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Pharmacology > Medications for Infectious and Neoplastic Diseases and Endocrine Disorders > Flashcards

Medications for Infectious and Neoplastic Diseases and Endocrine Disorders Flashcards

1
Q

What is the body’s response to a hypoglycemic state?

A

decreased glucose signals the pancreas to release glucagon. Glucagon stimulates gluconeogenesis and glycogenolysis to release glucose into the plasma to restore glucose plasma levels.
Glycogen is broken down in to glucose

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2
Q

What is the body’s response to a hyperglycemic state?

A

increased glucose plasma levels signals the pancreas to release insulin. Insulin stimulates Glucose take up by cells in the liver and forms glycogen (Glucose>glycogen= glycogenesis ) Glucose levels return to normal.

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3
Q

What is the age/speed of onset, family hx, primary defect , etiology for type 1 and 2 Diabetes

A

1: young onset, abrupt, negative family hx, autoimmune. Primary defect = destruction of Beta cells that secrete insulin
2: older onset, gradual, family hx usually present, unknown etiology heredity?, primary defect is tissue resistance and impaired insulin secretion. Majority of symptoms.

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4
Q

What are the insulin levels for Type 1 and 2 diabetes

A

I: reduced early in the disease and absent later

II: levels may be low (deficient) normal or high(resistance)

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5
Q

What is the treatment for type 1 DM and what makes glucose levels fluxuate?

A

insulin.

Infection, exercise caloric intake and insulin dose

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6
Q

what does a T1DM patient presentation look like ?

A

usually thin, malnourished
S/S: Polyuria, polydipsia, polyphagia, weight loss
keytosis is common 2/2 the break down of fats for energy utilization and keytones are left as byproduct

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7
Q

What are DM2 risk factors?

A

pro: obesity, sedentary, pro diabetes meds, aging, medical comorbidites
anti: balanced diet, lean, active, anti diabetes rx

risk fxs: fam hx, overweight
pacific islander, AA, Hispanic, pre diabetes, high BP, high lipids, diabetes with pregnancy >9lbs bb

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8
Q

What is the impairment in diabetes 2

A

impaired insulin secretion and tissue resistance

-As the dx progresses, secretion does not match the plasma glucose level
target tissue dont take up glucose
-Decr binding, receptors, and responsiveness
- beta cells decr production and secretion

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9
Q

what is the treatment for T2DM ?

A

ƒReduced caloric diet + exercise
ƒOral antidiabetic
ƒNon-insulin injectable agent with or without insulin

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10
Q

What does a T2DM presentation look like

A

Polyuria, polydipsia, polyphagia(may asymptomatic at first)
obese
keytosis in uncommon,

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11
Q

What are microvascular compilations of DM?

A 
Retinopathy
Nephropathy
-decr GFR and incr BP
Sensory and motor neuropathy
Gastroparesis
Amputations secondary to infection
Erectile dysfunction
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12
Q

What are macrovascular complications of DM?

A

CV risk
Peripheral vascular disease
Brain: TIA, Cognitive impatient, stroke, CVA

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13
Q

What are two acute medical emergencies you should watch out for with DM and how does this happen?

A
  • Diabetic Ketoacidosis (DKA)
  • Hyperosmolar Hyperglycemic State (HHS)

insulin circulation is poor which leads to counter regulatory levels of glucagon , catecholamines, growth hormone and cortisol. This leads to increase glucose production and impaired utilization by the peripheral tissues

  • Dehydration, E- abnormalities are caused 2/2 diuretic, lots of peeing.
  • coma seizure or death can happen by increased glucose levels
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14
Q

DKA is a concern for which population?

A

TYPE 1

  • blood glucose >250
  • pH <7.3
  • Plasma osmolality <320
  • large increase in keytones
  • breath may smell sweet, rotten apples or nail polish
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15
Q

HHS is a concern for which population?

