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1130 Cards in this Set
- Front
- Back
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Sodium
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Sodium 135-145 mEq/L
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Potassium
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Potassium 3.5-5 mEq/L
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Calcium 8.5-10.5
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Calcium 8.5-10.5 mmol/dl
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pH
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pH 7.35 – 7.45
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Oxygen saturation
|
95-100 mmHg
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PCO2
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35-45 mmHg
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HCO3
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18-23 mmol/L
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White Blood Cell Count (WBC)
|
4,500-10,000/mcL
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Glycosylated hemoglobin (HbA1c)
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4-5.9% >7=uncontroled glucose levels
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Total Cholesterol
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160-200
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Blood Urea Nitrogen (BUN)
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8-20
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Blood Glucose (fasting)
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70-120 mg/dL
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Serum Creatinine
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0.5-2.0 mg/dl
>2 signals Renal problems |
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GFR (Urinalysis)
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100-130 ml/min/1.73m2
< 90 stage 1 Renal failure |
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Urine Specific Gravity (Urinalysis)
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1.003-1.030
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INR
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0.8-1.2 (normal) 2-3 (therapeutic) INR and PT are used to determine therapeutic effectiveness of warfarin (Coumadin)
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Digoxin
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0.8 to 2.0 ng/ml
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Lithium
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0.5 to 1.5 mEq/L
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Dilantin
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10 - 20 mcg/mL
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Theophylline
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10 - 20 mcg/mL
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Temperature (PO)
|
36.3 - 37.3 °C (97.3-99.1 °F)
Above 100 = fever |
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Blood Pressure (adult systolic)
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90–120 mmHg
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Blood Pressure (adult diastolic)
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60–80 mmHg
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Heart Rate (adult)
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60-100 beats/min
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Respiration rate (adult)
|
12–20 breaths per minute
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Sodium
|
135-145 mEq/L
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Potassium
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3.5-5 mEq/L
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Chloride
|
95-105 mEq/L
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Calcium
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8.5-10.5 mmol/dl
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Magnesium
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1.5-2 mEq/L
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pH
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7.35 – 7.45
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PO2
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75-100 mmHg
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Oxygen Saturation
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95-100 mmHg
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PCO2
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35-45 mmHg
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HCO3
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18-23 mmol/L
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Alanine transaminase (ALT)
|
30- 65 U/L
In healthy individuals, ALT levels in the blood are low. When the liver is damaged, ALT is released into the blood stream, which results in high ALT levels. Causes: Hepatitis Cirrohosis Ischemia Tumor of liver Ischemia Viral hepatitis Infectious Mononucleosis, or myopathy. Congestive Heart Failure Liver damage Bile Duct problem |
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Aspartate transaminase (AST)
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6 - 40 IU/L
When liver or muscle cells are injured, AST is released into the blood. AST test detects liver damage. Causes: Alcoholic Hepatitis Cirrhosis Acute hepatitis Diabetes Hepatitis Viruses Jaundice |
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Alkaline phosphatase (ALP)
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20 to 140 IU/L
Maybe used to determine liver or bone disorders. Pregnant women, growing children and people with healing fractures may also show a temporary increase in ALP levels Causes: Liver cancer Cirrhosis Hepatitis Paget's disease Rheumatoid arthritis |
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Creatine kinase (CK)
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60 and 400 IU/L
Present in Muscle damage The doctor may order CK isoenzymes or a CK-MB as follow-up tests, to distinguish between the three types (isoenzymes) of CK: CK-MB (found primarily in heart muscle), CK-MM (found primarily in skeletal muscle), and CK-BB (found primarily in the brain; when present in the blood, it is primarily from smooth muscles, including those in intestines, uterus or placenta). |
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Myoglobin
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Female 1-66, male 17-106
Myoglobin may be ordered as a cardiac biomarker, along with troponin, to help diagnose or rule out a heart attack. Levels of myoglobin start to rise within 2-3 hours of a heart attack or other muscle injury, reach their highest levels within 8-12 hours, and generally fall back to normal within one day. An increase in myoglobin is detectable sooner than troponin, but it is not as specific for heart damage and it will not stay elevated as long as troponin. |
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Troponin-I
Troponin-T |
Troponin-I less than 10 µg/L
Troponin-T 0–0.1 µg/L Troponin tests are primarily ordered to evaluate people who have chest pain to see if they have had a heart attack or other damage to their heart. Either a cardiac-specific troponin I or troponin T test can be performed; usually a laboratory will offer one test or the other. Troponin tests are sometimes ordered along with other cardiac biomarkers, such as CK–MB or myoglobin. However, troponins are the preferred tests for a suspected heart attack because they are more specific for heart injury than other tests (which may become positive in skeletal muscle injury) and remain elevated for a longer period of time. |
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Brain natriuretic peptide (BNP)
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160-200
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HDL cholesterol
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35-80 mg/dL
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LDL cholesterol
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80-120 mg/dl
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Thyroid stimulating hormone
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(TSH) 0.3 to 3.0 μIU/mL
The TSH test is used to check thyroid function and/or symptoms of hyperthyroidism or hypothyroidism. It is usally ordered with a T4 test. A T3 may also be ordered. |
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Hemoglobin (Hb)
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men 138 to 180 g/L women 121 to 151 g/L
The hemoglobin test may be used to screen for, diagnose, or monitor a number of conditions and diseases that affect red blood cells (RBCs) and/or the amount of hemoglobin in blood. |
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Hematocrit (Hct)
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45% for men and 40% for women
To determine the proportion of the blood that is made up of red blood cells (RBCs), and help diagnose, or monitor conditions that affect RBCs. |
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Glycosylated hemoglobin(HbA1c)
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4-5.9 % Hb
Used to monitor glucose control of diabetics over a period of 2-3 months. The goal is to keep A1c 6% or under. |
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White Blood Cell Count (WBC)
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4,500-10,000 /mcL
High counts are associated with : Infections, Inflammation Leukemia Conditions that result in tissue death (necrosis) such as trauma, burns, surgery or heart attack Allergic responses Low counts are associated with: Bone marrow damage and disorders Lymphoma Autoimmune disorders Overwhelming infections |
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CD4+ cells
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500-1200 cells/mm3
CD4 is the main target of HIV, once the count is 200 or under a diagnosis of AIDS is given. |
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IgA
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70-360
one of the most common of the five major classes of immunoglobulins; the chief antibody in the membranes of the gastrointestinal and respiratory tracts |
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IgD
|
0.5-3.0
Not completely understood, but seems share the role of activating B-cells with IgM. |
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IgE
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0.01-0.04
IgE's main function is immunity to parasites such as parasitic worms. IgE also plays an essential role in type I hypersensitivity, which which include allergic diseases, such as allergic asthma, allergic rhinitis, food allergy, and some types of chronic urticaria and atopic dermatitis and anaphylactic reactions to certain drugs, bee stings, and antigen preparations used in specific desensitization immunotherapy. |
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IgG
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800-1800
Infection control of body tissues, including viruses, bacteria, and fungi. |
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IgM
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54-220
They are found in blood and lymph fluid and are the first type of antibody made in response to an infection. They also cause other immune system cells to destroy foreign substances |
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Thrombocyte/Platelet count
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(150 – 400) × 103 per mm3
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Prothrombin time (PT)
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12-13 seconds laboratory dependent
The prothrombin time (PT) and its derived measures of prothrombin ratio (PR) and international normalized ratio (INR) are measures of the extrinsic pathway of coagulation. Commonly used to check the therapeutic levels of warfarin (Coumadin), |
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INR
|
0.8-1.2 (normal) (therapeutic)2-3
The prothrombin time (PT) and its derived measures of prothrombin ratio (PR) and international normalized ratio (INR) are measures of the extrinsic pathway of coagulation. Commonly used to check the therapeutic levels of warfarin (Coumadin), |
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Activated partial thromboplastin time (PTT/ aPTT)
|
30-50s laboratory dependent
Used to monitor the treatment effects of heparin, and similar anticoagulant |
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Blood Urea Nitrogen
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8-20
The liver produces urea in the urea cycle as a waste product of the digestion of protein. BUN is an indication of renal health |
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Blood Glucose (fasting)
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70-120 mg/dL
8 hours after eating |
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Serum Creatinine
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100-130 ml/min/1.73m2
1) CKD Stage 1 – GFR >90mL/min/1.73m2 with evidence of kidney damage 2) CKD Stage 2 (Mild) – 60- 89 mL/min/1.73m2 with evidence of kidney damage 3) CKD Stage 3 (Moderate) – 30 - 59 mL/min/1.73m2 4) CKD Stage 4 (Severe) –15- 29 mL/min/1.73m2 5) CKD Stage 5 Kidney failure - GFR < 15 mL/min/1.73m2 |
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CKD Stage 1
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1) CKD Stage 1 – GFR >90mL/min/1.73m2 with evidence of kidney damage
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CKD Stage 2
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2) CKD Stage 2 (Mild) – 60- 89 mL/min/1.73m2 with evidence of kidney damage
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CKD Stage 3
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3) CKD Stage 3 (Moderate) – 30 - 59 mL/min/1.73m2
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CKD Stage 4
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4) CKD Stage 4 (Severe) –15- 29 mL/min/1.73m2
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CKD Stage 5
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5) CKD Stage 5 Kidney failure - GFR < 15 mL/min/1.73m2
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Urine Specific Gravity (Urinalysis)
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1.003-1.030
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Ketone Bodies (Urinalysis)
|
0
Its presence in urine is a sign of DKA |
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Digoxin
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0.8 to 2.0 ng/ml
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Lithium
|
0.5 to 1.5 mEq/L
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Dilantin
|
10 - 20 mcg/mL
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Theophylline
|
10 - 20 mcg/mL
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what is finkelstien test and what is it used to diagnose
|
pain with grasping thumb into palm_x000D_
_x000D_ used to dx de quervains tenosynovitis |
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a/w grape like vesicles in the vagina
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hyditiform mole
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a/w snow storm pattern on US of vagina
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hyditiform mole
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what are the two different type of hyditiform mole
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complete_x000D_
-46_x000D_ -empty egg and 2 sperm_x000D_ _x000D_ incomplete_x000D_ -69_x000D_ -egg and 2 sperm |
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what are the functions of B-hCG
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maintains the corpus luteum_x000D_
_x000D_ promotes male sexual differentiation_x000D_ _x000D_ stimulates maternal thyroid gland |
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what is the difference between gestational age and developmental age
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DA = since fertilization_x000D_
_x000D_ GA = since LNMP_x000D_ _x000D_ (GA is 2 weeks longer) |
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what is Nageles rules for dating
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LNMP - 3 months + 7 days
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what are the features of fetal hydantoin syndrome and what causes it
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caused by phenytoin or carbamazepine_x000D_
_x000D_ hypoplastic nails_x000D_ cleft palate_x000D_ vit K def |
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when is a baby considered term
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38-42 weeks
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when is a baby considered preterm
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25-37 weeks
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what type of somatoform disorder is pseudocyesis
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conversion
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what causes the damage in iron poisoning
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lipid peroxidation and free radicals
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what is the order that parity is written in
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T-PAL_x000D_
_x000D_ Term_x000D_ Pre term_x000D_ Abortions_x000D_ Living children |
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what must be ruled out in in hyperemesis gravidarum
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hyditiform mole_x000D_
_x000D_ choriocarcinoma |
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what cells produce B-hCG and where are they derived from
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syncytiotrophoblasts_x000D_
_x000D_ progenitor villous cytotrophoblast cells |
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when does B-hCG begin to be produced
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8 days after fertilization
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what is the best initial test to dx pregnancy
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B-hCG
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what test confirms a pregnancy
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US_x000D_
- transvaginal earlier than transabdominal |
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what is done to prevent or treat 1st trimester abortions caused by incompetent cervic
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cervical cerclage
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what cardiology physiologic changes are seen in pregnancy
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increased HR_x000D_
_x000D_ decreased BP |
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what respiratory physiologic changes are seen in pregnancy
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increased O2 consumption_x000D_
_x000D_ increased tidal volume and minute ventilation |
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what is a common SE of amniocentesis
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amniotic fluid embolism
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low PAPP-A is a/w
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trisomy 18 and 21
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what is a/w banana sign on US
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compressed cerebellum_x000D_
_x000D_ a/w neurotube defect |
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what should be done next is a triple or quad screen are found to be abnormal
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US to confirm date_x000D_
_x000D_ then an amniocentesis |
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a/w_x000D_
increased B-hCG_x000D_ decreased AFP_x000D_ decreased estriol |
trisomy 21
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a/w_x000D_
decreased B-hCG_x000D_ decreased AFP_x000D_ decreased estriol |
trisomy 18
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what are braxton hicks contractions
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contraction without dilation in the 3rd trimester
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why is chorionic villous sampling indication
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known genetic disease in parents_x000D_
mother > 35 yo_x000D_ abnormal US |
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why is amniocentesis indicated
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known genetic disease in parents_x000D_
mother > 35 yo_x000D_ abnormal quad screen |
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what test is used for rapid karyotype analysis
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cordocentesis
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when would MTX therapy for ectopic pregnancy be contraindicated
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immunodeficient px_x000D_
liver or renal disease_x000D_ ectopic larger than 3.5cm_x000D_ presence of fetal heart beat_x000D_ coexisting intrauterine pregnancy_x000D_ currently breast feeidng |
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what is intrauterine fetal demise
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fetal death after 20 weeks
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what is abortion
