemias characterized by abnormally small erythrocytes that contain abnormally reduced amounts of Hgb
microcytic-hypochromic anemias
2 types of microcytic-hypochromic anemias
- iron-deficiency anemia (IDA)- sideroblastic anemias (SA)
2 causes of IDA
- inadequate dietary intake- chronic blood loss
clinical manifestations of IDA
- typical anemia symptoms- nails become brittle and "spoon-shaped"- tongue papillae atrophy (soreness/redness/burning)- gastritis- neuromuscular changes (numbness/tingling)- irritability and headache
lab findings for IDA
- decreased iron levels- increased total iron binding capacity (TIBC) - transferrin is empty
heterogenous group of inherited or acquired disorders characterized by anemia of varying severity and presence of ringed sideroblasts in bone marrow
sideroblastic anemias (SAs)
clinical manifestations of SAs
- CV and respiratory manifestations- hemochromatosis (iron overload)- mild-moderate hepatosplenomegaly- bronze-tinted skin may occur
anemias characterized by erythrocytes that are relatively normal in size and Hgb content but insufficient in number
normocytic-normochromic anemias (NNAs)
5 types of normocytic-normochromic anemias
- aplastic - posthemorrhagic- acquired hemolytic- hereditary hemolytic- anemia of chronic inflammation
anemia due to damage to bone marrow erythropoiesis (bone marrow failure)
aplastic anemia
stem cell disorder w/ hyperplastic and neoplastic BM alterations that causes uncontrolled proliferation of RBCs (normally due to JAK2 mutation)
polycythemia vera (PV) or primary polycythemia
clinical manifestations of PV
- unique feature: aquagenic pruritus (painful itching when exposed to heat or water)- red color in face, hands, feet, ears, and mucous membranes- engorgement of retinal and cerebral veins -> cerebral thrombosis likely- HA, delirium, mania, psychotic depression, chorea, visual disturbances
common AR disorder of iron metabolism and is characterized by increased GI iron absorption and tissue deposition
hereditary hemochromatosis (HH)
lab findings of HH?
- elevations in serum iron levels and ferritin levels (iron in hepatocytes)- decreased TIBC (transferrin is saturated)
benign, acute, self-limiting, lymphoproliferative syndrome characterized by acute infection of B cells and usually transmitted through saliva; most commonly caused by EBV
infectious mononucleosis (IM)
classic symptoms of infectious mononucleosis
- pharyngitis- lymphadenopathy- fever- fatigue (may last 1-2 months after infection)- splenomegaly may occur
aggressive, fast growing leukemia with too many lymphoblasts (immature WBC) found in the blood and BM
acute lymphocytic leukemia (ALL)
aggressive, fast growing leukemia w/ too many myeloblasts (immature WBC that are not lymphoblasts) found in the blood and BM
acute myelogenous leukemia (AML)
leukemia most commonly seen in children
ALL
most common adult leukemia
AML
lymphoid progenitors
B cells and T cells
myeloid progenitors
- basophils- eosinophils- neutrophils- monocytes- erythrocytes- platelets
common clinical manifestations of leukemia
- anemia -> fatigue- bleeding -> skin, gums, MM, GI tract, petechiae, ecchymosis - infection -> fever- weight loss/anorexia- bone pain- liver, spleen, and lymph node enlargement- elevated uric acid levels
slowly progressing disease w/ too many blood cells (not lymphocytes) made in the BM
chronic myelogenous leukemia (CML)
slow-growing cancer in which too many immature lymphocytes are found mostly in the blood and BM
chronic lymphocytic leukemia (CLL)
leukemia caused by BCR-ABL fusion gene derived from reciprocal translocation of chromosomes 9 and 22 (Philadelphia chromosome)
CML
most common clinical finding in patients w/ CLL
lymphadenopathy (most are asymptomatic)
3 phases of CML
- chronic phase (asymptomatic)- accelerated phase (primary sxs develop)- termal blast phase (blast crisis) -> survival of 3-6 monthslater stages resemble acute leukemia but w/ more prominent and painful splenomegaly
malignant lymphoma that progresses from one group of lymph nodes to another, including systemic symptoms and presence of B cells called Reed-Sternberg (RS); peripheral nodes (cervical, axillary, inguinal)
Hodgkin lymphoma
progressive clonal expansion of B cells, T cells, or NK cells (mostly B cells); localized to single axial group of nodes
Non-Hodgkin lymphomas
fast-growing B cell tumor that is more common is Africa
Burkitt lymphoma
symptoms of B cell lymphomas (HL, NHL, can be seen in LL)
- fever- night sweats- weight loss
plasma cell (B cell) cancer characterized by slow proliferation of malignant cells w/ tumor cell masses in the BM usually resulting in destruction of the bone
multiple myeloma (MM)
common presentation of MM
- hypercalcemia- renal failure -> secondary to hypercalcemia and Bence Jones proteins- anemia- bone lesions- Bence Jones protein in urine (Ig fragments formed by bone lesions)
platelet count less than 150,000 platelets/uL
thrombocytopenia
immune mediated, adverse drug reaction caused by IgG antibodies against heparin-platelet factor 4 complex -> platelet activation -> platelet consumption
heparin-induced thrombocytopenia (HIT)
although the hallmark of HIT is thrombocytopenia, what else are patients at risk for?