A

type 2

  • blood glucose >600
  • pH >7.3
  • Plasma osmolality >320
  • minimal/ no change in keytones
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16
Q

A patient is weak, SOB, N/V, is hyperglycemic and has fruity breath. What your be wrong and what should you do?

A 
DKA - emergency situation 
Signs &amp; Symptoms 
•hyperglycemia
•High ketone levels in your urine &amp; blood
•Abdominal pain
•Weakness or fatigue
•Shortness of breath
•Fruity-scented breath
•Confusion
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17
Q

A patient has Blood sugar level of ≥ 600, what could be the cause and what shoudl you do?

A 
HSS, this is a medical emergency 
•Blood sugar level of  ≥ 600 mg/dL
•Excessive thirst
•Dry mouth
•Increased urination
•Warm, dry skin
•Fever
•Drowsiness, confusion
•Hallucinations
•Vision loss
•Convulsions
•Coma
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18
Q

How do you Dx Dm?

A 
Glucose levels are tested on 2 seprate occasions with HbA1c, a measuremetn of longterm glucose and no need to fast, or a fasting glucose test. 
Diabetes if:
HbA1c >6.5
Fasting >126
oral glucose> 200
Normal id 5.7, <99, <139
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19
Q

How often do patients check their blood glucose levels

A

Therapies vary widely:
ƒMetformin monotherapy: possibly ~1-2x/week
ƒT1DM on intensive insulin therapy: ≥ ~8x/day

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20
Q

What are target values for blood glucose?

A

ƒBefore meals: ~90-130 mg/dL

ƒAt bedtime: ~100-140 mg/dL

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21
Q

What are 4 different types of insulin preparation drugs?

A

ƒInsulin lispro (short, duration, rapid acting)
ƒRegular insulin (short duration, slower acting)
ƒNPH insulin (intermediate duration)
ƒInsulin glargine (long duration)

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22
Q

What drugs are Oral Insulin Secretagogues ?

A

ƒSulfonylureas

ƒMeglinitides (Glinides)

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23
Q

What does insulin do?

A

Insulin stimulates Glucose take up by cells in the liver and forms glycogen

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24
Q

What causes insulin to be released into the blood?

A

rise in blood glucose
- normally there is a close relationship btwn increased blood glucose and insulin secretion
-insulin has anabolic actions:
transport of G, Aminos, nucleotides and K

