Flashcards in Final Deck (54)
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1
Risk factors of Osteoporosis
Smoking
Alcohol
Rheumatoid Arthritis
Disease states (IBD, other malabsorption syndromes, chronic hepatic disease)
Advanced age
Low body weight
History of fractures (including family history of hip fracture)
History of steroid treatment
Vitamin D and calcium deficiency
2
Role of estrogen in preventing osteoporosis
Decreased osteoclast activity (osteoclasts break resorb bone) and increased osteoblast activity
(osteoblasts build bone)
3
What are the side effects of estrogen and under what conditions is it beneficial?
Cardiac problems if taken 10+ years after menopause, breast CA, DVT, gallbladder, stroke
Women within 10 years of menopause can take estrogen to decrease risk of osteoporosis w/o increased
risk of cardiac problems
Indicated for postmenopausal osteoporosis, hot flashes, colon cancer, vasomotor issues during
menopause
4
What are the side effects of bisphosphonates and what should you look for in patients who have taken them for a long period of time?
ADR’s: ulcers, esophagitis, osteonecrosis of the jaw when administered intravenously in cancer patients,
Patients taking drug for ~10 years: rare atypical fractures with minimal impact preceded by dull aching
pain in the the thigh and groin
5
How often should a patient with Type 1 diabetes check their blood glucose level.
6 - 10 times daily (Preprandial, 2 hr postprandial, pre-bedtime, pre-exercise, before critical tasks such as
driving, when suspecting and after treating hypoglycemia, middle of night {once a month})
6
Where are the injection sites for insulin? What activities should be avoided after insulin injection? What increases absorption of insulin?
Injection sites → Upper lateral arms, abdomen, buttocks, upper lateral thighs
Avoid exercising muscles or massage in the area of the injection (Guest slides)
Increase absorption → heat (ambient or local), abdomen > leg and arm, exercise in general and/or exercising muscles near injection site (Gladson slides)
7
Name the different types of insulins and when would each be used.
Ultra short acting: take 5 min before meal, duration 3-5 hours, peaks at one hour (Lispro, Aspart)
Regular insulin: take 30 min before meal, duration 6-8 hours. Often used with intermediate. Peaks in 2
hours
Intermediate: NPH (neutral protamine hagedo insulin); Onset is 1-4 hours, peaks in 6-12 hours, duration
14-24 hours.
Peakless-long acting : mean onset of action is within 1 hour with a duration of close to 24 hr; has no peak
and instead mimics continuous infusion of rapid-acting regular insulin from a pump (Glargine)
Inhaled insulin (hard to regulate how much of drug you are inhaling so hard to tell how effective it is)
8
Ultra short acting
5 min before meal
3-5 hours
Peaks 1 hr
Lispro, Aspart
9
Intermediate
NPH (neutral protamine hagedo insulin)
1-4 hours
Peaks 6-12
Duration 14-24
10
Regular insulin
30 mins before meal
Duration 6-8 hours
Peaks in 2 hours
Often used with intermediate
11
Peakless long acting
Mean onset 1 hour
Duration 24 hours
No peak (mimic continuous infusion of rapid- acting reg insulin from pump)
Glargine
12
Inhaled insulin
Hard to regulate how much you are inhaling
13
Describe the different insulin regimens: Split and mixed, split and mixed with bedtime intermediate, multiple pre-meal injections with bedtime long acting
Split and Mixed: regular or short-acting insulin mixed with intermediate, given before breakfast and
dinner (2 injections)
Split and mixed with bedtime intermediate: For purposes of improving morning fasting reading control
the second intermediate-acting insulin can be held until bedtime (9:00PM) (3 injections-1 at breakfast, 1
at dinner, 1 intermediate at bedtime)
Normal glucose level is 80-120
If next morning blood glucose is 60 (low), need to decrease insulin dose at bedtime
If next morning blood glucose is 150 (high), need to increase
Multiple pre-meal injections and Bedtime Long Acting: good for maintaining blood glucose level (best is
continuous insulin pump) (The more injections the person takes, the more controlled blood glucose
should be)
14
What are the adverse effects of insulin?
Hypoglycemia-if amt of insulin is too high, missed meal, strenuous exercise.
