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Nurs 323 > Final Exam > Flashcards

Final Exam Flashcards

1
Q

What is GERD

A

•Is the reflux of chime from the stomach through the lower esophageal sphincter to the esophagus. The LES may relax spontaneously and transiently 1 to 2 hours after eating, permitting gastric contents to regurgitate into the esophagus. May cause an inflammatory response called reflux esophagitis

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2
Q

What can cause GERD

A

-weak LES, irritation by acidic refluxate, abnormal esophageal clearance, hiatal hernia, delayed gastric emptying. Abdominal pressure (obesity, pregnancy, cough, etc can contribute to GERD)

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3
Q

Types of Ulcers

A

•Ulcers from ulcerative colitis (affecting rectum and sigmoid colon)
•Ulcers from Chron’s disease, affecting any part of GI
•Stress ulcers from PUD include:
Ischemic ulcers
Curling ulcers (burns)
Cushing’s ulcers (head trauma)

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4
Q

Factors that contribute to ulcer development

A
  • Infection with H. pylori
  • Chronic use of NSAIDS
  • Alcohol
  • Smoking
  • Advanced Age
  • Chronic diseases - emphysema, rheumatoid arthritis, cirrhosis and obesity & diabetes
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5
Q

Cause of hepatic encephalopathy

A

caused by an increase of ammonia in the blood. The loss of liver function prevents the ammonia from being converted to urea which is easily excreted by the kidneys.

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6
Q

Signs and symptoms of hepatic encephalopathy

A

confusion and an altered state of consciousness as ammonia easily crosses the blood brain barrier

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7
Q

Treatment for hepatic encephalopathy

A

Lactulose- increases the hydrogen ion concentration in the bowels which converts ammonia to ammonium. Ammonium can be easily secreted by the bowel.

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8
Q

Anti-ulcer drugs

A 
Antibiotics
Antisecretory
     -H2 antagonists
     -Proton pump inhibitors
Antacids
Mucosal protectants
Antisecretary/enhance mucosal defenses
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9
Q

Thrombotic stroke

A

Thrombotic strokes arise from arterial occlusions caused by thrombi formation in arteries supplying the brain or intracranial vessels.

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10
Q

Hemorrhagic stroke

A

Hemorrhagic (3rd most common) Hypertension, ruptured aneurysms or vascular malformation, bleeding into a tumor, or hemorrhage associated with anticoagulants or clotting disorder, head trauma, or illicit drug use are the most common causes. Hemorrhages can be massive, small, slit, or petechial.

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11
Q

Transient ischemic attack

A
  • Differentiate between ischemic and hemorrhagic with non-contrast CT scan
  • 24 hours or less with no permanent damage
  • A brief episode of neurologic dysfunction caused by a focal disturbance of brain or retinal ischemia with clinical symptoms typically lasting no more than 1 hour, no evidence of infarction, and complete clinical recovery.
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12
Q

Classes of anticonvulsant drugs

A
  • suppress sodium influx
  • suppress calcium influx
  • promote potassium efflux
  • potentiate GABA
  • antagonize glutamate
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13
Q

Suppress sodium influx

A 
•Suppress sodium influx: reversibly bind to sodium channels while they are in the inactivated state, thereby prolonging channel inactivation. By delaying return to the active state, these drugs decrease the ability of neurons to fire at high frequency.
Phenytoin (Dilantin)
Carbamazepine (Tegretol)
Valproic acid (Depakene)
Lamotrigine (Lamictal)
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14
Q

Suppress calcium influx

A 
•Suppress calcium influx: influx of calcium through votage-gated calcium channels promotes transmitter release. Hence, drugs that block these calcium channels can suppress transmission.
Ethosuxamide  (Zarontin)
Valproic acid (Depakene)
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15
Q

Promote potassium efflux

A

•Promote potassium efflux: during an action potential, influx of sodium causes neurons to depolarize (fire), and then efflux of potassium causes neurons to repolarize (relax). Ezogabine acts on voltage gated potassium channels to facilitate potassium efflux. This action is believed to underlie the drugs ability to slow repetitive neuronal firing and thereby provide seizure control.

