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Pharmacology > Spring Final Exam 2018 > Flashcards

Spring Final Exam 2018 Flashcards

1
Q

Most common neurotransmitters

A

Acetylcholine (Excitatory/Inhibitory)

Monoamines

  1. Norepinephrine (E)
  2. Serotonin (I)
  3. Dopamine (E)
  4. Histamine (I)

Amino Acids

  1. GABA (I)
  2. Glycine (I)
  3. Glutamate (E)

Neuropeptides

  1. Endorphins and Enkephalins (I)
  2. Substance P (E)

Purines-Adenosine

Gases-NO, CO

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2
Q

Ions involved in neuronal transmission and action potentials

A

Neuronal Transmission

Afferent Neuron: carrying information toward the CNS (ascending)

Efferent Neuron: carrying information away from the CNS to target organs (descending)

Interneuron: connecting areas within the brain

Membrane Potential

  • The Na-K ATPase pump maintains membrane potential
    • ~-90mV, “polarized”
  • More K+ IC; More Na+ EC
  • For each molecule of ATP used, 3 NA ions are pumped out of the cell, and 2 K+ ions are pumped into the cell
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3
Q

Normal intracranial pressure reading

and symptoms of increased intracranial pressure

A
  • Normal ICP 0-15mmHg (lateral ventricles)
  • Small changes with respiratory movements, coughing, straining, or sneezing
  • ICP above 20mmHg is seen as pathologic and should be treated

SYMPTOMS

  • Initial Symptoms: Headache, projectile vomiting, papilledema
  • Cushing’s Triad: Bradycardia, hypertension (with widening pulse pressure), and irregular respiratory pattern
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4
Q

Calculate and interpret a patient’s cerebral perfusion pressure (CPP)

A

CPP=MABP-ICP

MABP-mean arterial blood pressure

MABP and ICP commonly monitored

Normal CPP is 70-100mmHg

Brain ischemia at levels below 50-70mmHg

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5
Q

Cellular consequences of increased ICP or ischemia

A
  • MONROE-KELLIE HYPOTHESIS or DOCTRINE: Volumes of each of 3 compartments (brain, blood, CSF) can vary slightly without causing and marked increase in ICP. Increase in one compartment must be compensated by a decrease in another compartment, otherwise ICP will rise
  • Pathologic ICP levels can be caused by volume changes in any of the 3 compartments
  • Of the three compartments, brain tissue is least able to compensate.
  • Initial ICP changes buffered by CSF shunting to the spinal cord.
  • Only small amount of blood, blood flow tightly regulated.
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6
Q

PENUMBRA

A
  • Minimally perfused cells around central core of dead cells
  • Are in electrical failure but structure intact
  • Can recover if blood flow restored
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7
Q

Conditions associated with Ischemic Stroke

A

Thrombotic: Due to atherosclerotic plaques -lay off those lipids, hypercoagulation disorders (sickle cell, polycythemia); HTN

Embolic: Usually cardiac source-mural thrombi, valve vegetations, atrial fibrillation; carotid artery plaques; HTN

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8
Q

Conditions associated with Hemorrhagic Stroke

A
  • Most frequently fatal
  • Rupture of blood vessel-hemorrhage into brain tissue, edema, compression, spasm
  • Predisposing factors: age, HTN, aneurysm, trauma, tumor, AVM
  • Sudden onset, often with activity
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9
Q

Compare and contrast ischemic and hemorrhagic strokes

A
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10
Q

Secondary vs. Primary Seizure

A

Secondary: Known cause. Any disorder that alters the neuronal environment may cause seizure activity. Fever (especially in children), electrolyte imbalances, hypoglycemia, hypoxia, alkalosis, rapid withdrawal of sedatives, toxemia of pregnancy, water intoxication, CNS infections.

