Exam 2 Flashcards
Urinary Tract Obstructions
An interference with the flow of urine at any site along the urinary tract. Obstructions can be anatomical or functional.
Causes of upper urinary tract obstruction
- Stricture or congenital compression of a calyx or junctions of the ureters
- Compression from a tumor
- Stones
- Compression from abdominal inflammation and scarring
Obstructive uropathy
Anatomic changes in the urinary system caused by obstruction. Severity based on:
- Location
- Involvement of one or both sides
- Completeness of the blockage (still some function?)
- Duration
- Cause
Effects of upper urinary tract obstruction
-Early response: Dialation (of the ureter, renal pelvis, calyces, and renal parenchyma)=smooth muscle hypertrophy and accumulation of urine above level of blockage.
- If blockage nor relieved, dialation leads to enlargement
- Glomerular/kidney damage. Thinning of renal cortex.
Hydroureter
Dilation of the ureter. Accumulation of urine in the ureter.
Hydronephrosis
Dilation of the renal pelvis and calyces proximal to a blockage-Enlargement of the renal pelvis and calyces.
How the body is able to partially counteract the negative consequences of unilateral obstruction
- Compensatory hypertrophy
- Hyperfunction
Causes the unobstructed kidney to increase the size of individual glomeruli and tubules, but not total number of functioning nepherons.
Postobstructive diuresis
Marked polyuria after relief of obstruction. Can cause dehydration and fluid/electrolyte imbalances.
Risk factors for postobstructive diuresis
- Chronic, bilateral obstruction
- Impairment of one or both kidneys to concentrate urine or reabsorb sodium
- Hypertension
- Edema
- Congestive heart failure
- Uremic encephalopathy
Kidney Stone
Masses of crystals, protein, or other substances that form within and may obstruct the urinary tract. Classified according to the minerals that make up the stone.
Can be located in kidneys, urterers, and bladder
Causes of lower urinary tract obstruction
- Neurogenic bladder (Detrusor hyper-reflexia, Detruson areflex-inderactive)
- Tumors
- Prostate enlargement
- Pelvic organ prolapse
- Urethral stricture
Effects of lower urinary tract obstruction
- Incontenance (Stress, urge, overflow, mixed, functional)
- Frequent voiding
- Nocturia
- Poor force of stream
- Intermittent stream
- Feelings of incomplete bladder emptying
Pathophysiology of kidney stones
- Supersaturation of one or more salts
- Precipitation of a salt from liquid to solid state
- Growth into a stone via crystallization or aggregation
- Lack of crystal growth inhibitors
Types of stones
- Calcium oxalate/phosphate
- Struvite
- Uric acid stones
Manifestations of kidney stones
- Renal colic (moderate to severe flank pain that can radiate to the groin. Rhythmic contraction. )
- Urgency
- Frequent voiding
- Nausea and vomiting (sometimes)
Calcium oxalate stones
Formed in alkaline urine. Most common
Struvite stones
Formed in alkaline urine. Contain Magnesium, ammonium, varying levels of matrix, and phosphate. Form staghorn configuration.
Uric acid stones
Form in people who excrete excessive uric acid in the urine, such as people with gouty arthritis.
Neurogenic bladder
General term for bladder dysfunction caused by neuro disorders. Lead to dyssynergia.
Dyssynergia
Loss of coordinated neural muscle contraction.
Types of neurogenic bladder
- Detrusor hyperflexia
- Detrusor areflex
Detrusor hyperflexia
Overactive bladder syndrome. Bladder contracts before bladder is full.
Causes frequency, urgency, and nocturia
Detrusor areflex
Underactive bladder syndrome and may have symptoms of stress and overflow incontinence. Muscle not letting brain know it is full.
Causes of resistance to urine flow
- Urethral stricture
- Prostate enlargement (creates pockets where urine and bacteria sits/festers)
- Pelvic organ prolapse (Uterine prolapse–bladder falls due to no support)
Signs of urinary obstruction
- Frequent daytime voiding
- Nocturia
- Poor force of stream
- Intermittency of stream
- Urgency and hesitancy
- Feeling of incomplete bladder emptying
Renal Tumors
- Renal adenomas
- Renal cell carcinoma
Bladder tumors
-Transitional cell carcinoma: most common bladder malignancy. Most common in 60+ yr old men.