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fetal death before 20 weeks_x000D_
(or a fetus that weighs <500g) |
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how should intrauterine fetal demised be evacuated
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before 24 weeks D/C_x000D_
after 24 weeks PGE2, pisoprostal, oxytocin |
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what is the next step in diagnosing an abortion
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US
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what is the next step after threatened abortion is diagnosed
|
reassure_x000D_
_x000D_ follow up with US a week later |
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what is the Rx for septic abortion
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immediate surgical evacuation_x000D_
_x000D_ levofloxacin and metronidazole |
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what is used during twin delivery to convert 2nd twin from transverse to oblique position
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internal podalic version
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what is the only difference in monozygotic twins
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finger prints
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how is cervical length a/w preterm birth
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>35 mm = decreased risk_x000D_
_x000D_ <35 mm = increased risk |
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what is preterm labor
|
contractions and dilation before 37 weeks
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what is PROM
|
rupture of chorioamniotic membrane before 37 weeks_x000D_
_x000D_ gush of fluid from vagina)" |
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what is cervical incompetence
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painless dilation of cervix w/o contraction
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when should preterm labor NOT be stopped
|
preeclampsia and ecclampsia_x000D_
maternal cardiac disease or hemorrhage_x000D_ cervical dilation more than 4cm_x000D_ fetal death_x000D_ chorioamnionitis_x000D_ PROM |
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what should be done if preterm labor occurs and you dont want to deliver
|
give betamethasome or dexamethasone_x000D_
_x000D_ followed by Mg sulfate or CCB |
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how can Mg toxicity be checked for
|
depressed deep tendon reflexes
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what are the most feared complications of Mg toxicity
|
respiratory depression_x000D_
_x000D_ cardiac arrest |
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what are the complications of PROM
|
preterm labor_x000D_
_x000D_ cord prolapse_x000D_ _x000D_ placental abruption_x000D_ _x000D_ chorioamnionitis |
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how can chorioamnionitis risk be decreased in PROM
|
decreasing the amount of examinations
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Rx for chorioamnionitis
|
clindamycin and gentamycin
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how can maternal and fetal blood be differentiated
|
Apt test
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what heart tracings is vasa previa a/w
|
sinusoidal_x000D_
-tachycardia to bradycardia |
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Rx for vasa previa
|
crash c section
|
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what is the next step in placenta previa is preterm
|
betamethasone_x000D_
_x000D_ tocolytics |
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what is the next step in placenta previa in term
|
schedule c section
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how is placental invasion Rx
|
c section followed by hysterectomy
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what is invaded in placenta accreta
|
superficial uterine wall
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what is invaded in placenta increta
|
myometrium
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what is invaded in placenta percreta
|
uterine serosa with_x000D_
bladder wall or rectal wall |
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what is placental abruption
|
separation of placenta from decidua basalis
|
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what must be done if placental abruption occurs during delivery and why
|
rapid delivery to avoid retroplacental hemorrhage which could cause DIC
|
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what is a concealed placental abruption
|
completely detached placenta_x000D_
_x000D_ blood remains within uterine cavity |
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what is a external placental abruption
|
partially detached placenta_x000D_
_x000D_ blood drains through cervix |
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what are the serious complications of a concealed placental abruption
|
DIC_x000D_
uterine tetany_x000D_ fetal hypoxia_x000D_ sheehan syndrome |
|
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what is uterine rupture
|
complete transection of uterus from endometrium to the serosa
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what c section has the highest risk factor for uterine rupture
|
classical (longitudinal)
|
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what placental invasion has the highest risk for uterine rupture
|
placenta percreta
|
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how can uterine rupture present
|
abnormal bump in abdomen_x000D_
_x000D_ regression of fetus_x000D_ _x000D_ mother may have a sudden relief of pain that then becomes diffuse pain |
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Rx for uterine rupture
|
immediate laparotomy with delivery of the fetus_x000D_
_x000D_ all future deliveries must be at 36 weeks by c section |
|
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what type of reaction is Rh incompatibility
|
alloimmunization_x000D_
isoimmunization |
|
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what is the typical situation for ABO incompatibility
|
mother = O_x000D_
baby = A or B |
|
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what is the MCC for RhoGAM not to work
|
too low of a dose
|
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what is used as a qualitative test to see maternal fetal hemorrhage
|
rosette test
|
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what is used to determine the amount of fetal blood in maternal blood stream
|
klehauer betke stain
|
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what is transient or late HTN of pregnancy
|
HTN during second half of pregnancy or later_x000D_
_x000D_ w/o proteinuria |
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what is chronic HTN of pregnancy
|
HTN before 20 week of gestation_x000D_
_x000D_ w/o proteinura |
|
|
Dx_x000D_
chronic HTN of pregnancy that later develops prtoeinuria |
chronic HTN with superimposed preeclampsia
|
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what is gestational HTN
|
HTN that starts after 20 week of gestation
|
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what is preeclampsia
|
HTN after 20 week_x000D_
_x000D_ edema_x000D_ proteinuria |
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what must chronic HTN or pregnancy be differentiated from
|
molar pregnancy
|
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what are the symptoms for severe preeclampsia
|
>160/110_x000D_
_x000D_ >5g per 24 hours in urine_x000D_ _x000D_ impaired mental status, liver function and vision_x000D_ _x000D_ generalized edema_x000D_ _x000D_ oliguria_x000D_ _x000D_ thrombocytopenia |
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what is the pathophys of preeclampsia
|
vasospasm
|
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what causes the seizures in eclampsia
|
cerebral vasospasm leading to cerebral hypoxia
|
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Rx for ecclampsia
|
deliver if_x000D_
->34 weeks_x000D_ -lungs are mature_x000D_ -maternal or fetal deterioration |
|
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what causes the pain in HELLP syndrome
|
distention of hepatic (Glissons) capsule
|
|
|
what is seen histologically in the liver
|
centrilobular necrosis and hematoma formation
|
|
|
what causes fetal thyrotoxicosis in maternal graves disease
|
IgG autoAb cross placenta
|
|
|
how is gestational diabetes evaluated
|
screen 24-28 weeks with glucose load_x000D_
_x000D_ if >140 after 1 hour do glucose tolerance_x000D_ _x000D_ if any 2 are abnormal it is diagnostic_x000D_ -1 hour > 180_x000D_ -2 hour > 155_x000D_ -3 hour >140 |
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what is IUGR
|
fetus weighs in 10% for gestational age
|
|
|
what are the characteristics of symmetric IUGR
|
brain is proportional to body_x000D_
occurs before 20 weeks gestation_x000D_ caused by fetal factors |
|
|
what are the characteristics of asymmetric IUGR
|
brain weight is not decreased_x000D_
occurs after 20 weeks_x000D_ caused by maternal factors |
|
|
what is the most preventable cause of IUGR
|
smoking
|
|
|
how can IUGR be diagnosed
|
US_x000D_
-fundal hieght is atleast 3 cm smaller_x000D_ -abdominal circumference is best because it differentiates symmetric from asymmetric |
|
|
what is macrosomia
|
birth weight >4500g
|
|
|
what is the only way multiple gestations can be delivered
|
vertex vertex
|
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|
how is macrosomia Dx
|
screened with fundal height >3cm greater than gestation age_x000D_
_x000D_ confirmed with US |
|
|
how is macrosomia Rx
|
C section
|
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|
MCC of nonreassuring nonstress test
|
sleeping baby
|
|
|
what should be done in a nonreassuring nonstress test
|
vibroaccoustic stimulation
|
|
|
when and why is a NST performed
|
high risk pregnancy 32-34 weeks
|
|
|
when is a contraction stress test done
|
equivical NST or BPP_x000D_
_x000D_ assess uteroplacental dysfunctipn |
|
|
what is a contraction stress test
|
oxytocin challenge to see if it induces movement
|
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|
what is done if a BPP = 6
|
contraction stress test
|
|
|
what is done is BPP = 4
|
delivery
|
|
|
what is the next step in nonreassuring HR
|
oxygen_x000D_
change maternal position_x000D_ discontinue uterotonic drugs |
|
|
what is the most serious and dangerous deceleration
|
late
|
|
|
what is the cause of early decelerations
|
head compression -> vasovagal response
|
|
|
what is the cause of variable deceleration
|
umbilical cord compression
|
|
|
what is the cause of late decelerations
|
uteroplacental insufficiency ->hypoxia -> acidosis
|
|
|
what kind of contractions are not a/w with labor
|
irregular intervals_x000D_
_x000D_ do not shorten_x000D_ _x000D_ do not increase in intensity |
|
|
what are some epidural anesthesia SE
|
urinary retention_x000D_
hypotension_x000D_ decreased CO |
|
|
what is luchia rubra
|
first days bloody discharge
|
|
|
what is luchia serosa
|
3-4 days_x000D_
pale discharge |
|
|
what is luchia alba
|
3-4 days_x000D_
white yellow discharge |
|
|
what is prolonged latent stage
|
long time to reach 4 cm_x000D_
_x000D_ > 20 hours in primipara_x000D_ > 14 hours in multipara |
|
|
what is protracted cervical dilation
|
slow dilation during active stage_x000D_
_x000D_ < 1.2 cm per hour in primipara_x000D_ <1.5 cm per hour in multipara |
|
|
what is arrest of cervical dilation
|
no dilation for 2 hours
|
|
|
what is arrest of fetal descent
|
no descent for 1 hour
|
|
|
what is the MCC of arrest disorders
|
cephalopelvic disproportion
|
|
|
what is used to extract fetal head in breech delivery
|
piper forceps
|
|
|
Rx for breech
|
self correct by week 37_x000D_
_x000D_ if not perform external cephalic version_x000D_ _x000D_ if not perform c section |
|
|
Dx_x000D_
mother has bilateral discharge of clear, yellow, green or brown fluid |
galactorhea
|
|
|
what should be checked with suspected galactorrhea
|
prolactin TSH
|
|
|
what should be suspected in turtle sign_x000D_
(head is delivered and then retracts) |
shoulder dystocia
|
|
|
what is post partum hemorrhage
|
bleeding more than 500mL after delivery
|
|
|
MCC of postpartum hemorrhage
|
uterine atony
|
|
|
Rx for postpartem hemorrhage
|
1- check for ruptured uterus or retained placenta_x000D_
_x000D_ 2- compression massage_x000D_ _x000D_ 3- oxytocin_x000D_ _x000D_ 4- crystalloid fusion if BP is <90_x000D_ _x000D_ 5- blood products may be given (FFP, PRBC)_x000D_ _x000D_ 6- hysterectomy |
|
|
MC soft tissue sarcoma in children
|
rhabdomyosarcoma
|
|
|
what causes breast milk jaundice
|
factor in human milk increases bilirubin enterohepatic circulation
|
|
|
Rx for breast milk jaundice
|
switch to formula for a couple days
|
|
|
time period for breast milk jaundice
|
3 weeks and beyond
|
|
|
what causes breast feeding failure jaundice
|
insufficient coloric intake
|
|
|
time period for breast feeding failure jaundice
|
first week
|
|
|
Rx for breast feeding failure jaundice
|
increase breast feeds
|
|
|
presentation for milk protein intolerance
|
vominting and blooding diarrhea that contains RBCs and eosinophils
|
|
|
milk protein intolerance is a/w
|
atopic disorders
|
|
|
fractures highly suggestive of abuse
|
ribs_x000D_
skull_x000D_ various stages |
|
|
Dx_x000D_
child who was growing normally suddenly slows growth at 1 year but eventually reaches normal hieght |
constitutional growth delay
|
|
|
MCC of short stature and pubertal delay
|
constitutional growth delay
|
|
|
Dx_x000D_
8 yo child wakes up in the middle of the night with pain that resolves in the morning |
growing pains
|
|
|
Rx for growing pains
|
massage_x000D_
_x000D_ analgesics |
|
|
normal newborn respiratory rate
|
40-60
|
|
|
what is breast milk helps in gastric emptying
|
whey protein
|
|
|
what are the benefits of breast feeding
|
less reflux_x000D_
_x000D_ less colic_x000D_ _x000D_ better absorption |
|
|
what decreases in breast milk with each feed
|
protein
|
|
|
what is the main protein in breast milk
|
whey
|
|
|
what should be down if IV access cannot be obtained in pediatric px
|
intraosseous access_x000D_
_x000D_ can only be used for 24-48 hours |
|
|
what is dacrocystitis
|
nasolacrimal duct obstruction
|
|
|
Dx_x000D_
chronic tearing and mattering that resolves with massage of lacrimal duct |
dacrocystitis
|
|
|
when does chemical irritation of the eye occur
|
0-2 days
|
|
|
when does gonorrhea infection of the eye occur
|
2-7 days
|
|
|
when does chlamydia infection of the eye occur
|
7-21 days
|
|
|
when does herpes infection of the eye occur
|
over 21 days
|
|
|
what causes chemical irritation of the eye
|
silver nitrate
|
|
|
Rx for chemical irritation of the eye
|
resolve sin 24 hours
|
|
|
what eye problems are prevented with ointment given at birth
|
gonorrhea
|
|
|
what is put in eye soon after birth
|
erythromycon_x000D_
tetracycline_x000D_ silver nitrate |
|
|
what clotting factor deficiencies commonly cause purpura
|
vWD_x000D_
_x000D_ hemophilia A and B |
|
|
features of cephalohematoma
|
doesnt cross suture lines_x000D_
_x000D_ presents days later_x000D_ _x000D_ subperiosteal hemorrhage |
|
|
features of caput succedaneum
|
crosses suture lines_x000D_
_x000D_ seen immediately after birth_x000D_ _x000D_ echymotic swelling of the scalp |
|
|
what are nuclear remnants within RBC
|
howell jolly bodies
|
|
|
what do howell jolly bodies stain with
|
wright stain
|
|
|
what are oxidized hemoglobin
|
heinz bodies
|
|
|
what do heinz bodies stain with
|
crystal violet
|
|
|
what is deficient in galactosemia
|
G1PUT
|
|
|
features of galactossemia
|
cataracts_x000D_
jaundice_x000D_ hypoglycemia_x000D_ convulsions |
|
|
features of uridyl diphosphate galactose 4 epimerase def
|
cataracts_x000D_
jaundice_x000D_ hypoglycemia_x000D_ convulsions_x000D_ hypotonia_x000D_ nerve deafness |
|
|
what is used to detect Phe products in urine of those with PKU
|
gluthrie test
|
|
|
what causes redness, swelling and fever after a DTaP
|
pertussis part
|
|
|
when should the Hep B vaccine be given
|
shortly after birth_x000D_
_x000D_ except in those that wiegh less than 2kg (4lbs) |
|
|
what newborns should recieve the HBIG
|
those with HBaAg positive mothers
|
|
|
what causes transient polycythemia of newborn
|
hypoxia (MCC delayed cord clamping)
|
|
|
when does transient tachypnea require evaluation
|
if more than 4 hours work up for sepsis_x000D_
_x000D_ blood and urine cultrues |
|
|
MCC of brachial palsy
|
macrosomic baby
|
|
|
when do the sinuses develop
|
maxillary and ethmoid are present at birth_x000D_
_x000D_ sphenoid within first few years_x000D_ _x000D_ frontal by 9-10 yo |
|
|
which brachial palsy is a/w horner syndrome
|
klumpke
|
|
|
MCC of clavicular fracture
|
shoulder dystocia
|
|
|
biggest problem of oligohydramnios
|
cord compression
|
|
|
MCC of induced labor and c section
|
cord compression
|
|
|
until when is bed wetting normal
|
5 yo
|
|
|
what is the first step in management of a hiatal hernia
|
intubate _x000D_
_x000D_ orogastric tube placement |
|
|
where is AFP made
|
liver_x000D_
_x000D_ GI tract |
|
|
what is omphalocele a/w
|
trisomy 18
|
|
|
MCC of elevated AFP
|
incorrect dating
|
|
|
what is the cause of umbilical hernia
|
weakness of rectus abdominis
|
|
|
what is umbilical hernia a/w
|
congenit hypothyroidism
|
|
|
Rx for umbilical hernia
|
resolves spontaneously by 3_x000D_
_x000D_ surgical intervention by 4 |
|
|
MC abdominal mass in children
|
wilms
|
|
|
WAGR is caused by a deletion in
|
chromosome 11 PAX6
|
|
|
MC site of wilms metastasis
|
lungs
|
|
|
wilms tumor arises from
|
metanephrose
|
|
|
what is the best initial test to diagnose wilms
|
abdominal US
|
|
|
what is the most accurate test to diagnose wilms
|
CT with contrast
|
|
|
features of wilms
|
hematuria_x000D_
HTN_x000D_ doesnt cross midline_x000D_ no horners |
|
|
features of neuroblastoma
|
no hematuria_x000D_
no HTN_x000D_ horners syndorme_x000D_ crosses midline |
|
|
what is a/w wilms tumor
|
denys drash _x000D_
beckwith wiedemann |
|
|
features of beckwith weidemenn
|
hypoglycemia_x000D_
macroglossia_x000D_ visceromegaly_x000D_ omphalocele_x000D_ wilms tumor |
|
|
MC cancer of infancy
|
neuroblastoma
|
|
|
MC extracranial solid malignancy
|
neuroblastoma
|
|
|
a/w bag of worms
|
varicocele
|
|
|
what does neuroblastoma prognosis depend on
|
N-myc protooncogene and hyperdiploidy
|
|
|
what causes spermatocele
|
dilation of efferent ductules
|
|
|
Dx_x000D_
painless fluid filled cyst that transiluminates |
spermatocele
|
|
|
what causes vericocele
|
dilation of pampiniform plexus
|
|
|
what are hallmark signs of neuroblastoma
|
hypsarrythmia (dancing eyes)_x000D_
_x000D_ opsoclonus (dancing feet) |
|
|
cause of hydrocele
|
remnant tunica vaginalis
|
|
|
how is vesicoureteral reflux diagnosed
|
VCUG
|
|
|
how is posterior urethra valve diagnosed
|
VCUG
|
|
|
what is hypospadias a/w
|
cryptorchidism_x000D_
_x000D_ inguinal hernias_x000D_ _x000D_ 5a reductase def |
|
|
what is epispadias a/w
|
urinary incontinence_x000D_
_x000D_ bladder extrophy |
|
|
which cyanotic heart lesion depend on PDA
|
transposition of great vessels_x000D_
_x000D_ hypoplastic LH |
|
|
what are the cyanotic heart lesions
|
Ts
|
|
|
what are the R-L shunts
|
Ts
|
|
|
what are the acyanotic heart lesions
|
3 letters and coarctation
|
|
|
what are the L-R shunts
|
3 letters and coarctation
|
|
|
MC cyanotic heart lesion in children
|
TOF
|
|
|
what are at increased risk for TOF
|
cri du cht_x000D_
_x000D_ trisomys |
|
|
MCC of cerebral palsy
|
cerebral anoxia
|
|
|
child with trauma to soft palate is at increased risk for
|
acute stroke syndrome_x000D_
_x000D_ due to compression or dissection of carotid |
|
|
a/w boot shaped heart
|
TOF
|
|
|
how are all cyanotic heart lesions Dx
|
X ray_x000D_
_x000D_ most accurate is echocardiogram |
|
|
a/w single S2
|
TOGV_x000D_
TA_x000D_ TOF_x000D_ tricuspid atresia_x000D_ hypoplastic LH |
|
|
MC cyanotic heart lesion in neonates
|
TOGV
|
|
|
a/w egg on string x ray
|
TOGV
|
|
|
a/w pulsus bigeminus
|
hypertrophic obstructive cardiomyopathy
|
|
|
a/w pulsus bisferiens
|
aortic regurg
|
|
|
a/w pulsus tardus et parvus
|
aortic stenosis
|
|
|
a/w pulsus paradoxus
|
cardiac tamponade _x000D_
_x000D_ tension pneumothorax |
|
|
increased risk factor for TOGV
|
aperts_x000D_
cri du chat_x000D_ trisomys |
|
|
features of TOF
|
overriding aorta_x000D_
pulm stenosis_x000D_ right ventricular dilation_x000D_ VSD |
|
|
features of hypoplastic LH
|
LV hypoplasia_x000D_
mitral valve atresia_x000D_ aortic valve lesions |
|
|
presents with gray cyanosis at birth
|
hypoplastic LH
|
|
|
x ray shows globular shaped heart
|
hypoplastic LH
|
|
|
a/w biventricular hypertrophy
|
TA
|
|
|
what is the most severe sequela of TA
|
pulmonary HTN
|
|
|
MC congenital heart lesion
|
VSD
|
|
|
how are acyanotic heart lesions Dx
|
best initial is echcardiogram_x000D_
_x000D_ most diagnostic is cardiac catheterization |
|
|
a/w paradoxical splitting
|
LBBB
|
|
|
how is VSD treated
|
75% close by 10yo_x000D_
_x000D_ surveilence with echocardiogram until then |
|
|
MCC of ASD
|
osteum secundum defect
|
|
|
a/w fixed wide split S2
|
ASD
|
|
|
what is the only congenital heart defect that doesnt develop endocarditis
|
ASD
|
|
|
when is PDA a normal finding
|
forst 12 hours
|
|
|
which heart lesions radiate to the back
|
pulmonary and tricuspid
|
|
|
MCC of secondary HTN in children
|
fibromusculr displasia
|
|
|
Rx for kawasaki
|
aspirin for fever and arthralgia_x000D_
-if life long, needs influenza vaccine_x000D_ _x000D_ IVIG to prevent coronary aneurysms |