Primary: unknown cause. Frequent seizures of this type lead to diagnosis of seizure disorder

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11
Q

Simple Partial Seizures

A

Simple partial: one hemisphere, no impairment of consciousness

  • Jacksonian March: progressive motor

Complex partial: impairment of consciousness, often from temporal lobe. Automatisms common

Secondarily generalized Partial Seizure: starts as partial but spreads to both hemispheres, thalamus, reticular formation

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12
Q

Complex Seizures

A

Absence seizures: nonconvulsive disturbances in consciousness

Atonic Seizures: drop attacks

Myoclonic Seizures: Either tonic- rigid, violent contraction of muscles or clonic- repeated contractions and relaxations

Tonic-Clonic Seizures (grand mal): Loss of consciousness, incontinence common, possible cyanosis from constriction of airway and respiratory muscles. Tonic, followed by clonic then post-ictal period

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13
Q

Status Epilepticus

A

Seizure that will not stop on own, or multiple seizures in a row

  • Tonic-clonic status epilepticus can be fatal; leads to respiratory failure
  • If cause is known, must address otherwise may not stop seizure
  • IV Valium (diazepam) drug of choice
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14
Q

Basic concepts of anti-seizure medications

Old AEDs VS. New AEDs

A

Old AEDs: We know how and why they work; but have undesirable yet predectable side effects

New AEDs: They tend to have, for now, fewer side effects and are well tolerated; but can be more expensive and some of the side effects are un-predectable

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15
Q

Pathophysiology of Parkinson’s disease

A

Complex motor disorder accompanied by systemic non-motor and neurologic symptoms. One of the most common causes of neurologic disabilities in individuals over 60 years old

Primary PD: Usually begins after age 40, incidence increases after age 60.

  • More prevalent in males. Gene-environment.

Secondary Parkinsonism: caused by disorders other than PD

  • Head trauma, infection, neoplasm, atherosclerosis, toxins, medications or drugs

Degenerative disorder of the basal ganglia involving the dopaminergic nigrostriatal pathway

80% loss of dopamine before symptoms appear

Leads to imbalance of dopaminergic (I) and cholinergic (E) input in the caudate nucleus of the basal ganglia

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16
Q

Pathophysiology of Multiple scelrosis

A

T-cells, macrophages, and possibly antibodies react with myelin protein - BAD

  • Demyelination occurs, nerve fibers may be damaged
  • Demyelinating lesions (plaques) form in white matter and may extend into gray matter. Axonal conduction interrupted
  • Early exacerbations: edema and inflammation but return to baseline after exacerbation remits.
  • After many exacerbations, damage becomes permanent
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17
Q

Proto-oncogenes Vs. oncogenes

A

Proto-oncogenes: code for proteins that help regulate cell growth and differentiation

Tumor suppressor genes: inhibit cell proliferation

Proto-oncogenes become ONCOGENES when genetic mutations alter their activity-get excess proliferation: Growth Factor, Growth Factor receptor, Cytoplasmic Signaling Pathways, Transcription Factors

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18
Q

NADIR

A

Neutropenia-Nadir (10-14 days after chemo)

An abnormally low count of a type of white blood cell (neutrophils).

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19
Q

Benign Vs. Malignant growths

A
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20
Q

TNM grading system

A

Tumor (T)

  • Tx-tumor cannot be evaluated
  • T0-no evidence of tumor
  • T1, T2, T3, T4-size and/or extent of primary tumor

Regional Lymph Node Involvement (N)

  • Nx-regional lymph nodes cannot be evaluated
  • N0-no cancer in lymph nodes
  • N1, N2, N3-involvement of regional lymph nodes (number and/or extent of spread)

Distant Metastasis (M)

  • Mx-distant metastasis cannot be evaluated
  • M0-no distant metastasis
  • M1-distant metastasis
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21
Q

Side Effects of cytotoxic medications

focusing on bone marrow effects

A

Bone Marrow Suppression

  • Epoetin
    • Anemia
  • Colony stimulating factor (CSF)
    • Neutropenia-Nadir (10-14 days after chemo)
  • Neumega
    • Thrombocytopenia
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22
Q

Ways to overcome barriers in chemotherapy treatment

A
  • Intermittent Chemo: need time for normal cells to recover.
  • Combination of cytotoxic medications
    • Suppresses drug resistance-less likely to have multiple mutations
    • Increased rate of tumor cells kill
    • Decrease in injury to normal cells-use drugs with different toxicities
  • Specialized routes
    • Arterial, Intrathecal, Bladder, Peritoneal cavity
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23
Q