Renal adenomas
Benign. Encapsulated and located near the cortex of the kidney.
Renal cell carcinoma
50-60 year old man. Most common renal neoplasm.
Manifestations of renal tumors
- Hematuria
- Dull, aching flank pain
- Palpable flank mass
- Weight loss
Manifestations of Transitional cell carcinoma
-Gross painless hematuria
Metastisizes to lymph, liver, bones, and lungs.
Urinary tract infection
Inflammation of the urinary epithelium caused by bacteria
Types of UTI
- Acute cystitis
- Acute/Chronic pyelonephritis
- Painful bladder syndrome/Interstitial cystitis
Acute cystitis
Cause and manifestations
Inflammation of the bladder due to E Coli and Staph. Most common in women.
- Frequency
- Dysuria (painful peeing)
- Urgency
- Lower abdominal and or puprapubic pain
Urine can back travel to kidneys.
Pyelonephritis
Risks
Infection of one or both upper urinary tracts
Most common risks: Urinary obstruction and reflux of urine from the bladder
Acute pyelonephritis
Pathophysiology, evaluation, and Manifestations
Acute Infection of both tracts spread by microorganisms along the ureters. Evaluation done by urine culture and urinalysis.
Manifestations include:
- fever/chills
- Flank/groin pain
- Characteristic UTI symptoms: frequency, dysuria, and costovertebral tenderness may precede systemic symptoms
Chronic pyelonephritis
Pathophysiology, evaluation, and Manifestations
Persistent or recurrent infection of the kidney leading to scarring of one or both kidneys. Risk increases in people with renal infections and some type of obstructive pathogenic condition. Urinalysis and ultrasound used in evaluation.
Manifestations include:
- Hypertension
- Frequency
- Dysuria
- Flank Pain
- Progression leads to kidney failure
Glomerularnephritis
Inflammation of the golmerulus caused by:
- Primary glomerular injury (immunologic responses)
- Secondary glomerular injury (Systemic disease)
Primary glomerular injury
Includes immunologic responses, ischemia, free radicals, drugs, toxins, vascular disorders, and infection
Secondary glomerular injury
Consequence of systemic diseases including diabetes mellitus, lupus, congestive heart failure, and HIV related kidney diseases
Glomerulonephritis mechanisms of injury
Activation of biochemical mediators of inflammation:
- Deposition of immune complexes into the glomerulus
- Antigens reacting in situ against planted antigens within the glomerulus
-Non-immune injury is related to ischemia, toxin exposure, drugs, vasular disorders, and infection
Glomerulonephritis manifestations
Onset may be sudden or insidious. Symptoms may be silent, mild, moderate, or severe.
Severe:
-hematuria
-proteinuria
- oliguria (decreased output)
- hypertension
- edema
- nephrotic sediment
- nephritic sediment
Nephrotic sediment
Urine containing massive amounts of protein and lipids and either a microscopic amount of blood or no blood.
Nephritic sediment
Urine with the presence of blood with red cell casts, white cell casts, and varying degrees of protein (not severe)
Glomerular structure damages from Glomerulonephritis
Injury to the filtration membrane increaseing membrane permeability and reduces glomerular membrane surface area. GFR decreases.
Membranous nephropathy
Acute Glomerulonephritis. One of the most common causes of Glomerulonephritis. Caused by antibodies that cause inflammatory response.
Results in increased membrane permeability, thickening of glomerular membrane, and ultimately glomerular sclerosis.
Manifestations are proteinuria and nephrotic syndrome.
Chronic glomerulonephritis
Encompasses several glomerular diseases with a progressive course leading to chronic kidney failure. Diabetes mellitus and lupus are examples of secondary causes of chronic glomerular injury.
Manifestations include:
- hypercholestremia
- Proteinuria
- tubular injury
- Kidneys appear small with granular external surface
Nephrotic syndrome
The excretion of 3.5g or more of protein in the urine per day and is characteristic of glomerular injury. Often glomerular injury is permanent.
- Massive proteinuria
- Hypoalbuminemia
- Edema
- Hyperlipidemia (in blood) and hyperlipiduria (in urine)
- Frothy urine
Chronic and requires lifetime of medication and dialysis.