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16
Q

Potentiate GABA

A

•Potentiate GABA: these drugs potentiate the actions of GABA, an inhibitory neurotransmitter that is widely distributed thought the brain. These drugs decrease neuronal excitability. Drugs increase the influence of GABA by several mechanisms. Benzodiazepines and barbiturates engance the effects of GABA by direct binding to GABA receptors. Gabapentin promotes GABA release. Tiagabine inhibits GABA reuptake, and vigabatrin inhibits the enzyme that degrades GABA, thereby increasing its availability.

Benzodiazepines: Used in status epilepticus 
     -Diazepam (Valium)
     -Clonazepam (Rivotril, Klonopin)
     -Lorazepam (Ativan)
Barbiturates: 
     -Phenobarbital (Luminal)
     -Gabapentin (Neurontin)
Tiagabine
Vigabatrin
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17
Q

Antagaonize glutamate

A

Antagaonize glutamate: Glutamic acid (glutamate) is the prmary excitatory transmitter in the CNS working through two receptors NMDA and AMPA. Felbamate and topiramate block the actions of glutamate at NMDA and AMPA thereby suppressing neuronal excitation.

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18
Q

Drug of choice for tonic-clonic

A

phenytoin (Dilantin)

not effect in absence or myoclonic seizures

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19
Q

Used for partial seizures, tonic-clonic seizures, and bipolar disorders

A

Carbamazepine (Tegretol)

Lamotrigine (Lamictal)

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20
Q
  • Used for partial, generalized & absence seizures

- Used for bipolar disorders and migraine headache

A

Valproic acid (Depakene)

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21
Q

-Only indicated in absence seizures

A

Ethosuxamide (Zarontin)

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22
Q

Used in status epilepticus

A

Benzodiazepines

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23
Q

Used for partial and generalized tonic-clonic seizures. Not effective against absence seizures.

A

Barbiturates

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24
Q

Used for partial seizures, Also used for neuropathic pain and prevention of migraine headaches

A

Gabapentin (Neurontin)

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25
Q

Describe A1C

A

Diabetes can be diagnosed based on glycosylated hemoglobin (HbA1c). Glycosylated hemoglobin refers to the permanent attachment of glucose to hemoglobin molecules and reflects the average plasma glucose exposure over the life of a red blood cell. Test is critically dependent upon the method of measurement and must be related to established standards.

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26
Q

Somogyi effect and dawn phenomenon

A

Somogyi effect and dawn phenomenon are both AM diabetes. However, Somogyi effect is rebound in the AM from the patient having too much insulin at night. Dawn phenomenon is not rebound, and is because the patient did not get enough insulin.

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27
Q

Oral anti diabetic agents
Class
Names

A

Sulfonylureas
“ides” (not glinides)
-First generation: chlorpropamide (Diabinese),
tolazamide, acetohexamide (Dymelor),
tolbutamide (Orinase)
-Second generation: glyburide (Micronase,
Glynase, and DiaBeta), glimepiride (Amaryl),
glipizide (Glucotrol, Glucotrol XL)

Bigaunides
metaformin (Glucophage)

Thiazolidinediones
“zones”
pioglitazone (Actos), rosiglitazone (Avandia),

Meglitinides
“glinides”
-repaglinide (Prandin), nateglinide (Starlix)

Alpha-glucosidase Inhibitors
acarbose (Precose), miglitol (Glyset)

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28
Q

DKA

A
  • Main features: Hyperglycemia, dehydration, hemoconcentration, acidosis
  • For DKA to be diagnosed one must have 1) serum glucose level >250, 2) serum bicarb level< 7.3, 4)anion gap, 5) urine and serum ketones.

diabetic ketoacidosis. Normally found in type 1, insulin deficiency. Insulin normally stimulates lipogenesis and inhibits lipolysis, this preventing fat catabolism. With insulin deficiency, lipolysis is enhanced and there is an increase in the amount of nonesterified fatty acids delivered to the liver. Consequently there is an increase in glyconeogenisis contributing to hyperglycemia and production of ketone bodies. Symptoms of diabetic ketoacidosis include Kussmaul respirations, postural dizziness, central nervous system depression, ketonuria, anorexia, nausea, abdominal pain, thirst, and polyuria.