Tumor lysis syndrome

A

Commonly in rapidly growing cancers after administration of chemotherapy

  • Leukemias and lymphomas; rare in solid tumors
  • Starts within 1-3 days of chemotherapy

Massive number of cells killed in short period of time; release of intracellular ions, nucleic acids, proteins into circulation

  • Hyperuricemia, hyperkalemia, hyperphosphatemia, hypocalcemia

Kidneys damaged by uric acid and other intracellular contents

Cardiac arrhythmias

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24
Q

Inheritance patterns for autosomal dominant disorders

A
  • Father is carrying disease that’s autosomal dominant
  • 50% chance that the child will get disease
  • Each child is individual chance
  • If it’s passed on, it might be expressed in child
  • Can be a characteristic like brown eyes
  • Getting just one ”A”= expressing disease
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25
Q

Inheritance patterns for autosomal recessive disorders

A
  • Need two copies of gene to express disease process
  • Each of these parents are carrying this autosomal recessive disorder
    • Neither are expressing it b/c they only have one copy; May not know you’re a carrier for the disease b/c it’s not expressed
  • Need “aa” to express disease
  • 25% chance the child will express disease process
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26
Q

Inheritance of HLA proteins

Human Leukocyte Antigen

A

HLA: Human Leukocyte Antigen

Proteins that are present on the surface of cell that help you differentiate self from non self

Allows immune system to recognize own cells and makes sure it doesn’t attack your own body’s cells

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27
Q

Criteria for declaring brain death

A
  • No response to painful stimuli (Sternal rub-take knuckles and rub on sternum)
  • No spontaneous movement
    • Can have seizure activity or m. spasms, but no spontaneous mov’t
  • No spontaneous respirations
    • If pt gets up to 60 mmHg of CO2 in blood &still don’t take a breath, it’s criteria for brain death (remember CO2 is a driving force for respiration)
  • No cranial nerve response
    • EEG (Any brain waves that indicate thought/brain activity), cerebral angiography (see if blood flow to brain is adequate), apnea test (taking pt off ventilator and seeing if they breath on own)
  • Status unchanged for 6 hours
    • Wait 6 hours and do tests again to make sure pt is REALLY brain dead
28
Q

HLA system and the use of PRA in determining who can receive an organ

A

Panel Reactive Antibody

Test detects preformed HLA antibodies (antibodies in body already made against HLA protein)

  • From pregnancy, blood transfusions, previous transplantation
    • If you’ve never had any of these, you won’t have any antibodies against any other prot. b/c you’ve had no other person’s prot. In your body
  • Can restrict access to transplantation b/c it narrows your pool
    • Not only do you have to match these, you have to excluded other HLA protein
  • Given as a percentage – PRA of 50% means that the patient’s serum reacts with 50% of the donors in the panel
29
Q

Subacute Vs. acute Vs. chronic rejection

A
  • Hyperacute: Occurs minutes to hours after transplant. Kidney most susceptible. Due to pre-formed antibodies to organ’s HLA. Organ must be removed immediately
    • Happens very infrequently nowadays b/c we have figured this out and have good testing
  • Acute: Highest risk is in first 3 months, risk declines after 1 year. Must be treated (medically) promptly. T-cell mediated.
    • That’s why there’s intensive monitoring in the first year (looking for ANY sign of rejection)
  • Chronic: Long-term loss of organ function due to fibrosis (thickening/scarring) of vasculature which is due to poorly understood chronic inflammatory and immune response.
    • Over time blood supply to organ gets lower and lower and we have slow decline in function
    • Happens with even with best matching
    • When kid gets transplant, they will probably need another transplant later on
30
Q

Sensorineural Hearing Loss

A

From cochlear nerve damage

  • Sudden or progressive
  • Causes: trauma to 8th cranial nerve, trauma to cochlea, ototoxicity from medications (gentamycin); progressive from aging, noise, systemic disease (syphilis, diabetes)
  • Usually unilateral, may have tinnitus, dizziness, pain
31
Q

