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Patho/Pharm > Exam 1 > Flashcards

Exam 1 Flashcards

1
Q

Atrophy

A

Decrease in cellular size

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2
Q

Hypertrophy

A

Increase in cellular size

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3
Q

Hyperplasia

A

Increase in # of cells

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4
Q

Dysplasia

A

Deranged cellular growth

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5
Q

Metaplasia

A

Replacement of type of cell with another

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6
Q

Cellular Injury

A

Reversible and irreversible inability to maintain homeostasis

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7
Q

Hypoxic Injury

A

Reduced amt of O2 in the air, loss of hemoglobin, decreased RBC production, resp/cardio diseases, poison

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8
Q

Ischemia

A

Inadequate blood supply to an organ

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9
Q

Free Radicals and Reactive O2 Species (ROS)

A

Electrically uncharged atom or group of atoms having unpaired electron

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10
Q

Chemical Cellular Injury

A

Xenobiotics (Lead, CO Monoxide, Ethanol, Mercury)

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11
Q

Infectious Cellular Injury

A

Invasion/Destruction, Toxin production, hypersensitivity reactions

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12
Q

Necrosis

A

Cell death (sum of changes after local cell death)

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13
Q

Apoptosis

A

Programmed cellular death

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14
Q

Autophagy

A

Self-destructive/survival mechanism, aging!

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15
Q

Cellular Aging

A

Atrophy, decreased function, loss of cells

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16
Q

Tissue and systemic aging

A

Progressive stiffness and rigidity (sarcopenia)

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17
Q

Frailty

A

Mobility, balance, muscle strength, nutrition, falls, fractures, etc

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18
Q

Somatic Death

A

Death of an entire person

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19
Q

Postmortem Changes

A

Algor mortis (body temp), livor mortis (discoloration), rigor mortis (muscle stiffening), postmortem autolysis (enyme release)

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20
Q

DNA Replication

A

Untwisting and unzipping of DNA strand (DNA is template)

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21
Q

Mutation

A

Any alteration of genetic material

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22
Q

Mutagen

A

Agent known to increase the frequency of mutations (radiation/chemicals)

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23
Q

Central Dogma of Bio

A

DNA (transcription) - RNA (translation) - Protein

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24
Q

Proteins

A

One or more polypeptides - composed of amino acids (20 aa, directed by sequence of bases)

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25
Q

Somatic Cells/Gametes Chromosomes

A

Somatic: 46 chromosomes
Gametes: 26 chromosomes

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26
Q

Autosomes

A

First 22 of 23 pairs of chromosomes (virtually identical - homologous)

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27
Q

Sex Chromosomes

A

Remaining pair of chromosomes - XX (female) XY (male)

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28
Q

Aneupoidy

A

Somatic cell that does not have multiple of 23 chromosomes (better to have extra than less)

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29
Q

Locus

A

Position of gene on chromosome

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30
Q

Homozygous

A

Loci on a pair of chromosomes with IDENTICAL genes

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31
Q

Heterozygous

A

Loci on a pair of chromosomes with DIFFERENT genes

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32
Q

Allele

A

Different form of a gene at a given locus

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33
Q

Genotype

A

Composition of genes (what they have)

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34
Q

Phenotype

A

Appearance of the genetics (what they look like)

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35
Q

Penetrance

A

Percentage of individuals with genotype who express the phenotype

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36
Q

Expressivity

A

Extent of phenotype variation

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37
Q

3 properties of an ideal drug

A

Effectiveness, Safety, Selectivity

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38
Q

5 “rights” related to drugs

A

Drug, Patient, Dose, Route, Time

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39
Q

Absorption - affecting factors

A

Rate of dissolution, absorbing surface, blood flow, lipid solubility, pH partitioning

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40
Q

Parenteral Benefits

A

No barrier to absorption, rapid onset, large amts, dispersed quickly

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41
Q

Parenteral Problems

A

Cost, convenience, not reversible, infection, embolism, water solubility

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42
Q

Factors affecting enteral absorption

A

Solubility, GI pH, gastric emptying, stomach contents, drug coatings, etc

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43
Q

Disadvantages: Enteral

A

Variable absorption, food inactivation, awake/alert, GI upset

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44
Q

Distribution

A

Movement of drug through body

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45
Q

Distribution factors (med admin)