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29
Q

HHNKS

A
  • Main features: Severe hypoglycemia, hyperosmolality, dehydration
  • Diagnosis of HHNKS includes glucose level >600, serum ph >7.3, bicarb >15, serum osmolarity >320, absent or small number of ketones in the urine and serum.
  • HHNKS- (Hyperosmolar hyperglycemic nonketotic syndrome) uncommon complication of type 2. Mostly occurs in elderly with other comorbidities.HHNKS differs from DKA in the degree of insulin deficiency (which is more profound in DKA) and the degree of fluid deficiency (which is more marked in HHNKS).
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30
Q

DKN vs HHNKS

A

DKA has ketones in Type 1

HHNKS has severe dehydration in older adults in Type 2

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31
Q

Types of Insulin

A

Short duration: rapid acting
Short duration: slow acting
Intermediate duration
Long duration

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32
Q

Causes of UTI

A 
•Infection and inflammation of the urinary epithelium
•Can be lower or upper UTI
•Most UTI’s are bacterial caused by
     E. Coli (gram negative) most common cause
     Staphylococcus saprophyticus 
     Klebsiella 
     Proteus
     Can also be caused by Parasites
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33
Q

Cystitis
What is it?
Cause

A

-(lower) an inflammation of the bladder and is the most common site of UTI. Can range from mild to severe causing gangrenous cystitis, necrosis of the bladder wall.

Causes: Most common infecting microorganisms are uropathic strains of E.coli and the second most common is S. saprophyticus. Less common include Klebsiella, Proteus, Pseudomonas fungi, viruses, parasites, or tubercular bacilli. Schistosomiasis is the most common cause of parasitic invasions of the urinary tract on a global basis.

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34
Q

Cystitis
Patho
S/S

A

Pathophysiology: Bacterial contamination of the normally sterile urine usually occurs by retrograde movement of gram negative bacilli into the urethra and bladder and then to the ureter and kidney. Uropathic strains of e.coli have type 1 fimbriae that bind to catheters and receptors on uroepithelium and resist flushing during mictruition. These strains can bind to uroepithelial p blodd group antigen which is present in most of the human population. Some women may be genetically susceptible to certain strains of e. coli attachment. Hematogenous infections are uncommon and often preceded by septicemia. Infection initiates and inflammatory response and the symptoms of cystitis. The inflammatory edema in the bladder wall stimulates discharge of stretch receptors initiating symptoms of bladder fullness with small volumes of urine and producing the urgency and frequency of urination associate with cystitis.

Signs and Symptoms: frequency, urgency, dysuria, and suprapubic and low back pain. Hematuria, cloudy urine, and flank pain are more serious symptoms. Can be asymptomatic.

35
Q

Interstitial Cystitis

A

Also called painful bladder syndrome
Nonbacterial
Damage and irritation of bladder wall possibly due to autoimmune reaction
Same symptoms as acute cystitis, but no bacteria-does not respond to antibiotic therapy
Most common in women in their 20’s and 30’s
No effective treatment

36
Q

Pyelonephritis
What is it?
Causes

A

-is an infection of one or both upper urinary tracts. Can be acute or chronic

Causes: kidney stones, vesicoureteral reflux, pregnancy, neurogenic bladder, instrumentation, female sexual trama. Responsible microorganisms usually are e.coli, proteus, or pseudomonas

37
Q

Pyelonephritis
Patho
S/S

A

Pathophysiology:
acute: the infection is probably spread by ascending uropathic microorganisms along the ureters, but spread also may occur by way of the bloodstream. The inflammatory process is usually focal and irregular, primarily affecting the pelvis, calyces, and medulla. The infection causes medullary infiltration of white blood cells with renal inflammation, renal edema, and purulent urine. In severe infections, locatlized abscesses may form in the medulla and extend to the cortex. Primarily affected are the tubules; the glomeruli usually are spared. Necrosis of renal papillae can develop. After the actue phase, healing occurs with bibrosis and atrophy of affected tubules. The number of bacteria decreases until the urine again becomes sterile. Acute pyelonephritis rarely causes renal failure.
Chronic: starts as progressive inflammation, altered renal pelvis and calyces, destruction of the tubules, atrophy or dilation and iffuse scarring and finally impaired urine concentrating ability leading to chronic kidney failure

Signs and Symptoms:
acute: fever, chills, and flank or groin pain. Characterisitc symptoms of a UTI, including grequency, dysuria, and costobertebral tenderness, may precede systemic signs and symptoms. Older adults may have nonspecific symptoms.
Chronic: hypertension, frequency, dysuria, flank pain. Preogression leads to kidney failure, particularly in the presence of obstructive uropathy or diabetes mellitus.