Conductive Hearing Loss

A

Inability of sound to reach the inner ear from the middle ear or outer ear

  • Sudden or progressive
  • Causes: buildup of earwax, infection, foreign body; thickening, retracting, scarring, or perforation of tympanic membrane; fixing of ossicles
32
Q

Cataracts

A

Clouding of the normally clear lens of the eye

  • Oxidative damage to lens proteins and protein aggregation
  • Aging, diabetes, HTN, kidney disease, exposure to toxicities, congenital, steroid usage
  • Cardinal sign: halos around lights
  • Problem is with the lens only. Treatment is surgical excision of lens with replacement with an artificial lens
33
Q

Glaucoma

A
  • Normally, vitreous humor is created behind the lens, &fluid slowly leaks out through the spongy trabecular meshwork around the lens
  • Glaucoma is a problem with PRESSURE
  • As vitrious humor has a harder time getting out, more fluid stays in the posterior chamber, and pressure increases. Similar to the way that increased ICP damages brain tissue, increased intraocular pressure causes damage to the retina and optic nerve
34
Q

5 major causes of shock

A

Caused by any factor that alters heart function, blood volume, or blood pressure

  • Septic (caused by infection/inflammatory response)
  • Cardiogenic (caused by heart failure)
  • Anaphylactic (hypersensitivity)
  • Hypovolemic (insufficient intravascular volume)
  • Neurogenic (alterations in smooth muscle tone)
35
Q

Symptoms of septic shock

A
  • Culture and sensitivity does not always demonstrate a causative organism
  • Increased or very low WBCs
  • Tachypnea
  • Fever in 60% (commonly not present in those with advanced age, renal failure, or those taking anti-inflammatory medications)
  • Hypothermia (ominous sign)
  • Hypoxia
  • Hypotension
  • Tachycardia (nearly universal except those taking medications such as beta-blockers or those with cardiac abnormalities)
  • Elevated lactate levels=increased mortality
36
Q

Emergency medications used for anaphylactic shock

A

Epinephrine: First line drug. Alpha and beta agonist. Increases vascular resistance, reduces permeability, produces bronchodilation, increases CO

  • SubQ or IV (NOTE: Patients on beta-blockers may not respond appropriately and may need norepinephrine and dopamine)

Antihistamines: Benadryl

Corticosteroids: Not immediate acting but will shorten duration of symptoms and help prevent return-see below

Inhaled bronchodilators

Fluids

  • Note: risk for a second peak response to occur several hours after first-anyone with a severe anaphylactic response should be monitored overnight
37
Q

Superficial/1st Degree Burn

A
  • Destruction of epidermis only
  • Skin function intact
  • Tactile and pain sensors intact
  • Blisters only after 24 hours
  • Skin peels at 24-48 hours, normal or slightly reddened underneath
  • Healing time 3-5 days
  • No scarring
  • Commonly caused by sunburn
  • If large surface area involved, may have systemic responses (chills, edema, nausea, vomiting)
38
Q

Superficial Partial Thickness/2nd Degree

A
  • Destruction of epidermis and some dermis
  • Skin function absent
  • Tactile and pain sensors intact
  • Blisters within minutes; thin walled and fluid filled
  • After debridement, skin is red to pale ivory with moist surface
  • Healing time 21-28 days
  • Scarring may be present; genetically predetermined
39
Q

Deep Partial Thickness/2nd Degree

A
  • Destruction of epidermis and dermis, leaving only skin appendages (hair follicles, sweat glands)
  • Skin function absent
  • Tactile and pain sensors intact but diminished
  • Blisters may appear but most commonly is layer of flat, dehydrated “tissue paper” that lifts off in sheets
  • After debridement, wound is mottles w/ areas of waxy white, dry surfaces
  • Healing time 30 days to many months
  • High incidence of scarring, influenced by genetics; skin grafting may be necessary
40
Q

Full Thickness/3rd Degree

A

Destruction of epidermis, dermis, and underlying subcutaneous tissue. Very severe burns of this type can involve muscle and bone