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25
When should you take Lispro? Regular insulin? NPH? Lantus ?
Lispro- one meal at a time (15 mins before or after) Regular insulin- with breakfast lunch and dinner 30mins before NPH- 2x day with break and dinner Lantus - 1-2x day regardless of meals
26
how is insulin administered ?
Sub subcutaneously with needle or pump or IV infussion
27
What are the symptoms of low blood sugar?
``` trembling pounding heart sweating hunger numbness/ tingling sleepy irritable headache VERY LOW confusion, blurred vision, difficulty speaking, seizure/coma ```
28
Your patient has a hypoglycemic episode, what should you do?
``` •Fast-acting oral sugar: glucose tablets, orange juice, non-diet soda, sugar cubes, honey, corn syrup •Patients should always have oral carbohydrates available •15/15 rule ~15g of carbohydrates: ƒ3-4 glucose tablets ƒ1 tube of glucose gel ƒ4 oz of juice ƒ4 oz sweetened soda ƒ5 life savers ```
29
What are factors/ reasons that a hypoglycemic issue can go undetected and which symptom wont be masked ?
ƒDiabetic Autonomic Neuropathy (DAN) ƒFrequent hypoglycemia ƒPatients using beta-blockers Tachycardia, palpitations, tremors can be masked, but sweating wont be. DONT USE HR AS EX INDICATOR, RPE is better
30
What and Who is metformin used for?
1st line tx for T2DM ↓ hepatic glucose production ↑ tissue response to insulin ↑ anaerobic metabolism of glucose in intestine Side effects: weight loss, GI symptoms—decrease appetite, nausea, diarrhea NOT HYPOGLYCEMIA
31
What and Who is Glimepiride used for?
T2DM, 2nd choice Promotes insulin secretion by pancreas •Side effects: **Hypoglycemia**, weight gain
32
What and Who is Meglitinides (Glinides) used for?
T2DM - 2nd line Promote insulin secretion Side effects: Hypoglycemia, weight gain
33
What and Who is Thiazolidinediones (TZDs/Glitazones) used for?
T2DM - 2nd line ↓ insulin resistance (i.e. ↑ glucose uptake by muscle & adipose tissue) ↓ hepatic glucose production similar to metformin but has SE Adverse effects: worsens heart failure, bladder cx, fractures, ovulation
34
Do we have to know the oterh drugs?
``` DPP-4 Inhibitors (Gliptins) DPP-4 Inhibitors (Gliptins) GLP-1 Agonists (Incretin Mimetic)* Amylin Mimetics* * hypoG concern SE ```
35
Your patient has DM, what questions should you ask them?
When was the last time they exercised? What signs and symptoms does the patient usually experience during a hypoglycemic episode? Does the patient have rescue food readily available?
36
What should you do if the patient has S/S of DM ?
``` Send to PCP if they do have it and they come in - ask about non pharma options -is their DM well controlled? -are they compliant with med regimen? ```
37
what hormones do the thyroid gland produce
T3 and T4 that are synthesized from iodide eliminated by the liver
38
What does the thyroid gland do?
regulates metaboism, growth and regulates energy by hormone secretion. More hormone is secreted in the cold, pregancy, and growth spurts.
39
What is the main defect in Hypothyroidism ?
The pituitary fails at stimulating the thyroid to make T1 and T3 . Slow metabolism. -↑TSH, ↓T3 and/or T4
40
What is the main defect in Hyperthyroidism ?
The negative feedback loop is impaired and too much thyroid hormone is made. Instead if the hormone signaling TSH and TRH to stop, it continues to be secreted. Hypermetobolism ↓TSH, ↑T3 and/or T4
41
A patient comes in with Bradycardia,Cold skin,Brittle hair,Hair loss,Low HR & temperature,Lethargy,Fatigue and Intolerance to cold, she most likly has
Hypothyroidism
42
Hypothyroidism can be treated with
Levothyroxine (Synthroid) •Side effects: acute overdose—tachycardia, angina, tremor, nervousness, insomnia, heat intolerance, sweating (signs are opp. of hypo) •Key Points: ƒNarrow therapeutic window ƒTake medication 30-60 minute BEFORE eating
43
Graves disease is hypo or hyperthyroidism and how is it treated?
Hyper | -Thyroid stimulating immunoglobulins (TSI)
44
What is a thyroid storm ?
life threatening patient presentation of hyperthyroid ƒProfound hyperthermia (>105 F) ƒSevere tachycardia ƒRestlessness ƒAgitation ƒTremor ƒCan lead to unconsciousness, coma, and heart failure
45
A patient presents with Tachycardia, Dysrhythmias Angina, CNS stimulation: nervousness, insomnia, rapid thought & speech, Muscle weakness & atrophy, Increased heat & body temperature, Intolerance to heat Warm & moist skin,Exophthalmos