A

Blood flow, ability to exit and enter vascular system or cells

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46
Q

Excretion

A

Removal of drug from the body (filtration, reabsorption, secretion)

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47
Q

Factors effecting excretion

A

pH, competition for tubular transport, age

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48
Q

Aging effects on distribution of fluids

A

Decreased free fat mass, decreased muscle mass, renal decline, diminished thirst perception

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49
Q

Hydrostatic Pressure

A

PUSH: force exerted by water in the bloodstream (pushes water out of vascular)

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50
Q

Osmotic Pressure

A

Pressure by solutes in solution (low conc to high)

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51
Q

Oncotic Pressure

A

Force by albumin in blood stream

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52
Q

Pressures that favor filtration

A

Capillary hydrostatic pressure and intersititial oncotic pressure

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53
Q

Pressures that favor reabsorption

A

Capillary Oncotic Pressure and interstitial hydrostatic pressure

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54
Q

Causes of edema

A

Increase in capillary hydrostatic pressure, decrease in plasma oncotic pressure, increase in permeability, lymph obstruction

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55
Q

Different types of edema

A

Localized, Generalized, Dependent (legs dangling), Pitting edema

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56
Q

ADH

A

(from hypothalamus/pituitary gland) - water balance! Increases water reabsorption into the plasma

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57
Q

Aldosterone

A

(from adrenal cortex) - Na balance!

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58
Q

Renin-angiotensin-aldosterone system (RAAS)

A
  1. Decreased blood flow to kidney
  2. Juxtaglomerulus apparatus in kidney - secretes renin
  3. Renin changes angiotensinogen to angiotensin I
  4. Angiotensin-converting-enzyme (ACE) converts angiotensin I to angiotensin II
  5. Angiotensin stimulates release of aldosterone (Na + H2o retention) and vasoconstricts - raises BP!
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59
Q

Natriuretic Hormone

A

Protects from volume overload
Reduces BV/BP by excretion of Na and water
Increases vascular permeability

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60
Q

Isotonic alterations

A

Total body water (no change in electrolyte/water) eg. dehydration and hypovolemia

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61
Q

S/S of Isotonic Fluid Loss

A

Weight loss, increased thirst, dry skin

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62
Q

S/S of Isotonic Fluid Excess

A

Weight gain, decreased albumin, increased BP, increased neck veins, crackles, edema

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63
Q

Causes of isotonic fluid excess

A

IV therapy, aldosterone increase, drugs (cortisone)

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64
Q

Hyponatremia Causes

A

Pure sodium loss, low intake, dilutional hyponatremia

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65
Q

Hyponatremia S/S

A

Ability to polarize/repolarize, cell swelling, changes in LOC

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66
Q

Hypernatremia Causes

A

Gain in Na - IV, Cushing syndrome, fever, diabetes, sweating

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67
Q

Hypernatremia S/S

A

Thirst, weight gain, bounding pulse, increased BP, muscle twitching, coma, convulsions

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68
Q

Hypochloremia

A

(when bicarb increases, chloride decreases) ANION

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69
Q

Hypochloremia causes

A

Loss of Na, Increased Bicarb, Vomiting

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70
Q

Hyperchloremia causes

A

Hypernatremia, bicarb deficit (metabolic acidosis)

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71
Q

Potassium Role

A

Cellular membrane potential (cardiac/nerve) and buffering systems

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72
Q

Hypokalemia causes

A

Reduced intake of potassium, increased entry into cells, increased loss (upper gi - acid loss, lower gi - diarrhea, renal - diuretics)

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73
Q

Hypokalemia S/S

A

Dysrhythmias, Muscle weakness

74
Q

Hyperkalemia Causes

A

Increased intake, insulin deficiency, cell trauma

75
Q

Hyperkalemia S/S

A

Dysrhythmia, Neuromuscular irritability, loss of muscle tone, paralysis

76
Q

Volatile Acids

A

H2CO3 (eliminated as CO2)