Lipohypertrophy or lipoatrophy at injection site
Rebound hyperglycemia
Weight gain
15
Discuss the interaction between insulin and exercise and what type of exercise would have the least effect on glucose level?
What recommendations do you have for the newly diagnosed Type 1 patient who exercises every day
Exercise acts as insulin so take lower pre-exercise insulin dose and have a carb snack (40g) prior to
exercise
Aim for 150min aerobic exercise per week (non-consecutive days)
Blood sugar does NOT drop as much during sprint (less effect on glucose level) compared to aerobic
Hydrate during exercise
Check blood glucose levels before exercise and after
Might want to include 10s sprint at end of exercise to reduce post-exercise hypoglycemia
Exercise program must be individualized for particular pt
Pt must live a life of monotony (eat same food at same time of day, perform same exercises at the same time of day (helps pt predict/prepare for glycemic changes)
Always have simple sugar/glucose gel
16
Metformin
MOA
side effects
Metformin:
MOA: inhibits gene expression for gluconeogenesis (Improves glucose utilization in skeletal
muscle)
Side Effects: Modest weight loss; Does NOT cause hypoglycemia
17
Incretin Mimetics
Incretin Mimetics: glucagon-like peptide (GLP-1) analog, Protective effects on beta cells
Side Effects: nausea, vomiting, diarrhea, risk of mild to moderate hypoglycemia
18
Glitazones
MOA
side effects
Glitazones: Insulin sensitizers, Improves insulin resistance, Improves lipid and cholesterol levels (May alsodelay progression of disease)
○ Side Effects: Fluid retention, weight gain, inc risk of fxs
19
Pipeptidyl
MOA
Side effects
Pipeptidyl: competitively inhibit DPP-4 enzyme, slows incretin degradation-potentiating glucagon-like
peptide-1 (GLP-1) and glucose-dependent insulinotropic peptide (GIP)
○ Side Effects: nasopharynigitis, nausea
20
What is the tx for hypoglycemia
1. Eat 15 grams of carbohydrate
2. Recheck glucose level in 15 min
3. If reading is not above 70, eat another 15 g Test again in 15 min,
4. if not above 70 consume another 15 g of CHO and call MD
5. 15 grams = 4oz. Of juice or soda (not diet), 1Tbl of table sugar, honey, orange juice—any simple sugar
(non a complex CHO)
21
What confirms the diagnosis of diabetes?
Prediabetes: FBG 100-126, A1c 5.7-6.4%
Diabetes: FBG >126, A1C >6.5%
22
What is diabetic ketoacidosis?
Without insulin to shuttle sugar into cells for usage, the body breaks down fat as fuel, resulting in a
buildup of acid in the bloodstream called ketone, eventually leading to ketoacidosis; can be due to exercise because exercise decreases insulin release
23
What is the mechanism of action of commonly used antidepressants?
1. Inhibition of serotonin re-uptake
2. Inhibition of the re-uptake of both serotonin and norepinephrine
3. Stimulation of nor-adrenergic and dopaminergic activity
4. Alpha 2 antagonism of nor-adrenergic and serotonergic neurons.
24
What are the adverse effects of commonly used antidepressants-SSRIs vs. the TCAs?
SSRI ADRs: Insomnia, Sedation, Appetite Change, Nausea, Dry mouth, Headache, Sexual Dysfunction
TCA ADRs:
-Anticholinergic: dry eye, mouth, constipation, urinary retention, blurred vision, AMS
-Histaminic – sedation, weight gain
- Alpha -1 adrenergic blockade - orthostatic hypotension, falls
-Possible EKG changes, arrhythmias (prolonged QT and PR, AV block) * In OVERDOSE=widened
QRS
-Require diet modification to avoid HTN crisis (avoid tyramine containing foods)
-Cannot be combined with other antidepressants (risk of serotonin syndrome) or sympathomimetic drugs; avoid with cough syrup or Demerol
-SERIOUS RISK OF OD- even one week’s supply can be lethal!
25
What is Serotonin Syndrome?