Nephritic syndrome
Hematuria (usually microscopic) is present and red blood cell casts are present in the urine in addition to non-severe protein uria. Occurs due to inflammation of the glomeruli or glomerular membrane. Is reversible with control of inflammation.
- Dark, cola-colored urine
- Hematuria
- Oliguria (low output of urine)
- Azotemia
- Hypertension
Oliguria
Low output of urine
Dysuria
Painful urination
Acute Kidney Injury
A sudden decline in kidney function with a decrease in glomerular filtration rate (GFR) and increase of Blood Uria Nitrogen (BUN) and createnine. BUN and createnine proportionate and rise together. GFR inverse.
Vlassified as prerenal, intrarenal, and postrenal
Anuria
No urine output
Renal insufficiency
25% of normal GFR
Renal failure
Significant loss of renal function that requires dialysis
End-stage renal failure
Renal function of less than 10% requiring dialysis or transplant
Prerenal AKI
Most common reason for Acute Renal Failure and is caused by impaired renal blood flow (hemorrhage/trauma). “Interruption of blood flow before the kidneys.”
GFR declines because of the decrease in filtration pressure. Sudden/severe drop in pressure to kidney (trauma, blood loss, hypotension, hypovolemia)
Intrarenal AKI
Problem is inside the kidney. Direct damage to kidney by infection, reduced blood supply in kidney, inflammation, toxins, drugs. “Structural change inside the kidney causes problem even if there’s enough blood flow”
Most common cause: Acute tubular necrosis.
Acute tubular necrosis
Most common cause of Intrarenal AKI. Lack of O2 to tissues in kidney(ischemia)/nephrotoxic drugs. Damage to tubules.
Causes oliguria.
Postrenal AKI
Caused by urinary obstructions that affect the kidneys. “After kidneys”
- Stones
- Tumors
- Edema
Phases manifestations of AKI
Always 3 phases:
- Initiation phase
- Maintenance phase
- Recovery phase
Initiation phase of AKI
Kidney injury is evolving. Prevention of injury is possible (onset of trauma). Is reversible.
Maintenance phase of AKI
Established kidney injury and dysfunction.
-BUN/createnine increased and GFR decreased
-Low urine output
Lasts weeks/months
Recovery phase of AKI
Kidneys now functioning and injury is repaired. GFR rises and BUN/Createnine is decreasing.
- Normal output
- Can last 1-2 years depending on severity of injury
Chronic Kidney Disease
Progressive loss of renal function that affects nearly every organ in the body.
Associated with hypertension, diabetes, intrinsic kidney disease (chronic glomerularnephritis)
Chronic Kidney Disease requirement
3 months or more of less than 60ml/min GFR
Azotemia
Increased levels of waste in the body. Measured in part by BUN and createnine
Uremia
Systemic symptoms associated as a result of azotemia (buildup of waste and toxins)
Kidneys excrete too much sodium when GFR declines
Hyponatrimia in blood=neuro problems
When kidneys don’t excrete enough potassium (oliguria magnifies effects)
Hyperkalemia. Dysrhythmia/heart failure
Metabolic acidosis
Chronic kidney disease. Kidneys unable to balance out H+ elimination with bicarbonate resorption. Respiration system will try to compensate.
Risk when GFR less than 25ml/min
CKD patients and diet
Don’t have to moniter sodium, but must monitor Potassium
CKD affects vitamin D absorption
Hypocalcemia=fracture risks
Phosphate excretion lowers, so affects vit D synthesis.
CKD affects metabolism
Increases risk for heart disease.
CKD causes anemia
RBC production drops because eurethropoitin production drops. Fatigue, dizzy
CKD affects of cardiovascular system
- dislipidemia promotes buildup of plaque (cholesterol)
- hypertension result of imbalance of water/sodium
- Heart failure/stroke rates increase
- anemia increases workload on heart (heart pumps faster to get less O2 through body)
CKD affects of pulmonary system
-Fluid overload. Kidneys can’t get fluid out, so fluid gets dumped in your lungs.
CKD affects of hematologic system
- Anemia. Inadequate production of erythropoietin decreases RBC production.