38
Q

Complicated vs Uncomplicated UTI

A
  • Generally, UTIs are mild, without complications, and occur in individuals with a normal urinary tract, these infections are termed uncomplicated UTI.
  • A complicated UTI develops when there is an abnormality in the urinary system or a health problem that compromises host defenses or response to treatment
39
Q

Edema from renal disease

A

•Ultimately the kidney loses its ability to regulate sodium and water balance. Both sodium and water are retained, contributing to edema and hypertension

40
Q

Nephrotic symptoms

A

Protein > 3.5 g a day – most important symptom in nephrotic syndrome
Hypoalbuminemia, edema, hypertention
Hyperlipidemia (due to lipoproteins), lipiduria
Increased tendency for thrombotic events (especially renal) due to
loss of anicoagulant (e.g. antithrombin III) proteins in the urine
Hyperlipidemia (lipids injure platelets membrane and endothelial cells)
Hemoconcentration
High tendency for infection due to loss of complement proteins in the urine

41
Q

Nephritic symtoms

A

RBC casts – most important symptom in nephritic syndrome
Glomeruli inflamed, swollen and infiltrated with inflammatory cells leading to decreased blood flow through glomeruli leading to low GFR and oligurea
Hypertension Total protein loss is less than nephrotic syndrome
Azotemia
Uremia
Chronic renal failure

42
Q

glomerulonephritis

A

Acute
Associated with streptococcal infection
Abrupt onset, 7-10 days after infection of
throat or skin
Antigen/antibody reaction causes damage to
glomerular membrane
Chronic
Progressive destruction of glomeruli from
chronic inflammation, progresses to CRF
Caused by hypercholesterolemia causing
glomerulosclerosis, DM, lupus erythmatosus
Clinical Manifestations
Nephrotic or nephritic sediments
Edema
Periorbital
Around the ankles
HTN

43
Q

Acute Renal Failure
Patho
Causes

A

Patho
Abrupt and rapid reduction in kidney function
Associated with decreased glomerular filtration
and oliguria
Elevated BUN and creatinine
Reversible if diagnosed early and treated
Causes
Pre-renal
Most common
Caused by impaired renal blood flow
GFR declines due to decrease in filtration
pressure
Intrarenal
Acute tubular necrosis (ATN) is most common
cause
Postischemic
nephrotoxic
Post renal
Occurs with urinary tract obstructions that affect
the kidneys bilaterally

44
Q

Acute Renal Failure

clinical manifestations

A 
Clinical Manifestations
Oliguria
      Lasts 1-3 weeks
      Hyperkalemia
      Metabolic acidosis
      Anemia
      Fluid retention
      Elevated BUN and serum creatinine
Diuretic
      Lasts 24 hrs – 6 weeks
      Urinary output is >400 ml/day
      Hypokalemia
      Hyponatremia
      Dehydration
Recovery	
      Return of renal function to normal
      May take up to 12 months
45
Q

Chronic Renal Failure

Patho/causes

A

Pathophysiology/causes:

Irreversible loss of renal function that affects nearly all organ systems
Occurs over a continuum, patients may have few symptoms, as kidneys function even at 50% damage
Progression of chronic kidney disease is thought to be associated with common pathogenic processes regardless of the initial disease. These processes include the following:
Glomerular hypertension, hyperfiltration,
and hypertrophy
 Glomerulosclerosis
 Tubulointerstitial inflammation and
fibrosis
The factors that contribute to the pathogenesis of chronic kidney disease are complex and involve the interaction of many cells, cytokines, and structural alterations. Two factors that have consistently been recognized to advance renal disease are the presence of proteinuria and increased angiotensin II activity. Glomerular hyperfiltration and increased glomerular capillary permeability lead to proteinuria. Proteinuria contributes to tubulointerstitial injury by accumulating in the interstitial space and activating complement proteins and other mediators and cells that promote inflammation and progressive fibrosis. Angiotensin II activity is elevated with progressive nephron injury and promotes glomerular hypertension and hyperfiltration caused by efferent arteriolar vasoconstriction and also promotes systemic hypertension. The chronically high intraglomerular pressure increases glomerular capillary permeability, contributing to proteinuria.