Generally the cause of too many serotonergic agents (polypharmacy)
Signs: agitation, diaphoresis, tachycardia, autonomic instability (htn common), clonus (more in LEs),
tremor (more in LEs), hyperreflexia (unique – can distinguish from other syndromes; more in LEs),
increased bowel sounds
Management:
o Discontinue agent/drug
o Supportive care (IV fluids, intubation, induce paralysis)
o Control agitation (benzodiazepines)
o 5-HT2A antagonists: cyproheptadine, olanzapine
o Control autonomic instability and control of hyperthermia
o Propranolol, bromocriptine, and Dantrolene are NOT recommended
26
Indications for Lithium and its side effects. What other drugs can be used as mood stabilizers?
Indications: mood stabilizer (common for bi-polar)
Side Effects: Tremors, Lethargy, Confusion, Seizures, Coma, Gastrointestinal effects (Nausea, Vomiting,
Crampy abdominal pain, Diarrhea)
Signs of serious toxicity: Altered mental status; Muscle fasciculations; Stupor; Seizures, Coma, Hyperreflexia,Cardiovascular collapse.
Needs to be monitored every 6mo (can be toxic to kidneys/thyroid)
-Other Mood Stabilizers: anti-convulsants, 2nd generation anti-psychotics
27
What is the neurobiology of Schizophrenia?
Dopamine Hypothesis: dopamine hyperactivity in the mesolimbic pathway causes the positive symptoms
of psychosis.
Glutamate Hypothesis: Faulty NMDA synapses on GABA interneurons in PFC cause overstimulation of
glutamatergic cortico-brainstem neurons and downstream over activation of mesolimbic dopaminergic
neurons.
○ Corticobrainstem glutamatergic neurons indirectly innervate the mesocortical dopaminergic
pathway, so the same faulty NMDA synapses on GABA interneurons in PFC cause hypo-activation
in the mesolimbic circuit, and therefore the negative symptoms of schizophrenia
28
What are the side effects of D2 receptor blockers? What are the differences between first and second generation antipsychotics. What are the side effects of antipsychotics: weight gain, decreased sweating,
Side effects of D2 receptor blockers (1st generation): more likely to cause mvmt problems and
hyperprolactinemia
● 1st Generation Antipsychotics (typical receptors): D2 blockade drugs; target mesolimbic (affects pos.
symptoms like hallucination) and mesocortical (affects neg. symptoms like impaired speech/motor
function/depression) but also affects 2 other tracts which may lead to rigidity, dyskinesia
● 2nd Generation Antipsychotics (atypical receptors): work at D2 receptors and serotonergic receptors (less
likely to cause mvmt problems and hyperprolactinemia than 1st generation drugs)
● There was no significant differences in effectiveness between 1st and 2nd generation antipsychotics
● Side Effects of Antipsychotics:
- First generation: more likely to cause mvmt problems and hyperprolactinemia
- Second generation: more likely to cause: HTN, metabolic syndrome, diabetes, wt gain
29
What is Neuroleptic Malignant syndrome?
Rare, but life threatening reaction to neuroleptic medications
● Cardinal Features:
○ Severe muscular rigidity
○ Hyperthermia (temp > 38 deg C)
○ Autonomic instability
○ Changes in level of consciousness
30
What is Tardive Dyskinesia
Unwanted/involuntary movements of the mouth, jaw, and face
May be caused by use of antipsychotics (FGAs)
31
What is the mechanism of action of Baclofen and Botox and what would be the criteria for their use? How long does it take for Botox to start working?
Botox MOA: Prevent Ach release at alpha motor nerve ending
Botox Indications: spasticity, migraines, dystonia, eye mvmt abnormalities, comedic
How long does Botox start working: 48- 72 HOURS
Baclofen MOA: binds to GABAs receptor, blocks influx of Ca+ into presynaptic terminal → reduced neurotransmitter release and membrane hyperpolarization
Baclofen Indications: spasticity: spinal cord injury and MS in adults (No clear improvement of gait or ADL’s)
32
What is the pathophysiology of Alzheimers? What categories of drugs are used in its treatment?