- Uremia decreases RBC life span
- Alterations in thrombin and other clotting factors contribute to hypercoagulability (control of coagulation is essential during dialysis)
- Increased bleeding tendancies causes bruising
CKD affects of immune system
- Suppressed immune system
- WBCs might not respond appropriately to infections
CKD affects of neurological system
- headaches
- pain
- hyponatremia causes seizure/coma/muscle twitching
CKD affects of GI system
- Uremic gastroenteritis causes bleeding ulcers and hemorrhage
- anorexia
- nausea/vomiting
- constipation
- diarrhea
- Uremic fetor (bad breath. Wastes leaving body through your mouth)
- Malnutrition
CKD affects of endocrine/reproductive system
- Decreased testosterone (decreased libido)
- Infertility
- Insulin resistance in uremia(become diabetic)
- Half life of insulin increased
- Alterations of thyroid hormone metabolism
CKD affects of integumentary system
- Pallor from anemia
- bruising
Anemia commonalitles and general causes
Reduction of total # of erythrocytes (reduction in quality or quantity of hemoglobin)
- Impared erythrocyte production
- Acute or chronic blood loss
- Increased erythrocyte destruction
- Combination of above
Classic anemia manifestations
- Fatigue (less O2)
- Weakness (less O2)
- Dyspnea (shortness of breath–lungs trying to compensate)
- Increased heart rate (heart trying to pump a little O2 through the body)
- Pallor (pale skin)
Hypoxemia
Reduced oxygen level in the blood, further contributes to cardiovascular dysfunction by causing dilation of arterioles, capillaries and venules, thus increasing flow through them.
Pernicious anemia
Macrocytic-normochromic
Caused by a lack of intrinsic factor (required for B-12 absorption) from the gastric parietal cells. GI tract can’t absorb B-12. Vitamin b-12 deficiency.
Causes:
- atrophic gastritis
- alcoholism
Manifestations:
- Classic symptoms
- NEURAL manifestations (nerve demylination)
- –Gait issues, pins and needles feeling in toes and fingers, beefy red tounge, lemon-yellow skin
Folate deficiency anemia
Macrocytic-Normochromic
Causes:
-Pregnancy
-Alcoholism (dietary)
Manifestations: -Classic symptoms (NO neural symptoms) -Cheilosis -Stomatitis -Mouth ulcers
Microcytic-hypochromic anemias
RBC that are abnormally small and contain reduced amounts of hemoglobin
Macrocytic-normochromic
RBC that are abnormally large and contain normal amounts of hemoglobin
Iron deficiency anemia
Most common anemia. (Frequently associated with women of childbearing age due to periods)
Causes:
-Nutritional iron deficiency
Manifestations: -Fatigue -Weakness -Shortness of breath -pale ear lobes, palms, conjunctiva Progression: -Brittle, thin, coarsly ridged and spoon shaped nails -A red, sore, and painful tongue -Dry, sore corners of the mouth
Sideroblastic anemia
Functional problem with the iron. Iron is present, but not functioning correctly.
Manifestations:
- Common symptoms
- Iron overload (enlarged liver and spleen)
- Bronze colored skin
Normocytic-normochromic
Not sufficient number of RBC
Aplastic anemia
Pancytopenia. Reduction in all RBC, WBC, and platelets.
Manifestations:
- Classic anemia symptoms
- Reduced clotting
- Reduced immune function
Posthemorrhagic anemia
Acute blood loss. Lowers blood pressure. No symptoms are getting enough oxygen
Hemolytic anemia
RBCs getting destroyed. Many causes.
Manifestations
- Enlarged spleen
- Jaudice
- Hemolytic crisis
- CV and respiratory anemia manifestations
Relative Polycythemia
Overabundance of RBCs due to oversaturation because of dehydration (loss of fluid)
Absolute polycythemia (primary)
True overproduction of RBC. Abnormality of stem cells in the bone marrow (polycythemia vera)
Absolute polycythemia (secondary)
True overproduction of RBC. Increase in erythropoietin as a normal response to chronic hypoxia or in an inappropriate response to erythropoiten
Polycythemia
Overproduction of RBC
Manifestations of polycythemia
Manifestations due to increased blood volume which increases viscosity (blood becomes thicker) and leads to hypercoagubility.