thrombosis due to activation, aggregation, and consumption of platelets
most common cause of thrombocytopenia secondary to increased platelet destruction; usually secondary to infections or other conditions that cause large amounts of antigen in the blood -> immune complex w/ platelets -> destruction
immune thrombocytopenic purpura (ITP)
multisystem disorder (defect of ADAMS 13) characterized by thrombotic microangiopathy (TMA) -> platelets aggregate and cause occlusion of arterioles and capillaries within microcirculation -> increased platelet consumption and tissue ischemia
thrombotic thrombocytopenic purpura (TTP)
symptoms of TTP (5)
- extreme thrombocytopenia (<20,000)- intravascular hemolytic anemia- ischemic signs and symptoms (most often in CNS)- kidney failure- fever
acquired clinical syndrome characterized by widespread activation of coagulation resulting in formation of fibrin clots in microvasculature throughout body
disseminated intravascular coagulation (DIC)
causes of DIC (5)
- trauma- sepsis- cancer- products of conception- injury to endothelium
explain how DIC causes clots
massive activation of clotting cascade -> widespread microvascular thrombosis and vascular occlusion -> ischemic tissue damage
explain how DIC causes bleeding
- widespread thrombosis causes consumption of platelets and clotting factors- also causes activation of plasmin and fibrinolysis (try to break up clots) -> lysis of clotting factors and inhibition of platelet aggregationOVERALL: platelets and clotting factors all used up from clots but even if they were available -> clotting system would inhibit further clots from forming to stop potential bleeding
clinical manifestations of DIC
- oozing from puncture sites- GI bleeding- weakness/fatigue- cyanosis/hypoxiemia- hematuria/oliguria/renal failure
elevated fibrin degradation products (FDP) and D-dimer are hallmark findings of what?
DIC
EBV is linked to which lymphoma
Burkett's lymphoma
most treatable version of lymphoma
Hodgkin's lymphoma
elevated reticulocyte count
hemolytic anemia
group of bone marrow failure disorders where blood cells in BM don't mature; precursor to leukemia
myelodysplastic disorder (MDS)
Tx for sickle cell crisis
- pain control- O2- rehydrate (dehydration major cause)
Normal hematocrit (Hct) level
38-54%
Normal hemoglobin (Hgb) level
11.7-14.9 g/dL (lower end in females)
Normal RBC level
4.2-6.1 million cells/mcL
Normal WBC count
5,000-10,000
immature form of neutrophils; elevated in blood during infection (high production from BM)
bands
very early and immature form of WBC; sign of leukemia when increased numbers found on blood smear
blast cells
normal platelet (Plt) count
150,000-300,000
measure of the extrinsic clotting pathway
prothrombin time (PT)
Normal PT range
10-13 seconds
common cause of prolonged PT
Coumadin therapy
measure of the intrinsic clotting pathway
partial thromboplastin time (PTT)
Normal PTT range
30-45 seconds (other references say 25-35 seconds)
common causes of prolonged PTT
Heparin therapyHemophilia