46
Q

Chronic renal failure

clinical manifestations

A
  • Pulmonary symptoms related to pul edema
  • Anemia
  • LV hypertrophy
  • Anorexia, N & V,
  • Pruritis
47
Q

Renal failure tests

A

Evaluate severity of kidney disease/assess patient’s progress

Determine effectiveness of kidney excretory function

Results may be normal until GFR is reduced to < 50% of normal

Urinalysis: Color, appearance, odor

Standard Dipstick: Identifies gross levels of all protein

Urine Sediments: RBC, casts and WBC

Concentration tests
Specific gravity
Urine osmolality

Clearance tests: Creatinine clearance

Blood tests
Plasma creatinine concentration
BUN

Culture and sensitivity tests
Gram stain
Culture
Sensitivity

48
Q

Role of Von Willerand factor in primary hemostasis

A

adhesion

49
Q

Raynauds

A
  • PVD
  • Vasospastic disease involving the hands and the feet, usually precipitated by cold
  • Nifedipine (procardia) is the calcium channel blocker used to manage Raynauds disease
50
Q

Laboratory tests for monitoring patients on heparin and warfarin (Coumadin)

A
  • Heparin should be monitored with th6e aPPT test (Except LMWH, Lovenox/Enoxaparin)
  • Warfarin (Coumadin) should be monitored with a PT test and reported as INR (2-4.5)
51
Q

Antiplatelets drugs used

A
  • ASA (Aspirin)
  • Adenosine Diphosphate Receptor Blockers (ADP Blockers)
  • Glycoprotein IIb/IIIa Platelet Receptor Antagonist
52
Q

low v/q

A

•low V/q= low ventilation, but good perfusion
-very low ventilation = shunting, which
occurs in atelectasis, asthma, pulmonary
edema, and pneumonia

53
Q

high v/q

A

•high v/q= poor perfusion of well ventilated areas: common causes are pulmonary embolus impairing blood flow, a ventilated but not perfused area is termed alveolar dead space

54
Q

Diseases effecting ventilation/perfusion

A

•diffusion of oxygen through the alveolocapillary membrane is impaired if the membrane is thickened[as with edema or fibrosis] or the surface area available for diffusion is decreased[as with the destruction of alveoli in emphysema]

55
Q

Signs and symptoms of pulmonary embolism

A
  • Sudden onset of dyspnea, Tachypnea, tachycardia, chest pain, unexplained anxiety
  • Massive emboli leads to hypotension and shock
  • Altered ABGs: Hypoxemia, hypocapnia, hyperventilation (respiratory alkalosis)
56
Q

Treatment of pulmonary embolism

A

•Medications that treat pulmonary embolisms include: thrombolytics and anticoagulants.
•Surgical treatment includes:
-clot removal: threading a catheter through the
vein to clear out the clot.
- inserting a vein filter: this stops a clot from
entering the heart.
-surgery: this would be emergency surgery
where they remove the clot.

57
Q

Pathophysiology of emphysema

A

a.Irritants lead to structural damage to alveoli which leads to loss of elastic recoil of the lung which leads to air flow limitation
b.Centriacinar
-Initially affects distal bronchioles and then
affects alveoli
-seen in smokers
c.Panacinar
-Affects bronchioles & alveoli
-Occurs with alpha-1 antitrypsin deficiency

58
Q

chemotaxis

A

•Chemotaxis is the directional movement and attraction of microorganisms or phagocytes to the substances released in the environment or tissues (toward the inflammation). Primary chemotactic factors include any bacterial products, neutrophil, chemotactic factors by mast cells, complement fragments C3a and C5a, and products of the clotting and kinin systems

59
Q

Kinin pathway

A

•Kinin pathway: Activates and helps inflammatory cells by causing, vasodilation, vascular permeability, pain, endothelial smooth muscle contraction, leukocyte chemotaxis. Initiated through Hageman factor (factor XIIIor XIIa). The final product is called bradykinin which causes the dilation of blood vessels, acts with prostaglandins to induce pain, cases smooth muscle cell contraction, and increases vascular permeability.

60
Q

Prostaglandins

A

•Prostaglandins: cause increased vascular permeability, neutrophil chemotaxis, and pain by direct effects on nerves.

61
Q

Histamine

A

•Histamine: also called vasoactive amine. The molecules cause temporary, rapid constriction of smooth muscle and dilation of the postcapillary venules, which results in increased blood flow into the microcirculation. Histamine also causes increased vascular permeability resulting from retraction of endothelial cells lining the capillaries and increased adherence of leukocytes to the endothelium. Histamine affects cells by binding to histamine H1 and H2 receptors on the target cell surface. Antihistamines are drugs that block the binding of histamine to its receptors, resulting in decreased inflammation.

