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Pharmacy School 2015-16 > PHAR 720 Exam 1 > Flashcards

PHAR 720 Exam 1 Flashcards

1
Q

Regarding language barriers, what should pharmacists consider when dealing with patients?

A
  1. English may no be the patient’s first language
  2. Avoid scientific and medical jargon
  3. Use a 5-8th grade level of language when speaking with patients
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2
Q

What are the basic steps to the Patient Care Process?

A

Collect, Assess, Plan, Implement, Follow-up: Monitor and Evaluate

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3
Q

What is the LEARN model?

A

L - Listen with sympathy and understanding to the patients perception of the problem
E - Explain your perception of the problem
A - Acknowledge and discuss differences and similarities
R - Recommend treatment/solution
N - Negotiate a treatment plan that is mutually agreed upon

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4
Q

What are the 4 C’s of the “L”

A

What do you CALL the problem?
What do you think CAUSED the problem?
How do you COPE with the problem?
What CONCERNS do you have about the problem or treatment?

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5
Q

What is atherosclerosis and what does it commonly cause?

A

Atherosclerosis is a buildup of plaque on arterial walls, making it a specific type of arteriosclerosis (hardening of arterial walls).

Coronary Heart Disease (AKA CAD) is most commonly caused by atherosclerosis.

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6
Q

Describe the structure of blood vessels

A

Tunica Intima - Endothelium and Subendothelial layer

Tunica Media - Smooth muscle and Elastin which is very susceptible to damage from atherosclerosis

Tunic Adventitia (Externa) - connective tissue and arterioles in larger vessels

Lumen where blood flows

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7
Q

Describe the etiology of atherosclerosis

A

Deposit of cholesterol and lipids primarily within the intimal wall of blood vessels, leading to inflammation and alteration of endothelial lining.

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8
Q

Describe the pathogenesis of atherosclerosis

A
  1. Injury to endothelium causing increased vascular permeability
  2. Accumulation of lipoproteins, cholesterol and lipids into the intima
  3. Monocytes adhere to the endothelium and migrate to intima
  4. Platelet adhesion and smooth muscle proliferation
  5. Accumulated lipids engulfed by macrophages (foam cell after death) and smooth muscle cells
  6. Chronic inflammation causing damage over time
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9
Q

What specifically migrates to the site of damage in blood vessels causing loss of flexibility?

A

Calcium

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10
Q

What is CRP

A

C-reactive protein, a marker of inflammation and CAD; it is associated with unstable plaques and increased LDL oxidation

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11
Q

What problems might be associated with atherosclerosis of the renal arteries?

A

Fatigue, loss of appetite, nausea, edema, itching (CKD)

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12
Q

What are the high prevalence groups for CAD?

A

Primary ages between 40 and 60
Men have an increased risk after 45 and women after 55
Blacks, Whites and Asians/Pacific Islanders have higher percentages

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13
Q

Name the modifiable risk factors associated with atherosclerosis.

A

Hyperlipidemia, Hypertension, Cigarette smoking and Diabetes

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14
Q

Name the non-modifiable factors associated with atherosclerosis.

A

Genetics, age, gender and family history.

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15
Q

What factors negatively impact plasma lipid levels?

A

High dietary intake of cholesterol and saturated fats, trans-unsaturated fats produced by hydrogenation of polyunsaturated oils, obesity and smoking which lower HDL levels

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16
Q

What factors positively impact plasma lipid levels?

A

Diets low in cholesterol or higher ratios of polyunsaturated fats, diets rich in Omega-3 fatty acids, exercise and moderated consumption of ethanol which raise HDLs

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17
Q

How do fibrates work?

A

They lower triglycerides and raise HDL levels

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18
Q

What do the guidelines state for LDL cholesterol levels?

A 
Optimal = Less than 100
Near/Above Optimal = 100-129
Borderline high = 130-159
High = 160-189
Very High = 190 or above
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19
Q

What are the guideline total cholesterol values?

A

Desirable = under 200
Borderline high = 200-239
High = 240 or greater

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20
Q

What are the guideline HDL values?

A

Low under 40, high equal to or above 60

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21
Q

What do the ACC/AHA 2013 cholesterol guidelines emphasize? What do they de-emphasize?