|
|
a/w pear shaped heart
|
pericardial effusion
|
|
|
a/w jug handle appearance
|
primary pulmonary artery HTN
|
|
|
a/w 3 like appearance
|
coarctation of aorta
|
|
|
MC location for coarctation of aorta
|
ligamentum arteriosus
|
|
|
what happens if coarctation is proximal to left subclavian artery
|
pressure is higher in the right arm
|
|
|
when is jaundice pathologic in newborns
|
appears in first 24 hours_x000D_
rises by more than 5mg per day_x000D_ bilirubin rises above 19.5_x000D_ direct bilirubin rises above 2_x000D_ hyperbilirubin persist after 2 weeks of life |
|
|
Rx for pathologic jaundice of newborn
|
phototherapy_x000D_
_x000D_ exchage transfusion if rises above 20 |
|
|
Dx _x000D_
drooling, regurgitation or vomiting during feeds |
esophageal atresia
|
|
|
best initial test for esophageal atresia
|
coiling NG tube on x ray
|
|
|
Dx_x000D_
patient with recent URI follwed by sore throat, hot potatoe voice and neck stiffness |
retropharyngeal abscess
|
|
|
best initial test for retropharyngeal abscess
|
x ray shows widening between trachea and spine
|
|
|
what confirms a retropharyngeal abscess
|
CT
|
|
|
best initial test for pyloric stenosis
|
abdominal US
|
|
|
most accurate test for pyloric stenosis
|
GI series
|
|
|
Dx_x000D_
palpable olive shaped mass in epigastrium |
pyloric stenosis
|
|
|
what can be seen in upper GI series of pyloric stenosis
|
string sign_x000D_
shoulder sign_x000D_ mushroom sign_x000D_ railroad track sign |
|
|
a/w doughnut sign
|
intussusception
|
|
|
what is choanal atresia
|
membrane between nostrils and pharyngeal space prevents breathing during feeding
|
|
|
Dx_x000D_
child turns blue when feeding and pink when crying |
choanal atresia
|
|
|
best initial test for choanal atresia
|
passing NG tube
|
|
|
confirmation test for choanal atresia
|
CT with intranasal contrast shows narrowing of pterygoid plate
|
|
|
first step in management of choanal atresia
|
secure airway
|
|
|
a/w explosive stool on rectal exame
|
hirschsprung
|
|
|
what is charge syndrome
|
coloboma of the eye_x000D_
heart defect_x000D_ atresia of chanae_x000D_ retardation in growth and development_x000D_ genitalurinary defects_x000D_ ear anomolies |
|
|
best initial test for hirschsprung
|
x ray
|
|
|
best diagnostic test for hirschsprung
|
full thickness biopsy
|
|
|
what is vecterl syndrome
|
vertebral anomolies_x000D_
anal atresia_x000D_ cardiovascular anomolies_x000D_ tracheoesophageal fistula_x000D_ esophageal atresia_x000D_ renal anomolies_x000D_ limb anomolies |
|
|
choanal atresia is a/w
|
charge syndrome
|
|
|
imperforate anus is a/w
|
vacterl syndrome
|
|
|
defect in duodenal atresia
|
improper canalization
|
|
|
what isduodenal atresia a/w
|
annular pancreas_x000D_
_x000D_ down syndrome |
|
|
what is the best initial test for duodenal atresia
|
x ray
|
|
|
a/w double bubble
|
duodenal atresia_x000D_
_x000D_ volvulus |
|
|
first step in management of duodenal atresia
|
IVF
|
|
|
presentation in volvulus
|
vomiting with bile_x000D_
blood stained stools_x000D_ abdominal distention |
|
|
a/w birds beak
|
volvulus
|
|
|
best initial treatment for volvulus
|
endoscopic decompression
|
|
|
most effective therapy for volvulus
|
surgical decompression_x000D_
(used if endoscopic decompression fails) |
|
|
a/w currant jelly stools
|
intussusception
|
|
|
a/w sausage mass
|
intussusception
|
|
|
MC location for intussusception
|
ileocecal junction
|
|
|
common causes of intussusception
|
polyp_x000D_
lymphoma_x000D_ hamartoma_x000D_ enlarged mesenteric node_x000D_ enlarged peyer patches_x000D_ meckels diverticulum |
|
|
best initial test for intussusception
|
US
|
|
|
a/w target sign
|
intussusception
|
|
|
most accurate test for intussusception
|
barium/air enema
|
|
|
therapeutic steps in intussusception
|
1- fluid resuscitation_x000D_
_x000D_ 2- NGT decompression_x000D_ _x000D_ 3- barium/air enema_x000D_ _x000D_ 4- surgery |
|
|
what kind of tissue is found in meckels diverticulum
|
gastric or pancreatic
|
|
|
what is meckels diverticulum
|
incomplete obliteration of omphalomesenteric duct (viterlline duct)
|
|
|
Dx_x000D_
1 year old boy with painless rectal bleeding |
meckels diverticulum
|
|
|
what is the most accuarate test for meckels diverticulum
|
technetium 99m scan
|
|
|
Dx_x000D_
infant with excessive crying for more than 3 hours, more than 3 days, for more than 3 months |
infantile colic
|
|
|
Rx for infantile colic
|
probiotics_x000D_
_x000D_ simethicone |
|
|
a/w increased gastric residual volume
|
necrotizing enterocolitis
|
|
|
a/w pneumatosis intestinalis
|
necrotizing enterocolitis
|
|
|
how does IDM develop RDS
|
hyperinsulin antagonizes the actions of cortisol on the lungs
|
|
|
what pathologies are a/w IDM
|
caudal regression_x000D_
TOGV_x000D_ duodenal atresia_x000D_ small left colon_x000D_ anencephaly_x000D_ neurotube defects |
|
|
what is increased in 21 hydroxylase def
|
17 a hydroxyprogesterone
|
|
|
how can 21 hydroxylase def be confirmed
|
ACTH stimulation test
|
|
|
MCC of congenital hypothyroidism
|
thyroid dysgenesis
|
|
|
a/w palpable step off at lumbosacral area
|
spondyllolisthesis
|
|
|
what is spondylolithessi
|
forward slip of vertebral L5 over S1_x000D_
_x000D_ slow development of back pain and neurological dysfunction |
|
|
what are some common findings of rickets
|
craniotabes_x000D_
_x000D_ rachitic rosary (beading of ribs)_x000D_ _x000D_ large anterior fontanelle_x000D_ _x000D_ harrison groove (horizontal depression on lower border of chest) |
|
|
Rx for rickets
|
calcitrol_x000D_
_x000D_ ergocalciferol |
|
|
MCC of neonatal sepis
|
GBS
|
|
|
how can GBS be diagnosed in a mother who has already recieved antibiotics
|
latex agglutination
|
|
|
what should be done in a new born suspected of having sepsis
|
lumbar puncture and blood cultures
|
|
|
best initial test to diagnose toxoplasmosis
|
IgM
|
|
|
best initial test to diagnose syphilis
|
VDRL or RPR
|
|
|
best initial test to diagnose CMV
|
urine or saliva viral titers
|
|
|
best initial test to diagnose herpes
|
tzanck smear
|
|
|
best initial test to diagnose varicella
|
tzanck smear
|
|
|
most accurate test to diagnose toxoplasmosis
|
PCR
|
|
|
most accurate test to diagnose syphilis
|
FTA ABS or dark field microscopy
|
|
|
most accurate test to diagnose CMV
|
urine or saliva PCR
|
|
|
most accurate test to diagnose herpes
|
PCR
|
|
|
most accurate test to diagnose varicella
|
viral culture
|
|
|
most accurate test to diagnose measles (rubeola)
|
IgM Ab
|
|
|
MCC of infantile febrile seizures
|
HSV 6 (roseola)
|
|
|
features of measle (rubeola)
|
cough coryza conjunctivitis_x000D_
_x000D_ rash spreads from head to toe_x000D_ _x000D_ koplik spots |
|
|
what can cause upper airway compression by a vascular ring
|
double aortic arch_x000D_
right sided aorta_x000D_ pulmonary sling |
|
|
tracheal compression symptoms that are worse when supine and relieved by extending the neck
|
upper airway compression by vascular ring
|
|
|
how is foreign body aspiration treated and diagnosed
|
direct laryngoscopy and rigid bronchoscopy
|
|
|
what causes croup
|
parainfluenza
|
|
|
triad of croup
|
barking cough (horseness)_x000D_
_x000D_ caryza_x000D_ _x000D_ inspiratory stridor |
|
|
a/w steeple sign
|
croup
|
|
|
a/w narrowing of air column in the trachea on x ray
|
croup
|
|
|
a/w lateral x ray showing subglottic narrowing
|
croup
|
|
|
how is croup Rx
|
mild symptoms = steroids_x000D_
_x000D_ severe symptoms = racemic epi_x000D_ _x000D_ finally intubate if all fail |
|
|
a/w unilateral tonsilar swelling with uvualr deviation
|
peritonsilar abscess
|
|
|
when is HiB vaccine needed
|
those younger than 5_x000D_
_x000D_ asplenics |
|
|
MCC of epiglotitis in unvaccinated
|
HiB
|
|
|
MCC of epiglotitis in vaccinated
|
Strep
|
|
|
presentation of epiglotitis
|
hot potatoe voice_x000D_
_x000D_ drooling in tripod position_x000D_ _x000D_ cherry red epiglotis |
|
|
a/w thumb print sign
|
epiglotitis
|
|
|
Rx for epiglotitis
|
intubate_x000D_
_x000D_ ceftriaxone |
|
|
prophylaxis for epiglotitis close contacts
|
rifampin
|
|
|
MCC of chronic inspiratory noise in infants
|
laryngomalacia
|
|
|
Rx for laryngomalacia
|
improves slowly_x000D_
_x000D_ disappears by 2 years |
|
|
how is laryngomalacia diagnosed
|
laryngoscopy
|
|
|
what is seen in laryngoscopy of laryngomalacia
|
rolling in from side to side
|
|
|
what is the most contagious stage of whooping cough
|
catarrhal stage
|
|
|
when does post tussive emesis occur
|
paroxysmal stage
|
|
|
a/w butterfly pattern on xray
|
whooping cough
|
|
|
when should a px with whooping cough be isolated
|
first 5 days of Rx
|
|
|
how is whooping cough diagnosed
|
PCR of nasal secretions_x000D_
_x000D_ or _x000D_ _x000D_ toxin ELISA |
|
|
pathophys of whooping cough
|
causes ciliary paralysis
|
|
|
prophylaxis to close contacts of whooping cough
|
macrolides
|
|
|
Rx for whooping cough
|
erythromycin or azithromycin_x000D_
_x000D_ initially decrease infection_x000D_ after 2 weeks they reduce transmission |
|
|
what should never be done in diptheria infection
|
scrape
|
|
|
a/w productive cough lasting 7-10 days with fever
|
bronchitis
|
|
|
MCC of bronchitis in smokers
|
s pneumo_x000D_
_x000D_ H influ |
|
|
MCC of bronchitis in nonsmokers
|
viral
|
|
|
Rx for diptheria
|
antitoxin
|
|
|
a/w gray pseudomembrane plaques on back of throat
|
diptheria
|
|
|
a/w think greenish amniotic fluid
|
meconium aspiration syndrome
|
|
|
a/w displaced femoral epiphysis in obese adolescents
|
slipped capital femoral epiphysis
|
|
|
a/w a painful limp and an externally rotated leg
|
slipped capital femoral epiphysis
|
|
|
Rx for Slipped capital femoral epiphysis
|
internal fixation with pinning
|
|
|
a/w avascular necrosis of the femoral head
|
legg calve perthes disease
|
|
|
a/w asymmetric hips in a child
|
legg calve perthes disease
|
|
|
a/w proximal thigh atrophy in child
|
legg calve perthes disease
|
|
|
a/w breech infants with difficulty walking
|
congenital hip dysplasia
|
|
|
Rx for congenital hip dysplasia
|
<6m = pavlik harness_x000D_
_x000D_ 6m - 1 y = reduction with spica cast_x000D_ _x000D_ >2y reduction |
|
|
how is congenital hip dysplasia Dx
|
ortolani and Barlow meneuver_x000D_
_x000D_ causes click or clunk |
|
|
endocrine disfunction in prader willis
|
hypothalamic dysfunction_x000D_
-GH def_x000D_ -hypogonadism |
|
|
how is SIDS most prevented
|
sleepin in supine position
|
|
|
Rx for reyes syndrome
|
glucose_x000D_
_x000D_ FFP_x000D_ _x000D_ mannitol |
|
|
pathophys of reyes syndrome
|
diffuse mitochondrial injury_x000D_
-extensive fatty vacuolization of liver without inflammation |
|
|
barbiturates
|
phenobarbital_x000D_
pentobarbital_x000D_ methohexital_x000D_ thiopental_x000D_ thiamylal |
|
|
alpha-2 agonists
|
xylazine_x000D_
medetomidine_x000D_ detomidine |
|
|
benzodiazepines
|
diazepam_x000D_
clonazepam_x000D_ zolazepam_x000D_ midazolam |
|
|
dissociative anesthetics
|
ketamine_x000D_
tiletamine |
|
|
neuroleptics
|
phenothiazines: acepromazine, chlorpromazine_x000D_
_x000D_ butyrophenones: droperidol |
|
|
pure opioid agonists
|
morphine_x000D_
hydromorphone (oxymorphone)_x000D_ etorphine_x000D_ codeine_x000D_ dextromethorphan_x000D_ methadone_x000D_ carfentanil_x000D_ sufentanil_x000D_ fentanyl |
|
|
pure opioid antagonists
|
naloxone_x000D_
naltrexone_x000D_ diprenorphine |
|
|
mixed opioid agonists/antagonists
|
butorphanol_x000D_
buprenorphine |
|
|
miscellaneous opioids
|
loperamide_x000D_
apomorphine |
|
|
inhalational anesthesetics
|
halothane_x000D_
isoflurane_x000D_ sevoflurane_x000D_ nitrous oxide |
|
|
analeptics
|
doxapram_x000D_
strychnine_x000D_ theophylline_x000D_ aminophylline_x000D_ theobromine |
|
|
local anesthetics
|
esters: cocaine, proparacaine_x000D_
amides: lidocaine, bupivacaine, mepivacaine |
|
|
anticonvulsants
|
phenobarbital_x000D_
primidone_x000D_ diazepam_x000D_ clonazepam_x000D_ potassium bromide_x000D_ felbamate_x000D_ gabapentin |
|
|
phenobarbital
|
barbiturate_x000D_
_x000D_ used to tx seizure disorders in dogs & cats; occasionally used as oral sedative |
|
|
pentobarbital
|
barbiturate_x000D_
_x000D_ sedative agent, drug of choice for tx of intractable seizures in dogs & cats d/t convulsant agents (ex. strychnine poisoning) or CNS toxins (ex. tetanus), major active ingredient in several euthanasia solutions_x000D_ _x000D_ largely replaced by ultra-short acting barbiturates b/c of slow induction, long duration of action, inactivated primarily by metabolism (don't use w/ liver dz) |
|
|
thiopental
|
barbiturate_x000D_
_x000D_ ultra short acting _x000D_ excellent IV induction agent in young, healthy animals, or alone for very short procedures |
|
|
thiamylal
|
barbiturate_x000D_
_x000D_ ultra short acting_x000D_ no longer available in US; replaced by thiopental |
|
|
methohexital
|
barbiturate_x000D_
_x000D_ ultra-short acting anesthetic agent often used in sight hounds b/c it does not depend on redistribution to fat to reverse effect |
|
|
etomidate
|
ultrashort acting, hypnotic non-barbiturate induction agent_x000D_
_x000D_ excellent induction agent for patients w/ CV, respiratory, or liver dz_x000D_ _x000D_ safe for use in sighthounds_x000D_ _x000D_ depresses cortisol production_x000D_ can't use in horses (excitement) |
|
|
propofol: facts + pros
|
non-barbiturate sedative-hypnotic agent_x000D_
_x000D_ used for induction &/or maintenance of anesthesia, to produce prolonged sedation of patients in ICU_x000D_ _x000D_ pros: rapidly metabolized & redistributed --> very rapid recovery_x000D_ does NOT accumulate in body w/ chronic dosing |
|
|
barbiturates & lipid solubility
|
thiobarbiturate always more lipid soluble than oxybarbiturate_x000D_
_x000D_ phenobarb<pentobarb<thiopental_x000D_ _x000D_ as lipid solubility increases:_x000D_ 1. duration of action decreases_x000D_ 2. quicker onset_x000D_ 3. increased rate of distribution, metabolism_x000D_ 4. more hypnotic potency_x000D_ 5. more protein binding |
|
|
barbiturates: metabolism & redistribution
|
renal excretion: if highly lipid soluble, completely reabsorbed --> metabolized in liver (caution w/ liver dz)_x000D_
_x000D_ redistribution occurs if drug given rapidly (ex. IV), highly lipid soluble: drug goes to high flow organs 1st, then rapid reversal to muscle, adipose |
|
|
clinical uses of barbiturates
|
induction_x000D_
tx of seizures_x000D_ to decrease ICP & tx cerebral edema_x000D_ euthanasia |
|
|
cons of barbiturates
|
NOT analgesic (HYPERalgesic at subanesthetic doses)_x000D_
contraindicated w/ liver dz d/t metabolism, inc. free drug if hypoproteinemia is present_x000D_ can't use thiobarbiturates in sighthounds_x000D_ induce liver microsomal enzymes --> incr. metabolism of other drugs (phenobarb most potent)_x000D_ given only IV or PO_x000D_ w/ multiple dosing --> longer duration_x000D_ no pharmalogical antagonist (phenobarb OD: give bicarb to alkaline urine --> increased rate of excretion of parent drug) |
|
|
CV, resp. effects of barbiturates
|
brief hypotension, reflex tachycardia_x000D_
transient resp. depression (+/- apnea)_x000D_ arrhythmias, esp. in excited animals |
|
|
clinical uses of alpha-2 agonists
|
preanesthetic agent_x000D_
chemical restraint_x000D_ _x000D_ selectivity: xylazine < detomidine < medetomidine_x000D_ _x000D_ duration: detomidine longest |
|
|
effects of alpha-2 agonists
|
increases potency of other anasthetic drugs_x000D_
sedation/hypnosis_x000D_ analgesia_x000D_ muscle relaxation |
|
|
adverse effects of alpha-2 agonists
|
emesis_x000D_
resp. depression_x000D_ CV effects (vary b'twn drugs)_x000D_ bloat_x000D_ hyperglycemia_x000D_ increased urine output_x000D_ don't use xylazine during last mo. of pregnancy |
|
|
CV effects of xylazine
|
transient hypertension followed by prolonged hypotension_x000D_
bradycardia_x000D_ arrhythmias |
|
|
clinical uses of guaifenesin
|
adjunct to anesthesia in horses (IV)
|
|
|
effects of guaifenesin
|
sedation/hypnosis_x000D_
analgesia_x000D_ muscle relaxation_x000D_ antipyretic_x000D_ antitussive |
|
|
pros & cons of guifenesin
|
pros: inc. potency of barbiturates_x000D_
dec. hypertonicity assoc. w/ ketamine_x000D_ little cardiopulmonary depression_x000D_ _x000D_ cons: not very H2O soluble --> large vols. required_x000D_ may hemolyze RBCs (esp. in cattle) |
|
|
clinical uses of benzodiazepines
|
pre-anesthetic med (often w/ opioids)_x000D_
tx of seizures (midazolam: neonatal seizures in foals)_x000D_ tx anorexia in cats_x000D_ tx fears & phobias |
|
|
pros of benzodiazepines
|
dec. dose of other anesthetic drugs_x000D_
muscle relaxant_x000D_ weak resp. depression_x000D_ minor CV effects |
|
|
cons of benzodiazepines
|
cannot give IM (except midazolam)_x000D_
weaker sedative/hypnotic effects than other meds_x000D_ amnesia_x000D_ can't give oral diazepam to cats --> idiopathic hepatic necrosis_x000D_ avoid ending chronic tx abruptly_x000D_ tolerance w/ chronic use_x000D_ IV midazolam in cats --> profound tachycardia |
|
|
pharmacokinetics of benzodiazepines
|
lipid soluble --> extensive redistribution when given IV_x000D_
_x000D_ metabolism:_x000D_ oxidative pathway --> many active metabolites_x000D_ reductive path --> inactive compounds_x000D_ _x000D_ midazolam: short duration d/t rapid metab & distribution |
|
|
mechanism of action of benzodiazpines
|
facilitates GABA by binding to site on GABA receptor --> inc. affinity of GABA for receptor & vice versa --> GABA produces inc. in chloride conductance
|
|
|
flumazenil
|
benzodiazepine receptor antagonist_x000D_
_x000D_ useful in sick animals, esp. cats, to speed up recovery from anesthesia |
|
|
mechanism of action of barbiturates
|
low doses: facilitates GABA by binding to site on GABA receptor (separate site from benzos)_x000D_
_x000D_ higher doses (anesthetic): _x000D_ decreases presynaptic release of NTs_x000D_ blocks postsynaptic action of excitatory NTs_x000D_ GABA-mimetic effect |
|
|
dissociative anesthetic state
|
eyes open_x000D_
involuntary movements_x000D_ vocalization_x000D_ hallucinations_x000D_ feel separated from body |
|
|
physiological effects of dissociatives
|
analgesia (mostly somatic, less visceral)_x000D_
sympathetic activation_x000D_ hypertonicity (use w/ benzos, alpha-2s, or guaifenesin)_x000D_ inc. ICP, IOP_x000D_ convulsions (use w/ benzos)_x000D_ apneustic breathing_x000D_ retention of near normal pharyngeal & laryngeal reflexes |
|
|
mechanism of acation of dissociatives
|
noncompetitive antagonists of NMDA glutamate receptor --> inc. activity of layer V pyramidal output neurons (that release glutamate) --> disruption of thalamic & cerebral functions
|
|
|
tiletamine
|
similar to ketamine, but longer duration of action_x000D_
_x000D_ can only be bought mixed w/ benzo zolazepam = Telazol (recoveries may be prolonged & rough) |
|
|
clinical uses of neuroleptics
|
chemical restraint_x000D_
preanesthetic meds (dec. dose of other meds)_x000D_ antiemetic |
|
|
neuroleptic syndrome
|
sedation_x000D_
tranquilization_x000D_ dec. emotional behavior_x000D_ dec. responsiveness to external stimuli_x000D_ dec. spontaneous movement_x000D_ NOT hypnotic_x000D_ NO analgesia alone |
|
|
adverse effects of neurolpetics
|
extrapyramidal effects: dyskinesia, dystonia, muscle tremors_x000D_
higher doses --> catalepsy_x000D_ hypotension_x000D_ hypothermia_x000D_ mild neg. inotropic effect_x000D_ dec. seizure threshold_x000D_ weak resp. depression, but can inc. resp. depression w/ other drugs |
|
|
mechanism of action of neuroleptics
|
antagonize dopaminergic, alpha-adrenergic, muscarinic, H1, certain serotonergic receptors
|
|
|
phenothiazine neuroleptics: effects in horses
|
ace, chlorpromazine_x000D_
_x000D_ can cause violent incoordination & excitement _x000D_ _x000D_ penile prolapse & priapism |
|
|
droperidol
|
butyrophenone neuroleptic_x000D_
_x000D_ used in various preps in SA, swine_x000D_ don't use in horses d/t bizarre rxns_x000D_ shorter duration than phenothiazine neuroleptics_x000D_ potent dopamine receptor antagonists --> more likely to produce extrapyramidal effects |
|
|
mechanism of action of opioids & opiopeptins
|
decrease release of substance P --> dec. transmission of nociceptive info
|
|
|
species dependent effects of morphine
|
dogs, monkey, man: analgesia, sedation, euphoria, pupillary miosis_x000D_
_x000D_ horses, cats, pigs, ruminants: analgesia, excitement, dysphoria, mydriasis (use low doses) |
|
|
pros of morphine
|
valuable premed b/c dec. amt. of other drugs_x000D_
antitussive_x000D_ mild hypotension, bradycardia |
|
|
cons of morphine
|
dose dependent resp. depression: CAUTION w/ lung dz, neonates_x000D_
constipation, esp. w/ chronic use_x000D_ emetic_x000D_ SEVERE hypotension if in shock or w/ volume depletion |
|
|
hydromorphone
|
pure opioid agonist_x000D_
_x000D_ similar to morphine, but 5x more potent_x000D_ _x000D_ less GI upset & vomiting than morphine in dogs |
|
|
etorphine
|
pure opioid agonist_x000D_
_x000D_ agonist at all receptors, 1000x more potent than morphine_x000D_ _x000D_ used only to immobilize wild animals |
|
|
codeine
|
pure opioid agonist_x000D_
_x000D_ 10x weaker than morphine_x000D_ protected from 1st pass metabolism in liver --> converted to morphine_x000D_ _x000D_ uses:_x000D_ antitussive_x000D_ w/ acetaminophen to relieve pain in dogs |
|
|
dextromethorphan
|
pure opioid agonist_x000D_
_x000D_ devoid of all opioid properties except ANTITUSSIVE effect |
|
|
meperidine
|
pure opioid agonist (=Demerol)_x000D_
_x000D_ effective analgesic, maintains much of potency when given PO_x000D_ less constipating than morphine |
|
|
methadone
|
pure opioid agonist_x000D_
_x000D_ accumulates in body --> inc. duration of action w/ multiple doses_x000D_ retains most analgesic potency when given orally_x000D_ tolerance, dependence develop slowly_x000D_ also NMBA glutamate antagonist --> dec. opioid dependence |