77
Q

Nonvolatile Acids

A

Organic acids, eliminated by renal tubules

78
Q

Bicarbonate Carbonic Acid Buffering System

A

In lungs and kidneys - extracellular - carbonic acid

79
Q

Bicarbonate Carbonic Acid Buffering System (Lungs)

A

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)

80
Q

Kidneys (Bicarbonate Carbonic Acid Buffering)

A

HCO3- excretion adjusts pH to bring back to normal

81
Q

Respiratory Acidosis

A

Increase in pCO2 (Ventilation Depression)

82
Q

Respiratory Alkalosis

A

Decrease of CO2 (Alveolar Hyperventilation)

83
Q

Metabolic Acidosis

A

Decrease in HCO3

84
Q

Metabolic Alkalosis

A

Increase in HCO3

85
Q

Metabolic Acidosis Causes

A

Ketoacidosis, Lactic Acid, Renal Failure, Diarrhea

86
Q

Metabolic Acidosis compensation

A

BiCarb Buffering, Increased ventilation, Eliminate H+

87
Q

Metabolic Acidosis Treatment

A

IV Ringers Lactate, Na Bicarb IV

88
Q

Metabolic Alkalosis Causes

A

Loss of Acid, Accumulation of Bicarb

89
Q

Metabolic Alkalosis compensation

A

Decreased ventitlation, eliminate HCO3, retain H+

90
Q

Metabolic Alkalosis Treatment

A

IV Saline

91
Q

Respiratory Acidosis

A

HYPOventilation

92
Q

Respiratory Acidosis Treatment

A

Restore ventilation, mechanical ventilation, administer O2

93
Q

Respiratory Alkalosis

A

HYPERventilation (initial response to hypoxia)

94
Q

Goal of Renal System

A

Balance H2O/Solutes, Excrete waste, conserve nutrients, regulate acid/base

95
Q

Endocrine Function of Renal System

A

Regulate BP (Renin), Erythrocyte Production (Erythropoietin), Calcium Metabolism (vitamin D)

96
Q

How much urine does a bladder hold before it senses the urge to urinate?

A

250-300

97
Q

Urge to void

A

Parasympathetic fibers of ANS

98
Q

Length of Urethra (Female)

A

3-4cm

99
Q

Length of Urethra (Male)

A

18-20 cm

100
Q

Parts of kidney that collect urine

A

Calyx

101
Q

Structure unit of kidneys

A

Lobes (14-18 per kidney)

102
Q

Functional unit of kidneys

A

Nephron (1.2 mill)

103
Q

Proximal Tubule function

A

Reabsorption of Na, Glucose, K+, AA
Secretion of H+, drugs

104
Q

Loop of Henle function

A

Concentration of urine
Water Absorption
Urea secretion

105
Q

Distal Tubule

A

Reabsorption of Na, H2O, HCO3
Secretion of urea, K+, H+
Aldosterone

106
Q

Collecting Duct

A

Reabsorption of H2O (ADH required)
Secretion of Na+, H+, K+

107
Q

Nephron Function

A

Filters plasma, reabsorbs different substances, forms a filtrate, regulates body fluid volume, electrolytes, and pH

108
Q

Renal Blood Flow

A

20-25% of C/O
1-2 L of Urine

109
Q

Glomerular Filtration Rate (GFR)

A

Filtration of plasma per unit of time
Movement of solutes across capillary membrane

110
Q

GFR is related to:

A

Perfusion pressure of capillaries, renal blood flow

111
Q

What is the minimal urine output?

