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80 Cards in this Set
- Front
- Back
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What are 4 types of healing? |
1. Keloid: hypertrophic scar tissue formation 2. Contracture: joints and visceral organs not properly sliding 3. 1st intention healing: sutured, small scar 4. 2nd intention healing: open, bigger scar |
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The three "R"s of cellular healing and what are the exceptions |
1. Resolution - heals quick with minimal damage 2. Regeneration - tissue regenerated with new cells 3. Replacement - original cells can't regenerate resulting in scar tissue - Cardiac, Nerve and burn tissue |
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Patho and treatment of burns: |
-Hypovolemia shock: fluid loss in one part of body due to massive fluid shift to injured area causing BP to drop. Respiratory: always look at patient airway to see if they inhaled burn Pain: immense due to skin nerve endings Infection: Beware due to 2nd intention healing Metabolic needs: patient needs high calorie/protein diet Nurse Implication: kidney failure possible due to increased protein in blood, need to check heart in the case of electrical burn, if hands/face affected >5% then patient transferred to burn unit |
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What are the 3 classifications of Burns? |
1. Superficial thickness (1st degree): doesn't penetrate past epidermis, no blisters, resolves quickly (ex = sunburn) 2. Partial thickness (2nd degree): complete epidermis penetration and partial dermis penetration resulting in blistering (may leave scar and may mean increased risk of cancer) 3. Full thickness (3rd degree): damage all the way through dermis and going into connective tissue (result in permanent disability) |
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Negative vs Positive feedback loop (give example for positive) |
Negative: output of system acts to keep homeostasis Positive: output unable to keep homeostasis ex) heart failure |
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What is Necrosis and what are the different types (6)? |
Cell death 1. Liquefaction: liquified tissue from enzymes 2. Coagulative: dead tissue retains form 3. Fat: broken down fatty acids (induce inflammation) 4. Caseous: cheesy 5. Infarction: cell death from hypoxia 6. Gangrene: bacterial infected necrotic tissue |
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Acute vs Chronic Inflammation |
Acute: massive swelling and exudate Chronic: more lymphocytes and marcophages, potential for larger scar |
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Type IV: Cell Mediated/delayed hypersensitivity |
-Mediated by T-cells when they become sensitized to antigens causing cell destruction through cytokines -Causes: contact dermatitis (latex, nickel, poison ivy), Graft host reaction (transplant rejection), positive TB test -Chest X-ray ordered if + TB test |
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Type I: Allergic reaction |
-IgE mediated mast cell reaction (histamine) -Results in: VD (causing low BP), cap perm, edema, airway obstruction, hypoxia. allergies, anaphylaxis -Caused by: stings, nuts, shellfish, antibiotics, anesthetics -Nursing Imp: Anaphylaxis due to low BP and bronchial edema (swelling) can both be life threatening early signs/Sx: pruritus, tingling, soughing, SOB Late signs/sx: dizziness, fainting, low bp, hives, edema |
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Treatments for Type 1 Allergic reactions |
Epinephrine = vasoconstrictor
Diphenhydramine = antihistamine
Glucocorticoids = decrease immune response |
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Type II: Cytotoxic (ABO incompatibility) |
-Blood typing - the type of antigen (or lack of) on RBCs determines your blood type - If incompatible blood is transfused then hemolysis occurs -Signs/sx: SOB, CP, diaphoresis, Jandice -Can result in death |
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Type III: Ag-Ab complex (immune complex) |
-Occurs when Ag-ab complex fails to be removed after phagocytosis and debris is deposited into tissue, this then results in complement activation causing damage to host tissue/organ -Causes: Serum sickness, post-strep, rheumatic fever -Rheumatic fever: when strep isnt properly treated and heart tissue is damaged causing lifelong heart murmurs. -Autoimmune disorder: Lupus, Rheumatoid arthritis, MS |
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Spreading of cancer |