|
|
carfentanil
|
pure opioid agonist_x000D_
_x000D_ most potent of fentanil family (all are short acting, w/ rapid onset)_x000D_ _x000D_ used to immobilize wild animals |
|
|
sufentanil
|
pure opioid agonist_x000D_
_x000D_ anesthetic adjunct in dogs |
|
|
fentanyl
|
pure opioid agonist_x000D_
_x000D_ anesthetic adjunct in dogs_x000D_ patches: control of chronic pain (absorption can be unreliable) |
|
|
naloxone
|
pure opioid antagonist_x000D_
_x000D_ most commonly used opioid antagonist in vet med_x000D_ _x000D_ parenteral use only (usually IV), slightly shorter acting than morphine |
|
|
diprenorphine
|
pure opioid antagonist_x000D_
_x000D_ parenteral only (usually IM)_x000D_ _x000D_ used only to reverse etorphine-induced immobilization |
|
|
naltrexone
|
pure opioid antagonist_x000D_
_x000D_ uses:_x000D_ control crib biting in horses_x000D_ reverse carfentanil-induced immobilization_x000D_ _x000D_ long duration of action_x000D_ oral or parenteral use |
|
|
butorphanol
|
mixed opioid agonist/antagonist_x000D_
_x000D_ uses:_x000D_ analgesic_x000D_ antitussive_x000D_ preanesthetic med_x000D_ chemical restraint (w/ alpha-2 agonist)_x000D_ _x000D_ popular in horses d/t low incidence of excitatory effects_x000D_ weak resp. depression, less constipation |
|
|
buprenorphine
|
mixed opioid agonist/antagonist_x000D_
_x000D_ uses:_x000D_ analgesic in dogs & cats_x000D_ alternative to methadone for addicts_x000D_ _x000D_ longer duration of action than torb, morphine_x000D_ reverse w/ naloxone given PRIOR to buprenorphine_x000D_ well tolerated in horses |
|
|
loperamide
|
misc. opioid agent (=Immodium)_x000D_
_x000D_ used to tx diarrhea_x000D_ _x000D_ avoid repeated use --> constipation_x000D_ can cause profound sedation in certain dog breeds (collies, Australian shepherds, etc.) |
|
|
apomorphine
|
misc. opioid agents_x000D_
strong dopaminergic agonist _x000D_ _x000D_ emetic of choice in dogs_x000D_ give conjunctivally (or SQ) |
|
|
innovar
|
neuroleptanalgesic_x000D_
_x000D_ = droperidol + fentanyl |
|
|
midazolam + morphine
|
benzo/opioid combo_x000D_
_x000D_ given IM as pre-med to dogs that can't be handled easily &/or are in pain_x000D_ often given to cats as alternative to ketamine (ex. w/ intracranial mass, etc.) |
|
|
diazepam + morphine
|
benzo/opioid combo_x000D_
_x000D_ given IV as pre-med to calm depressed &/or sick dogs |
|
|
neuroleptanalgesia
|
(+): sedation, dec. anxiety, intense analgesia, dec. movement, NO emesis, dec. dose of other drugs_x000D_
_x000D_ (-): resp. depression, extrapyramidal effects, chest rigidity, change in autonomic fn |
|
|
benzodiazepine/opioid combos
|
(+): sedation, dec. anxiety, intense analgesia, amnesia, minimal autonomic effects, NO extrapyramidal effects_x000D_
_x000D_ (-): resp. depression (easily reversed w/ opioid antagonist) |
|
|
determinants of tension of gas in alveoli (FA)
|
rate of delivery of gas TO alveoli: _x000D_
1. tension of anesthetic gas in inspired gas (FI)_x000D_ 2. minute volume_x000D_ _x000D_ rate of removal of gas FROM alveoli:_x000D_ 1. cardiac output_x000D_ 2. blood solubility (Fblood)* |
|
|
blood solubility & induction/recovery
|
LOW blood solubility: _x000D_
fast induction & recovery_x000D_ _x000D_ HIGH blood solubility: slow induction & recovery |
|
|
effects of inhalational anesthetics
|
all produce dose dependent depression of respiration & MAP_x000D_
minimal skeletal muscle relaxation_x000D_ _x000D_ halothane is most potent (lowest MAC)_x000D_ sevo has fastest induction/recovery (lowest max vapor conc.) |
|
|
cons of halothane
|
hypotension d/t dec. myocardial contractility_x000D_
arrhythmias_x000D_ significant hepatic biotransformation (hepatotoxic metabolites)_x000D_ _x000D_ alters Ca++ movements_x000D_ 1. intearctions w/ aminoglycoside Abs, Ca channel blockers --> severe CV depression_x000D_ 2. can produce malignant hyperthermia (esp. in pigs), caused by failure of Ca uptake in SR |
|
|
dantrolene sodium
|
used to tx malignant hyperthermia_x000D_
_x000D_ decreases Ca++ release from SR |
|
|
sevoflurane
|
hypotension d/t vasodilation, esp. in muscle & skin (same w/ iso)_x000D_
unstable in soda lime_x000D_ excellent for sea turtles_x000D_ expensive |
|
|
nitrous oxide
|
used as adjunct to anesthesia in small animals b/c:_x000D_
1. concentration & 2nd gas effects_x000D_ 2. decreases dose of primary anesthetic_x000D_ 3. mild stimulation of symp. nervous system_x000D_ 4. ANALGESIC_x000D_ _x000D_ avoid conc. > 70-75%_x000D_ do not give to patients w/ any condition where air is trapped in viscera --> will cause air pocket to expand (ex. pneumothorax) |
|
|
concentration effect
|
only seen w/ high conc. of nitrous oxide_x000D_
_x000D_ when higher conc. of anesthetic gas is inhaled, FA (& therefore Fblood), inc. at a slightly greater rate than if a lesser conc. were inhaled |
|
|
2nd gas effect
|
occurs when a 2nd gas (ex. 1% halothane) is inspired w/ 75% nitrous & 24% O2_x000D_
_x000D_ conc. effect produced by 75% N2O not only concentrates O2, but also halothane --> inc. rate of movement of halothane from alveolar air to pulm. blood --> faster induction |
|
|
uses of analeptics
|
used to reverse drug-induced CNS depression (esp. respiratory depression)_x000D_
_x000D_ cause general CNS stimulation --> can result in convulsions |
|
|
doxapram
|
most commonly used analeptic_x000D_
_x000D_ used to stimulate respiration during or after gen. anesthesia, in newborns, in cases of cardiopulm. arrest_x000D_ _x000D_ stimulates carotid & aortic chemoreceptors --> reflux stimulation of medullary resp. centers_x000D_ _x000D_ short duration: 5-10 m._x000D_ excessive doses --> hypertension, hyperventilation, seizures (rare) |
|
|
strychnine
|
analeptic; used as a pesticide_x000D_
_x000D_ glycine receptor antagonist --> CNS stimulation_x000D_ _x000D_ strychnine poisoning --> severe & extremely painful convulsions |
|
|
theophylline
|
methylxanthine (weak analpetic)_x000D_
_x000D_ used in tx of asthma, adjunct to digoxin to tx CHF (dilates coronary aa.) |
|
|
aminophylline
|
methylxanthine (weak analpetic)_x000D_
_x000D_ H2O sol. salt of theophylline (better oral absorption)_x000D_ _x000D_ used in tx of asthma, adjunct to digoxin to tx CHF (dilates coronary aa.) |
|
|
theobromine
|
methylxanthine (weak analpetic)_x000D_
_x000D_ in chocolate |
|
|
cocaine
|
local anesthetic (ester)_x000D_
_x000D_ only one to cause vasoconstriction |
|
|
proparacaine
|
local anesthetic (ester)_x000D_
_x000D_ used to anesthetize cornea_x000D_ lasts 15-30 m. |
|
|
lidocaine
|
local anesthetic (amide)_x000D_
_x000D_ most widely used local anesthetic_x000D_ _x000D_ used to tx post-op ileus in horse_x000D_ _x000D_ may cause local irritation & swelling, esp. in horse |
|
|
bupivacaine
|
local anesthetic (amide)_x000D_
_x000D_ useful for post-op analgesia_x000D_ duration up to 8 hrs |
|
|
mepivacaine
|
local anesthetic (amide)_x000D_
_x000D_ most widely used local in horses b/c it causes little swelling & edema |
|
|
mechanism of action of local anesthetics
|
block initiation & propagation of AP by preventing voltage-dep. inc. in Na permeability that accompanies a small inc. in mem depolarization
|
|
|
factors influencing sensitivity of nerves to blockade by local anesthetics
|
firing rate of nerve: resting Na channels least susceptible, then open channels, inactivated channels most susceptible _x000D_
_x000D_ pH of body fluids & pKa of local anesthetic: uncharged mols penetrate mem, but CHARGED mols bind receptors (if pH dec. d/t inflammation --> more drug needed to block)_x000D_ _x000D_ anatomical structure of nerve: small diameter n. easier to block |
|
|
local anesthetics: determinants of absorption from site of administration
|
dosage_x000D_
site of injection: absorbed more quickly in highly vascular area_x000D_ extent of tissue binding: keeps drug at site of admin --> inc. duration of action_x000D_ concurrent admin of vasoconstricting substances: locals are vasodilators & usually sold w/ vasoconstrictor (ex. epi); vasoconstriction --> inc. efficacy b/c systemic absorption is decreased d/t low blood flow |
|
|
metabolism of local anesthetics
|
esters: shorter half life d/t rapid hydrolysis by plasma & liver cholinesterases_x000D_
amides: hydrolyzed by liver microsomal enzymes (DO NOT USE w/ liver dz) |
|
|
systemic effects of cocaine
|
restlessness, euphoria --> tremors --> convulsions_x000D_
_x000D_ vasoconstriction, hypertension, arrhythmias |
|
|
systemic effects of local anesthetics (except cocaine)
|
only w/ HIGH plasma levels:_x000D_
_x000D_ marked hypotension d/t dec. cardiac contractility --> dec. CO & vasodilation by dec. symp. tone |
|
|
mechanisms of action of seizures
|
seizure focus activated, seizure discharge from focal area may synchronize w/ other neurons & propagate to surrounding areas of brain_x000D_
_x000D_ dec. GABA activity & inc. glutamate activity important |
|
|
3 ways anticonvulsants inhibit seizures
|
1. dec. excessive discharge of seizure focus_x000D_
2. inc. seizure threshold required for discharge_x000D_ 3. dec. spread of discharge to surrounding neurons_x000D_ _x000D_ most drugs work by 2 & 3 |
|
|
tx for chronic seizures in dogs & cats
|
Dogs:_x000D_
1. phenobarb_x000D_ 2. phenobarb + KBr_x000D_ 3. KBr alone_x000D_ _x000D_ Cats:_x000D_ 1. phenobarb_x000D_ 2. benzodiazepine_x000D_ 3. third level drugs |
|
|
when to start tx for seizures
|
> 1 seizure/month_x000D_
very intense seizures w/ breathing difficulties_x000D_ clusters of seizures |
|
|
pros of phenobarbital for tx of seizures
|
effective against wide spectrum of epilepsies_x000D_
inexpensive_x000D_ relatively non-toxic_x000D_ easy to measure blood levels_x000D_ relatively little sedation |
|
|
cons of phenobarbital for tx of seizures
|
polyphagia --> wt. gain_x000D_
PU/PD_x000D_ hepatotoxicity_x000D_ _x000D_ w/ chronic use:_x000D_ altered bone metabolism_x000D_ inc. metabolism of other drugs using liver microsomal enzymes_x000D_ blood dyscrasias_x000D_ inc. liver enzymes |
|
|
mechanism of action of phenobarb for tx seizures
|
inc. seizure threshold, dec. spread of discharge d/t facilitation of GABA, then also inhibition of glutamate_x000D_
_x000D_ at higher doses, may dec. Ca flux across neuronal mem |
|
|
primidone
|
anticonvulsant (dogs only)_x000D_
_x000D_ congener of phenobarb _x000D_ more expensive, more hepatotoxic, quite sedative intially_x000D_ _x000D_ it & 2 metabs all anti-convulsant |
|
|
benzodiazepines to tx seizures
|
orally ineffective in dogs_x000D_
tolerance to anticonvulsant properties can develop over time_x000D_ most potent elevator of seizure threshold: facilitates GABA_x000D_ _x000D_ diazepam: used in cats that are refractory to phenobarb (don't give orally)_x000D_ _x000D_ clonazepam: not metab. by liver microsomal enzymes (no active metabolites), longer half life, doesn't cause hepatic necrosis |
|
|
cons of potassium bromide
|
vomiting_x000D_
pancreatitis (rare)_x000D_ takes ~1 mo. to reach therapeutical plasma levels_x000D_ in emergency, would have to give large loading dose --> potentially cardiotoxic (can use sodium bromide IV instead) |
|
|
third level drugs used to tx seizures
|
felbamate (dogs)_x000D_
gabapentin (dogs, cats) |
|
|
tx of status epilepticus
|
1. IV diazepam (2-3 doses if needed)_x000D_
2. IV phenobarbital_x000D_ 3. if still seizing, IV pentobarbital to produce anesthesia (or IV propofol)_x000D_ _x000D_ if seizures result of strychnine poisoning: tx of choice is anesthetic dose of IV pentobarbital |
|
|
cons of propofol
|
-some pain w/ IV administration_x000D_
-can damage tissue if given extravascularly_x000D_ -apnea common after administration_x000D_ -dose dependent vasodilation --> dec. MAP (do NOT use in hypotensive patients)_x000D_ -cats: chronic admin can cause oxidative injury to RBCs |
|
|
ALS
|
Amyotrophic lateral sclerosis AKA Lou Gahrig’s Disease
|
|
|
ALS Pathophysiology
|
Rapidly Progressive neurodegenerative disease that attacks upper and lower motor neurons.
|
|
|
What neurotransmitter do ALS pts have in excess? How is it harmful?
|
Glutamate- it's toxicity is apparently due to Ca flooding the cell. Ca is supposed to briefly enter the neuron with each signal and triggers the cell to fire off its own signals and adjust its own activities accordingly. But prolonged Ca inside the cell evidently can do damage, and will even activate programmed cell death
|
|
|
Is ALS slow or quick onset?
|
Very quick progression and very short lifespan
|
|
|
Major problems for ALS pts?
|
No known cause, cure, specific treatment, standard pattern of progression, and no method of prevention.
|
|
|
What is the suspected cause of ALS?
|
Genetic (10%)- small gene mutation maybe overstimulation by glutamate→ cell injury degeneration (ALS patients have higher levels of glutamate)
|
|
|
Age and gender ALS usually affects?
|
ages 40-60_x000D_
Men > women |
|
|
ALS: what is the overall problem?
|
Brain can no longer send impulses to muscles (therefore can no longer control muscle movement)
|
|
|
Does ALS start as being widespread throughout the body?
|
Starts in one area of body and spreads until entire body is involved
|
|
|
Major clinical manifestations of ALS
|
Atrophy → Progressive muscle weakness_x000D_
Muscle wasting_x000D_ Spasticity → paralysis_x000D_ Fatigue_x000D_ Cramps_x000D_ Twitching especially of face (fasciculation)_x000D_ Less motor control in hands and arms_x000D_ Talk, swallow, and breathing affected (will eventually need to be put on a ventilator) |
|
|
What are the biggest concerns for ALS pts?
|
• Compromised respiratory_x000D_
• Pneumonia |
|
|
Does ALS cause death?
|
Not from ALS itself, but death due to respiratory failure
|
|
|
What is the avg lifespan for ALS pt?
|
3-5 yrs d/t respiratory failure
|
|
|
Are cognitive/intellictual functinos affected by ALS?
|
No- Intellectual functioning remains intact! Worst part of this desease ☹ (Think Steven Hawkings)_x000D_
_x000D_ May see cognitive changes in thinking and planning processes |
|
|
Are the senses affected by ALS?
|
No- Does not affect sight, sound, smell, taste, hearing_x000D_
_x000D_ • Control of eyes, bladder, etc. will be lost |
|
|
How to diagnose ALS?
|
No Specific test to diagnose ALS (all tests are used only to rule out other diseases )
|
|
|
Tests used to determine if pt has ALS?
|
• Electromyelogram (EMG): Looks at fibrillations and muscle twitching_x000D_
• Muscle Biopsy: Shows abnormalities_x000D_ • PFTs: To make sure no other respiratory problems are the cause of fatigue |
|
|
Why do we want to diagnose ALS early on?
|
The earlier it is diagnosed, the slower the disease progresses = can have longer lifespan (d/t lifestyle and environmental changes)
|
|
|
Can ALS be treated to stop progressing>
|
No- no matter what, the disease WILL progress _x000D_
100% fatal |
|
|
How to manage ALS?
|
No specific treatment
|
|
|
What is the only drug approved by the FDA to manage ALS?
|
Rilutek
|
|
|
What type of drug is Rilutek?
|
glutamine antagonists
|
|
|
What labs to monitor for pts on Rilutek?
|
LFTs- drugs harsh on liver_x000D_
_x000D_ AST/ALT |
|
|
How long does Rilutek work for ALS pts?
|
Only 2-3 months!
|
|
|
What does Rilutek do for the ALS pt?
|
slows progression and may prolong need to be trached- Does not relieve symptoms
|
|
|
What other meds will ALS pts be Rx?
|
Meds also prescribed for pain, fatigue, spasticity, excessive secretions, sleep disturbances, and other complications as they occur
|
|
|
What nursing care for ALS pts?
|
Support!_x000D_
Patient may feel pain, depression, panic attacks, fear, etc._x000D_ Pastoral care? Palliative/comfort care, refer to support groups, hospice programs, help w/ spasticity, help/advise about putting final affairs in order |
|
|
What are some of the issues ALS pts and families will have to deal with?
|
Adaptive devices to maintain independence_x000D_
Alternative means of communication_x000D_ Consider mechanical ventilator (up to patient and family)_x000D_ Remember- No Cure |
|
|
GB- Guillan Barre
|
It is demylination/INFLAMMATION OF THE PERIPHERAL NERVES AFFECTS NODES OF RANVIER, SLOWS TRANSMISSION OF IMPULSES→progressive motor weakness and sensory abnormalities.
|
|
|
How common is Guillan Barre?
|
Rare!
|
|
|
Does Guillan Barre affect more men or women?
|
Men- esp middle aged
|
|
|
Most common form of Guillan Barre?
|
ASCENDING PARALYSIS, _x000D_
LEGS UPWARD _x000D_ DTR (deep tendon reflexes)s, flaccid paralysis, paresthesias |
|
|
Descending type of Guillan Barre affects...
|
Starts in the jaw, tongue larynx- on its way down compromises respiratory function_x000D_
Facial weakness, dysphagia, difficulty speaking, diplopia_x000D_ As it goes down cranial nerve 10 is affected- difficulty swallowing and BP drops d/t vagal, bradycardia, orthostatic BP, bottom out, arrhythmias, shock |
|
|
IF GB STARTS TO AFFECT AUTONOMIC NERVOUS SYSTEM AND RESP. SYSTEM...
|
MAJOR COMPLICATIONS AND EVENTUALLY RESP FAILURE→DEATH!!!!
|
|
|
How does GB happen?
|
Acute illness causes an autoimmune response that interferes with T-suppressor cell circuits. Causative antigen has similar cell markers as myelin. Body mistakes myelin for causative agent and attacks= invasion of spinal and cranial nerves.
|
|
|
Three acute stages of GB
|
Acute/Initial period_x000D_
Plateau_x000D_ Recovery phase |
|
|
What is the Acute/Initial period of GB?
|
1-4 weeks- onset of symptoms (NUMBNESS AND TINGLING), PROGRESSIVE WEAKNESS) and ends when no further deterioration occurs _x000D_
Can Cause complete paralysis_x000D_ If spread to Resp & ANS- pt in danger- on vent in ICU |
|
|
Plateau phase of GB?
|
Several days to 2 weeks- NO RECOVERY, NO FURTHER PROGRESSION OF DISEASE→ Most discouraging phase to patients- they need complete emotional support, and information from HCP they are very frustrated and need help in moving forward
|
|
|
Recovery phase for GB
|
4-6 months ,sometimes up to 2 years- HEALING OCCURS IN REVERSE ORDER (whatever was affected last heals first), CAN BE PAINFUL WHEN NERVES REMYELINATE, SOME PTS MAY HAVE RESIDUAL DEFICITS THAT NEVER HEAL.
|
|
|
Cause of GB?
|
NO actual known cause
|
|
|
What are potential causes linked to GB?
|
1. ACUTE ILLNESS_x000D_
2. UPPER RESP INFECTIONS_x000D_ 3. TRAUMA_x000D_ 4. IMMUNIZATIONS_x000D_ 5. SURGERY_x000D_ 6. INFECTION→VIRAL EXPOSURE→EPSTEIN BARR (GET IT? GUILLAN BARRE)_x000D_ 7. SYSTEMIC LUPUS_x000D_ 8. UNDERCOOKED CHICKEN…NASTY. :/ |
|
|
S/S of GB
|
• DECREASED DEEP TENDON REFLEXES_x000D_
• FLACCID PARALYSIS_x000D_ • TONE REMAINS INTACT_x000D_ • PARESTHESIAS_x000D_ • WEAKNESS_x000D_ • FATIGUE_x000D_ • FACIAL PARALYSIS_x000D_ • DYSPHAGIA_x000D_ • DIFFICULTY SPEAKING_x000D_ • DIPLOPLIA (DOUBLE VISION)_x000D_ • LABILE BP_x000D_ • CARDIAC ARRYTHMIAS_x000D_ • TACHYCARDIA_x000D_ • LOSS OF BOWEL AND BLADDER FUNCTION_x000D_ • ATAXIA |
|
|
Most dangerous symptom of GB in severe cases?
|
IN SEVERE CASES→RESP FAILURE→PNEUMONIA→DEATH!!!!!
|
|
|
What test to diagnose GB?
|
NO SINGLE DEFINITIVE TEST- tests are only used to rule out other diseases/disorders
|
|
|
Tests to help diagnose GB?
|
Lumbar puncture_x000D_
Blood Studies_x000D_ EMG_x000D_ NCV_x000D_ Hx of viral illenss in past few weeks or immunization |
|
|
If pt has GB, what will Lumbar Puncture show?
|
Cerebral Spinal Fluid will have proteins (from inflammation)
|
|
|
What will blood studies show if pt has GB?
|
Leukocytosis (only in early phase of illness)
|
|
|
What will EMG show if pt has GB?
|
electromyelogram MEASURES THE MUSCLES ABILITY TO FIRE IMPULSES (ACTIVITY)- will be diminished
|
|
|
What will NCV show if pt has GB?
|
Nerve Conduction Velocity (MEASURES THE SPEED AT WHICH MUSCLES/NERVES CONDUCT AN IMPULSE) will be slowed
|
|
|
What is the cure for GB?
|
No known Cure
|
|
|
What are treatments for GB?
|
Plasmapharesis_x000D_
IV Immunoglobulins |
|
|
What is Plasmapharesis?
|
Plasma Is Removed From Whole Blood, Antibodies That Circulate In Plasma Are Thus Removed, And The Pt Receives The Remaining Blood Cells. Done Several Days After Onset Of Symptoms. 3-4 Treatments 1-2days Apart
|
|
|
How does Plasmapharesis work to help GB?
|
Limits the amount of circulating antibodies that are attacking the myelin
|
|
|
What nursing responsibilities for pts undergoing plasmapheresis?
|
Support/Reassurance_x000D_
Weigh The Pt_x000D_ Monitor Shunt (Patency, Bleeding, Obstructions Listen For The Bruits!!!!)_x000D_ Pt May Experience Bradycardia Because Of Loss Of Plasma |
|
|
What do we give pt if they are experiencing bradycardia d/t loss of plasma?
|
Atropine!
|
|
|
Atropine
|
atropine counters the rest and digest" activity of all muscles and glands regulated by the PNS. This occurs because atropine is a competitive antagonist of the muscarinic acetylcholine receptors (acetylcholine being the main neurotransmitter used by the parasympathetic nervous system). Atropine dilates the pupils, increases HR, and reduces salivation and other secretions."
|
|
|
Major A/E of plasmaphresis?
|
1. Hypovolemia_x000D_
2. Hypokalemia_x000D_ _x000D_ These both can lead to cardiac problems! |
|
|
What is Iv Immunoglobulin therapy?
|
Pt Is Treated With Immunoglobulins From A Pool Of Donors, When Given Can Lessen Attack On Nervous System
|
|
|
Major A/E of Iv Immunoglobulin therapy?
|
1. Chills_x000D_
2. Fever_x000D_ 3. Headache_x000D_ 4. Myalgia |
|
|
Interventions for GB?
|
Monitor Resp status_x000D_
Monitor for cardiac dysfunction_x000D_ Improve mobility_x000D_ Manage Pain_x000D_ Promote communication_x000D_ Nutrition_x000D_ Provide Support |
|
|
What to give for hypotension (GB)?
|
IVF
|
|
|
What to give for Bradycardia (GB)?
|
Atropine
|
|
|
What to give for Hypertension (GB)?
|
Beta Blockers (Nitroprusside)
|
|
|
Hot to improve mobility (GB)?
|
ROM exercises- active and passive, PT, OT, Assist w/ transfers, assistive devices, balance rest with activity
|
|
|
How to manage pain (GB)?