A

30ml

112
Q

Favoring force in GFR

A

Glomerular hydrostatic pressure (is impermeable too large molecules)

113
Q

Opposing forces in GFR

A

Hydrostatic pressure
Plasma oncotic pressure

114
Q

Filtration

A

Water, free of proteins, blood cells, electrolytes, organic molecules

115
Q

Reabsorption

A

Movement of particles and water into plasma

116
Q

Secretion

A

Movement of particles from plasma into tubules

117
Q

Nephron Hormones

A

ADH, Aldosterone, Natriuretic Peptides (Urodilantin - distal tubules and collecting duct)

118
Q

Kidney Hormones

A

Vitamin D, Erythropoietin

119
Q

Erythropoietin

A

Stimulates production of RBCs
Senses low Oxygen
Anemia - Low production of Epo

120
Q

Urea

A

Protein metabolism (50% urine, 50% in kidneys) - Individuals w/ protein deprivation do not maximally concentrate urine

121
Q

Urinary Tract Obstruction (Upper)

A

Smooth muscle, urine above blockage (common is renal calculi)

122
Q

Hydroureter

A

Dilation of ureter

123
Q

Hydronephrosis

A

Kidney swells and cannot get rid of pee

124
Q

Renal Calculi - Stones

A

Nephrolithiasis (mass of crystals/protein) - cause infection

125
Q

Types of Renal Calculi

A

Calcium (70-80)
Struvite (15%)
Uric (7%)

126
Q

Stone Formation

A

Supersaturation/Precipitation - Crystallization - Growth - No inhibitors

127
Q

Renal Calculi Risk Factors

A

Immobilization, Diet (high sodium, lots of nuts and coffee, supplements), lack of H2O

128
Q

Infection from Renal Calculi

A

Increases saturation of substance, bacteria, staghorn formation

129
Q

Renal Calculi Symptoms

A

Pain (flank, cva, groin), hematuria, oliguria

130
Q

Renal Calculi Treatment

A

Pain management, lithotripsy (laser), nephrolitotomy

131
Q

Lower Urinary Tract Obstruction

A

Storage/Emptying of Urine

132
Q

Incontinence Examples

A

Urge
Stress
Overflow
Mixed
Functional

133
Q

Urinary Tract Infection

A

Infection of any part of the urinary tract, diagnosed by presence of microorganism

134
Q

Defense mechanisms to UTI

A
  1. Urine flow, pH, osmolality, uromodulin
  2. Antibaterial effect of mucosa
  3. Bacterioocidal of prostatic fluid
  4. Ureterovesical junction
  5. Length of urethra
135
Q

Acute Cystitis

A

Bladder Infection

136
Q

Acute Cystitis Risk Factors

A

Sexual activity, poor hygiene, neurogenic bladder, obstruction, diabetes mellitus

137
Q

Acute Cystitis Symptoms

A

Asymptomatic, Dysuria, Frequency, Urgency, Suprapubic pain, hematuria

138
Q

Acute Cystitis Treatment

A

1-3 days of antibiotic (may develop into pyelonephritis)

139
Q

Pyelonephritis

A

Inflammation of renal pelvis and interstitium

140
Q

Most common bacteria of pyelonephritis

A

E. Coli

141
Q

Glomerular Disorder

A
  1. Inflammation of glomerulus
    Damaged by:
  2. Chemicals, radiation, hypoxemia, infection, etc.
  3. Damaged/Inflamed glomerulus resulting in sediment (nephrotic, nephritic)
142
Q

Nephrotic Syndrome

A

Protein, lipids
- Glomerulonephritis

143
Q

Nephritic Sediment

A

Blood
- Infection

144
Q

Glomerulonephritis Symptoms

A

Hematuria with RBC, Proteinuria, HTN, Decreased GFR

145
Q

Nephrotic Syndrome (Progressive Glomerulonephritis)

A

Group of symptoms caused by loss of protein (greater than 3.5 of protein), edema, hyperlipidemia, infection

146
Q

Acute Kidney Injury (Acute Renal Failure)

A

Abrupt reduction in GFR and increase in BUN + Creatinine
- Oliguria

147
Q

Prerenal AKI

A

Hypoperfusion (hypotension in kidneys)
- Hypovolemia
- Vasodilation
- Renal vascular obstruction
- Inadequate C/O

148
Q

Intrarenal - Intrinsic AKI

A

Caused by Acute Tubular Necrosis
- Ischemic or Nephrotoxic

149
Q

Postrenal AKI

A

Obstruction to outflow
- Benign Prostatic Hypertrophy
- Nephrolithiasis
- Tumors

150
Q

Most common kind of AKI

A

Acute Tubular Necrosis (ATN) caused by ischemia and nephrotoxins

151
Q

AKI risk factors

A

Increased in volume depletion
Elderly
Pre-existing renal disease
Post-Op
Anesthesia

