Exam 1 Flashcards
Atrophy
Decrease in cellular size
Hypertrophy
Increase in cellular size
Hyperplasia
Increase in # of cells
Dysplasia
Deranged cellular growth
Metaplasia
Replacement of type of cell with another
Cellular Injury
Reversible and irreversible inability to maintain homeostasis
Hypoxic Injury
Reduced amt of O2 in the air, loss of hemoglobin, decreased RBC production, resp/cardio diseases, poison
Ischemia
Inadequate blood supply to an organ
Free Radicals and Reactive O2 Species (ROS)
Electrically uncharged atom or group of atoms having unpaired electron
Chemical Cellular Injury
Xenobiotics (Lead, CO Monoxide, Ethanol, Mercury)
Infectious Cellular Injury
Invasion/Destruction, Toxin production, hypersensitivity reactions
Necrosis
Cell death (sum of changes after local cell death)
Apoptosis
Programmed cellular death
Autophagy
Self-destructive/survival mechanism, aging!
Cellular Aging
Atrophy, decreased function, loss of cells
Tissue and systemic aging
Progressive stiffness and rigidity (sarcopenia)
Frailty
Mobility, balance, muscle strength, nutrition, falls, fractures, etc
Somatic Death
Death of an entire person
Postmortem Changes
Algor mortis (body temp), livor mortis (discoloration), rigor mortis (muscle stiffening), postmortem autolysis (enyme release)
DNA Replication
Untwisting and unzipping of DNA strand (DNA is template)
Mutation
Any alteration of genetic material
Mutagen
Agent known to increase the frequency of mutations (radiation/chemicals)
Central Dogma of Bio
DNA (transcription) - RNA (translation) - Protein
Proteins
One or more polypeptides - composed of amino acids (20 aa, directed by sequence of bases)
Somatic Cells/Gametes Chromosomes
Somatic: 46 chromosomes
Gametes: 26 chromosomes
Autosomes
First 22 of 23 pairs of chromosomes (virtually identical - homologous)
Sex Chromosomes
Remaining pair of chromosomes - XX (female) XY (male)
Aneupoidy
Somatic cell that does not have multiple of 23 chromosomes (better to have extra than less)
Locus
Position of gene on chromosome
Homozygous
Loci on a pair of chromosomes with IDENTICAL genes
Heterozygous
Loci on a pair of chromosomes with DIFFERENT genes
Allele
Different form of a gene at a given locus
Genotype
Composition of genes (what they have)
Phenotype
Appearance of the genetics (what they look like)
Penetrance
Percentage of individuals with genotype who express the phenotype
Expressivity
Extent of phenotype variation
3 properties of an ideal drug
Effectiveness, Safety, Selectivity
5 “rights” related to drugs
Drug, Patient, Dose, Route, Time
Absorption - affecting factors
Rate of dissolution, absorbing surface, blood flow, lipid solubility, pH partitioning
Parenteral Benefits
No barrier to absorption, rapid onset, large amts, dispersed quickly
Parenteral Problems
Cost, convenience, not reversible, infection, embolism, water solubility
Factors affecting enteral absorption
Solubility, GI pH, gastric emptying, stomach contents, drug coatings, etc
Disadvantages: Enteral
Variable absorption, food inactivation, awake/alert, GI upset
Distribution
Movement of drug through body
Distribution factors (med admin)
Blood flow, ability to exit and enter vascular system or cells
Excretion
Removal of drug from the body (filtration, reabsorption, secretion)
Factors effecting excretion
pH, competition for tubular transport, age
Aging effects on distribution of fluids
Decreased free fat mass, decreased muscle mass, renal decline, diminished thirst perception
Hydrostatic Pressure
PUSH: force exerted by water in the bloodstream (pushes water out of vascular)
Osmotic Pressure
Pressure by solutes in solution (low conc to high)
Oncotic Pressure
Force by albumin in blood stream
Pressures that favor filtration
Capillary hydrostatic pressure and intersititial oncotic pressure
Pressures that favor reabsorption
Capillary Oncotic Pressure and interstitial hydrostatic pressure
Causes of edema
Increase in capillary hydrostatic pressure, decrease in plasma oncotic pressure, increase in permeability, lymph obstruction
Different types of edema
Localized, Generalized, Dependent (legs dangling), Pitting edema
ADH
(from hypothalamus/pituitary gland) - water balance! Increases water reabsorption into the plasma
Aldosterone
(from adrenal cortex) - Na balance!