|
Opiates With A Pca Pump, Positioning, Deep Breathing, Distraction, Humor, Guided Imagery, Ice, Heat (Not Excessive!!!!!), Massage
|
|
|
What is MS?
|
Multiple Sclerosis is a chronic autoimmune disease that affects the myelin sheath and conduction pathway of the CNS. It’s one of the leading causes of neurological disability in persons 20-40yrs
|
|
|
Cause of MS?
|
Unknown- may have genetic predisposition and environmental factors (also geographic)_x000D_
_x000D_ Viral- inflammation process could be a cause |
|
|
MS is an ______ response that destroys the ___ ___ (______-)
|
inflammatory_x000D_
myelin sheath (demylination) |
|
|
Pathway of MS-_x000D_
_x000D_ ___________--> _________--> ________--> interference of normal ______ _________ |
Inflammation --> Scarring --> plaques --> interference of normal nerve transmission
|
|
|
MS is characterized by an ______ response that results in diffuse random or patchy areas of _____ in the white matter of the CNS. When this happens, the ____ ______ is damaged and its thickness is reduced (__________).
|
inflammatory_x000D_
plaque_x000D_ myelin sheath_x000D_ (demyelinated) |
|
|
Myelin is responsible for...
|
The electrochemical transmission of impulses between the brain and spinal cord and the rest of the body.
|
|
|
Are impulses still transmitted in MS pts?
|
Yes- but they are less effective
|
|
|
What areas are most affected by MS?
|
optic nerves, pyramidal tracts, posterior columns, brainstem nuclei and the periventricular regions of the brain
|
|
|
4 types of MS?
|
Relapsing Remitting (RRMS)_x000D_
Primary Progressive (PPMS)_x000D_ Secondary progressive (SPMS)_x000D_ Progressive Relapsing (PRMS) |
|
|
Relapsing Remitting (RRMS):
|
MOST COMMON. periods of exacerbation and remission- clearly defined for about 4-5 yrs. The course of the disease may be mild or moderate, depending on the degree of disability. Symptoms may develop and resolve in a few weeks to months after which the patient returns to baseline.
|
|
|
Primary Progressive (PPMS):
|
continuous progressive worsening of mobility, balance, increased spasticity and pain involves a steady and gradual neurological deterioration without remission of symptoms. The patient has progressive disability with no acute attacks. Patients with this type of MS tend to be between 40-60yrs at onset of disease.
|
|
|
Secondary progressive (SPMS):
|
begins with relapsing-remitting course that later becomes steadily progressive. Functioning begins to decline with no clear times of remission
|
|
|
Progressive Relapsing (PRMS):
|
characterized by frequent relapse with some partial recovery but not a return to baseline. Progressive, cumulative symptoms and deterioration occur over several years.
|
|
|
MS S/S
|
Fatigue/weakness_x000D_
Visual disturbances_x000D_ Cognitive changes_x000D_ Mental Health_x000D_ Spinal Cord dysfunctions |
|
|
What type of visual disturbances with MS?
|
Blind spots (holes in vision)_x000D_
Blurred vision_x000D_ Diplopia (double vision)_x000D_ Decreased visual acuity_x000D_ Scotomas (change in peripheral vision)_x000D_ Nystagmus (involuntary, rapid eye movement) |
|
|
What type of cognitive changes with MS?
|
Intention tremor (tremor when performing an activity)_x000D_
Cognitive changes usually seen late in the course of the disease: decreased short term memory, concentration, and ability to perform calculations; inattentiveness; and impaired judgment |
|
|
What type of mental health issues with MS?
|
• depression_x000D_
• isolation |
|
|
What type of Spinal Cord Changes/dysfunctions with MS?
|
• Bowel and bladder dysfunction_x000D_
• Constipation and INCONTINENCE _x000D_ • Sexual dysfunction _x000D_ • muscle spasms (SPASTICITY)_x000D_ • tingling/numbness_x000D_ • decreased motor coordination (ATAXIA) |
|
|
What is important to teach the pt about any type of MS medication therapy?
|
***medications that work well now may not work later, and medications that do not work now may work later- it is all trial and error***
|
|
|
What is the acronym for MS medical treatment?
|
A-B-C_x000D_
Avonex, Betaserone, Copoxone |
|
|
Avonex or Betaserone
|
MS med- interferons (Very expensive)_x000D_
_x000D_ FIGHTS VIRAL INFECTION and regulates the immune system_x000D_ -mechanism of action is very unclear but it does help to FIGHT RELAPSE of symptoms-every other day SQ inj fights viral infections and regulates the immune system |
|
|
Copoxone
|
MS med- a glutimer acetate_x000D_
_x000D_ decreases relapse rate and progression of disease. Blocks immune system’s attack of myelin. |
|
|
Baclofen
|
for the muscle spasms (muscle relaxer) (MS)
|
|
|
Baclofen Most Common A/E?
|
Sedation
|
|
|
Gabapentin (Neurontin)
|
decreases spasticity (MS)
|
|
|
What labs to monitor for pts on Gabapentin?
|
monitor renal function tests (BUN, CR)
|
|
|
MS- Overall goals of meds?
|
increase self care ability with ADLs
|
|
|
What drugs are useful to decrease spasticity?
|
Baclofen and valium
|
|
|
What type of history to assess for MS pts?
|
relatives with MS?_x000D_
type of symptoms?_x000D_ how long do they last? _x000D_ triggers? |
|
|
What is a neurological exam used for in pts with MS?
|
TO see the progressino of the disease and any cognitive changes
|
|
|
What is and EMG used for in pts with MS?
|
looks at neurological electrical activity and conduction through muscle stimulation
|
|
|
What are the two gold tests for MS???
|
MRI and VEP (Visual Evoke Potential)
|
|
|
what type of MRI and what are they looking for in pts with MS?
|
MRI of Brain w/ contrast- looking for plaque
|
|
|
What is the Visual Evoke Potential (VEP) and why is it used to help diagnose MS?
|
measures electrical activity of brain in response to visual sensory input (demyelination will slow conduction)- in MS it will be severely slowed
|
|
|
What is the overall goal for MS pts?
|
GOAL= ↑ independence and self-care with ADL’s
|
|
|
What pt teaching for MS pts?
|
Energy Banking_x000D_
Diet_x000D_ Prevent exacerbations_x000D_ Make appts later in morning to allow time for mobility |
|
|
What diet is helpful for MS pts?
|
↓ simple carbs, saturated fats_x000D_
use of mustard under tongue to decrease spasticity |
|
|
What can MS pts do to help avoid exacerbations?
|
Avoid:_x000D_
_x000D_ Over exertion_x000D_ Stress- physical and emotional_x000D_ Heat intolerance _x000D_ Sick people (Immunosuppressants)_x000D_ Sudden body changes |
|
|
What are the three Movement Disorders?
|
Multiple Sclerosis_x000D_
Parkinson's Disease_x000D_ ALS |
|
|
What system is responsible for coarse control of voluntary muscles (And is affected in movement disorders?)
|
The EPS- Extrapyramidal System
|
|
|
What is Dopamine?
|
A neurotransmitter that is produced in the Substantia Nigra (basal ganglia) and adrenal glands. DA sends info to parts of the brain that control movement and coordination
|
|
|
What other neurotransmitter is important in smooth movement, and communicates with DA?
|
ACh
|
|
|
what type of disorder is Parkinson's?
|
A movement disorder
|
|
|
Is Parkinson's curable?
|
No
|
|
|
What are causes of Parkinson's?
|
Causes are UNKNOWN, but genetics and exposure to PESTICIDES and other chemical agents are suspected to have a role.
|
|
|
What happens at a cellular level Parkinson's Disease?
|
here is Death of the neuron (substantia nigra cells) that produce dopamine
|
|
|
The substantia nigra is responsible for
|
the production of dopamine.
|
|
|
Dopamine (DA) and Acetylcholine (Ach) work together to
|
to initiate and control smooth purposeful movement.
|
|
|
What happens to Dopamine and ACh in Parkinson's Disease?
|
Because there is a decrease in Dopamine, and a normal level of ACh there is now an imbalance between the two. The imbalance causes increased GABA action (an inhibitory neurotransmitter) which decreases signal conduction which leads to the manifestations of the disease.
|
|
|
What are the 4 CLASSIC manifestations/symptoms of Parkinson's Disease?
|
1) Tremors at rest (tremors when not engaged in purposeful movement)_x000D_
2) Muscle rigidity (stiffness)_x000D_ 3) Slow movement (shuffling)_x000D_ 4) Postural instability (stooped posture) |
|
|
Do Classic symptoms occur more at rest or during purposeful movement?
|
At rest, during purposeful movement symptoms subside
|
|
|
What are other symptoms of Parkinson's disease?
|
orthostatic hypotension, “mask-face”, may get dementia, excessive perspiration
|
|
|
Is Ach increased in Parkinson's?
|
No, it stays the same, but because DA is deceased, there is now an imbalance
|
|
|
What happens when ACh and DA become unbalanced?
|
Movement becomes jerky
|
|
|
Why does the imbalance of DA and ACh cause this type of jerky movement?
|
The UNOPPOSED Ach causes a stimulation of GABA, and DECREASES the CELLS ABILITY TO FIRE
|
|
|
Is Parkinsons Progressive?
|
Yes
|
|
|
Is Parkinson's fatal?
|
No, and life expectancy is not decreased
|
|
|
What types of drugs are used to treat Parkinson's?
|
dopaminergics, dopamine agonists, anticholinergics, and COMT inhibitor
|
|
|
What Dopaminergics are used to treat Parkinson's?
|
Carbidopa and Levodopa
|
|
|
Why is carbidopa and levodopa given in combination?
|
Levadopa is a precursor to dopamine. It can cross the BBB but only 2% makes it past the BBB to be converted to dopamine where it can do its work. Levadopa is deactivated by DDC and COMT (enzymes)_x000D_
•Carbidopa inhibits DDC, which allows a greater 10% of the levodopa to reach the BBB, allowing for smaller amounts of Levadopa to be administered, which decreases the chances for adverse effects. |
|
|
Why can't Dopamine be given for Parkinson's?
|
It cannot cross the BBB
|
|
|
What two enzymes in the body break down Levodopa?
|
Dopamine decarboxylase (DDC) & _x000D_
catechol-O-methyl transferase (COMT) |
|
|
How does Carbidopa work to increase the amount of Levodopa available to cross the BBB?
|
Carbidopa inhibits the DDC enzyme- stops it from breaking down the levodopa
|
|
|
How long does the Carbidopa-Levodopa combo take to see effects?
|
1-2 months, sometimes up to six months.
|
|
|
Where is Carbidopa-Levodopa metabolized into Dopamine?
|
In the periphery of the body
|
|
|
What disease can Carbidopa-Levodopa activate (if the person is already genetically predisposed to?)
|
Malignant melanoma
|
|
|
What pts is the Carbidopa-Levodopa combo contraindicated in?
|
In pts with undiagnosed pigmented lesions, hx of melanoma,
|
|
|
What effect can carbidopa-levodopa have on pts with preexisting conditions?
|
Anyone with past cardiac disease, pulmonary disease, Peptic ulcer disease and DM may have exacerbation of symptoms_x000D_
_x000D_ Can also cause mental status changes in pts with mental health hx (Depression, SI) |
|
|
Why is it a goal to get more levodopa to the BBB?
|
So that we can give less medication to begin with and decrease the A/E
|
|
|
What are A/E of carbidopa-Levodopa?
|
GI upset- N/V/D, anorexia, wt loss, orthostatic hypotension_x000D_
Abnormal movements |
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|
What is the most serious A/E of carbidopa-Levodopa?
|
Neuroleptic malignant syndrome (AKA parkinsonian crisis)- happens when drug is STOPPED ABRUPTLY-extreme rigidity/tremors
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|
Simultaneous admin of Carbidopa-Levodopa with MAOIs can result in...
|
hypertensive crisis- MAOIs should be D/Cd 2-4 weeks before start of therapy
|
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What effect does B6 (pyroxidine) have on Carbidopa-Levodopa?
|
It increases levadopa destruction.
|
|
|
What (7) foods contain B6?
|
bananas, avocado, oatmeal, sunflower seeds, chicken, halibut
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What Drug interaction happens with Carbidopa-Levodopa and TCAs?
|
delays absorption
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What happens when Hydantions (aka phenytoin- dilantin) are given with Carbidopa-Levodopa?
|
decreases effectiveness of levadopa
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|
|
What is very important to assess before giving Carbidopa-Levodopa as drug therapy?
|
Psych Hx_x000D_
Malignant melanoma- skin lesions?_x000D_ Cardiac Hx |
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|
What diet to follow while on Carbidopa-Levodopa?
|
High protein diet can slow or prevent absorption of carbidopa-levodopa- therefore need to take protein in high amts- eat equally throughout the day_x000D_
•Take on an empty stomach, but take food 15-30 mins after to decrease GI distess. |
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Is Carbidopa-Levodopa less effective for certain races/ethnicities ?
|
Yes- Due to increased COMT in Chinese, Filipino, and Thai populations, this drug is less effective for them.
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|
How long does Carbidopa-Levodopa work for?
|
2-5 years, so they need to alert HCP when symptoms start to worsen so they can be switched to something else
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Should pts on Carbidopa-Levodopa reduce their dietary intake of Vit B6?
|
No! They need to eat the foods high in B6 or take supplements because they still need that vitamin for the body. Plus, only Levodopa ALONE interacts with B6- not the combo drug because the carbidopa inhibits the action of B6
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If taking Levodopa alone should pts avoid foods high in Vit B6?
|
Yes!
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|
|
What are surgical treatments for Parkinson's?
|
Pallidotomy_x000D_
Fetal-Cells- Stem Cell implantation (still in research)_x000D_ Beep Brain Stimulation |
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|
Pallidotomy
|
Can be very effective for controlling Parkinson's Symptoms- go in and destroy brain tissue
|
|
|
Beep Brain Stimulation
|
Put a pacemaker into the brain to interfere with the part of brain causing tremors and to inactivate parts of the brain that causes theose symptoms without purposly destroying the brain like pallidotomy
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|
What are 2 major nursing responsibility with Parkinson's patients?
|
Aspiration precautions and_x000D_
Maintain movement- Keep pt. as mobile & _x000D_ independent as possible |
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What is Meningitis?
|
Inflammation of the meninges- the tissue that surrounds the brain and the spinal cord
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|
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What causes meningitis?
|
Inflammation is caused by viral, bacterial, fungal, or protozoal infection
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|
|
How do organisms enter the brain/meninges?
|
Organisms enter brain via BBB- opened connection between the CSF and the organism following a trauma injury, surgery, ruptured cerebral abscess, or other open entry
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When will we see exudate with meningitis?
|
If infection is bacterial
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What is something that must be constantly monitored with meningitis?
|
Increased ICP d/t blockage of CSF flow that results in a change in blood flow leading to increased ICP, hypoxia, and infarction (stroke)
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|
How common and severe is viral meningitis?
|
It is the most common; it is self-limiting and can get better on it's own.
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How does one get viral meningitis?
|
results from viral illness- measles, mumps, herpes simplex, zoster (shingles) virus
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Is there anything found in the CSF to diagnose meningitis when it is a viral infection?
|
No
|
|
|
Viral menigitis AKA
|
Aseptic Meningitis
|
|
|
S/S Viral meningitis
|
fever, photophobia, HA, myalgias, nausea
|
|
|
Treatment for viral meningitis?
|
symptomatic cases treated only- usually with acyclovir
|
|
|
How serious is bacterial meningitis?
|
VERY SERIOUS- MEDICAL EMERGENCY
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|
|
When do we see a lot of bacterial meningitis cases coming into the hospital?
|
Seasonal when upper resp. infections are common (colds)
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What are the common organisms that cause bacterial meningitis?
|
Bacteria organisms that cause meningitis: Neisseria meningitides (most often), Streptococcus pneumoniae, H. influenza
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|
Outbreaks of Meningococcal meningitis occurs in areas of increased populations in...
|
Close quarters ex: college dorms, military barracks
|
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|
What is the classic triad of symptoms that are associated with bacterial meningitis?
|
Fever_x000D_
Nuchal Rigidity_x000D_ Decreased LOC |
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|
What other S/S are associated with Bacterial Meningitis?
|
Seizures_x000D_
ICP → decreased LOC_x000D_ Brudzinski’s sign_x000D_ Kernig’s Sign |
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|
Brudzinski’s sign
|
neck and hip flexion
|
|
|
Kernig’s Sign
|
SEVERE cases only, passive extension of the knee while hips are flexed
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|
What causes the ICP in bacterial meningitis?
|
exudate and abnormal stimulation of hypothalamic area
|
|
|
If bacterial meningitis is left un-treated...
|
If left untreated → herniation of brain → DEATH
|
|
|
Infant S/S meningitis
|
“flu-like”, increased irritability, arching, decreased feeding, nuchal rigidity,_x000D_
**can be hospitalized for up to 6 months, lose all motor skills- relearn how to walk, talk, eat, etc. |
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|
What will we see when assessing Pupil reaction & Eye movements in bacterial meningitis?
|
nystagmus, photophobia
|
|
|
What cranial nerve responsible for pupil reaction and eye movement?
|
Cranial nerves 2,3,4,6,
|
|
|
What motor response will we see when assessing bacterial meningitis?
|
decreased muscle tone
|
|
|
What cranial nerves are involved in progression to decreased muscle tone?
|
Cranial nerves 3, 4, 6, 7, 8
|
|
|
Will we see memory and behavioral changes with bacterial meningitis?
|
Yes
|
|
|
What type of HA with bacterial meningitis?
|
Severe HA that will not go away
|
|
|
What is the best way to diagnose bacterial meningitis?
|
Analysis of CSF
|
|
|
What will results of CSF analysis be if pt has bacterial meningitis?
|
Appearance cloudy_x000D_
High WBCs and High protein_x000D_ Low Glucose_x000D_ CSF pressure will be elevated |
|
|
What will results of CSF analysis be if pt has viral meningitis?
|
Appearance clear_x000D_
High WBCs and slightly High protein_x000D_ normal or low Glucose_x000D_ CSF pressure varies |
|
|
What is the VERY FIRST thing that is prescribed when bacterial meningitis is even suspected?
|
Broad spectrum Antibiotic – 1st thing!!! prophylaxis_x000D_
very important, patient can die during testing |
|
|
What position should a pt be in after a LP?
|
patient MUST lay flat for 8 hrs after procedure to avoid CSF leakage
|
|
|
What nursing interventions for bacterial meningitis?
|
• monitor VS_x000D_
• FREQUENT neuro and vascular assessments- Q2Hr_x000D_ **change in neuro may indicate increased ICP- esp. LOC changes_x000D_ • reduce environmental stimuli_x000D_ • monitor peripheral pulses_x000D_ • medication management |
|
|
What meds are prescribed for bacterial meningitis?
|
antibiotics, steroids, hyperosmolor, anti epileptics (seizures d/t increased ICP)
|
|
|
The increased ICP in bacterial meningitis increases the likelihood of what?
|
seizures
|
|
|
Encephalitis
|
inflammation of the brain tissue itself and meninges
|
|
|
What is encephalitis usually caused by?
|
Viral infection
|
|
|
What is encephalitis patho?
|
inflammation of the brain tissue and meninges, usually caused by viral infection which causes inflammation which leads to the 2D’s ( neurological degeneration and demylination) where white matter can be destroyed, then swelling or edema occurs resulting in compression and increased ICP, herniation of the brain and ultimately DEATH
|
|
|
Is encephalitis serious?
|
YES LIFE THREATENING-leads to neurological deficits, motor issues, learning disabilities, memory problems, and epilepsy
|
|
|
**CLASSIC TRIAD of clinical manifestations of encephalitis**
|
**FEVER, N/V, STIFF NECK **
|
|
|
Other s/s encephalitis
|
change in mental status_x000D_
neurological deficits_x000D_ motor dysfunction_x000D_ light and/or noise sensitivity_x000D_ fatigue |
|
|
What changes in mental status come with encephalitis?
|
more severe change than meningitis- personality and behavioral
|
|
|
What neurological defecits happen in encephalitis?
|
optic nerve paralysis, nystagmus, facial weakness
|
|
|
optic nerve paralysis, nystagmus, facial weakness in encephalitis- what cranial nerves are involved?
|
Cranial nerves 2, 4, 6
|
|
|
What type of motor dysfunction comes with encephalitis?
|
difficulty swallowing
|
|
|
What cranial nerve is affected if there is difficulty swallowing?
|
Cranial nerve 10
|
|
|
How to diagnose encephalitis?
|
CSF specimen _x000D_
Polymerase Chain Reaction (PCR) |
|
|
What information will CSF give in the case of encephalitis?
|
obtained via lumbar puncture, determines specific infection organism
|
|
|
What information will PCR give in the case of encephalitis?
|
detects viral DNA/RNA chains in CSF
|
|
|
What is the number 1 intervention for encephalitis?
|
Prompt recognition and treatment for increased ICP
|
|
|
Other interventions for encephalitis?
|
frequent VS including O2 sat and neuro checks – Q2Hr_x000D_
HOB elevated between 35-45- not too high to reduce risk of increasing ICP_x000D_ darkened, quiet environment to reduce stimuli |
|
|
What med to give to pts with encephalitis?
|
antiviral medication therapy- acyclovir
|
|
|
What to teach pts and family about encephalitis?