152
Q

Initiation Phase - AKI

A

24-48 hr post event (period of reduced perfusion is evolving)

153
Q

Maintenance Phase - AKI

A

“Oliguric state”
- Hyperkalemia
- Metabolic Acidosis
- Anemia
- Fluid retention

154
Q

Recovery Phase - AKI

A

Diuretic stage
- Output: >400cc/day
- Dehydration
- Hypokalemia/Hyponatremia

155
Q

Chronic Kidney Disease (CRF)

A

Maintain function when 50% is damaged
- Progressive loss of kidney function

156
Q

Stages of Disease

A

Stage I - Normal (90ml/min)
Stage II - 60-89
Stage III - 30-59
Stage 4 - (15-29)
Stage V - Dialysis/Transplant

157
Q

CKD Clinical Manifestations

A

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

158
Q

CKD Treatment

A

Dietary Control,Medications, Dialysis/Transplant

159
Q

Uses of Diuretics

A

Treatment of HTN
Mobilization of Fluid
Prevent renal failure

160
Q

Osmotics (Mannitol) Site

A

Proximal Convoluted Tubule

161
Q

Loops (Furosemide) Site

A

Thick Ascending Henles Loop

162
Q

Thiazides Site

A

Convoluted Tubule

163
Q

K+ Sparing (spironolactone or triamterene)

A

Distal Convoluted Tubule and Collecting Duct

164
Q

Loop Diuretics Action

A

Block amounts of NaCl reabsorption

165
Q

Loop Diuretics Pharmacology

A

60 min - PO / 5 min - IV
5 hr - PO / 2 hr - IV

166
Q

Loop Diuretics Use

A

Conditions required significant fluid loss
Edema

167
Q

Loop Diuretics adverse drug reactions

A

Dehydration
Hypotension
Electrolyte Imbalance
Ototoxicity
Hyperuricemia

168
Q

Loop Diuretics Drug Interactions

A

Digoxin - Lithium levels
Ototoxic Drugs - NSAID, K+ Sparing, Antihypertensives

169
Q

Loop Diuretics Examples

A

Furosemide (Lasix), Ethacrynic Acid (Edecrin), Bumetanide (Bumex)

170
Q

Thiazide Diuretics Action

A

Block absorption of Na/Cl in distal CT
Dependent on renal function **

171
Q

Thiazide Diuretics Pharm

A

Po - 1-2hr (lasts 6-12)
Slow release available

172
Q

Thiazide ADR

A

Same as loops (hypokalemia)
Hyperlipidemia (increased cholesterol)
Hypersensitivity
Not ototoxic

173
Q

Thiazide Diuretics Drug Interactions

A

Same as Loop (except for ototoxic)
Bile acid resins can bind to drug

174
Q

Thiazide Drugs Examples

A

8 - End in Thiazide (hydrochlorothiazide)
All PO except Chlorothiazide

175
Q

K+ Sparing diuretics action (Sprinolactone - Aldactone)

A

Blocks action of aldosterone in collecting duct
Causes excretion of Na and retention of K
Minimal diuresis

176
Q

K+ Sparing Uses

A

HTN + Edema
Used with thiazides or loops (prevent hypokalemia)
Block effects of aldosterone in pts with hyperaldosteronism

177
Q

K+ Sparing - ADR

A

Hyperkalemia
Hormone irregularities
Drug reactions - elevate potassium levels

178
Q

Osmotic Diuretics (Mannitol) Action

A

Sugar that creates osmotic force in glomerulus
Increases osmotic pressure (water is not reabsorbed)
Little effect on electrolytes
**ICP

179
Q

Osmotic - Mannitol Pharm

A

IV only
Does not cross GI endothelium
Crosses Capillary endothelium but not in brain

180
Q

Mannitol - ADR

A

Edema

181
Q

Mannitol - Uses

A

Renal Failure, Reduction of ICP, Reduction of intraocular pressure

Patho/Pharm (2 decks)

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