62
Q

B lymphocytes

A
  • Humoral
  • Antibody producing cells
  • Can only recognize 1 pathogen due to the receptor on the cell
  • When antigen binds to antibody on B cell surface, antigen goes into cell, gets broken down and parts of antigen mix with MHC and gets displaced on the cell wall and presented to T cell
  • Do not have the power to attack the pathogen
  • Develop into plasma or memory cells
63
Q

T Lymphocytes

A

-Cell-mediated

-Helper T Cells, Killer/Cytotoxic T Cells, NK Cells, T Regulatory Cells
Helper T: control cell mediation and humoral immune response
Memory T: induce 2nd immunse response faster when next encountered
Cytotoxic T: attack antigens directly

  • Do not produce antibodies, do the actual attacking of the pathogen
  • Require B lymphocytes or NK cells to present antigen information
64
Q

Neutrophils

A

•Neutrophils (type of a granulocyte, which is a white blood cell) are the predominant cell needed to kill bacteria in early stages of inflammation, they arrive 6-12 hours after initial injury (first responders). They are short lived (24 hours) and become a part of the purulent exudates (pus); the primary role is the removal of debris and dead cells in sterile legions such as burns, and the destruction of bacteria in nonsterile lesions.

65
Q

Pharmacokinetics

A
  • Pharmacokinetics: movement of the drug throughout the body

* 4 phases: absorption, distribution, metabolism, and excretion

66
Q

Absorption

A

Absorption: the process of moving the drug from site of administration across body membranes and into the blood stream. This determines the length of time it takes the drug to produce its effect. The more rapid the absorption the faster the onset of action. The fastest route is an IV because it is put directly into the blood stream, the safest but slowest route is the oral. The factors that affect absorption include the dose, dosage form (syrup is faster than a tablet), blood flow in site of administration, degree of ionization, route of administration. Factors that specifically effect enteral route includes food/fluids administered, dosage formulation, status of the absorptive surface, rate of blood flow, gastric ph, and status of GI motility.

67
Q

Distribution

A

Distribution: the transport of a drug in the body by the bloodstream to its site of action. Factors affecting distribution include amount of blood flow, physical properities (drug-lipid soluble is more readily distributed), ability to exit vascular system (protein binding, plasma protein sites, barriers: blood brain and fetal placental).

68
Q

Metabolism

A

Metabolism (biotransformation): the process of enzymatically converting the drug to a form that is more easily removed from the body. The liver is the primary site for the drug metabolism (cytochrome P-450), kidneys and intestinal tract are also involved in the drug metabolism. Factors affecting metabolism rate include enzyme induction (accelerates hepatic metabolism), enzyme inhibition (decreases hepatic metabolism), hepatic conditions that decrease hepatic metabolic activity, malnutrition decreases hepatic enzyme availability. Accelerate metabolism causes therapeutic failure and delayed metabolism causes increased toxicity.

69
Q

Excretion

A

Excretion: Removal of drugs from the body via the kidneys (main organ), liver, and bowel. Kidneys: the glomerulus filters free drugs from the blood into renal tubule, passive tubular reabsorption (ionized and water soluble drugs will remain in the filtrate and get excreted), active tubular secretion removes drugs from the blood into the tubules (pglycoprotein helps transfer drugs back into filtrate that may have been kicked out because they were non ionized or fat soluble). Factors affecting excretion include acid drugs and alkaline drugs and effects of ionization (urinary ph can be manipulated to get a drug excreted quicker), age can effect excretion, as well as renal disease.

70
Q

Pharmacodynamic

A

The mechanism of drug action in living tissue. Pharmacodynamics affect the therapeutic range (ED50 is the median effect dose), it includes drug receptor interactions (agaonists, partial agonist, antagonist)

71
Q

Half life

A

•Half-life is the time it takes for one half of the original amount of a drug in the body to be removed. Half-life varies among different drugs. If the dose of drugs remains constant it takes 4 half-lives to reach steady state (plateau) and 4 to rid the body of the drug after the last dose. Half-life is prolonged in patients with liver and kidney disease, in this case half-life is increased and dosage should be adjusted as appropriate to prevent toxicity. If half-life is decreased the drug will be metabolized and removed from your system more quickly than usual, again dosage should be modified as appropriate

72
Q

Function of P53

A

P53 is a tumor suppressor gene that tells the cell to stop dividing. It can repair the cell or send it to apoptosis when it can’t repair.