|
family support and care- possibility of long term care: fall precautions, signs and symptoms of decreased LOC and mental status changes, aspiration, swallowing precautions, etc.
|
|
|
What are the outcomes of encephalitis?
|
recovery VERY SLOW, may have full recovery or may have some permanent disabilities_x000D_
_x000D_ Medical management is long term therapy |
|
|
What is a seizure?
|
Abnormal, sudden, excessive, uncontrolled electrical discharge of neurons w/in brain
|
|
|
What is epilepsy?
|
two or more seizures_x000D_
Chronic disorder, repeated unprovoked seizures occur |
|
|
What can be causes of epilepsy?
|
May be caused by:_x000D_
An abnormality in electrical neuronal activity_x000D_ Imbalance of neurotransmitters (GABA)_x000D_ both |
|
|
Triggers for seizures?
|
Increased physical exertion_x000D_
Emotional stress_x000D_ Stimulants (caffeine)_x000D_ Fatigue_x000D_ Foods_x000D_ Chemicals_x000D_ Bright lights, strobes |
|
|
Three broad categories of seizures
|
1. Generalized seizures- both hemispheres_x000D_
_x000D_ 2. Partial seizures- one hemisphere_x000D_ _x000D_ 3. Unclassified seizures |
|
|
Generalized Types of seizures affect which hemisphere?
|
Affects Both Hemispheres
|
|
|
4 types of generalized seizures
|
Tonic Clonic (Grand Mal)_x000D_
Absent _x000D_ Myoclonic_x000D_ Atonic |
|
|
Tonic Clonic (Grand Mal) seizure
|
(generalized-both hemi)_x000D_
_x000D_ Lasts 2-5 Mins_x000D_ Tonic Phase→Stiff, Rigid, LOC_x000D_ Clonic Phase→Jerky Uncontrolled Movements_x000D_ Post-Ictal→Resting Phase May Last Up To 2 Hours, Do Not Wake The Pt, Allow Them To Wake Up On Their Own! |
|
|
What is the tonic phase?
|
Stiff, Rigid, LOC
|
|
|
What is the clonic phase?
|
Jerky Uncontrolled Movements of extremities, biting down, sometimes incontinence
|
|
|
What is the post-ictal phase?
|
Lethargy Phase after seizure. May Last Up To 2 Hours, Do Not Wake The Pt, Allow Them To Wake Up On Their Own!
|
|
|
What sometimes happens right before a seizure?
|
Person will feel an aura or sensation that something is about to happen
|
|
|
Absent (Petite Mal) seizure
|
Mostly Children _x000D_
Day-Dreamers_x000D_ Short Seizure Activity_x000D_ Blank Stare Brief Loss Of Consciousness Automatisms→Lip Smacking, Picking At Clothing_x000D_ Abrupt Return To Baseline_x000D_ _x000D_ (generalized-both hemi) |
|
|
Automatisms
|
Lip Smacking, Picking At Clothing
|
|
|
Why does it sometimes take a long time for absent seizures to be diagnosed in children?
|
This can take a long time to be diagnosed because parents think their kids just dayderam, the longer it goes on the more and more it can happen and can start to interfere of their activities and daily lives
|
|
|
What can happen if absent seizures are left untreated?
|
If Untreated May Result In Learning Disabilites And Problems In School
|
|
|
Myoclonic seizures
|
(generalized-both hemi)_x000D_
_x000D_ Short In Duration seconds to minutes_x000D_ Jerky/Stiff/Rigid Movements of extremities_x000D_ Unilateral and/or Bilateral_x000D_ _x000D_ (generalized-both hemi) |
|
|
Atonic seizure
|
Rapid Loss Of Muscle Tone_x000D_
Pt Loses Consciousness_x000D_ Post-ictal Confusion Upon Awakening_x000D_ _x000D_ (generalized-both hemi) |
|
|
What is the biggest danger of atonic seizures?
|
Injury! They have falls
|
|
|
Partial seizures affect how many hemispheres?
|
1
|
|
|
Are partial seizures common in adults or children?
|
adults
|
|
|
Are partial seizures more responsive or less responsive to treatment?
|
Less responsive
|
|
|
Types of partial seizures?
|
Complex Partial_x000D_
_x000D_ Simple Partial |
|
|
Complex Partial seizure
|
1-3 Minutes In Duration_x000D_
Loss Of Consciousness_x000D_ Amnesia Afterwards_x000D_ Automatisms |
|
|
Simple Partial Seizure
|
1-2 minutes (+ or-)_x000D_
Aura beforehand_x000D_ Unilateral Movement Of Extremity_x000D_ Pt Is Conscious_x000D_ Weird Sensations- Metallic Taste, Pain, Offensive Smells_x000D_ Memory intact afterward |
|
|
Standard Seizure precautions
|
Pad The Side Rails (Side Rails Up X 4)_x000D_
Have O2 w/ face mask ready_x000D_ IV access Ready to go_x000D_ Suction ready to go_x000D_ Remove Restrictive Clothing |
|
|
What to do for pt during seizure?
|
Do Not Restrict Their Movements_x000D_
Turn Pt On Side_x000D_ Time The Seizure_x000D_ Notice Characteristics |
|
|
What to do immediately after a seizure?
|
Supplemental O2 Via Mask, Not Nasal Cannula_x000D_
Suction After The Pt Is Done Seizing |
|
|
Why do we NOT put anything in persons mouth during a seizure?
|
Chipped Teeth→Airway Obstruction
|
|
|
What to do with family during their loved ones seizure?
|
If Family Is Present→ Keep Them Busy With Helpful Jobs, “Hold My Pen”, “Please Time The Seizure”, “Sit And Relax, Talk To Your Family Member In Postictal Period”
|
|
|
Status Epilepticus
|
Seizure Activity Lasting Longer Than 5 Minutes Or Recurring Seizures Lasting Longer Than 30 Minutes
|
|
|
Is Status Epilepticus serious?
|
Yes! This Is A Medical Emergency_x000D_
Medications Are Required |
|
|
What meds to give in status epileptics?
|
Benzos (Short Acting)_x000D_
Dilantin_x000D_ Tegretal/Depakote |
|
|
Meds used to treat seizures?
|
Dilantin_x000D_
Benzos_x000D_ Tegretal_x000D_ Valporic Acid (Depakote/Depakene) |
|
|
What is one of the oldest drugs used to treat seizures?
|
Dilantin
|
|
|
Which seizures is Dilantin useful for?
|
Status epilepticus and tonic-clonic (grand mal)
|
|
|
What drug classification is Dilantin (phenytoin)?
|
Anti-epileptic- HYDANTOINS the toins""
|
|
|
What is the action of Dilantin?
|
Controls seizures by reducing the amount of sodium influx into the cells. This causes decreased Depolarization and activity of the cells to fire
|
|
|
How long does Dilantin take to take effect?
|
Long Half Life 7-10 Days To Trake Effect
|
|
|
If Dilantin given PO...
|
TAKE WITH MEALS
|
|
|
If Dilantin given NGT
|
Dilute
|
|
|
If Dilantin given IV/IVP...
|
Give SLOWLY!!! Can Cause Cardiovascular Collapse!!!!! Give 50mg/Min
|
|
|
What rate to give Dilantin IV/IVP?
|
50mg/Min
|
|
|
What drugs does Dilantin interact with?
|
ETOH, Benzos, Ibuprofen_x000D_
Barbiturates_x000D_ Acetaminophen |
|
|
What is the effect if Dilantin interacts with ETOH, Benzos, Ibuprofen?
|
Inhibit The Metabolism Of Dilantin=Drug Toxicity
|
|
|
What is the effect if Dilantin interacts with Barbiturates?
|
Inhibit Absorption Of Dilantin=Decreased Effects
|
|
|
What is the effect if Dilantin interacts with Acetaminophen?
|
Accelerates The Metab Of Aceta. Causing Decreased Analgesic Effects Of Acetaminophen and more Aceta circulating so more liver damage potential
|
|
|
Dilantin most common A/E?
|
Nausea, Dizziness, Blurred Vision, Ataxia
|
|
|
Dilantin most SERIOUS A/E?
|
Cardiovascular Collapse
|
|
|
Can Dilantin and Benzos be given in the same IV line?
|
No- they will precipitate
|
|
|
What medications can be used to ABORT a seizure?
|
Dilantin_x000D_
Benzos_x000D_ Tegretal_x000D_ Valporic Acid (Depakote/Depakene) |
|
|
Examples of Benzos?
|
Valium/Ativan/Lorazepam
|
|
|
How do Benzos work to stop seizures?
|
They increase the effect of the neuro-inhibitor GABA
|
|
|
What is GABA?
|
inhibitory neurotransmittor that works in opposition to glutamate
|
|
|
Benzos action
|
Keep Chloride Channels Open Longer→ Raises Cells Threshold To Fire→Produces Inhibitory Effect Decreasing Electrical Activity In The Brain
|
|
|
In what case is Benzo the first choice when having to do with seizures?
|
In status epilepticus they are the first choice before any other seizure aborting drug
|
|
|
Are the Benzos given over long periods of time for seizures?
|
No- they are on the BEERs criteris of meds to watch out for- they have a very high addictive rate, so only used short term
|
|
|
What drugs to avoid when giving benzos?
|
Any other sedative drugs- ETOH and CNS depressants!
|
|
|
What to closely monitor with Benzos?
|
ABGs
|
|
|
A/E of benzos?
|
Cann
|
|
|
How does Tegretal (Carbamazipine) work to control seizures?
|
Reduces Influx Of Na Ions, Thus Decreases Cells Ability To Fire
|
|
|
What is important to monitor when ot taking Tegretal?
|
Monitor Blood Levels 2-4mcg/Ml,
|
|
|
When is Tegretal used for seizures?
|
When other meds are ineffective
|
|
|
How does Valporic Acid (Depakote/Depakene) work to reduce seizures? (Action)
|
Reduces Influx Of Na Ions, Thus Decreases Cells Ability To Fire
|
|
|
What is important to monitor for in pts taking Valporic Acid?
|
Monitor Blood Levels 50-150mcg/Ml, Monitor Liver (Hepatotoxic Alt, Ast) And Renal Function Tests)
|
|
|
A/E of Valporic Acid?
|
Sedation, Dizziness, Agitation
|
|
|
What should nurses teach pts that have seizures... a good way to document for complete hx?
|
Patients Should Keep A Seizure Diary (Characteristics, Triggers, Reactions To Meds)
|
|
|
If pts miss a dose of their seizure meds, can they double up the next time?
|
NO
|
|
|
Should seizure pts wear anything special on a day to day basis?
|
Wear a medic alert bracelet
|
|
|
What is the antidote to Heparin (and should be on hand during dialysis?)
|
Protamine Sulfate
|
|
|
MG
|
Myasthenia Gravis “Grave Muscle Weakness"_x000D_
What type of disease?" |
|
|
What happens in Myasthenia gravis?
|
Skeletal/voluntary muscles cannot hold a contraction.
|
|
|
What happens at the cellular level in Myasthenia gravis?
|
• Normally ACh is the neurotransmitter that causes muscles to contract, Cholinesterase comes in to break down Ach in the synapse, causing muscles to contract._x000D_
• In the case of MG there is an autoantibody attack on the Ach receptors in muscle end plate membranes, limiting the number of receptors, and so those nerve impulses are not transmitted to the muscles. |
|
|
Causes of Myasthenia gravis?
|
o Over growth (hyperplasia) of the Thymus Gland_x000D_
o Thymoma (encapsulated thymus gland tumor)_x000D_ o Strong relationship with hyperthyroidism |
|
|
Myasthenia gravis symptoms?
|
o Weakness and fatigue (esp. muscles that are innervated by cranial nerves, skeletal, and respiratory muscles)_x000D_
o Ocular muscles affected- Ptosis (drooping eyelids- like Sleepy), diplopia- dbl vision_x000D_ o Bulbar involvement (muscles used for facial expression)_x000D_ o Chewing, swallowing, speech difficulty_x000D_ o Muscle weakness that increases w/ exertion and improves with rest |
|
|
What is a blood test looking for in Myasthenia Gravis?
|
To detect Ach receptor antibodies- will be increased
|
|
|
What pharmacology test is used to diagnose Myasthenia Gravis?
|
Tensilon Test (Challenge)-
|
|
|
Why is the Tensilon Test (Challenge)- used to help diagnose Myasthenia Gravis?
|
It is a Cholinesterase inhibitor and within minutes with will temporarily increase levels of ACh and relieve weakness- this tells us that there is a problem with ACh and it is MG
|
|
|
What is the antidote to Tensilon?
|
Atropine
|
|
|
What diagnostic tests are used to help diagnose MG?
|
EMG_x000D_
CT_x000D_ PFT |
|
|
What will EMG tests show in cases of MG?
|
nerve conduction study which tests for specific muscle “fatigue” be repetitive nerve stimulation- shows muscles decreased response to repetitive stimulation
|
|
|
What will CT tests show in cases of MG?
|
Abnormal thymus gland- useful to identify if there is any thymus gland present or a thymoma
|
|
|
What will PFT tests show in cases of MG?
|
measure breathing strength- helps predict whether respiratory system may fail and lead to myasthenic crisis
|
|
|
What two Anticholinesterase/ cholinesterase hinibitor/ cholinergic agonist drugs are used to treat Myasthenia Gravis?
|
neostigmine (Prostigmin)_x000D_
and_x000D_ pyridostigmine (Mestinon) |
|
|
What is the drug of choice for Mysathenia Gravis?
|
pyridostigmine (Mestinon)
|
|
|
Ho do the anticholinesterase drugs work to treat MG?
|
ONLY FOR SYMPTOMS_x000D_
increases amount of Ach available at the receptor site- resulting in enhanced muscle contraction. |
|
|
Most common A/E of the Anticholinesterase drugs?
|
N/V/D, bradycardia, miosis, diaphoresis
|
|
|
Most serious A/E of the Anticholinesterase drugs?
|
cholinergic crisis
|
|
|
How to admin Anticholinesterase drugs?
|
PO- Admin with small amount of food to minimize GI effects- 45 min to 1 hr after taking med to prevent aspiration
|
|
|
What other drugs to avoid while pt is on Anticholinesterase drugs?
|
Mg, morphine, hypnotics, etc. should be avoided- they may increase pts weakness
|
|
|
What is the antidote to the Anticholinesterase drugs?
|
Atropine
|
|
|
How does the dosing of Pyridostigmine (Mestonin) work?
|
the dose depends on that say’s symptoms- like a sliding scale. Given PO. A/E and antidote same as Neostigmine
|
|
|
Why are Corticosteroid Meds given to treat Myasthenia Gravis?
|
• Used to induce remission_x000D_
• Immunosuppression _x000D_ • Used if pt doesn’t respond well to Anticholinesterase drugs |
|
|
Why are Immunosuppression Meds (Imuran, Cytoxin) given to treat Myasthenia Gravis?
|
Used to induce remission
|
|
|
How do immunosuppression meds improve muscle strength in myasthenia gravis?
|
• Improves muscle strength by suppressing the production of abnormal antibodies
|
|
|
Major side effects of Immunosuppressant Meds (Imuran, Cytoxin)?
|
• Infection_x000D_
• Leukocytosis (Low WBC count)_x000D_ • Liver Dysfunction (Monitor LFTs- AST/ALT)_x000D_ • Hair loss |
|
|
What medications are used to induce remission in Myasthenia Gravis?
|
Corticosteroids_x000D_
and _x000D_ Immunosuppressants |
|
|
What medications are used to relieve symptoms in Myasthenia Gravis?
|
the anticholinesterase drugs
|
|
|
What surgeries have been helpful in treating myasthenia gravis?
|
Thymectomy
|
|
|
How does the Thymectomy help with Myasthenia Gravis?
|
removing the thymus in order to (hopefully) rebalance the immune system- takes about 2 year post op to be effective
|
|
|
What is important nursing care post op thymectomy?
|
• Post op- pay extra attention to pulmonary hygiene (suction PRN)_x000D_
• Provide chest tube care_x000D_ • Sterile technique for wound care_x000D_ • Observe for s/s pneumothorax or hemothorax (Major Complications!) |
|
|
What are s/s pneumothorax or hemothorax?
|
• Chest pain, SOB, dim chest wall expansion, dim breath sounds, change in V/S
|
|
|
What to do if nurse suspects pneumothorax or hemothorax?
|
• Call surgeon STAT, Provide O2, raise HOB 45 degrees
|
|
|
How does plasmaphoresis helpin Myasthenia Gravis?
|
• Plasma taken out and replaced. Done to DECREASE the amount of Ach ANTIBODIES
|
|
|
How long does plasmaphoresis relieve Myasthenia Gravis symptoms?
|
only lasts a couple months if treatment done alone- that is why thymectomy is usually done after this
|
|
|
What is a Myasthenic Crisis
|
• Sudden worsening of symptoms
|
|
|
What causes a myasthenic crisis?
|
TOO LITTLE cholinesterase inhibitor drugs
|
|
|
S/S Myasthenic crisis?
|
• Increase HR, BP, absence of cough, swallow reflex absent or decreased
|
|
|
Nursing focus during myasthenic crisis?
|
• Treatment- focus on respiratory support. Most pts on mechanical vent
|
|
|
Do we give more cholinesterase drugs during myasthenic crisis?
|
• Even though this is due to too little cholinesterase drugs, we still do not want to increase drugs during crisis because it would cause an increase in secretions and the pt is already having respiratory problems.
|
|
|
What is a Cholinergic Crisis
|
• Acute exacerbation of symptoms
|
|
|
What causes a Cholinergic Crisis
|
TOO MUCH cholinesterase inhibitor drugs
|
|
|
S/S Cholinergic Crisis
|
• Increase in weakness, Twitching especially around the eyes, general facial weakness_x000D_
• Inability to clear secretions, swallow, or breathe adequately |
|
|
Do we give more cholinesterase drugs during Cholinergic Crisis?
|
we do not want to increase drugs during crisis because it would cause an increase in secretions and the pt is already having respiratory problems.
|
|
|
What to do during a myasthenic or cholinergic crisis??
|
Do not give MG Drugs- Monitor Respiratory Status- Call DR, going to so the Tensilon Test
|
|
|
How to distinguish between myasthenic or cholinergic crisis
|
Tensilon Test
|
|
|
What will the Tessilon test show if it is myasthenic crisis?
|
a TEMPORARY IMPROVEMENT of symptoms in Myasthenic crisis
|
|
|
What will the Tessilon test show if it is Cholinergic crisis?
|
NO IMPROVEMENT of symptoms in Cholinergic Crisis
|
|
|
What nursing interventions if tensilon tests shows that it is myasthenic crisis?
|
• Monitor Resp status, mech vent possibly, drugs w/held, takes few days to recover
|
|
|
What nursing interventions if tensilon tests shows that it is cholinergic crisis?
|
• Give antidote- Atropine 1mg IV, repeat if necessary_x000D_
• Monitor airway- secretions can thicken_x000D_ • Improves rapidly after antidote is given |
|
|
What is the overall goal for Myasthena Gravis?
|
Goal: Maintain muscle strength!
|
|
|
When should meds be given to Myasthenia Gravis pts?
|
Give meds before eating to prevent aspiration, but because some meds should be given with food to prevent GI upset, provide meal as soon as medication kicks in
|
|
|
When should myasthenia gravis pts expect peak activity?
|
peak activity in the morning- Weakness will increase throughout the day
|
|
|
Pt teaching for myasthenia gravis?
|
Teach that disease has exacerbations and remissions_x000D_
Things that may cause exacerbation_x000D_ Take drugs at same time to maintain therapeutic level |
|
|
Things that may cause exacerbation of myasthenia gravis
|
fever, stress, infection, surgery, exercise, extreme heat/weather change, change in sleep habits (sedatives)- any sudden change in body
|
|
|
Is there a cure for MG... Can MG pts live long lives?
|
NO CURE FOR MG BUT LONG TERM REMISSION IS POSSIBLE, they can still live normal or near normal lives
|
|
|
What are the cranial nerve diseases?
|
Trigeminal _x000D_
Bell’s Palsy |
|
|
What is Trigeminal Nerve Disease?
|
“tic douloureux”- PAINFUL TWITCH_x000D_
_x000D_ Unilateral, sudden, intense facial spasms |
|
|
What facial nerve is affected in Trigeminal Nerve Disease?
|
affects Cranial Nerve 5- Trigeminal Nerve
|
|
|
What is the likely cause of trigeminal verve disease?
|
Cause is uncertain but most likely due to vascular compression.
|
|
|
Clinical Manfiestatios of Trigeminal Nerve Diasease
|
• unilateral sudden onset intense facial spasms _x000D_
• sharp, shooting, piercing, burning pain |
|
|
What usually brings the onset of painful facial twitch?
|
provoked by stimulation at trigger zone_x000D_
pt usually aware of what causes pain |
|
|
How long does the painful twitch last in Trigeminal nerve disease?
|
may go on for weeks to months- then no pain for a period of time
|
|
|
Trigeminal Nerve Disease- does it ever go away?
|
rarely does it go away forever
|
|
|
Medications to manage Trigeminal Nerve Disease?
|
Antiseizure Meds and_x000D_
Pain Meds |
|
|
What antiseizure meds to help with Trigeminal Nerve Disease?
|
carbamazepine (Tegretol), phenytoin (Dilantin)_x000D_
meds decrease nerve transmission_x000D_ TAKE WITH MEALS |
|
|
A/E of carbamazepine (Tegretol), phenytoin (Dilantin)
|
Adverse Effects: dizzy, drowsy
|
|
|
What types of pain medications are used for trigeminal nerve disease?