AD pathophysiology: Excessive amount of tau/inadequate Tau clearance; Excessive beta amyloid
production
-Brain shrinkage, loss of cholinergic neurons in frontal cortex, amyloid plaques, and intraneuronal
neurofibrillary triangles made up of Tau protein
Treatment: Blocking acetylcholinesterase enzyme to make more Ach present
-Acetylcholinesterase inhibitors (AChEI’s): prevents breakdown of ACh
-Glutamate modulators: modulates glutamine by antagonizing NMDA receptor
Behavioral treatments:
-Environment: quiet, familiar, with labels on doors, and good lighting
-Depression: Use SSRI’s
-Agitation: use neuroleptics
33
What are the major categories of drugs used to treat Parkinson’s Disease(Dopamine agonists, L-dopa/carbidopa, anticholinergics)? Know their mechanism of action. What is the difference between L-dopa and dopamine? Why is carbidopa added to L-Dopa?
Dopamine agonist MOA:
- Activates dopamine receptors?
L-Dopa/Carbidopa MOA: replaces dopamine in CNS, with dopa decarboxylase inhibitor, which doesn’t cross the BBB and inhibits the conversion of levodopa to dopamine outside the brain ·
Anticholinergics MOA: decreases CNS acetylcholine and restores the balance between dopamine and acetylcholine
Diff b/w L-dopa and dopamine: Pure dopamine cannot cross the blood brain barrier, but L-dopa can.
Carbidopa added to L dopa: carbidopa inhibits enzymes that break down L-dopa
34
What are the common side effects of AEDs? Besides seizures, what other indication is there for AEDs.
Side effects of AEDs: SEDATION, Drowsiness, “Brain fog”, Depression, Dizziness
Other Uses of AEDs: Bipolar disorder, neuropathic pain, migraines, bipolar disorder
35
What is a positive screening test for intrathecal baclofen?
Drop in spasticity scale or hypotonia without respiratory difficulty
36
What is the difference between gram positive organisms and gram negative organisms? Be able to name the parts of the organism’s cell wall. What is a beta lactamase enzyme?
Gram positive: many layers of peptidoglycan strands (contain penicillin binding proteins and beta
lactamases
-Beta lactamase: bacterial enzymes that inactivate drugs (THIS IS BAD)
Gram negative: contains 2 membranes separated by periplasmic space; beta lactamases located in periplasmic space; outer membrane has aqueous channels where drugs can enter
Gram-negative is more difficult organism to treat than gram-positive organism
37
What is the major side effect of antimicrobials
C-diff
38
Know the difference between Bacterial cell wall inhibitors, Inhibitors of bacterial cell membrane function, and inhibitors of bacterial DNA/RNA synthesis in terms of their function
Bacterial cell wall inhibitors (beta lactams): inhibits linking of peptide and prevents linkage of structural
components of cell wall
Inhibitors of bacterial cell membrane function: destroys cell membrane allowing escape of nutrients
Inhibitors of bacterial DNA/RNA synthesis:
-Fluoroquinolones: inhibit DNA gyrase enzyme preventing relaxation of supercoiled DNA (useful
against gram neg)
-Sulfonamides: interfere w/ production of folate which is necessary for production of purines and
DNA
39
Know the indications for Vancomycin.
Restart streptococci, staphylococci, c-diff, doc for methicillin resistant staphyococi
40
What is MRSA
MRSA: methicillin-resistant staphylococcus aureus (spreads through direct contact and can live on surface for 70+ days)
41
What are the side effects of fluoroquinolones.
Fluoroquinolones Side Effects: Cystic lesion in articular cartilage, tendon ruptures, long Q-T interval
42
Describe the lifecycle of the HIV virus.
HIV Lifecycle:
- Fusion of virus to the host cell surface receptor
- Surface glycoprotein (gp120) on HIV binds to receptors on T cells, macrophages, and dendritic
cells
-Penetration and un-coating exposing RNA
-Viral RNA converted to viral DNA by reverse transcriptase enzyme - Transcription of the host cell’s DNA and the viral DNA occurs and is followed by translation and production of viral proteins
-Protease enzyme hydrolyzes the newly formed proteins into smaller units and assembles them w/ viral RNA to produce new virions
-Budding and release of new HIV particles
43
Major drug classification used to control HIV
Fusion inhibitors, nucleoside reverse transcriptase inhibitors, non-nucleoside reverse transcriptase inhibitors, protease inhibitors, integrase inhibitors
44
What is the role of beta lactamase inhibitors?