Invasion: local spread where tumor grows into adjacent tissues and destroys normal cells Metatasis: spreading via blood/lymph -"hot nodes" = cancer containing nodes Seeding: movement of neoplastic cells in body fluids or along membranes usually in cavity. -can also occur iatrogenically |
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TNM Cancer staging |
-determines extent of disease and is monitored through out the course of the disease. -basis for treatment and prognosis T: size of primary Tumor N: extent of regional Node involvement M: signs of Metatasis |
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Metaplasia and who does this happen to? |
change from one cell type to another cell type
Smokers will see this due to chronic irritation of the airway, this eventually leads to cancer |
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Dysplasia |
Deformed cells, precursor to cancer |
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Anaplasia |
undifferentiated and overgrowing cells without form aka CANCER |
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Benign Vs Malignant |
Benign: slow growing encapsulated mass of differentiated cells. similar to normal cells with fairly normal mitosis. remains localized and life threatening if in brain. Malignant: rapidly growing anaplastic cells that invade nearby tissue and spread through blood and lymph system. |
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What are the 6 types of Exudate? |
1. Serous: clear yellow fluid 2. Fibrinous: fibrin (clotting factor) 3. Purulent: "Pus" - many dead WBCs 4. Abcess: "walled off" to protect health areas. Ucusually needs to be I&D 5. Hemorrhagic: compromised artery/vein resulting in blood collection 6. Necrotizing Faciitis: skin eating disease |
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What is Hemolytic Anemia cased by (2) and what can it lead to (3)? |
-Caused by the rapid destruction of RBCs or Liver dz (when there is decreased ability to conjugate bilirubin)
-Unconjugated bilirubin in blood = jaudice, pruritis, icteric sclera |
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What is Valine? |
The amino acid that replaces glutamic on the Hgb beta chain. -this small change causes Sickle cell anemia |
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What is pancytopenia and what is an example? |
-systemic bone marrow suppression (reduction in RBCs, WBCs and platelets) Ex) Aplastic anemia's |
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What is going on with Anemias, what are normal RBC levels and what are the symptoms if low? |
-reduction in O2 carrying capacity of blood = cellular hypoxia -women: 12-14 -men: 14-16 -CNS irritability, decreased energy, metabolism, reproduction, Erythropoiesis, tachycardia, peripheral vasoconstriction, decreased GI regeneration |
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The 4 Types of Anemia |
1. Iron deficiency 2. Pernicious 3. aplastic 4. hemolytic (sickle cell, Thalassemia, polycythemia) |
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Iron Defiency anemia (Patho, CBC, Causes, S/sx) |
Patho: lack of Fe+ impedes production of RBCs CBC: hypochromic, microcytic, decreased Hgb, MCV, MCHC (RDW unaffected) Causes: diet lacking green veg/red meat, chronic blood loss, bad duodenal absorption of Fe+, liver dz S/Sx: regular anemia s/sx, stomatitis, amenrrhea, delayed healing |
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Pernicious Anemia aka megaloblastic anemia (patho, CBC, causes, s/sx) |
Patho: malabsorption of B-12 that is needed for RBC production in bone marrow CBC: macrocytic reticuloctes, increased RDW Causes: diet (rare), destroyed parietal cells due to autoimmune reaction or chronic gastritis (alcoholics), gastroectomy due to surgery S/sx: macroglossia, acholorhydria. ataxia, tingling, burning due to peripheral demylination |
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Pernicious anemia diagnosis and tx |
Diagnosis tests: achlorhydria (decreased production of HCL confirms diagnosis), large megaloblastic cells, decreased b-12 Tx: B-12 injection, oral for prophylaxis only, cannot treat with oral supplement |
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Aplastic Anemia aka pantocytopenia (patho, CBC, cuases, S/sx, Tx) |
Patho: impairment of bone marrow leading to lack of stem cells to make RBCs, WBCs, platelets CBC: neutorphilia, MCV, Hgb/Hct/Plt all low Causes: idiopathic (most common), myelotoxins, SLE (autoimmune dz), Fanconi's (hereditary dz) S/sx: regular anemia s/sx, leukopenia, opportunitic infections, thrombocytopenia Tx: tx underlying causes, bone marrow trans |
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Hemolytic Anemias (3 types, patho, causes) |