Renin-angiotensin-aldosterone system (RAAS)
- Decreased blood flow to kidney
- Juxtaglomerulus apparatus in kidney - secretes renin
- Renin changes angiotensinogen to angiotensin I
- Angiotensin-converting-enzyme (ACE) converts angiotensin I to angiotensin II
- Angiotensin stimulates release of aldosterone (Na + H2o retention) and vasoconstricts - raises BP!
Natriuretic Hormone
Protects from volume overload
Reduces BV/BP by excretion of Na and water
Increases vascular permeability
Isotonic alterations
Total body water (no change in electrolyte/water) eg. dehydration and hypovolemia
S/S of Isotonic Fluid Loss
Weight loss, increased thirst, dry skin
S/S of Isotonic Fluid Excess
Weight gain, decreased albumin, increased BP, increased neck veins, crackles, edema
Causes of isotonic fluid excess
IV therapy, aldosterone increase, drugs (cortisone)
Hyponatremia Causes
Pure sodium loss, low intake, dilutional hyponatremia
Hyponatremia S/S
Ability to polarize/repolarize, cell swelling, changes in LOC
Hypernatremia Causes
Gain in Na - IV, Cushing syndrome, fever, diabetes, sweating
Hypernatremia S/S
Thirst, weight gain, bounding pulse, increased BP, muscle twitching, coma, convulsions
Hypochloremia
(when bicarb increases, chloride decreases) ANION
Hypochloremia causes
Loss of Na, Increased Bicarb, Vomiting
Hyperchloremia causes
Hypernatremia, bicarb deficit (metabolic acidosis)
Potassium Role
Cellular membrane potential (cardiac/nerve) and buffering systems
Hypokalemia causes
Reduced intake of potassium, increased entry into cells, increased loss (upper gi - acid loss, lower gi - diarrhea, renal - diuretics)
Hypokalemia S/S
Dysrhythmias, Muscle weakness
Hyperkalemia Causes
Increased intake, insulin deficiency, cell trauma
Hyperkalemia S/S
Dysrhythmia, Neuromuscular irritability, loss of muscle tone, paralysis
Volatile Acids
H2CO3 (eliminated as CO2)
Nonvolatile Acids
Organic acids, eliminated by renal tubules
Bicarbonate Carbonic Acid Buffering System
In lungs and kidneys - extracellular - carbonic acid
Bicarbonate Carbonic Acid Buffering System (Lungs)
CO2 excretion adjusts pH (reduce carbonic acid by blowing off CO2 and leaving H2O OR increase carbonic acid by holding CO2 and combining with H2O)
Kidneys (Bicarbonate Carbonic Acid Buffering)
HCO3- excretion adjusts pH to bring back to normal
Respiratory Acidosis
Increase in pCO2 (Ventilation Depression)
Respiratory Alkalosis
Decrease of CO2 (Alveolar Hyperventilation)
Metabolic Acidosis
Decrease in HCO3
Metabolic Alkalosis
Increase in HCO3
Metabolic Acidosis Causes
Ketoacidosis, Lactic Acid, Renal Failure, Diarrhea
Metabolic Acidosis compensation
BiCarb Buffering, Increased ventilation, Eliminate H+
Metabolic Acidosis Treatment
IV Ringers Lactate, Na Bicarb IV
Metabolic Alkalosis Causes
Loss of Acid, Accumulation of Bicarb
Metabolic Alkalosis compensation
Decreased ventitlation, eliminate HCO3, retain H+
Metabolic Alkalosis Treatment
IV Saline
Respiratory Acidosis
HYPOventilation
Respiratory Acidosis Treatment
Restore ventilation, mechanical ventilation, administer O2
Respiratory Alkalosis
HYPERventilation (initial response to hypoxia)
Goal of Renal System
Balance H2O/Solutes, Excrete waste, conserve nutrients, regulate acid/base
Endocrine Function of Renal System
Regulate BP (Renin), Erythrocyte Production (Erythropoietin), Calcium Metabolism (vitamin D)
How much urine does a bladder hold before it senses the urge to urinate?