Block the beta lactamase enzymes that attack our drugs (inhibitors prevent the breakdown of these bad
enzymes)
45
What is the difference between adjuvant and neoadjuvant therapies?
Neoadjuvant therapy: when CA mass is too large to eliminate initially w/ surgery, so therapy is used to shrink tumor so that they can do radiation therapy or surgery once the mass is smaller (done with breast and colon cancers)
Adjuvant therapy: for pts who are diagnosed w/ CA and have surgery to remove it
46
What are the main side effects of almost all chemotherapy agents, acute and long term?
1. Malnourishment
2. Nausea/ diarrhea
3. Alopecia (hair loss)
4. Damage of GI epithelium
5. Fatigue, pain
6. Sterility
7. Cardiotoxicity
8. Depression in growth in children
9. Organ toxicity
47
Why might a PT treat someone on a Plant alkaloid (Taxanes)?
Plant alkaloids often produce paresthesias and foot or wrist drop.
48
What is the difference between tyrosine Kinase inhibitors and Mammaliam target of rapamycin?
-Tyrosine kinase inhibitors: work inside the cell to inhibit tyrosine kinase receptors (inhibit signaling
system that would lead to cell division)
-Mammalian target of rapamycin (MTOR) inhibitor: prevent MTOR from activating signaling pathways involved in angiogenesis and cell growth (inhibits angiogenesis so CA can’t feed itself)
49
What serious side effect of anthracycline should the PT be aware of?
Cardiac toxicity (can lead to heart problems over time) (pts get no more than 4 doses)
50
In very general terms, what is the role of Mabs, cytokines, cancer vaccines and colony stimulating factors in the treatment of cancer?
MABs (monoclonal antibodies): flag CA cells for destruction, block growth signals and receptors (prevents
angiogenesis-cuts off cell’s food supply
Cytokines: stimulate T cell growth and help them get “revved” up (provides immune system boost)
CA vaccines: delay/stop CA cell growth, cause tumor shrinkage, prevent CA from recurring, eliminate CA cells that have not been killed by other treatments
-Autologous CA vaccines: derived from pt-specific materials/cells (customized to pt-most costly)
-Allogeneic CA vaccines: not-pt specific (off the shelf) (target tumor-specific antigen common to
CA)
Colony stimulating factors: helps regenerate neutrophil recovery following myelosuppressive therapy to
minimze extent of pt’s nadir and reduce infection
51
What is neutropenia? When should chemotherapy be held? What are risk factors for neutropenia?
Neutropenia – low white blood cell count, most common chemo dose-limiting side effect
When should chemo be held: when neutrophil count drops below 500mm^3 and/or platelet count below
100,000/mm^3
Do NOT treat if you (therapist) have an active active infection/cough/fever
Risk Factors: age, female, malnutrition, open wounds, comorbidities (hepatic and renal dysfunction), hx of
neutropenia, type of chemo (combined modality), dose intensity, extensive previous chemo, radiation
52
What signs of infection should you be looking for when treating patients on chemotherapy?
GI (mucositis, diarrhea), Respiratory tract (cough, dyspnea, abnormal breath sounds), Urinary tract
(dysuria, frequency, urgency, color/odor changes), indwelling devices (site redness, edema, tenderness, warmth), skin/mucous membranes (redness, edema, tenderness, warmth), generalized (flu-like, fever, chills, myalgia, malaise, fatigue)
Fever >38dgrC is most reliable sign of infection in pts with neutropenia
Septic shock from neutropenia has high mortality rate so do NOT let a fever go untreated!
53
What are risk factors for thrombocytopenia? What are some clinical signs of this condition?
Thrombocytopenia: low platelet count
Risk factors: myelosuppressive chemotherapy, radiation therapy, bone marrow involvement, DIC, fever,
concomitant disease, nutrition deficiencies
Clinical Signs: petechiae/bruising, overt bleeding, enlarged liver/spleen, occult/overt blood in stool/urine, headaches, hypotension, tachycardia, prolonged menstruation
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