Cell Biology
 Nucleus: cell division and storage of genetic material
 Rough ER: protein synthesis
 Smooth ER: lipid synthesis
 Ribosomes: protein synthesis
 Golgi body: pack proteins into secretory vesicles
 Lysosomes: digestion
 Peroxisomes: cell digestion
 Plasma membrane: storage, protection, cell activation, controls what goes in and out of
the cell
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8 major functions
1. Conductivity
2. Communication
3. Metabolism
4. Secretion
5. Excretion
6. Respiration
7. Reproduction
8. Movement
Altered Cell Biology
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Atrophy: decrease in cell size
Hypertrophy: increase in cell size
Hyperplasia: increase in cell #
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Metaplasia: replacing one mature cell type with another
Dysplasia: disorganized cell growth
Causes of cell injury: hypoxia (most common), ischemia, free radicals/ reactive oxidative
species, chemicals, unintentional/ intentional injuries
Genetics
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Central dogma of biology: DNA->RNA->Protein
Locus: location of a gene on a chromosomes
Allele: different gene at a specific locus
Heterozygous: identical allele
Homozygous: different allele
Introduction to Pharmacology
 3 main characteristics of ideal drug: safety, selectivity (no side effects), effectiveness
 IV’s are IRREVERSIBLE
 Absorption
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Movement from site into bloodstream
Quickest w/ IV because there is no barrier
Determined by surface area, blood flow, dissolution rate, lipid solubility (better
absorption)
Barriers: epithelial cells, GI tract, endothelial capillary walls
Distribution
- Movement from bloodstream to target cell
- Affected by blood flow
- Affected by ability to exit capillaries-> blood brain barrier and protein binding
- When a medication binds to a protein it cannot exit the vascular system because it
becomes too big
- Affected by ability to enter cells
Metabolism
- Biotransformation: enzyme alterations of a drug
- First pass effect: oral meds are rapidly inactivated by the liver
- Slower in infants and older adults
Excretion
- Removal of drugs from the body
1. Filtration
2. Reabsorption
3. Secretion
ED50: dose needed to achieve therapeutic response in 50% of the population; standard
dose
Minimal concentration effect (MEC): minimal concentration of a drug for it to have a
therapeutic effect
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5 rights of medication administration
- Right pt
- Right drug
- Right route
- Right time
- Right dose
Drugs can only mimic or block actions of a substance and CANNOT give cells new
function
Fluid and Electrolytes
 Types of fluid: ICF, ECF (intravascular, interstitial)
 Hypertonic imbalance: water leaves the cell H20-> cell shrinks
 Hypotonic imbalance: water enters the cell-> cell swells
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HYDROSTATIC=PUSH
ONCOTICS= PULL W/ PROTEINS
OSMOTICS= PULL W/ ELECTROLYTES
Pressures inside the capillary favors filtration and rebsorption
Capillary hydrostatic pressure: pushing water out of the capillary into interstitial
Interstitial oncotic pressure: pulling water out of capillary into interstitial using proteins
decreased BP= increased HR (the heart pumps harder and more to move the blood)
Hypovolemia
- Weight loss
- Decreased BP
- Increased HR
- Thirst
- Dry skin
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- Increased hematocrit
- Decreased neck veins
Hypervolemia
- Edema
- Weight gain
- Increased BP
- Decreased HR
- Crackles in the lungs
- Decreased albumin
- Increased neck veins
Edema
- Increased capillary hydrostatic pressure
- Decreased plasma oncotic pressure
- Increase in capillary permeability (leaky)
- Lymphedema