250-300
Urge to void
Parasympathetic fibers of ANS
Length of Urethra (Female)
3-4cm
Length of Urethra (Male)
18-20 cm
Parts of kidney that collect urine
Calyx
Structure unit of kidneys
Lobes (14-18 per kidney)
Functional unit of kidneys
Nephron (1.2 mill)
Proximal Tubule function
Reabsorption of Na, Glucose, K+, AA
Secretion of H+, drugs
Loop of Henle function
Concentration of urine
Water Absorption
Urea secretion
Distal Tubule
Reabsorption of Na, H2O, HCO3
Secretion of urea, K+, H+
Aldosterone
Collecting Duct
Reabsorption of H2O (ADH required)
Secretion of Na+, H+, K+
Nephron Function
Filters plasma, reabsorbs different substances, forms a filtrate, regulates body fluid volume, electrolytes, and pH
Renal Blood Flow
20-25% of C/O
1-2 L of Urine
Glomerular Filtration Rate (GFR)
Filtration of plasma per unit of time
Movement of solutes across capillary membrane
GFR is related to:
Perfusion pressure of capillaries, renal blood flow
What is the minimal urine output?
30ml
Favoring force in GFR
Glomerular hydrostatic pressure (is impermeable too large molecules)
Opposing forces in GFR
Hydrostatic pressure
Plasma oncotic pressure
Filtration
Water, free of proteins, blood cells, electrolytes, organic molecules
Reabsorption
Movement of particles and water into plasma
Secretion
Movement of particles from plasma into tubules
Nephron Hormones
ADH, Aldosterone, Natriuretic Peptides (Urodilantin - distal tubules and collecting duct)
Kidney Hormones
Vitamin D, Erythropoietin
Erythropoietin
Stimulates production of RBCs
Senses low Oxygen
Anemia - Low production of Epo
Urea
Protein metabolism (50% urine, 50% in kidneys) - Individuals w/ protein deprivation do not maximally concentrate urine
Urinary Tract Obstruction (Upper)
Smooth muscle, urine above blockage (common is renal calculi)
Hydroureter
Dilation of ureter
Hydronephrosis
Kidney swells and cannot get rid of pee
Renal Calculi - Stones
Nephrolithiasis (mass of crystals/protein) - cause infection
Types of Renal Calculi
Calcium (70-80)
Struvite (15%)
Uric (7%)
Stone Formation
Supersaturation/Precipitation - Crystallization - Growth - No inhibitors
Renal Calculi Risk Factors
Immobilization, Diet (high sodium, lots of nuts and coffee, supplements), lack of H2O
Infection from Renal Calculi
Increases saturation of substance, bacteria, staghorn formation
Renal Calculi Symptoms
Pain (flank, cva, groin), hematuria, oliguria
Renal Calculi Treatment
Pain management, lithotripsy (laser), nephrolitotomy
Lower Urinary Tract Obstruction
Storage/Emptying of Urine
Incontinence Examples
Urge
Stress
Overflow
Mixed
Functional
Urinary Tract Infection
Infection of any part of the urinary tract, diagnosed by presence of microorganism
Defense mechanisms to UTI
- Urine flow, pH, osmolality, uromodulin
- Antibaterial effect of mucosa
- Bacterioocidal of prostatic fluid
- Ureterovesical junction
- Length of urethra
Acute Cystitis
Bladder Infection
Acute Cystitis Risk Factors
Sexual activity, poor hygiene, neurogenic bladder, obstruction, diabetes mellitus
Acute Cystitis Symptoms
Asymptomatic, Dysuria, Frequency, Urgency, Suprapubic pain, hematuria
Acute Cystitis Treatment
1-3 days of antibiotic (may develop into pyelonephritis)
Pyelonephritis
Inflammation of renal pelvis and interstitium
Most common bacteria of pyelonephritis
E. Coli
Glomerular Disorder
- Inflammation of glomerulus
Damaged by: - Chemicals, radiation, hypoxemia, infection, etc.