  • Skin function absent
  • Tactile and pain sensors absent
  • No blisters
  • Appearance after debridement varies
  • Will not heal on own, skin grafting necessary
41
Q

Primary MODS

Multiple organ dysfunction syndrome

A

Organ injury directly associated with specific insult (ischemia or impaired perfusion from an episode of shock or trauma, thermal injury, soft tissue necrosis, invasive infection)

  • Stress response initiated
  • Neutrophils and macrophages “primed” by cytokines, which can be activated by a secondary insult, resulting in……Secondary MODS
  • These neutrophils and macrophages are putting on all their gear and are ready to fight
42
Q

Secondary MODS

Multiple organ dysfunction syndrome

A

Progressive organ dysfunction as a result of excessive inflammatory reaction in organs distant from the site of initial injury

  • Often the second insult is mild but produces an immense and disproportionate response due to the previous priming of leukocytes
  • Interaction of injured organs leads to self-perpetuating inflammation
43
Q

Neurotransmitters involved in schizophrenia

A

Etiology: Exact cause is unknown

Neurodevelopmental/Neuroanatomic factors

  • Synapse formation and maintenance; white matter connectivity
  • Enlargement of lateral and third ventricles; widening of frontal cortical fissures and sulci
  • Reductions in the thalamus and temporal lobe (which includes the amygdala, hippocampus, and parahippocampal gyrus)

Excessive activation of CNS receptors for dopamine

Insufficient activation of CNS receptors for glutamate

44
Q

Neurotransmitters involved in depression

A

Monoamine hypothesis of depression

  • Functional insufficiency of monoamine neurotransmitters

Neuroendocrine dysregulation

  • Hypothalamic-pituitary-adrenal (HPA) system dysregulation
  • Hypothalamic-pituitary-thyroid (HPT) system dysregulation
  • Hypothalamic-pituitary-gonadal (HPG) system dysregulation
45
Q

Positive symptoms of schizophrenia

A

Positive symptoms -too much of something-

  • Exaggeration or distortion of normal function
  • Hallucinations
  • Delusions
  • Agitation
  • Tension
  • Paranoia
46
Q

Negative symptoms of schizophrenia

A

Negative symptoms -too little of something-

  • Loss or diminution of normal function
  • Lack of motivation
  • Poverty of speech
  • Blunted affect
  • Poor self-care
  • Social withdrawal
47
Q

Depression

A

Most common psychiatric disorder

1 in 8 adults is depressed at any given time in the US

  • Incidence in women twice as high as that in men

Risk of suicide is high with depression

Often untreated

Symptoms:

  • Depressed mood
  • Loss of pleasure or interest
  • Insomnia (or sometimes hypersomnia)
  • Anorexia (or sometimes hyperphagia)
  • Mental slowing and loss of concentration
  • Feelings of guilt, worthlessness, and helplessness
  • Thoughts of death and suicide
  • Overt suicidal behavior
  • Symptoms must be present most of the day, nearly every day, for at least 2 weeks
48
Q

Bipolar

A
  • Formerly known as manic-depressive illness, etiology unknown
    • Cause may be disruption of neuronal growth and survival
  • Afflicts an estimated 3.7% of the adult population
  • Requires chronic-lifelong therapy
  • Characterized by recurrent fluctuations in mood
    • Cyclic disorder
    • Recurrent fluctuations in mood
    • Episodes of mania and depression persist for months without treatment
  • Presents in adolescents, early adulthood
  • Four mood episodes: pure manic, hypomanic, major depressive, mixed
49
Q

ANTIPSYCHOTICS

A

Used for diverse spectrum of psychotic disorders

  • Schizophrenia, delusional disorders, bipolar disorders, depressive psychoses, and drug-induced psychoses
  • Also used to suppress emesis and to treat Tourette’s syndrome and Huntington’s chorea

Should not be used to treat dementia in the older adult

First-generation antipsychotics (FGAs) or conventional antipsychotics

  • Block receptors for dopamine in CNS
  • Cause serious movement disorders known as extrapyramidal symptoms (EPS)
  • Classification by potency
    • Low potency; Medium potency, High potency