- Headaches
- Increased blood pressure because of increased volume
- Chest pain
- Angina–myocardial infarctions (signs of clots)
- Intense painful itchiness
Neutrophilia
More neutrophils (evident in the first stages of an infection-left shift) Immature neutrophils are released into blood. Immature cells not able to do as much as a mature cell
Neutropenia
Reduced neutrophils, mature or immature.
Causes:
- Prolonged severe infection
- decreased neutrophil production
- Reduced survival
- Abnormal neutrophil distribution and sequestrian
Infectious monocucleosis
Infection of B lymphocytes. Commonly caused by Epstein-Barr virus.
Manifestations start mildly and progress:
- Fever
- Sore throat
- Swollen cervical lymph nodes
- Fatigue (can take several months to get over)
Leukemia
Malignant disorder of the blood and blood forming organs.
Excessive accumulation of leukemic cells. Pancytopenia of cells crowd bone marrow because leukemic cells take all the room.
Acute leukemia
Presence of undifferentialted or immature cells
Chronic leukemia
Predominant cell is mature but doesn’t function normally
85% of childhood leukemia
ALL
Causes/risks of leukemia
- Associated with other genetic disorders
- Genetic translocations
- Cigarette smokine, exposure to benzene, ionizing radiation
- Infections with HIV or hep C
- Drugs that cause bone marrow depression (cancer treatment)
Manifestations of leukemia
*Remember: reduction of all blood cells, so manifestations are a hodgepodge of results from decreased RBC, WBC, and platelets.
- Anemia
- bleeding
- Purpura-big spots
- Petechiae-small pinpoint spots
- Ecchymosis-decreased platelets
- Hemorrhage-decreased platelets
- DIC-Decreased platelets
- Infection-Reduced WBC
- Weight loss
- Bone pain
- Elevated uric acid
- Liver, spleen, and lymph node enlargement
Chronic anemia more slowly and stealthily (insidious)
Malignant lymphoma
Malignant transformation of a lymphocyte and proliferation of lymphocytes, histiocytes, their precursors, and derivitaves in lymphoid tissues
Two categories:
-Hodgkin
-Non-hodgkin
Hodgkin lymphoma
Characterized by presence of Reed-Sternberg cells in lymph nodes. Spreads in an orderly fashion-from the neck down
Manifestations:
-Enlarged spleen
-Cervical, axillary, inguinal retroperitoneal nodes enlarged
-**Intermittant fever, weight loss, night sweats, pruritus(itchiness)
Non-hodgkin lymphoma
Generic term for a diverse group of lymphomas. Doesn’t spread in an orderly fashion. Cancers of B, T, or NK cells. Includes multiple myloma.
Multiple myeloma
Malignant proliferation of plasma cells-B cells
Infiltrate bone marrow and aggregate into tumor masses in skeletal system.
Manifestations:
-Hypercalcemia
-Renal failure secondary to hypercalcemia
-Proteinuria
-Bone leisions and bone pain
Normal platelet count
<150,000/mm^3
Platelet count that would cause hemorrhage from minor trauma
<50,000/mm^3
Platelet count that would cause spontaneous bleeding
<15,000/mm^3
Platelet count that would cause severe bleeding situations
<10,000/mm^3
Causes of thrombocytopenia
Results from decreased platelet production, increased consumption, or both.
- Hypersplenism
- Autoimune diesease
- Viral or bacterial infections that cause disseminated intravascular coagulation (DIC)
Thrombosis
Blood clot in deep vein
Characterizations and manifestations of alterations of platelet function
Increased bleeding time in the presence of a normal platelet count
Manifestations:
- petechiae
- purpura
- Bleeding from GI tract
Types of alterations of coagulation
- Vitamin K deficiency
- Liver disease
Impairs homeostasis-inability to promote coagulation and the developement of a stable fibrin clot
Vitamin K deficiency
Necessary for synthesis and regulation of anticoagulants. Causes liver disfunction
Liver disease
Causes a broad range of homeostatic dosorders
- Defects in coagulation
- Fibrinolysis
- Platelet number and function
Disseminated Intravascular Coagulation (DIC)
Clots and bleeding. Widespread activation of coagulation, resulting in formation of clots in medium/small vessels throughout the body. Clotting may cause consumption of platelets and clotting factors leading to severe bleeding.