|
gabapentin ( Neurontin)_x000D_
lidocaine- numbs pain _x000D_ calcitonin intranasal spray- temporary relief |
|
|
Are opioids effective for nerve pain?
|
No
|
|
|
How can Microvascular Decompression work to relieve trigeminal nerve disease?
|
posterior craniotomy done microscopically_x000D_
artery pressing is lifted to relieve pressure by use of a small prosthetic device |
|
|
How can Radiofrequency Thermal Regulation work to relieve trigeminal nerve disease?
|
small heat lesions made in nerve to stop conduction of pain; affected side will be permanently unresponsive to pain
|
|
|
How can Balloon Microcompression work to relieve trigeminal nerve disease?
|
balloon compresses the nerve root and vascular structures
|
|
|
For balloon microcompression- what nursing int pre op
|
no eating hot or cold foods or washing face with hot or cold water which can trigger pain
|
|
|
For balloon microcompression- what nursing int post op
|
CN ASSESMENT- ALL CRANIAL NERVES_x000D_
ice pack to site – monitor closely d/t decreased sensations_x000D_ prevent chewing, rubbing eyes on affected side- can bite through tongue, can injure eye_x000D_ regular dental visits d/t absence of pain |
|
|
What is Bell’s Palsy
|
A Cranial Nerve Disease that causes Facial Paralysis
|
|
|
How does Bells Palsy Manifest?
|
unilateral paralysis of Cranial Nerve VII- Facial Nerve, can also affect Cranial Nerve V(Facial)
|
|
|
Which cranial nerve is affected in Bells Palsy?
|
7- facial Nerve (can also affect 5)
|
|
|
Bells Palsy is caused by __________ which weakens or paralyzes facial muscles on affected side
|
inflammation
|
|
|
What can trigger Bells Palsy?
|
inflammation process may be triggered by herpes simplex virus (HSV-1)
|
|
|
Clinical Manifestations of Bells Palsy
|
• pain: face, ear, eye_x000D_
• quick onset of paralysis- full extent within 2-5days_x000D_ • distorted face- cannot move anything on affected side, increased tearing, speech and eating affected |
|
|
Do pts ever recover from Bells Palsy?
|
MOST recover completely with no residual effects_x000D_
80% fully recover within a few weeks to months |
|
|
What part of face is important to protect in cases of Bells Palsy?
|
protection of eye- artificial tears, taped or shield at bedtime, goggles or sunglasses to protect from debris and sunburn
|
|
|
What nsg interventions in regard to facial muscles for bells palsy?
|
eat and drink on unaffected side to reduce injury- small meals are easier to tolerate_x000D_
prevent facial muscle atrophy- massage, facila exercises_x000D_ facial exercises: wrinkling forehead, blowing out cheeks, whistling |
|
|
Glasgow coma scale (GCS)
|
tool used to help describe the patient’s level of consciousness. It has been shown to be very reliable for most patients
|
|
|
What do the scores of Glasgow Come Scale mean?
|
A score of 15 means the patient has normal neurologic function, where a score of 7 means the patient is comatose. The lower the score, the lower the patient’s level of consciousness.
|
|
|
The GCS establishes baseline data in each of these areas (3):
|
• Eye opening_x000D_
• Motor response_x000D_ • Verbal response |
|
|
Definition of a stroke (Brain Attack)?
|
Infarction of brain cells caused by a reduction in cerebral blood flow & oxygen
|
|
|
What does complete recovery depend on after a stroke- what is the time frame for optimal results and treatment options?
|
circulation returning to normal, 3 hour window
|
|
|
Transient ischemic attack (TIA) and s/s?
|
a brief period of neurological deficit (visual loss, hemiparesis, slurred speech, aphasia, &vertigo)
|
|
|
How long do transient ischemic attacks last?
|
30 seconds to 24 hours (w/ complete resolution of symptoms)--> but generally a warning sign of a stroke in near future
|
|
|
List the three common causes of a stroke (brain attack)?
|
Thrombosis, embolus, hemorrhage
|
|
|
What is the most common cause of a brain attack (stroke)?
|
Thrombosis (60-80%) due to atherosclerosis
|
|
|
What causes an embolus, that causes a stroke?
|
clot of: fat, air tumor, or bacteria that occludes blood vessels in the brain
|
|
|
Who is at risk for a stroke caused by an embolus?
|
a-fib, orthopedic surgery pts
|
|
|
The third common cause of a stroke is hemorrhage rt what?
|
sudden rupture of a cerebral blood vessel from chronic HTN or aneurysm.
|
|
|
What are the modifiable risk factors for a stroke?
|
1. HTN (3/4 rt HTN)_x000D_
2. BMI >30, increased ab fat_x000D_ 3. A-Fib (5X greater risk, causes stasis) |
|
|
What are the main non-modifiable risk for having a stroke?
|
1. age_x000D_
2. race (African, Hispanic, Indian) |
|
|
List Subjective Clinical manifestations:
|
syncope, changes in LOC, TIAs, HA, mood swings
|
|
|
Objective, hemiplegia?
|
paralysis; on side opposite lesion _x000D_
(initially flaccid) |
|
|
Objective, hemiparesis?
|
muscular weakness on one side of body
|
|
|
Objective, dysphagia?
|
impaired swallowing_x000D_
(aspiration, PNA, NPO, until gag reflex assessed, speech therapy) |
|
|
Objective, _x000D_
alexia?_x000D_ dyslexia?_x000D_ agraphia? |
1. inability to comprehend written words_x000D_
2. inability to read written words_x000D_ 3. loss of ability to write |
|
|
Objective, _x000D_
expressive aphasia?_x000D_ receptive aphasia?_x000D_ expressive-receptive aphasia? |
1. difficulty making thoughts known to others, speak & write incorrect words_x000D_
2. DIFFICULTY UNDERSTANDING what others communicate_x000D_ 3. equal difficult speaking, writing, interpretting speech or reading |
|
|
Objective, dysarthia?
|
paralysis of facial muscles, difficulty speaking
|
|
|
Objective, homonymous hemianopia?
|
loss of half of visual field, affected side of vision corresponds to the paralyzed side of body.
|
|
|
Objective, _x000D_
diplopia?_x000D_ ptosis? |
1. double vision_x000D_
2. drooping eyelids (same side as lesion) |
|
|
Objective, sensory changes, proprioception?
|
impairment of touch, awareness of body position in space, spatial/ balance difficulties
|
|
|
Objective, alternation in reflexes?
|
initially pt may be flaccid/paralysis or loss of deep tended reflexes. Reflexes reappear by 48 hours accompained by increased tone & spasticity
|
|
|
Objective, cognitive?
|
loss of memory, poor judgement, decrease in attention span
|
|
|
Objective, emotional deficits?
|
frustration, anger, confusion, depression, w/drawal, feeling of isolation
|
|
|
What does the extent of injury depend on with a stroke pt?
|
artery location
|
|
|
Explain the thrombolytic therapy, rtPA?
|
Recombinant tissue plasminogen activator dramatically improves the chances of survival. Must be administered w/in 3 hours of s/s. (need Ct or MRI scan)
|
|
|
What are the contraindications of using rtPA?
|
1. s/s longer than 3 hours_x000D_
2. active hx. of bleeding_x000D_ 3. low platelet count_x000D_ 4. taking anticoagulatnts |
|
|
Antiplatelet agents (ASA) are used for tx of?
|
non cardioembolics causes of TIA & carotid stenosis
|
|
|
The main medical interventions are based on what care plan theories?
|
maintaining life, reducing ICP, limiting extension of stroke, preventing complications
|
|
|
The acute phase 48-72 hours for a stroke pt is the same as?
|
caring for an unconscious client
|
|
|
Explain the main neuro assessment for a stroke pt?
|
ICP, GCS, facial symmetry, arm drift
|
|
|
Why is it so important for speech therapy to assess gag reflex?
|
PNA aspiration
|
|
|
Name the nursing interventions when it comes to nutrition for a stroke victim?
|
1. place food in unaffected side of mouth_x000D_
2. semi-solid foods _x000D_ 3. offer solids & liquids at diff times_x000D_ 4. High Fowlers_x000D_ 5. keep pt in upright pos. for 45 to 60 min |
|
|
Where should pts belongings be placed?
|
on unaffected side. Always approach on unaffected side.
|
|
|
What should we teach pts about SAFETY?
|
to compensate by scanning (turning head to see things on affected side)
|
|
|
List for nursing interventions used to increase mobility?
|
1. proper pos. to prevent deformities (support with pillow or sling)_x000D_
2. elevate extremities to prevent edema_x000D_ 3. ROM Q4, use of muscles may return if complications involving muscoskeletal system have been prevented_x000D_ 4. REHABILITATION SHOULD BEGIN ON DAY 1. PT, OT, ST, SW, NURSING WORK TOGETHER |
|
|
What should be considered for bowel & bladder control for a stroke pt?
|
adequate fluids, diet w/ roughage, monitor for fecal impaction
|
|
|
For emotional lability what should be done for stroke pts?
|
maintain quiet, restful environment, Cal, non-threatening manner
|
|
|
Nursing interventions for pt with expressive aphasia?
|
associate words with physical objects, anticipate pts need to express helplessness
|
|
|
Nursing interventions for pt with receptive aphasia?
|
slow directions, allow adequate time, nonverbal techniques of communication
|
|
|
Why is anticoagulant therapy used in brain attack medical interventions?
|
used if atrial fib present though research doesn't show benefit
|
|
|
Describe the implications thrombolytic therapy rtPA as a medical intervention for stroke victims?
|
Recombinant tissue plasminogen activator dramatically improves chances of survival. Must be given w/in 3 hours of s/s (need MRI or CT scan)
|
|
|
What are the contraindications of using rtPA (tissue plasminogen activator)?
|
active/ hx of bleeding, low platelet count, already taking anticoagulatns
|
|
|
When is ASA (antiplatelet agents) used?
|
tx for non-caridoembolic of TIA & carotid stenosis
|
|
|
Medical interventions are guided by what 4 implications when txing stroke victims?
|
maintaining life_x000D_
reducing ICP_x000D_ limiting extension of stroke_x000D_ preventing complications |
|
|
The nursing interventions for a stroke victim in the acute phase is the same as?
|
caring for the unconscious client_x000D_
(Neuro checks, s/s of I ICP, facial symmetry, arm drift, GCS) |
|
|
Why is it so important to evaluate swallowing and gag reflexes?
|
risk for aspiration PNA
|
|
|
Who evaluates gag reflex?
|
speech therapy
|
|
|
Nutrition education for a stroke victim?
|
1. place food in unaffected side of mouth_x000D_
2. semi-solid foods are best_x000D_ 3. offer solid/ liquids at diff times_x000D_ 4. high fowlers for eating_x000D_ 5. upright for 45 after eating |
|
|
Safety implications for stroke patients include?
|
organize enviornemnt, place items where they can be reached, unclutter environment
|
|
|
Do to homonymous hemianopia where should patient personal belongings be placed?
|
on unaffected side, approach on unaffected side. TEACH pt to compensate by scanning room
|
|
|
Do to homonymous hemianopia where should patient personal belongings be placed?
|
on unaffected side, approach on unaffected side. TEACH pt to compensate by scanning room
|
|
|
Define Peripheral Vascular Disease?
|
Progressive narrowing & degeneratie dz of the blood vessels in peripheral circulation (thick arteries).
|
|
|
Describe patho of PAD/ PVD?
|
occluded arterial blodo flow due to atherosclerosis, thrombus, embolus
|
|
|
Leading cause of PAD?
|
atherosclerosis, diabetes, obesity, smoking
|
|
|
List common s/s of PVD?
|
1. intermittent claudation, pain described as burning, achy, cramps_x000D_
2. skin smooth, shinny w/ hair loss_x000D_ 3. nails thicken_x000D_ 4. no edema present_x000D_ 5. skin cool, pale, cyanotic, ulcerated, gangreen_x000D_ 6. D peripheral pulses |
|
|
How are diabetic and PVD ulcers different?
|
PVD on surface, diabetic on pressure points
|
|
|
#1 predisposing factor for PVD?
|
HTN
|
|
|
How does ankle brachial pressure index help identify severity of occlusive dz?
|
BP in lower extremeties should be higher than upper
|
|
|
Why should legs be kept level w/ heart but not above with arterial problems?
|
bc legs will completely loose blood flow
|
|
|
Foot care and well footed shoes help reduce injury in PVD pts, should ted hose be used?
|
NO
|
|
|
In what kind of leg problems should legs be elevated and ted hose be used?
|
Venous ulcers
|
|
|
Describe proper exercise in pvd pts?
|
walk 34 to 45 min, stop at onset of claudication, resting until the symptoms resolve
|
|
|
What has been reported to decrease progression of atherosclerosis in pts w peripheral arterial occlusive dz?
|
antiplatelet agents: _x000D_
plavix & aspirin |
|
|
Describe proper exercise in pvd pts?
|
walk 34 to 45 min, stop at onset of claudication, resting until the symptoms resolve
|
|
|
What has been reported to decrease progression of atherosclerosis in pts w peripheral arterial occlusive dz?
|
antiplatelet agents: _x000D_
plavix & aspirin |
|
|
Define Raynaud's Dz?
|
vasospasms fo digital arteries
|
|
|
Individuals w/ Raynaud's dz may later develop what dz?
|
connective tissue
|
|
|
Precipitaiton factors for Raynaud's?
|
cold, stress, smoking
|
|
|
How does Nifedipine help Raynaud's?
|
helps w/ arterial vasodilation
|
|
|
Patho of DVT?
|
Superficial thrombophlebitis begins w/ localized inflammation alone; inflammatory process causes thrombus formation. PLATELETS, RBC, FIBRIN form a clot in vein
|
|
|
Causes & incidence of DVT?
|
stasis, vascular damage & hypercoagulability = VIRCHOW'S TRIAD
|
|
|
Causes of venous stasis that may lead to DVT?
|
a-fib_x000D_
orthopedic surgery_x000D_ prolonged immobility |
|
|
What can lead to hypercoagulability contributing to DVT?
|
smoking, pregnancy, estrogen therapy, sepsis
|
|
|
S/S of DVT only when clot completely obstructs blood flow?
|
1. swelling/ edema_x000D_
2. muscle tenderness_x000D_ 3. warmth on affected side_x000D_ 4. pain (calf, when ankle is bent dorsiflexion- Homan's)_x000D_ 5. malaise & fever_x000D_ 6. 50% have no s/s--> unexplained tachycardia, tachypnea, anxiety, hypoxia |
|
|
Posts-thrombotic syndrome develops in 40-60% of pts w/ DVT and is characterized by?
|
skin changes, ankle reddish-brown dicoloration, ulceration, chronic, hard to heal
|
|
|
Name the diagnostic tools used for DVT?
|
Venous ultrasonography_x000D_
Homan's sign_x000D_ D-Dimer (thrombotic process) |
|
|
Prevention of PE is most important reason for treating DVT, how is this accomplished?
|
1. anticoagulants (heparin, lovenox, coumadin)
|
|
|
Name the low-molecular weight heparin therapy that has a lower half life which makes monitoring CBC and platelet count easier?
|
Lovenox_x000D_
(small purple hemorrhage area on upper abdomen) |
|
|
Why is it important to overlap heparin tx with Coumadin for at least 4 to 5 days?
|
Full effect of coumadin is delayed. Coumadin blocks prothrombin synthesis by interfering w/ Vit K. Pts need to monitor Vit K rich foods * have their INR checked every 4-6 weeks. Pts should avoid invasive procedures & surgery while on Coumadin
|
|
|
How does elevating the DVT involved extremity help?
|
I venous return & D edema
|
|
|
What labs should be monitored for:_x000D_
Heparin:_x000D_ Coumadin:_x000D_ Lovenox: |
1. PT & PTT (kept at 1.5-2.5 > N)_x000D_
2. INR_x000D_ 3. CBC, platelets |
|
|
Antidotes for:_x000D_
Heparin:_x000D_ Coumadin: |
1. Protamine Sulfate_x000D_
2. Vit. K |
|
|
What is HIT?
|
Heparin induced thrombocytopenia: 50% decrease in plateletes
|
|
|
S/s of PE?
|
pleuritic chest pain, tachycardia, anxiety
|
|
|
How surgery is used to tx emboli's?
|
vena cava surgery is done (insertion of umbrella filter cap)
|
|
|
Label as R-apid, S-hort, I-termed, or L-ong acting:_x000D_
_x000D_ Aspart_x000D_ Detemir_x000D_ Glargine_x000D_ Humulin NPH_x000D_ Novolin NPH_x000D_ Novolin R_x000D_ Glulisine_x000D_ Humulin R_x000D_ Lispro |
Aspart - R = 5-15m_x000D_
Detemir - L = 20-24h_x000D_ Glargine - L_x000D_ Humulin NPH - I = 4-14_x000D_ Novolin NPH - I_x000D_ Novolin Reg - S = 2-4h_x000D_ Glulisine - R_x000D_ Humulin Reg - S_x000D_ Lispro - R |
|
|
How long do these last in hours?_x000D_
_x000D_ Rapid_x000D_ Short_x000D_ Intermed_x000D_ Long |
Rapid 5-15h_x000D_
Short 1-4h_x000D_ Intermed 4-12h_x000D_ Long 20-24h |
|
|
Which insulin type can't you mix?
|
long acting = detemir, glargine
|
|
|
Which insulin type is cloudy?
|
NPH's = novolin and humulin
|
|
|
Take glargine ____x000D_
when converting NPH → glargine_x000D_ ↓ dose by ____% |
qhs_x000D_
20% |
|
|
____ binds to albumin_x000D_
daily - BID_x000D_ NPH → _____x000D_ unit to unit |
detemir
|
|
|
admin ____ qhs,_x000D_
acB and acD |
NPH's, humulin NPH, novolin NPH
|
|
|
Admin ____ 30 min b4 meal_x000D_
BID - TID_x000D_ can mix ____ w/ NPH |
Regulars_x000D_
Humulin-R_x000D_ Novolin-R |
|
|
Admin ____ w/in 15 min b4 meal or w 1st bite of food_x000D_
can mix ____ w/ NPH (protoamine) |
Rapid acting insulins:_x000D_
aspart, lispro, glulisine |
|
|
Peak times for: _x000D_
_x000D_ R_x000D_ S_x000D_ I_x000D_ L |
R = 0.5-2h_x000D_
S = 5-8h (double DoA)_x000D_ I = 10-16L = NONE NONE NONE_x000D_ _x000D_ Rapid Short Inter_x000D_ 0.5, 5, 10_x000D_ 2h 8h 16h |
|
|
The pH reqd by glargine is ___
|
4
|
|
|
Goals per Dr. Foepple_x000D_
_x000D_ Fasting (also pre-meals) = ____ mg/dL*_x000D_ 2 hours post-prandial <____ mg/dL*_x000D_ Bedtime <____mg/dL_x000D_ Lower limit? ~____mg/dL |
Fasting (also pre-meals) = 70-130 mg/dL*_x000D_
2 hours post-prandial <180 mg/dL*_x000D_ Bedtime <150 mg/dL_x000D_ Lower limit? ~110 mg/dL_x000D_ _x000D_ it goes up 50 from fasting to meals, then drops 30 before bed |
|
|
Goals per Dr. Vo for inpatient care_x000D_
_x000D_ Critically ill patients:_x000D_ Maintain BG between ____ mg/dL_x000D_ _x000D_ BG between ____mg/dL is acceptable_x000D_ < ___ or ___ 180 is not recommended |
140-180_x000D_
110-140_x000D_ <110 or >180 mg/dL |
|
|
Goals per Dr. Vo for inpatient pt_x000D_
_x000D_ Pre-meals BG < ____mg/dL_x000D_ Random BG < ____mg/dL |
140 mg/dL_x000D_
180 mg/dL |
|
|
Which medications should be discontinued when insulin is started?
|
Base decision on medication MOA_x000D_
Continue insulin sensitizers_x000D_ Discontinue insulin secretagogues |
|
|
Example treatment algorithm:
|
Lifestyle / Dietary changes _x000D_
Add metformin _x000D_ Add sulfonylurea_x000D_ Add thiazoladinedione_x000D_ Add DPP4 or other options_x000D_ Add once daily basal insulin_x000D_ Add multiple daily prandial insulin |
|
|
Usual starting basal dose for type 2 DM = _____x000D_
Consider ____ for elderly. |
10 units_x000D_
5 units |
|
|
Possible basal regimens for_x000D_
NPH, Glargine_x000D_ _x000D_ Continue to increase basal insulin until.... |
NPH at dinner or bedtime_x000D_
Glargine or detemir at bedtime _x000D_ _x000D_ FBG AT GOAL |
|
|
When do you consider use of prandials?