Second-generation antipsychotics (SGAs) or atypical antipsychotics

  • Produce only the moderate blockade of dopamine receptors; stronger blockade for serotonin
  • LOWER EPS risk, high metabolic effects
50
Q

SELECTIVE SEROTONIN REUPTAKE INHIBITORS (SSRIS)

A

Most commonly prescribed antidepressants

  • Bipolar disorder, Obsessive-compulsive disorder, Panic disorder, Bulimia nervosa, Premenstrual dysphoric disorder
  • Off-label uses: Post-traumatic stress disorder, social phobia, alcoholism, attention-deficit/hyperactivity disorder, Tourette’s syndrome, and obesity

Side effects: nausea, weight gain, agitation/insomnia, sexual dysfunction, serotonin syndrome (2-72 hours after treatment)

  • Altered mental status (for example, agitation, confusion, disorientation, anxiety, hallucinations, and poor concentration)
  • Incoordination, myoclonus, hyperreflexia, excessive sweating, tremor, and fever
  • Deaths have occurred
  • Syndrome resolves spontaneously after discontinuing the drug
  • Risk increased by concurrent use of MAOIs and other drugs
51
Q

BARBITURATES

A

CNS Depression

  • With increasing dosage, responses progress from sedation to sleep to general anesthesia

Cardiovascular Effects

  • At hypnotic doses, barbiturates produce modest reduction in blood pressure and heart rate.
  • Toxic doses can cause profound hypotension and shock
  • High doses depress the myocardium and vascular smooth muscle, along with other electrically excitable tissues

Induction of hepatic Drug-Metabolizing Enzymes

  • Stimulate synthesis of hepatic microsomal enzymes, the principal drug-metabolizing enzymes of the liver
  • As result, they can accelerate their own metabolism and the metabolism of many other drugs (this is achieved by promoting synthesis of porphyrin, which is converted to heme, which is incorporated unto cytochrome p450)
52
Q

BENZODIAZEPINES

A
  • Reduction of anxiety, anticonvulsant properties, muscle relaxant properties
  • Safe, effective and lack the undesirable properties that typify barbiturates and other hypnotics
  • Benzos have low abuse potential, cause minimal tolerance and physical dependence, present a minimal risk of suicide, and undergo few interactions with other drugs
  • Tolerance to hypnotic actions develops slowly, allowing them to be used nightly for several weeks without a noticeable loss in hypnotic effects
53
Q

Physical and psychological components of anxiety disorders

A

5 types:

  • Generalized anxiety disorder (GAD)
  • Panic disorder
  • OCD
  • Social anxiety disorder
  • PTSD

2 components:

  • Psychological (fear, apprehension, dread, uneasiness, tension)
  • Physical (tachycardia, dry mouth, fatigue, shortness of breath)
54
Q

Extrapyramidal symptoms

A

Due to blockade of D2 receptors

4 types of EPS3 are treatable with a variety of drugs (dystonias, Parkinsonism, akathisia)

  • Treat with Anticholinergic medication (e.g., benztropine and diphenhydramine)
  • Tardive dyskinesia (TD) - has no treatment

1. Acute dystonia (involuntary muscle contractions)

  • Oculogyric crisis (prolong involuntary upward deviation of eyes)
  • Opisthotonus (spasm of the muscles causing backward arching of the head, neck, and spine)
  • Joint dislocation
  • Impaired respiration

2. Parkinsonism: tremor, bradykinesia, rigidity, and postural instability

3. Akathisia: Pacing & squirming brought on by an uncontrollable need to be in motion

4. Tardive dyskinesia: Choreoathetoid movements of the tongue and face; lip-smacking movements; tongue flicks out in a “fly-catching” motion; slow, worm-like movement of the tongue; and involuntary movements of the limbs, toes, fingers, and trunk

55
Q

Prerenal AKI

A
  • Most common cause of AKI
  • Usually due to renal hypoperfusion (hypotension, hypovolemia, hemorrhage, low CO)
    • Shock, dehydration, vasoconstriction
  • Failure to restore blood volume (or BP) can cause cell injury and ATN (acute tubular necrosis)
56
Q