73
Q

Function of telomeres and telomerase

A
  • A telomere is a region of repetitive DNA at each end of a chromosome, which protects the end of the chromosome from deterioration. Every time a cell replicates, the telomeres shorten. Because of this, cells can only replicate a limited number of times. This is normal for cells.
  • Telomerase is an enzyme that repairs the telomeres of a cell after cell division, rendering the cell immortal. The lengthened life-span of the cell allows for more time to acquire mutations, greatly increasing the risk for cancer. In cancer cells, telomerase is switched on all the time
74
Q

oncogene

A

•Oncogene- mutant genes (causes over expression or amplification causing gain of function; driver mutation) oncogenes must be activated to produce cancer (i.e. gene amplification) (can be activated by mutation or loss of silencing)

75
Q

Proto-oncogene

A

•Proto-oncogene- directs synthesis of proteins that regulate [accelerate] proliferation. Examples of proto-oncogenes include growth factors (i.e. epidermal growth factor), growth factors receptors, or positive regulators of proliferation in the signal transduction pathways signaling growth (i.e. RAS).

76
Q

Metaplasia

A

•Metaplasia- Replacement of one type of mature tissue with a different type of mature tissue Example, if you smoke you will not have normal epithelial cells (they were not made to withstand the smoking), the system changes the cells to handle the nicotine (squamous metaplasia). This is reversible, so if a smoker stops the cells can return back to normal; unless the patient waits so long the cells turn to dysplasia and then to cancer. Can lead to dysplasia.

77
Q

Hyperplasia

A

•Hyperplasia (aka hypergenesis)- increase in the number of cells, but the cells are normal, and still function normally and remain under normal regulatory mechanisms (i.e. prostate hyperplasia).
3 types: hormonal, compensatory, and pathologic.

Causes can be hormonal, inflammatory response, or compensatory.

Examples, uterine expansion during pregnancy from hormones. Liver grows back after damage, compensatory. Prostate hyperplasia is an example of pathologic, its not normal, but not cancerous…occurs from aging and hormonal changes. Hyperplasia is reversible.

78
Q 
PH
PaCO2
HCO3
PaO2
O2sat
A
  • PH = 7.35-7.45
  • PaCO2= 35-45
  • HCO3 = 22-26
  • PaO2 = 80-100
  • O2sat = 95-100
79
Q

Metabolic acidosis

A 
•Metabolic acidosis is caused by an increase in the levels of non carbonic acids or by loss of bicarbonate from the extracellular fluid
Increased H+load
   -Ketoacidosis (dm, starvation)
   -Lactic acidosis (shock, hypoxemia)
   -Ingestion
Decreased renal H+ excretion
Renal Bicarb loss
Diarrhea
80
Q

Metabolic alkalosis

A

•Metabolic alkalosis occurs with an increase in bicarbonate concentration, which is usually caused by loss of metabolic acids from conditions such as vomiting or gastrointestinal suctioning or by excessive bicarbonate intake, hyperaldosteronism, and diuretic therapy, which increase plasma bicarbonate concentration.

81
Q

Respiratory acidosis

A

•Respiratory acidosis occurs with decreased alveolar ventilation, which in turn causes hypercapnia and increased carbonic acid concentration. Causes include hypoventilation, paralysis of lungs, chest wall disorder, respiratory depression, etc.

82
Q

Respiratory alkalosis

A

•Respiratory alkalosis occurs with alveolar hyperventilation and excessive reduction of carbon dioxide level, or hypocapnia with decreases in carbonic acid concentration. Also can be caused by exercise, kidney problems, and anxiety.

83
Q

Compensation for:
Metabolic acidosis
Metabolic alkalosis

A

Metabolic acidosis: hyperventilation

Metabolic alkalosis: hypoventilation

84
Q

Compensation for:
Respiratory acidosis
Respiratory alkalosis

A

Respiratory acidosis: increased excretion of H+, retain bicarb
Respiratory alkalosis: retain H+, excretion of bicarb

Nurs 323 (2 decks)

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