|
Once FBGs at goal, consider prandial coverage if needed
|
|
|
Typical prandial starting dose: ____ units with meals
|
5 units
|
|
|
Describe insulin dosing:_x000D_
_x000D_ Average daily insulin requirement = ____ units/kg_x000D_ _x000D_ Total daily insulin requirement (in units of insulin) = <eqn>_x000D_ _x000D_ Basal dose = <eqn>_x000D_ _x000D_ FIXED Preprandial dose = <eqn>_x000D_ _x000D_ FLEXIBLE Preprandial dose = rule of ____ = |
0.5-1 units/kg_x000D_
_x000D_ = 0.5(TBW in kg)_x000D_ _x000D_ = rule of 500 = 500/total daily dose = 1 unit of insulin will cover __g of carbs eaten" |
|
|
High blood glucose correction factor (aka insulin sensitivity factor, Rule of ____ or ____)
|
Rule of 1500 or 1800 for high BG Correction factor
|
|
|
Rule of 1800 = use if patient is taking _____x000D_
_x000D_ Rule of 1500 = use if patient is taking ____ |
1800 : rapid acting insulin_x000D_
1500 : regular insulin_x000D_ _x000D_ = 1800/total daily insulin dose = _x__x000D_ _x000D_ “1 unit of aspart will reduce blood glucose by _x_ mg/dL” |
|
|
Insulin dosing wrap up:_x000D_
_x000D_ daily = wt_kg (0.5) units_x000D_ 1/2 basal_x000D_ 1/2 preprandial _x000D_ fixed = divided amongst meals_x000D_ flexible = 500/daily insulin dose per gram carbs_x000D_ _x000D_ high BG_x000D_ --rapid acting = 1800/total daily dose_x000D_ --regular = 1500/total daily dose |
na
|
|
|
When do these insulins peak and how long do they last?_x000D_
_x000D_ R_x000D_ S_x000D_ I_x000D_ L |
When do these insulins peak and how long do they last?_x000D_
_x000D_ onset peak doa dirctions_x000D_ R 5-15m 0.5-2h 3-5h 15m b4 meal or 1st bite_x000D_ S 30-60m 2-4h 5-8h 30m b4 meal, avail OTC_x000D_ I 1-2h 4-12h 10-16h avail OTC, CLOUDY_x000D_ L 1-2h no pk 20-24 can't mix |
|
|
how to convert NPH -> Glargine_x000D_
_x000D_ How often is Glarg dosed?_x000D_ _x000D_ What's special about its solubility? |
decr. NPH by 20%_x000D_
_x000D_ qday_x000D_ _x000D_ completely soluble in pH4, but tissue is 7.4 = slow release throughout day |
|
|
What type of insulin is highly protein bou
|
Detemir
|
|
|
Detemir DoA_x000D_
_x000D_ Conversion from NPH? |
20h max, may be dosed 2x daily_x000D_
_x000D_ same, unit to unit |
|
|
Adverse effects of insulin
|
Hypoglycemia (see later slides)_x000D_
_x000D_ Injection site pain_x000D_ Possibly less if insulin is warmed to room temp_x000D_ _x000D_ Lipohypertrophy_x000D_ Decrease risk by rotating injection sites_x000D_ _x000D_ Weight gain_x000D_ Encourage lifestyle changes |
|
|
How to Pick a syringe
|
30-31 gauge preferred_x000D_
1 cc syringes for doses > 10 units_x000D_ --Small lines = 2 units_x000D_ 0.5 cc syringes for doses < 10 units |
|
|
when do insulin vials expire?
|
28 days
|
|
|
method for injection
|
. Pick a syringe_x000D_
30-31 gauge preferred_x000D_ 1 cc syringes for doses > 10 units_x000D_ Small lines = 2 units_x000D_ 0.5 cc syringes for doses < 10 units_x000D_ 2. Date insulin vial after opening_x000D_ Most insulin vials expire after 28 days_x000D_ Expiration date for pens tend to be shorter_x000D_ 3. Alcohol swab the top of the bottle each time_x000D_ No need for alcohol on skin if clean_x000D_ 4. Draw back syringe to correct dose_x000D_ Pinch a fold of skin for SC administration_x000D_ 6. Insert needle in skin and inject_x000D_ ---Syringe at 90 degrees if plump_x000D_ ---Syringe at 45 degrees if lean_x000D_ 7. Count to 5 slowly then pull needle straight out_x000D_ 8. Dispose of syringe in sharps container_x000D_ 9. Use the same injection technique for pens. You may need to prime (dial up to 2 units, then waste), then dial to correct dose |
|
|
mj diff betw inj w/need vs pens?
|
pens may need priming
|
|
|
Fastest site of injection is:
|
gut,/waist > upper arm > anywhere else
|
|
|
How can one increase rate of abs of insulin?
|
exercise_x000D_
heat or massage |
|
|
Mixed preparations_x000D_
L/S = NPH / Regular_x000D_ L/R = Long actin / Lispro or aspart_x000D_ _x000D_ Choose between:_x000D_ 70/30, 75/25, 50/50 |
NPH/Regular = 70/30, 50/50_x000D_
Intermed/short_x000D_ _x000D_ aspart protamine / aspart = 70/30, 75/25, 50/50, |
|
|
is aspart protamine rapid or intermed, or long acting?
|
protamine = intermediate
|
|
|
Insulin Pumps_x000D_
_x000D_ what type of insulin_x000D_ infusion rate_x000D_ bolus avail? |
RAPID ACTING_x000D_
every 5 min_x000D_ bolus based on carb ration and correction factor |
|
|
use _x000D_
Rule of 1800 = _x000D_ Rule of 1500 = _x000D_ _x000D_ should this amt BE ADDED TO MEAL INSULIN (fixed dose/rule of 500?) |
Rule of 1800 = use if patient is taking rapid acting insulin_x000D_
Rule of 1500 = use if patient is taking regular insulin_x000D_ _x000D_ YES MUST BE ADDED TO MEAL TIME INSULIN_x000D_ _x000D_ SO, Type1 60kg = 30units/day_x000D_ 15 basal_x000D_ 15 prandial = 5U / meal_x000D_ ...now add rule of 1800 for fast acting = 1800/30 = 6units_x000D_ total = 5U (meal) + 6U (rapid) = 11U |
|
|
Usual starting basal dose for type 2 DM = _x000D_
_x000D_ Typical prandial starting dose: ____ with meals |
10 units _x000D_
5 units |
|
|
We usually give detemir at ____._x000D_
_x000D_ Glargine can be given at _____ or _____ |
bedtime_x000D_
bedtime or morning |
|
|
How do we treat (strat) DM2 w/insulin?
|
1. Get FBG (basal) to goal_x000D_
2. Consider prandial |
|
|
Keep total daily insulin adjustment to ≤____ units at any one time
|
5-8 units at a time
|
|
|
Some patients taking ≥ ____ units may tolerate a 10-20% change in dose
|
100
|
|
|
BG Goals:_x000D_
Fasting (also pre-meals) =_x000D_ 2 hours post-prandial =_x000D_ Bedtime = |
FBG (incl pre-meal) = 70-130 mg/dL*_x000D_
<180 mg/dL_x000D_ 110-150 mg/dL |
|
|
Dawn phenomenon_x000D_
Describe._x000D_ How does it work?_x000D_ How to manage it? |
Caused by nocturnal surges of growth hormone, cortisol, glucagon, epinephrine_x000D_
Results in transient hyperglycemia – since no insulin to counter the effects of counterregulatory hormones_x000D_ _x000D_ viz graph_x000D_ starts low at pm, slowly ramps to hyperG but still LOW at 2-3am_x000D_ _x000D_ increase PM BASAL insulin |
|
|
Somogyi effect_x000D_
Describe._x000D_ How does it work?_x000D_ How to manage it? |
REBOUND HYPERG_x000D_
_x000D_ Caused by overcompensation _x000D_ of nocturnal hypoglycemia_x000D_ _x000D_ viz graph_x000D_ starts low at pm, FAST RAMP to hyperG and HIGH at 2-3am_x000D_ _x000D_ REDUCE PM BASAL insulin |
|
|
What to look for when identifying Somogyi/Dawn effects
|
Excessive night time carb intake_x000D_
Low night BG --> High morning_x000D_ Sxs of HYPOglycemia at night_x000D_ -dizzi_x000D_ -nausea_x000D_ -sweating_x000D_ -polyuria |
|
|
TX of _x000D_
Dawn =_x000D_ Somogyi = |
incr bedtime basal _x000D_
reduce bedtime basal_x000D_ _x000D_ DAWN = SUN RISES FAST! |
|
|
If you saw low BG at night but high a.m. =_x000D_
_x000D_ high BG at night and high in a.m. = |
somogyi (rebound)_x000D_
_x000D_ dawn |
|
|
Signs and Symptoms of Hypoglycemia_x000D_
<3 stages> |
First stage_x000D_
Adrenergic system – catecholamine release_x000D_ _x000D_ Anxiety_x000D_ Shakiness_x000D_ Sweating_x000D_ Hunger tremors_x000D_ Tachycardia_x000D_ _x000D_ Second stage_x000D_ Neuroglycopenic – CNS response to lack of glucose supply_x000D_ Confusion_x000D_ Irritability_x000D_ Headache_x000D_ Impaired mental function_x000D_ Impaired vision_x000D_ Motor in-coordination_x000D_ Convulsion_x000D_ Coma_x000D_ _x000D_ _x000D_ Nocturnal hypoglycemia_x000D_ Usually because of excess insulin therapy_x000D_ Symptoms usually do not awaken the patient_x000D_ Night sweats_x000D_ Nightmares_x000D_ Morning headaches_x000D_ Difficulty in awakening_x000D_ Restless during sleep |
|
|
Hypoglycemia Treatment Approach _x000D_
_x000D_ conscious:_x000D_ how soon after do you test?_x000D_ _x000D_ When call 911?_x000D_ _x000D_ What if not sched to eat in next hr? |
CONSCIOUS:_x000D_
Eat or drink 10 to 15 g of glucose or carbohydrate-containing foods or beverages _x000D_ May need 20 to 30 g if blood glucose level < 50 mg/dL_x000D_ _x000D_ 15m_x000D_ _x000D_ Call 911 if blood glucose not back to normal after 3 treatments_x000D_ _x000D_ If not scheduled to eat within the next hour, pt should be cautious about additional hypoglycemia _x000D_ Strongly consider protein+carb snack (i.e. PB&J sandwich) |
|
|
HypoG tx_x000D_
_x000D_ how many Gluc tabs?_x000D_ gel?_x000D_ juice and soda?_x000D_ milk? |
3-4 gluc tabs_x000D_
1 tube gluc gel_x000D_ 1/2 cup_x000D_ 1 cup |
|
|
When use glucagon injection?
|
Use when patient cannot take oral fluids, is unconscious, or is seizing
|
|
|
Glucagon Injection Instructions
|
Inject entire liquid contents of syringe into the glucagon bottle_x000D_
Swirl contents until mixture is fully dissolved_x000D_ Using the same syringe, withdraw the contents from the bottle_x000D_ Turn the individual onto their side_x000D_ Inject glucagon into arm, leg, or buttock_x000D_ 1 mg for adults_x000D_ 0.5 mg for children weighing <44 lbs (though there is no danger of overdose)_x000D_ Feed patient as soon as they awaken and can swallow |
|
|
Antidepressants_x000D_
General |
therapetuci resposne may take weeks_x000D_
no therapeutic diff between classes |
|
|
Antidepressants_x000D_
Main Indications_x000D_ 4 |
MDD_x000D_
bipolar_x000D_ anxiety - SSRI, SNRI (long term)_x000D_ post traumatic stress - not benzos_x000D_ OCD - not benzos_x000D_ neuropathic pain SNRI |
|
|
Antidepressants_x000D_
Other Indications |
smoking - Bupropion_x000D_
premenstrual dysphoric disorder - SSRI_x000D_ ADHD - TCA_x000D_ bulimia - fluoxetine |
|
|
Antidepressants_x000D_
Mech |
all inc levels of NE and 5-HT_x000D_
monoamine hypothesis - block neuronal pre--jxnal membrane transport into NE and 5-Ht |
|
|
Antidepressants_x000D_
monoamine hypothesis - |
block neuronal pre--jxnal membrane transport into NE and 5-Ht
|
|
|
Antidepressants_x000D_
neurotrophic hypothesis |
brain derived neurotrophic factors inc neurogenesisi and plasticity_x000D_
in depression vol loss and decreased BDNF |
|
|
SSRI_x000D_
Mech |
block serotonin reuptake
|
|
|
SSRI_x000D_
Advantage |
minimal sedation/hypotension/anticholinergic effects_x000D_
no cardiotoxicity or lethality with overdose |
|
|
SSRI_x000D_
Side E |
headache_x000D_
sex dysfxn!_x000D_ wt changes_x000D_ anxiety_x000D_ rebound effect (shorter half life more likely, paroxetine) |
|
|
SSRI_x000D_
Toxicity |
Sertonin syndrome - severe agitation; sweating, diarrhea, hyperpyrexia, coma/death_x000D_
inc risk with MAOI or another agent |
|
|
SSRI_x000D_
Fluoxetine |
least specific_x000D_
long half life of metabolite (norfluoxetine, 14 days)_x000D_ inhibit liver microsomal enz |
|
|
SSRI_x000D_
drugs |
Fluoxetine_x000D_
Seratraline_x000D_ Paroxetine |
|
|
Atypical Antidepressants_x000D_
Hypericum (St. John's Wort)3_x000D_ features |
treats mild depression_x000D_
affects liver metab of other drugs for HD, depression, seizures |
|
|
Atypical Antidepressants_x000D_
Amoxapine (TCA)_x000D_ Features |
blocks DA, _x000D_
hyperprolactinemia, EPS |
|
|
Serotonin 5TH2 antagonists_x000D_
Drugs |
Trazodone_x000D_
nefazodone |
|
|
Serotonin 5TH2 antagonists_x000D_
nefazodone |
moderate sedation_x000D_
liver failure |
|
|
Serotonin 5TH2 antagonists_x000D_
Trazodone |
severe sedation
|
|
|
Serotonin 5TH2 antagonists_x000D_
Trazodone_x000D_ nefazodone_x000D_ Side E |
nausea/vomiting_x000D_
priapism_x000D_ hypotension |
|
|
Serotonin 5TH2 antagonists_x000D_
Trazodone_x000D_ nefazodone_x000D_ ADV |
mild hypotensive_x000D_
mild GI/sexual_x000D_ safter than TCA in overdose |
|
|
Serotonin NE RI (SNRIs)_x000D_
Drugs |
Venlafaxine_x000D_
Duloxetine |
|
|
Serotonin NE RI (SNRIs)_x000D_
Venlafaxine_x000D_ Duloxetine_x000D_ indication |
MDD when SSRIs don't work_x000D_
neuropathic pain/fibromyalgia |
|
|
Serotonin NE RI (SNRIs)_x000D_
Venlafaxine_x000D_ Duloxetine_x000D_ Side E |
seizures;more than SSRI
|
|
|
AD_x000D_
Bupropion_x000D_ Features |
less side E; (sedation, hypotensive, sexual, antiach)_x000D_
smoking cessation_x000D_ lowers seizure threshold |
|
|
AD_x000D_
Bupropion_x000D_ Side E |
agitation/insomnea_x000D_
seizures |
|
|
AD_x000D_
Maprotiline_x000D_ Mech |
Blocks NE uptake_x000D_
no adv over TCA |
|
|
AD_x000D_
Maprotiline_x000D_ Side E |
wt gain_x000D_
seizures_x000D_ lethal in overdose |
|
|
AD_x000D_
Mirtazapine_x000D_ mech |
blocks prejxnal alpha 2 receptors thus inc NE and 5-HT_x000D_
blocks serotonin receptors |
|
|
AD_x000D_
Mirtazapine_x000D_ Side E |
fewer than SSRIs_x000D_
sedation and wt gain main ones_x000D_ minimal sexual |
|
|
AD _x000D_
Clomipramine_x000D_ Features |
OCD_x000D_
moderate Side E_x000D_ hihg seizures |
|
|
TCA_x000D_
Mech |
block reuptake of catacholamines into prejxnal endings
|
|
|
TCA_x000D_
Properties |
lipid sol. with long half life (days)_x000D_
2 rings - 2ndary or tertiary amine side chains_x000D_ metabolized by ring hydroxylation and glucuronide conjgation_x000D_ can be made into active metabolite |
|
|
TCA_x000D_
Side E - general |
antagonit at alpha, M, and H receptors
|
|
|
TCA_x000D_
Side E_x000D_ CNS |
sedation - H_x000D_
confusion/delirium - cholinoceptor block_x000D_ seizure; mania_x000D_ tremor - propranolol_x000D_ amoxapine - movement (EPS) (dopamine antag) |
|
|
TCA_x000D_
Side E_x000D_ CV |
post hypoT - alpha1_x000D_
tachycardia |
|
|
TCA_x000D_
Side E_x000D_ Periph activity |
dry mouth, blurred vision, constipation, urinary retention
|
|
|
TCA_x000D_
Side E_x000D_ Others_x000D_ 3 |
Wt gain_x000D_
sexual dysfxn_x000D_ rebound |
|
|
TCA_x000D_
Overdose |
M and alpha antag. activity_x000D_
excitement, seizures_x000D_ slowed conduction (quinidine-like effect)_x000D_ supportive treatment - respiration_x000D_ benzos for seizures |
|
|
TCA_x000D_
Drug Interactions |
alcohol_x000D_
block antihypertensive (clonidine)_x000D_ block antihistamines_x000D_ MAOIs - serotonin syndrome |
|
|
TCA_x000D_
Drugs |
Imipramine_x000D_
Amitriptyline_x000D_ Nortriptyline_x000D_ Desipramine |
|
|
MAOI_x000D_
Phenelzine_x000D_ Mech |
inhib MAO A and B_x000D_
suicide inhib; knocks enz out until more is made - weeks_x000D_ actaully has short half life but works for longer |
|
|
MAOI_x000D_
Phenelzine_x000D_ Indications |
no response to TCAs and SSRI
|
|
|
MAOI_x000D_
Phenelzine_x000D_ Side E |
hypotension_x000D_
headache, dry mouth sex, wt gain_x000D_ CNS stim |
|
|
MAOI_x000D_
Phenelzine_x000D_ Interactions |
serotonin syndrome_x000D_
CNS depressant, sympathomimetic amine |
|
|
MAOI_x000D_
Phenelzine_x000D_ Interactions_x000D_ Tyramine |
Tyr releases NE_x000D_
is in many foods_x000D_ typically broken down but when MAO is deficient, leads to nausea and vomiting_x000D_ leads to inc in NE release = arrhythmias, HTN crisis, subarachnoid bleeding, stroke |
|
|
Lithium_x000D_
Indications |
mania or bipolar_x000D_
onset is 2-3 weeks |
|
|
Lithium_x000D_
Mech |
pict. in notes_x000D_
inhib phospholipid turnover, and therefore lowers amt PIP2, IP3 and DAG |
|
|
Lithium_x000D_
excretion |
amt in blood determine efficacy_x000D_
elminated unchanged by kidney, 80% reab in prox tubule_x000D_ competes with tubule_x000D_ low TI |
|
|
Lithium_x000D_
Side E |
low plasma levels .5-.9 normal_x000D_
0.9-2.5 more severe_x000D_ nausea, fine tremore, polyuria,polydipsia_x000D_ wt gain/ rash/thyroid_x000D_ fetal malformation |
|
|
Lithium_x000D_
Side E - high dose |
confusion first sign of toxicity_x000D_
collapse coma_x000D_ treat with hemodialysis and anticonvulsants |
|
|
Lithium_x000D_
Interactions |
sodium depletion (thiazide diuretics)_x000D_
renal clearance dec by NSAIDs - not aspirin or acetaminophen |
|
|
Valproic acid_x000D_
Carbamazepine |
treat mania and bipolar with or without lithium
|
|
|
Special Dietary Considerations: Pancreatitis
|
Avoid Alcohol
Bland Foods Small, frequent meals Decrease Fat |
|
|
Special Dietary Considerations: Cholecystitis
|
• Decrease Fat
• small, frequent meals |
|
|
Special Dietary Considerations: Hepatitis
|
• NPO initially
• low Fat • High protein/carbohydrates |
|
|
Special Dietary Considerations: Cirrhosis
|
Small, frequent meals
Low sodium/protein |
|
|
Special Dietary Considerations: Diaphragmatic Hernia
|
• Decrease portion sizes
• Decrease Fat • increase frequency of meals • increase protein |
|
|
Special Dietary Considerations: Dumping Syndrome
|
• increase fat/protein/fiber
• increase frequency of meals • Decrease portion size/fluid with meals • Decrease carbohydrate intake |
|
|
Special Dietary Considerations: Diverticulosis
|
• NPO initially
• increase fluids • Bland/soft foods • High-fiber foods, but avoid foods that are difficult to digest such as corn, seeds, and nuts |
|
|
Special Dietary Considerations: Ulcerative Colitis
|
• AVOID coarse, high-fiber, raw fruits/veggies,
cold beverages • increase bland foods • increase protein • increase calories |
|
|
Special Dietary Considerations: Celiac Disease
|
No gluten
increase calories increase protein |
|
|
Special Dietary Considerations: Renal failure (Acute)
|
increase carbohydrates
limit protein (good rule ol thumb for anyone with kidney failure until otherwise specified by physician) Decrease sodium Fluid restriction |
|
|
Special Dietary Considerations: Renal failure (Chronic)
|
Avoid high potassium foods
Low sodium High iron High calcium, vitamins B, C, D |
|
|
Special Dietary Considerations: Cushing’ Syndrome
|
Increase Protein
Increase Potassium Decrease Sodium Decrease calories |
|
|
Special Dietary Considerations: Addison’s Disease
|
Increase Sodium
Low Potassium |
|
|
Special Dietary Considerations: Meniere’s Disease
|
No alcohol
Low Sodium |
|
|
Special Dietary Considerations: Heart Failure
|
Low sodium
Low fat Fluid restriction in some patients |