WATER FOLLOWS SODIUM
Cl- FOLLOWS Na+
Na+ and K+ are OPPOSITES
Cl- and Bicarb are OPPOSITES
Normal sodium levels: 135-145
SODIUM= NEUROMUSCULAR IRRITABILITY
Hypernatremia
- Na+ >145
- GAIN IN SODIUM AND LOSS OF WATER
- Causes: excessive IV therapy, excessive Na+ intake, fluid loss (sweating, fever, lung
infection), hyperaldosteronism (cushing syndrome), intracellular dehydration,
diabetes
- Symptoms: weight gain, thirst, bounding pulse, increased BP, muscle twitching,
hyperreflexia, changes in LOC
 Think “FRIED”
(F) atigue
(R) estless, really confused
(I) ncreased reflexes
(E) xtreme thirst
(D) ecreased urine, Dry mouth
Hyponatremia
- Na+ <135
- LOSS OF SODIUM AND CELL SWELLING
- Causes: vomiting, diarrhea, GI suction, diuretics, low intake, renal failure, SIADG (too
much ADH= body holds onto water)
- Symptoms: cerebral cell swelling, lethargy, confusion, seizures, coma
Normal Cl- levels 95-105
Hypochloremia
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- Causes: hyponatremia, metabolic alkalosis, vomiting (loss of HCl)
Hyperchloremia
- Causes: hypernatremia, metabolic acidosis
Normal K+ levels 3.5-5
MAIN ROLE IN CARDIAC AND NERVE CELLS and BUFFER FOR ACIDOSIS AND ALKALOSIS
Hyperkalemia
- K+ >5.5
- Causes: increased intake, cell trauma (cells burst open so K+ spreads into ECF),
decreased renal excretion, insulin deficiency (hyperglycemia)
- Symptoms (think heart and muscles): Increased neuromuscular irritability->muscles
stay contracted leads to restlessness, cramping, loss of muscle tone, paralysis,
dysrhythmias
Hypokalemia
- K+ <3.5
- Causes: reduced intake, movement of K+ from ECF to ICF, loss if K+
- Symptoms: dysrhythmias, muscle weakness (not enough K+ to contract=weak)
Acid-Base Imbalances
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Normal pH range 7.35-7.45
pH is low= H+ is high
pH is high= H+ is low
Volatile acids= secreted by lungs (carbonic acid)
Nonvolatile acids= secreted by kidneys
Acidosis (H+ is high) = Hyperkalemia
Alkalosis (H+ is low)= Hypokalemia
When H+ comes out of the cell to compensate for alkalosis (more HCO3- in the blood
than the cells), K+ enters the cell
When H+ enters the cell to compensate for acidosis (more H+ in the blood), K+ leaves
the cell
Normal HCO3- levels 22-26
Normal PaCO2 levels 35-45
Normal PaO2 levels 80-100
Metabolic acidosis
- Loss of bicarb (base)
- pH <7.35
- HCO3- <22
- Causes: diarrhea, ketoacidosis, lactic acids, RENAL FAILURE
- Compensation: Kussmaul breathing (deep, rapid breaths) causing you to breath out
more CO2 (acid) to increase pH
Metabolic alkalosis
- Increased bicarb
- pH >7.45
- HCO3- >26
- Causes: accumulation of bicarb, loss of acid (vomiting, diarrhea)
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Compensation: Hypoventilation, paper bag breathing (you breath CO2 into the bag
but then you breath the CO2 (acid) back in causing increase pH)
Respiratory acidosis
- Accumulation of CO2 (acid)
- pH <7.35
- CO2 >45
- Causes: HYPOVENTILATION
- Compensation: kidneys excrete more H+ and reabsorb HCO3Respiratory alkalosis
- Loss of CO2
- pH >7.45
- CO <35
- Causes: HYPERVENTILATION (pain and anxiety may lead to hyperventilation)
- Compensation: kidneys excrete HCO3-
Renal System
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Structural unit= lobe
Functional unit= nephron
Each nephron consists of the renal corpuscle, proximal convoluted tubule, loop of henle,
distal convoluted tube, and collecting duct
- Glomerulus: filters plasma
- Proximal tubule: big one to focus on-> secretes drugs/foreign substances
- Loop of henle: urine concentration
- Distal tubule: reabsorption of H2O with ADH; reabsorption of Na+ and excretion of
K+ with aldosterone
- Collecting duct: reabsorption of H2O with ADH
GFR
- Increased perfusion pressure and Increased renal blood flow=