hyperthyroidism- graves
46
What drugs would you expect to see in a patient's case for hyperthyroidism
•Drug: Methimazole(Tapazole), Propylthiouracil •MOA: ƒPrevents oxidation of iodide, thereby inhibiting incorporation of iodine into tyrosine ƒPrevents iodinated tyrosine from coupling SE: none really
47
what is the leading cancer caise of death in men and women
lungs
48
What is a common type of hormaonal drug used for breast cancer
tamoxifen- estrogen targeted
49
What characterizes a cell as a neoplastic cell
proliferation invasiveness formation of metastases immortality- 2/2 telomerase that perseveres telemeres and allows for repetitive division
50
How does cancer damage DNA ?
-activation of onco genes inactivation of tumor -suppression genes -carcinogens
51
what us the ratio of proliferating cells to G0 cells
The growth fraction high= proliferating cells > G0 low growth fraction= G0> proliferating cells - growth fraction is important bc cytotoxic drugs impact DNA synthesis and mitosis - bone marrow, hair, GI,have high growth fx and are inpacted by cytotoxic drugs
52
When should cancer tx be stopped
hard to tell when to stop, remission hits when signs are not clinically detectable - an obstacle to killing cancer is the simmilarity of host cells and cx cells
53
Is early detection hard to achieve ?
Cancers are usually advance by the time of detection. cervical cancer is caught early
54
Do solid tumors resping better or worse to treatment?
•Solid Tumors Respond Poorly: ƒLow growth fraction ƒpoor drug response ƒLarger tumors less responsive than smaller ones ƒDrug sensitivity can be improved with debulking ƒMore cells leave G0 and re-enter cycle: recruitment
55
What are p-glycoproteins ?
drug resistance can happen over the course of cancer tx - p-glycoproteins pump drugs out of cells and can cause drug resistance - Increased repair of drug-induced damage to DNA - this is a bad thing that leads to resistance
56
What are obstacles to successful chemo?
our own host defense cells are similar to cancer cells making detection and fighting difficult (same surface antigens) - solid tumors - drug resistance - normal cell toxicity - chemo may not work against dissimilar cells making broad spectrum drugs less effective
57
combo VS intermittent chemo
intermittent chemo focuses on cell repopulation and combo chemo is the admin of several drugs with diff MOAs and Side effects for minimal overlapping toxicities
58
What is Myelosuppression and what does it cause
↓ WBC, RBC, platelets due to bone marrow suppression
59
What is Neutropenia and what does it cause
↑ incidence & severity of infection 2/2 ↓ WBC | - this is one of the most serious complcation of chemo anddevelops a few days after dose lasting days for the NADIR -
60
What is the nadir ?
essentail time of ↓ WBC where infection may occur. Look for fever and refer. Normal for chemotherapy: 2500 –7500 cells/mm3
61
What is Thrombocytopeniaand what does it cause
↓ platelets can lead to nose and gum bleeds | - make sure pts dont fall and dont give NSAIDS
62
What are other side effects of chemo ?
Anemia, less common, V/N, diarrhea, stomatitis, Alopecia, Fetal malformation, reproductive toxicity
63
CLINICAL PEARLS for Pt and Chemo
- screen, report is somthing suspicious is found - have compassion - communicate with oncologist - rehab is complex, be flexible - Practice clean hand hygien and clean surfaces and equipment - watch for red flags - sometimes care is palliative
64
what is Hyperuricemia
↑ uric acid | formed by breakdown of DNA following cell death
65
what is a Local Injury from Extravasation of Vesicants?
Iv meds must be placed properly bc leakage can lead to necrosis.
66
Can selective toxicity target 1 type of cell?
yes - no injury to host no injury to other cells
67
how does selective toxicity work?
- breaks cell wall - enzyme inhibition - stops bacterial protein synthesis
68
Antimicrobial drugs can be classified by narrow and broad, whats the difference?
Narrow (ideal )vs. broad spectrum (sepsis with blood culture)
69
What is the difference btwn bacterialcidal and Bacteriostatic
Bactericidal- directly lethal with right concentration | Bacteriostatic- slows bacteria growth then host defenses kick in
70
How do microbes form resistance?
- ↓ drug concentration - altered molecules that drug targets - antagonist production - drug inactivation