Include Sickle cell, thalassemia, polycythemia Patho: excessive hemolysis Causes: genetic, neoplastic, cytotoxic immune reaction, toxins, malaria |
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Sickle cell anemia (causes, fact, s/sx, diagnosis, tx) |
Causes: HgS gene inherited from parents as homoxygous recessive. needs to be from both parents for abnormal Hgb (african/middle eastern) Fact:inherit from one parent (heterozygous) its protective against malaria S/sx: regular anemia s/sx, hyperbilirubinemia, splenomegaly, vascular occlusions causing sickle cell crisis, growth/development delays, CHF Diagnosis: hemoglobin eletophoresis, DNA test for HgS Tx: hydrea, avoid high altitudes/infections/stress, prophylactic meds, 20 year life expectancy |
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Thalassemia (causes, s/sx, CBC, tx) |
Causes: genetic defect where one or more genes of globin (protein portion of Hgb) are variant/ missing = premature destruction of RBCs S/sx: reg anemia s/sx, hyperbilirubinemia, hyperactive bone marrow, growth retardation CBC: microcytic, hypochromic RBCs, increased erythropoietin/reticulocytes, high iron levels Tx: transfusion, iron chelation, splenectomy, survive into 30s |
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More about Thalassemia |
-Thalassemia minor when only one globin unit -Thalassemia major (cooley's dz) when 2+ globin units -Named after which globin affected (alpha or beta -Alpha: seen more in Indian, Chinese, South Asian -Beta: Mediterranean |
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Polycythemia (patho, causes, CBC, S/sx, Tx) |
Patho: increased bone marrow stimulation Causes: neoplastic/idiopathic (primary/vera type), lung dz, high altitudes, increased excretion of erythorpoietin due to renal tumor (secondary) CBC:high RBC/granulocytes/platelets, low erythropoietin, hyperuricemia S/sx: high viscosity blood, increase throbocytes, cyanosis, hepatomegaly, plenomegaly, full/bounding pulse, visual probs Tx: phlebotomy, marrow suppression, meds, radiation |
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Gout (patho, etiology, s/sx, tx) |
Patho: uric acid metabolism defect causing it to deposit in soft tissue an and form crystals initiating acute inflammatory response Etiology: Renal dx, dm, illness, stress S/sx: tophi, pain, inflamed/rubor/calor joint tx: meds, low purine diet, increase fluid, increase pH of urine to excrete uric acid
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Rheumatoid Arthritis (patho, etiology, s/sx) |
Patho: type IV (autoimmune) disorder causing systematic/symmetrical inflammation of synovial membrane in joints Etiology: female, increased age, genetic, virus link S/sx: joint stiffness, synotivtis, muscle atrophy, painful pannus, ulnar deviation, boutonnieire deformity |
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Osteoarthritis (Patho, etiology, s/sx) |
Patho: fissure of weight-bearing articular cartilage in joints causing decreased joint function due to abnormal healing of bone Etiology: idiopathic, wear and tear S/sx: NON-INFLAMMATORY but there may be secondary inflammation, pain, decreased mobility, crepitus |
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Osteoporosis (Patho, Etiology, s/sx) |
Patho: decreased bone density due to osteoclast destruction outdoing osteoblast construction Etiology: women, small/light structure, lack of Ca+/Vit D as child, smoking, post-menopausal due to decrease in estrogen, >50, sedentary/immobile, hyperparathyroidism, cushing's, glucocotricoids, diet drinks b/c of excessive phosphates S/sx: fracture, delayed bone healing, DEXA scan to confirm |
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Huntington's Dz (patho, etiology, s/sx, tx) |
Patho: N-terminal proteins accumulate causing progressive atrophy of brain = decreased GABA and acetylcholine levels Etiology: autosomal dominant (chrom 4) S/sx: 50-60s, mood changes, restlessness, dementia, choreiform, milkmaids grip, harlequins tongue, rigidity, akinesia, dystonia tx: only for symptoms |
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Myesthenia Gravis (patho, eti, s/sx, dx, crisis) |
Patho: IgG antibodies block acetylcholine receptor site, preventing muscle stimulation leading to weekness/fatigue Etiology: authoimmune, more in women 20-30, men 50+ S/sx: starts in face and moves down, facial/eye muscle weakness, diplopia, ptosis, flat affect, disphagia, unproductive cough = resp infections Dx: Positive tensilon test = immediate relief of symptoms Crisis: from infection, stress, alcohol |
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Amyotrophic Lateral Sclerosis aka ALS aka Lou Gehrig's Dz (Patho, eti, s/sx, dx,tx,mortality) |