Clotting factors and platelets all being used to form clots.
Manifestations:
- Hemorrhage
- Bleeding from venipuncture sites/arterial lines
- Purpura, petechiae, and hematomas
- Cyanosis of fingers and toes (blue tint)
Thrombus
Clot
Embolus
Clot that has broken free and is moving in the bloodstream
Virchow triad
The risk for developing spontaneous thrombi. 3 factors:
- Injury to the blood vessel endothelium
- Abnormalities to blood flow
- hypercoagulabiltiy of the blood
Examples of injury to blood vessel endothelium in relation to Virchow triad
- Atherosclerosis
- Smoking
- Endotoxins
- Hypertension
Examples of abnormalities to blood flow in relation to Virchow triad
- Atherosclerosis
- Bedrest
- Malignancy
- Surgery
- Sickle cell anemia
- Myocardial infraction
Examples of hypercoagulability of blood in relation to Virchow triad
-Polycythemia
Symbiosis between humans and microorganisms
Benefits only the human; no harm to microorganism
Mutualism between humans and microorganisms
Benefits the human and the microorganism
Commensalism between humans and microorganisms
Benefits only the microorganism; no harm to the human
Pathogenicity between humans and microorganisms
Benefits the microorganism; harms the human
Oppoortunism between humans and microorganisms
Situation that occurs when benign organisms become pathogenic because of decreased human host resistance
Communicability
Ability to spread from one individual to others and cause disease-for example, measles and pertussis spread very easily. HIV is of lower communicability
Immunogenicity
Ability of pathogens to induce an immune response
Infectivity
Ability of the pathogen to invade and multiply in the host
Mechanism of action
Manner in which the microorganisms damages tissues
Pathogenicity
Ability of an agent to produce disease—success depends on communicability, infectivity, extent of tissue damage, and virulence
Portal of entry
Route by which a pathogenic microorganism infects the host
Toxigenicity
Ability to produce soluble toxins or endotoxins, factors that greatly influence the pathogen’s degree of virulence
Virulence
Severity of affect—for example, measles virus is of low virulence; rabies virus is highly virulent
Endotoxins
Released during destruction of bacteria. Contained in cell wall of some bacteria. Breaks down>enters blood stream
Bacteria that produce endotoxins cause fever from inflammatory process
Exotoxins
Released during bacterial growth. Enzymes with specific target cells.
Immunogenic and elicit production of antibodies
Bacteremia
Presence of bacteria in the blood
Septicemia
Growth of bacteria in the blood. Results from breakdown of body’s defense mechanisms
6 Phases of viral replication
- Adsorption-Virion adds itself to cell membrane
- Penetration-enzymes break through membrane
- Uncoating-virus exposed
- Replication
- Assembly and maturation of replicas
- Release-spreads to other host cells
Clinical manifestations of infection
Begins with nonspecific symptoms
- FEVER
- fatigue
- malaise
- weakness
- loss of concentration
Predictable stages of infection
- infection
- incubation
- symptom stage
- shedding of microorganism
Vaccines
Preparation of weakened or dead pathogens
Types of vaccines
- Attenuated (live virus)
- Killed (inactivated virus)
- Toxoids (purified toxins that are used against the disease toxins)
Primary (congenital) immune deficiency
Caused by a sporadic genetic defect. Most manifest in childhood.
Secondary (aquired) immune deficiency
Caused by cancer, infection, or normal changes (aging)
Usually doesn’t greatly increase infection (HIV exception)
Typical routes of transmission for HIV
Blood borne pathogen.
- blood/blood products
- IV drug abuse
- sexual activity
- maternal-child transmission
HIV/AIDS manifestations
- At first, symptoms mimic flu like symptoms
- Susceptible to opportunistic infections (fungal, bacterial, viral, neoplasms)
Treatment and prevention of HIV
- HAART medications (antiretrovirals)
- Safe sex
- No drugs
Allergy
Hypersensitivity to environmental antigens
Hypersensitivity
Altered immunologic reactions to an antigen that results in disease or damage to the individual
Autoimmunity
Disturbance in the immunologic tolerance of self-antigens
Alloimmunity
Individual produces reactions against tissues of another (blood transfusions/fetus during pregnancy/transplant)
Type I hypersensitivity reactions
Allergies. Mast cell products: histamine
Type II hypersensitivity reactions
Tissue specific reactions. Symptoms determined by what tissue is being attacked.