71
How does the use of an antibiotic form Drug-Resistant Microbes?
naturally, there is competitve environment that balances out microbies; no single microbe dominates bc they kill each other off - the introduction of a antibiotic favorable select one microbe to thrive bc the drug will kill off sensitive microbes. - selection pressure favors over growth of resistant microbes.
72
Shoudl we use narrow or broad spectrum antibiotics
narrow- so we kill less completing organisms without narrow, health associated infections can occur and lead to super infections. Therfore we need to ID the infecting organism and employ choice drug 1st
73
Penicillin - can it be used on MRSA? Is it safe for a majority or Patients?
-PCN -usually safe -1% have adverse rxns to cephalosporins - cross reactivity -Very effective - does not work on MRSA -As cephalosporin generations go up (1st to use vs 5th to use) ↑ activity against gram-negative bacteria and anaerobes ↑ ability to reach cerebrospinal fluid (CSF)
74
What is MRSA? is it the same as HCS-MRSA?
Gram postive bacteria - genetically different from MRSA - transmitted thro person - person contact •(Health care)HCA-MRSA is more prevalent than CA-MRSA (community based)
75
Who would you be more concerned to contract MRSA ?
``` A patient that is -compromised - old -dialysis - ICU prolonged antibiotic therapy - catheter - in longterm care facility ```
76
Is Ca-MRSA commonly found on the skin?
yes, most young people are carriers but show no symptoms - spread peron- person or infected surfaces - manifests as bois, abcess, impetigo
77
What types of patient profile would you expect to see CA-MRSA in?
contact sports men who have sex with men people in close quarters
78
Can good hand hygine kill MRSA and fight infection rates
Yes. Soap and water are enough. | C-diff infections needs bleach.
79
Is a Carbapenem the same as a Cephalosporins
no. Diff MOAs SE for carba include GI iratation and have more adverse rxns vs cephalo - carba are broad spectrum
80
When should vancomyosin be used
severe c-diff, MRSA, serious infections
81
When is someone susceptible to c-diff?
After prolonged antibiotic use
82
when is Doxycycline used and for what?
- infection bacterial -Tetracyclines MOA protein synthesis inhibitor -Bacterial growth suppressor - bacterio static - SE: GI symptoms: N/V/D, C. diff infection - take with water avoid milk
83
What is Erythromycin, what is it used for?
- infection bacterial like in Upper respiratory tract - Macrolides - MOA protein synthesis inhibitor - SE: GI effects—epigastric pain, N/V/D
84
What is Clindamycin, what is it used for?
Use: severe strep throat, MOA:inhibits protein synthesis Adverse effects: C. diff infection diaherra
85
What is Gentamicin, what is it used for?
Aminoglycosides E-coli infections MOA: bacterial protein disruption -Adverse effects: Ototoxicity, renal toxicityƒHigh-pitched tinnitus, HA, impaired balance
86
What are Fluoroquinolones adn thier associated risks?
the -"Cins" - enzyme inhibotor - Se: c-diff, tendinopathy, phototoxicity - median time of onset of tendon effects 6 days (early as 2 hours as late as 6 months) - majority in 1 month - DISCONTINUE USE AND CALL PCP -Achilles tendon is the most commonly affected, but others are susceptible -
87
which Fluoroquinolones has the highest risk for tendon rupture? least? what is the rehab like ?
most: Ciprofloxacin least: Levofloxacin •Rehabilitation should involve a 2-phase approach ƒ1stphase: bracing and support to allow the tendon to recover from the chemical injury ƒ2nd phase: progressive loading
88
What are 2 red glaf to look out for when dealing with infections?
Osteomylitis and cellulitis
89
What is cellulitis ?
Pathogen gains entry into dermis through breaks in the skin - pt may have fever (100.4) and pimple looking thing, warmth, TTP, redness - **Unilateral **
90
How can you prevent and treat cellulitis?
``` 5-10 days of antibiotics prevent with regular foot checks dry skin care tx fungal infections - use compression socks for lymphedema - proper wound care ```
91
what is Osteomyelitis?
Inflammation of the bone caused by an infecting organism - LE most often affected - S/S, fever, drainage, redness, TTP, warmth loss of ROM,
92
How can you tx Osteomyelitis?
debridement, ID and use correct antibiotic,

Pharmacology (5 decks)

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