Patho: nonremissive and non inflammatory muscle wasting of lateral corticospinal motor neuron tracks in cerebrum, brainstem and spine Etiology: ideopathic, men 40-60, chrom abnormalities, 10% familial S/sx: extremity weakness, hyperflexia, flaccid paralysis, falls, twitching, dysphagia Dx: no tests Tx: none to stop/slow, exercise may help Mortality: 2-5 yrs due to resp failure |
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Parkinson's Dz (patho, primary and secondary eti, s/sx, dx, tx) |
Patho: decreased dopamine due to changes in substantia nigra basal nuclei causing loss of motor control Primary etiology: 60+ Secondary: post-encephalitis, trauma, vascular dz, phenothiaizine meds S/sx: weakness, hand tremors at rest and decrease with vol movement/sleep, flat affect, slumped, dementia Dx: none, only history/physical s/sx Tx: Levodopa |
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MS (patho, etiology, s/sx, dx, tx) |
Patho: demyelination of CNS motor, sensory and autonomic neurons interfering with conduction first causing inflammation in white matter then later causing permanent plaques Etiology: 20-40, S/sx: tingling, numb, burning, diplopia, paralysis Dx: MRI shows plaqued CNS, CSF will have elevated proteins and WBCs Tx: glucocorticoids for INF, PT to max function |
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Autonomic Dysreflexia (causes, process, complications) |
Cause: spinal cord injury Process: spine lesion below injury prevents message to brain --> SNS stimulation below block --> Vasoconstriction --> HTN --> stimulated baroreceptors send PNS signal to SNS to shut off but can't due to lesion --> baroreceptors send PNS to SA node to slow down HR = bradycardia --> since SNS stimulus not blocked and original stimulus not stopped then more severe vasoconstiction and HTN occurs Complication: malignant HTN, Stoke, MI, aneurysm, resp failure |
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Meningitis (patho, eti, s/sx) |
Patho: inflammation, ICP and exudate covering PIA matter and sulci of brain due to bacteria/virus attaching to choroid plexus Etiology: trauma/surgery, Haemophilus influenza in kids, E. coli in babies due to difficult delivery - BACTERIA TYPE more severe S/sx: HA, photophobia, nuchal rigidity, Kernig's-Brudzinski's signs, exudate/leukocytosis in spinal tap |
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ICP (early and later s/sx) |
First s/sx: LOC change including lethargy, decreased responsiveness Later s/sx: Cushing's Triad = HTN with widening pulse pressure, bradycardia, bradypnea |
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Aphasia and its 3 subtypes |
-Inability to comprehend or express language 1. Expressive: ptn can't speak or write language due to broca's area damage 2. Receptive: ptn can't understand written/spoken language due to wernicke's area damage 3. Global: both of the above
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Dysarthia |
words can't be articulated clearly as result of motor dysfunction due to cranial nerve damage |
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Agraphia, Alexia, Agnosia |
-Impaired Writing ability -impaired readying ability -loss of recognition of association |
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Coma |
-patient doesn't resond to painful or verbal stimuli, body flaccid but some reflexes still may be present. Slow and irregular pulse and respirations. -3 on coma scale Deep: no reflexes, dilated pupils, slow pulse |
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Vegetative state |
loss of awareness and mental capabilities due to brain damage but due to brainstem still being intact the fucntions of the resp, circulatory, cardio and autonomic systems still function |
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Acute renal failure (patho, eti, s/sx) |
Patho: ischemia from renal artery damage, HTN, DM, shock, inflammation/obstruction of tubules Etiology: acute bilateral dz, nephrotoxic meds, mechanical obstuction (calculi, clot, tumor) S/sx: increased BUN and creatinine, metabolic acidosis, hyperkalemia Complications: chronic renal failure |
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Chronic Renal Failure (patho, eti, tx) |
Patho: more insidious/systemic ischemia of both kidneys Etiology: pyelonephritis, HTN, DM, vancomycin Complications: metabolic acidosis, fluid overload, hyperkalemia Tx: dialysis, transplant |
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The 3 S/sx stages of chronic renal failure |