- Damaged/Inflamed glomerulus resulting in sediment (nephrotic, nephritic)
Nephrotic Syndrome
Protein, lipids
- Glomerulonephritis
Nephritic Sediment
Blood
- Infection
Glomerulonephritis Symptoms
Hematuria with RBC, Proteinuria, HTN, Decreased GFR
Nephrotic Syndrome (Progressive Glomerulonephritis)
Group of symptoms caused by loss of protein (greater than 3.5 of protein), edema, hyperlipidemia, infection
Acute Kidney Injury (Acute Renal Failure)
Abrupt reduction in GFR and increase in BUN + Creatinine
- Oliguria
Prerenal AKI
Hypoperfusion (hypotension in kidneys)
- Hypovolemia
- Vasodilation
- Renal vascular obstruction
- Inadequate C/O
Intrarenal - Intrinsic AKI
Caused by Acute Tubular Necrosis
- Ischemic or Nephrotoxic
Postrenal AKI
Obstruction to outflow
- Benign Prostatic Hypertrophy
- Nephrolithiasis
- Tumors
Most common kind of AKI
Acute Tubular Necrosis (ATN) caused by ischemia and nephrotoxins
AKI risk factors
Increased in volume depletion
Elderly
Pre-existing renal disease
Post-Op
Anesthesia
Initiation Phase - AKI
24-48 hr post event (period of reduced perfusion is evolving)
Maintenance Phase - AKI
“Oliguric state”
- Hyperkalemia
- Metabolic Acidosis
- Anemia
- Fluid retention
Recovery Phase - AKI
Diuretic stage
- Output: >400cc/day
- Dehydration
- Hypokalemia/Hyponatremia
Chronic Kidney Disease (CRF)
Maintain function when 50% is damaged
- Progressive loss of kidney function
Stages of Disease
Stage I - Normal (90ml/min)
Stage II - 60-89
Stage III - 30-59
Stage 4 - (15-29)
Stage V - Dialysis/Transplant
CKD Clinical Manifestations
Azotemia/Uremia (irritates all body parts)
Atherosclerosis, HTN, Pericarditis, CHF
Kussmaul, Pneumonitis
Anemia (reduced EPO, increase bleeding, risk for clots)
Skin pallor, pruritis, uremic frost
Hiccups, Anorexia, Ulcers
Drowsiness, Concentration, Seizures, Asterixis
Osteodystrophy
CKD Treatment
Dietary Control,Medications, Dialysis/Transplant
Uses of Diuretics
Treatment of HTN
Mobilization of Fluid
Prevent renal failure
Osmotics (Mannitol) Site
Proximal Convoluted Tubule
Loops (Furosemide) Site
Thick Ascending Henles Loop
Thiazides Site
Convoluted Tubule
K+ Sparing (spironolactone or triamterene)
Distal Convoluted Tubule and Collecting Duct
Loop Diuretics Action
Block amounts of NaCl reabsorption
Loop Diuretics Pharmacology
60 min - PO / 5 min - IV
5 hr - PO / 2 hr - IV
Loop Diuretics Use
Conditions required significant fluid loss
Edema
Loop Diuretics adverse drug reactions
Dehydration
Hypotension
Electrolyte Imbalance
Ototoxicity
Hyperuricemia
Loop Diuretics Drug Interactions
Digoxin - Lithium levels
Ototoxic Drugs - NSAID, K+ Sparing, Antihypertensives
Loop Diuretics Examples
Furosemide (Lasix), Ethacrynic Acid (Edecrin), Bumetanide (Bumex)
Thiazide Diuretics Action
Block absorption of Na/Cl in distal CT
Dependent on renal function **
Thiazide Diuretics Pharm
Po - 1-2hr (lasts 6-12)
Slow release available
Thiazide ADR
Same as loops (hypokalemia)
Hyperlipidemia (increased cholesterol)
Hypersensitivity
Not ototoxic
Thiazide Diuretics Drug Interactions
Same as Loop (except for ototoxic)
Bile acid resins can bind to drug
Thiazide Drugs Examples
8 - End in Thiazide (hydrochlorothiazide)
All PO except Chlorothiazide
K+ Sparing diuretics action (Sprinolactone - Aldactone)
Blocks action of aldosterone in collecting duct
Causes excretion of Na and retention of K
Minimal diuresis
K+ Sparing Uses
HTN + Edema
Used with thiazides or loops (prevent hypokalemia)
Block effects of aldosterone in pts with hyperaldosteronism
K+ Sparing - ADR
Hyperkalemia
Hormone irregularities
Drug reactions - elevate potassium levels
Osmotic Diuretics (Mannitol) Action
Sugar that creates osmotic force in glomerulus
Increases osmotic pressure (water is not reabsorbed)
Little effect on electrolytes
**ICP
Osmotic - Mannitol Pharm
IV only
Does not cross GI endothelium
Crosses Capillary endothelium but not in brain
Mannitol - ADR
Edema
Mannitol - Uses
Renal Failure, Reduction of ICP, Reduction of intraocular pressure