increased GFR
- Favoring pressure: glomerular hydrostatic pressure (pushing blood out
of glomerulus)
- Opposing pressures: hydrostatic pressure in Bowman’s capsule (wants
to push blood back into glomerulus) and plasma oncotic pressure
Renin: RAAS Net effect, low blood volume and blood pressure stimulates
the kidneys to produce renin which turns angiotensinogen into
angiotensin I, which eventually leads to production of aldosterone
Erythropoietin: produced by the kidneys to stimulate production of RBCs (which is why
you may see anemia with kidney failure)
Kidneys activate Vitamin D
Normal BUN levels 7-20
Normal Creatinine levels 0.6-1.2
Normal GFR 90-120
Increased BUN and Creatinine= renal failure, dehydration
Decreased GFR= renal failure, dehydration
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Azotemia: elevated blood urea nitrogen (BUN)
MINIMUM URINE OUTPUT= 30 ML/ HR
Anuria: complete lack of urine
Oliguria: decrease in urine output
Dysuria: painful/difficult urination
Polyuria: increased urine output
Hematuria: blood in the urine
Pyuria: WBCs in urine
Nephrotic syndrome: more than 3.5g of protein found in the urine
Nephritic syndrome: RBC casts found in the urine
Cystitis (bladder infection)
- Causes: sexual activity, pregnancy, backflow of urine from urethra into bladder
(vesicoureteral reflux), poor hygiene, neurogenic bladder, obstruction, diabetes
- Symptoms: dysuria, urinary frequency and urgency, suprapubic pain, hematuria
- CAN DEVELOP INTO PYELONEPHRITIS
Pyelonephritis (inflammation of renal pelvis)
- Causes: infection from the bladder up to the kidneys or blood stream
- Signs and symptoms: increased WBCs, renal edema, purulent urine,
medullary/cortical necrosis
Acute tubular necrosis: lack of blood flow and oxygen to the kidneys
Acute Kidney Injury: abrupt reduction in GFR and increase In BUN and Creatinine
Prerenal Classification
- Poor perfusion to the kidneys
- Causes: hypovolemia, vascular pooling/vasodilation, increased renal vascular
resistance (remember decreased pressure and vascular resistance= decreased renal
blood flow), inadequate cardiac output
Intrarenal classification
- Acute tubular necrosis
- Causes: ischemia or nephrotoxicity (like overuse of antibiotics)
Postrenal classification
- Obstruction to outflow as seen by anuria followed by polyuria
- Causes: prostatic hypertrophy, kidney stones (nephroliths), tumors, catherization of
the ureters causing edema
Chronic Kidney Disease: Progressive loss of kidney function
- Stage I= GFR 90+ NORMAL
- Stage II= GFR 60-89
- Stage III+ GFR 30-59
- Stage IV+ GFR 15-29
- Stage V (kidney failure) = less than 15
- Aztomia and Uremia are present (increased BUN and creatinine)
- Metabolic acidosis
- Hyperkalemia
- Pulmonary edema
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Diet control: restrict protein, phosphorus, and potassium; maintain sodium and
water intake; vitamin D supplement
Renal dysfunction/failure decreases absorption
Nephrolithiasis: masses of crystals and proteins
- Renal colic pain (at flank, CVA, groin)
- Hematuria
- Oliguria
Urinary tract infections
- Symptoms: dysuria, urinary frequency, urinary urgency, suprapubic pain, hematuria,
CONFUSION in older adults
- Microorganisms: E. coli, proteus, pseudomonas
Diuretics
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Loop diuretics (furosemide)
- Blocks significant amounts of NaCl reabsorption
- Hyponatremia, hypochloremia, hypokalemia
- Ototoxicity (ringing in the ears)
Thiazides
- Block absorption of Na+ and Cl- in the distal convoluted tubule
- May cause hypokalemia
K+ sparing (spironolactone, triamterene)
- Blocks aldosterone causing Na+ to be excreted and K+ to be reabsorbed
- May cause hyperkalemia
Osmotics (mannitol)
- Creates osmotic force in glomerulus
- Little effect on electrolytesc