1. 60% loss of nephron, BUN/creatinine normal, decreased GFR 2. 75% loss of nephron aka "renal insufficiency", increased BUN/creatinine, 20% GFR, electrolyte imbalance, anemia, HTN 3. 90% nephron loss, GFR negligible, increased BUN/Creatinine = Axotemia aka uremic frost and urine smelling breath, hypocalcemia, fractures |
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Glomerulonephritis (s/sx, eti) |
S/sx: smokey/coffee colored urine, proteinuria, gross hematuria, RBC casts, HTN, facial/orbital edema later anasaric Etiology: kids 3-7 about 10-14 days after strep infection |
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Pyelonephritis (patho, s/sx) |
Patho: inflammed and purulent filled kidney(s) where tubule tissue sloughs off forming "casts" of tubule walls S/sx: dysuria, bad smelling urine, CVA tenderness, fever, malaise, leukocytosis with casts in urinalysis |
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Seizure disorder |
Patho: hyperexcitiable neurons have lower stimulation threshold resulting in brainwide motor/sensory activity Etiology: kids, familial, idiopathic Precipitating factors: hypoglycemia, meds, hyperventilation Tx: meds to increase action potential threshold, meds that end in -pam, benzodiazepines, avoid triggers |
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Partial vs. Generalized Seizure |
Partial: single focus often unilateral, ptn sometimes doesn't lose conciousness, may progress to generalized Generalized: involves multiple foci and both hemispheres of brain and brainstem, will result in LOC, can result in tonic-clonic (grand mal), status epilepticus |
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Types of Generalized Seizures (2) |
Petit mal (absent): 5-10 secs, mult times/day, brief LOC, transient facial movement, eyelid twitch Grand mal (tonic clonic): spontaneous, ptn may have prodromal sign/Aura, strong muscle contractions with cry noise, erratic extremity movement followed by postictal stage (ptn out cold) |
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Partial Seizure (aka simple or focal) |
S/sx: repeated jerking movement, clapping, tingling, hallucination, deja vu, unresponsive, amnesia, NO LOC |
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Transient Ischemic Attach - TIA |
Patho: temporary + partial blockage of artery that is often warning of eimpending CVA Etiology: atherosclerosis, emboli, vascular spasm S/sx: no more than 24 hrs, location ischemia, intermittent impaired functioning that is not perm. patient remains conscious Risk factors: DM, smoking, CAD, HTN |
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Cerebral Vascular Accident (aka Stroke) |
Patho: infarction of brain tissue causing tissue necrosis Etiology: thromus, embolus, hemorrhage S/sx: first flaccid paralysis directed related to part/size of infaction followed by increasing deficits for 48 hrs due to inflammation, HEMMORRHAGIC STOKES ptns will have blinding HAs Risk factors: DM, Smoking, CAD, HTN
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The 3 types of CVAs |
Thrombus: gradual + localized effects caused by atherosclerosis in cerebral or carotid artery Embolus: sudden + localized effects caused by atherosclerosis in carotid from systemic source Hemorrhage: sudden, widespread + severe effects due to HTN causing rupture of cerebral artery |
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Pancreatitis (Patho, Eti, complications) |
Paho: INF of pancreas due to autodigestion of tissue b/c of premature activation of proenzyme turning trypinogen into trypsin Etiology: gallstones, alc abuse, sphincter of odd obstruction Complications: Acute can be med emerency leading to shock, ARDS, hemorrhage, peritonitis, tachycardia, hypotension |
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Tuberculosis (patho and primary infection) |
Patho: AFB invades lung tissue Primary : non-contagious time when organism gets englufed by macrophages and there is some inflammation of upper lung lobes ->some of theses bacilli reach lymph nodes causing a type IV delayed hypersensitivity response (TB skin test would recognize) and local infection gets walled off and creates "Ghon Complexes" |
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Tuberculosis (secondary, etiology) |
Secondary: "active infection" causing orgnaism to multiply and cuase necrosis, cavitation and hemoptysis, GI can then become infected due to swallowing Etiology: close quarters, immunocompromised, immigrants, recent travelers |
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Tuberculosis (diagnosis, tx) |
Diagnosis: TB skin test (mantoux) if +, then CXR/culture taken Tx: INH for up to 12 months - compliance very important or else MDR-TB (superbug) can occur |