Type III hypersensitivity reactions
Immune complex reactions. Antibodies formed in circulation cause damaging inflammation. Systemic affects all over. (serum sickness)
Type IV hypersensitivity reactions
Cell mediated reactions. Mediated by T lymphocytes and don’t involve antibodies.
Hyperacute rejection reactions
- Immediate and rare
- usually happen due to preexisting antibody toward grafted tissue (occurs when circulation reestablished to graft site)
- Type 2 hypersensitivity reaction
Acute rejection reaction
- Cell mediated
- Happens days to months after transplant
- Body develops an immune response against unmatched HLA antigens
Chronic rejection reactions
- Slow progressive organ failure
- Months to years after transplant
- Type 4 hypersensitivity reaction
Cancer
Refers to malignant tumors
Tumor/Neoplasm
New growth
Benign
Not cancer. Well differentiated cells and encased in stoma. Do not spread
Malignant
Tumors with more rapid growth rates and specific microscopic alterations. Lack of organization
Metastasis
Spread of cancer cells to distant tissues & organs of the body
Carcinoma in situ
Early stage growths, may:
- Remain stable
- Progress to metastatic cancer
- regress and disappear
Common in cervix
Anaplasia
Loss of differentiation in malignant neoplasms
Pleomorphia
Variety of sizes and shapes of cancer cells in malignant neoplasms
Tumor markers
Produced by both benign and malignant tumors. Present in or on tumor cells. May be found in blood, spinal fluid, or urine. Helps healthcare workers screen and ID people at high risk and diagnose specific cancers.
- Hormones
- enzymes
- genes
- antigens
- antibodies
Characteristics of cancer cells in the lab
- Transformed cells (created from normal cells.)
- Contact inhibition (crowd and grow on each other)
- Anchorage independent (Continue to divide when suspended)
- Immortality (evade apoptosis)
Changes in genes occurring in cancer
- Point mutations (small scale changes in DNA)
- Translocations & duplication (large scale changes in chromosomal structure.)
- Gene amplification (Epigenetic changes. Activates oncogenes and results in increased expression of oncogene)
Oncogene
Mutant gene which accelerate proliferation
Tumor-suppressor genes
Put the brakes on cell proliferation
Epigenetic silencing
Chemical modifications that alter expression of genes
Loss of heterozygosity
Loss of one copy of a chromosome region in a tumor-unmasks mutations
Apoptosis
Self-destruction of cells
Telomeres
Protective ends of each chromosome
Cancer metabolism
- Cancer cells divide rapidly
- Most often grow in hypoxic and acidic environments
- Cancer loves glucose
- Cancers are parasites
Chronic inflammation and cancer
- Active immune response in chronic inflammation predisposes to cancer
- Inflammation and cancer have a lot in common
- Combating inflammation leads to cancer eventually
Bacterial causes of cancer
- H. Pylori infection
- Gastric carcinoma
- Peptic ulcer disease
Viral causes of cancer
- Hep B/Hep C
- Ebstein-Barr virus
- Herpes
- HPV
Paraneoplastic syndromes
Symptom complexes triggered by cancer but not caused by direct local effects of the tumor mass.
Caused by biologic substances released due to the tumor.
(examples: crushing syndrome, hypoglycemia, hypercalcemia)
Stages of cancer
1: confines to the organ of origin
2: Cancer that is locally invasive
3: cancer that has spread to regional structures such as lymph nodes
4: Cancer that has spread to distant sites, such as liver cancer which has spread to the lungs
Manifestations of cancer
- Pain *most feared
- Fatigue
- Cachexia
- Anemia
- Low platelets and blood count
- Infection (most sig cause of death and disease)
- GI problems
- Hair and skin problems
Cancer treatment options
- Chemo
- Radiation therapy
- Surgery
Carcinogens
Cancer causing substances.
- Chemical
- Radiation
- Sexual practices
- Dietary
- Air pollution
- Obesity
- Electromagnetic radiation
- Smoking