Intrarenal (Intrinsic) AKI

A

Results from ATN, acute glomerularnephritis, vascular disease, use of nephrotoxins, interstitial disease (drug allergy, infection, tumor)

  • Kidney tubule function decreased
  • Ischemia, toxins, intratubular obstruction
57
Q

Postrenal AKI

A

Rare

  • Caused by urinary tract obstruction
  • enlarged prostate
  • neurogenic bladder
58
Q

Acute Cystitis

A
  • Inflammation of the bladder, most common site of UTI in women of childbearing age
  • Bacteria: E.coli (80%)
  • S&S: urinary frequency, urgency, dysuria, suprapubic discomfort and LBP
  • Diagnosis: urinalysis (+ bacteria > 100k,+leukocyte esterase, + nitrite reductase), urine culture for species
  • Oral antibiotics
    • Treatment ranges from 1 day to 7 days
59
Q

Acute Bacterial Prostatitis

A
  • Causes: Indwelling catheter, instrumentation from urethral or prostate surgery
  • S&S: High fever, chills, myalgias, localized pain as well as UTI symptoms
  • Responds well to antimicrobial therapy usually a fluoroquinolone
60
Q

Acute Uncomplicated Pyelonephritis

A
  • Usually women of childbearing age, kids, elderly
  • Infection in one or both urinary tracts (ureter, renal pelvis, interstitium)
  • Shorter course of treatment
  • Usually symptomatic
  • Pathogen: E.coli (90%)
  • Treatment: oral antibiotics
61
Q

Complicated UTI

A
  • Males & females
  • Associated with a predisposing factor
    • Renal stones
    • Enlarged prostate
    • Indwelling catheter
    • Impediment to flow of urine
  • Longer course of treatment 3-7 days, may take as long as 14 days
  • Pathogen: E. coli
62
Q

Lab values commonly seen in patients w/ chronic renal failure (GFR, BUN, Creat)

A
  • Risk: 1.5-fold increase in serum creatinine, or GFR decreased by 25%, or UO <0.5 mL/kg/hr for 6 hrs
  • Injury: 2-fold increase in serum creatinine, or GFR decreased by 50%, or UO <0.5 mL/kg/hr for 12 hrs
  • Failure: 3-fold increase in serum creatinine, or GFR decreased by 75%, or UO <0.3 mL/kg/hr for 24 hrs or no UO for 12 hrs
  • End-stage renal failure: Complete loss of kidney function >3 mo (requiring dialysis or transplant)
63
Q

Functional units of the kidney

A

All the components of the nephrons contribute to URINE formation

  • Filtration
  • Reabsorption
  • Secretion
  • FiltersECF at glomerulus
  • Reabsorbsand secretesdifferent substances along tubular structures
  • Each kidney contains 1.2 million nephrons

Nephrons are the functional unit of the kidney

  • Renal corpuscle (Glomerulus + Bowman capsule)
  • Proximal convoluted tubule  Reabsorbs Na, K, Cl, H2O
  • Loop of Henle  Reabsorbs Na, K, Cl, H2O
  • Early distal convoluted tubule Reabsorbs Na, Cl
  • Late distal convoluted tubule/Collecting duct Reabsorbs H2O: exchange of Na for K with aldosterone; and with ADH
64
Q

Pathogens that most commonly cause UTIs

A

Community associated

  • E.coli (80%)

Hospital associated

  • Klebsiella, Enterobacter, Proteus
  • Catheter-associated urinary tract infection (CAUTI)
65
Q

Treatment for hyperphosphatemia in renal patients

A

Phosphate Binders for Dialysis Patients

Blood phosphate is high because glomerular filtration of phosphate is reduced

Can cause hyperparathyroidism—hypercalcemiaadded CV risk

Tx:

  • Reduce phosphate intake
  • Remove phosphate with dialysis
  • Use a phosphate binding drug

Phosphate Binding Drugs

  • Calcium-based
    • Ie. Calcium carbonate
    • Ie. Calcium acetate (PhosLo)
  • Calcium-free
    • Ie. Sevelamer hydrochloride (Renagel)
  • Both equally effective, all pose a risk for GI upset

Pharmacology (13 decks)

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