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Peptic ulcer dz (patho, etiology, who, s/sx) |
patho: acidic stomach juices creating cavities typically seen in proximal duodenum that can eventually lead to peritonitis Etiology: H-pylori, inadequate blood supply, ASA,, ibuprogen, alcohol, stress, glucocorticoids Who: men, western countries, type O blood S/sx: 2-3 hrs after meal at night, relieved by eating/antacids, melena (black tarry stools) |
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ARF |
pH: <7.3 aka resp acidosis Etiology: body unable to blow off enough CO2 or get enough O2 S/sx: CNS depression, resp arrest |
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Respiratory Acidosis (levels, causes, effects, compensation) |
-pH less than 7.35 Causes: Pneumonia, airway obstruction, opioids, COPD, emphysema, chronic bronchitis Effects: HA, lethargy, drowsiness, confusion, CNS depression, coma/death Compensation: acidic urine |
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Metaboilc Acidosis (levels, causes, effects, compensation) |
-pH less than 7.35 Causes: loss of bicarb ions in diarrhea, dehydration, internal bleeding, DKA, Renal disease Effects: HA, lethargy, drowsiness, confusion, CNS depression, coma/death Compensation: increased RR |
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Respiratory Alkalosis (levels, causes, effects, compensation) |
-pH > 7.45 Causes: hyperventilation caused by anxiety, fever, ASA OD, brainstem disease, brain injury Effects: CNS irritability, restlessness, twitching, tingling, numbness of fingers, tetany, seizure coma Compensation: bicarb exretion |
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Metabolic Alkalosis (levels, causes, effects, compensation) |
-pH > 7.45 Causes: early vomiting, NG suction, iatrogenically (overcorrection of acidosis) Effects: CNS irritablity, restlessness, muscle twitching, numbness, tetany, seizure, coma Compensation: decreased RR |
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Type I Diabetes Mellitus (action, onset, ptn, tx) |
Action: autoimmune reaction that completely stops insulin production in pancreas Onset: Acute, patients usually in a state of DKA at diagnosis Patient: younger, thin frame Treatment: insulin replacement |
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Type II Diabetes Mellitus (action, onset, ptn, tx) |
Action: insulin resistance Onset: insidious taking years Patient: middle age usually, high BMI, high glucose diet. higher rate in black, latino, American Indian populations. Treatment: diet, exercise, oral drugs, insulin replacement |
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8 Signs and Symptoms of Diabetes |
2. hyperglycemia 3. Glucosuria 4. Polydipsia 5. Polyphagia 6. weight gain 7. nocturia 8. elevated HgB A1C (should be below 11) |
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DKA (patho, complications) |
Patho: type 1 patient has prolonged/severe insulin deficit caused by stress, infection, overindulgence in carbs = catabolism = using fats/proteins for energy = FFA and Ketones Complications: kassmaul respirations, fruity breath, decreased LOC, resp depression, hyperkalemia |
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Myocardial Infarction (S/sx, dx, complications) |
S/sx: sudden CP that going into jaw/shoulder/arm, silent in DM ptns, women have atypical s/sx, SNS iritibility, N/V, fever Dx: ST elevation dx's occluded arteries (aka stemi vs nstemi), CK-MG, Troponin-I, K+/Na+ abnormal, Leukocytosis Complications: Arrhythmias (in first hours after), shock, CHF, aneurysm, thromboembolism |
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Cushing's reflex |
As ICP increases vasomotor centers are stimulated = systemic vasoconstriction to increase cerebral blood supply = temporarily increases cerebral blood supply = baroreceptors in carotid arteries respond to increased BP = PSN stimulation to SA node = bradycardia = chemorecpetors respond to low cerebral CO2 levels = bradypnea = cerebral ischemia temp improves but returns from high ICP = cycle retarts = cushings triad (HTN w/ increasingly widening pulse pressure, bradycardia/pnea) |
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Cholelithiasis aka gallstones |
Causes: fatty meal, cholesterol, infection, e.coli S/sx: RUQ pain Complications: jaundice, leukocytosis, fever Cholesterol stones: obese, women, estrogen Bile stones: anemia, alcohol cirrhosis, biliary infection
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Cholangitis vs Choledocholithiasis |
-INF of gallbladder -obstruction of biliary tract |