A

Use of statins

Use of non-statins

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22
Q

What lifestyle changes should be suggested to reduce risk of Cardiovascular disease?

A
  1. Heart healthy diet (eat veggies, fruits, whole grains, low-fat dairy, avoid red meat, limit sugary drinks and sweets, limit saturated trans fat to 5-6 percent of calories, limit sodium intake to 2400mg/day)
  2. Exercise regularly (40 minutes 3-4 times/week)
  3. Avoid tobacco
  4. Maintain healthy weigh
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23
Q

What are the 4 major benefit groups for Statin therapy?

A
  1. Patients with clinical atherosclerosis or CVD
  2. Patients with LDL higher than 190
  3. Patients 40-75 years of age with diabetes and LDL 70-189
  4. Patients with atherosclerotic CVD or diabetes with LDL 70-189 with an estimated 10 year risk of atherosclerotic CVD of 7.5 percent or higher
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24
Q

How is cardiac output (CO) calculated?

A

CO = HR x Stroke Volume (SV)

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25
Q

How is Mean Arterial Pressure (MAP) calculated?

A

MAP = CO x Peripheral Resistance (PR)

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26
Q

What are some factors that effect peripheral resistance?

A

Collagen buildup with age, Endothelial dysfunction, vasoactive substances, sympathetic nervous system stimulation.

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27
Q

Name some vasodilators

A
  1. Parasympathetic nervous system
  2. Bradykinin which is inactivated by ACE
  3. Prostaglandins
  4. NO in vascular endothelial cells
  5. Atrial natriuretic factor - leads to increased blood volume causing sodium and water excretion in kidneys
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28
Q

Name vasoconstricting systems

A
  1. Sympathetic (adrenergic) nervous system
  2. Calcium channels
  3. Renin-angiotensin aldosterone
  4. Endothelins
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29
Q

What are the different types of adrenergic receptors?

A

Alpha respond to norepinephrine and lead to smooth muscle contraction.

B1 in heart causes contraction of smooth muscle
B2 in lungs, liver and vascular smooth muscle causes relaxation

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30
Q

Describe the Renin-Angiotensin Aldosterone system

A

Decreased blood flow to kidneys causes release of renin which converts angiotensinogen to angiotensin 1. Angiotensin 1 converted to 2 by ACE. Angiotensin 2 is a potent vasoconstrictor that stimulates the release of aldosterone, causing resorption of water and sodium.

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31
Q

How do endothelins work and who is most susceptible?

A

Influence sodium and water homeostasis, blacks typically have higher levels.

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32
Q

What is secondary hypertension?

A

Accounts for 5 to 10 percent of diagnoses cases of hypertension. Results from renal, endocrine, neoplastic, neurological or cardiovascular problems.

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33
Q

Typical onset age of hypertension?

A

20 - 50 years of age

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34
Q

What are the systolic and diastolic JNC 7 classifications of blood pressure?

A

Normal (

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35
Q

What are the etiologic factors of hypertension?

A

Genetics and age

Hypertensinogenic factors (body mass, insulin resistance, high alcohol or sodium intake, sedentary lifestyle, low potassium or calcium intake, stress)

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36
Q

What are some other factors contributing to hypertension?

A

Oral contraceptives, inadequate sleep (under 5 hours), frequent use of analgesics and/or diet high in red meat (females only), increased lead levels

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37
Q

Cardiovascular disease risk factors

A

Genetics

Framingham Risk Factors (Total cholesterol above 240, HDL above 40, smoking, high BP, age and sex)

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38
Q

What are the JNC 8 guidelines for BP treatment levels?

A

Age 60 or above treat to goal of

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39
Q

What are the JNC 8 guidelines for initial treatment of hypertension?

A

General non-black:

  1. Thiazide-type diuretic
  2. CCB
  3. ACE inhibitor
  4. ARB

General Black:

  1. Thiazide type diuretic
  2. CCB

Adults with CKD: ACE Inhibitor or ARB

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40
Q

What are the JNC guidelines for attaining and maintaining hypertension goals>

A

If goal not reached in 1 month, increase dose or add drug from another class; if goal not reached with 2 drugs, add and titrate (DO NOT USE ACEI AND ARB TOGETHER); if goal not reached with 3 drugs, may use drugs from other classes or refer to specialist

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41
Q

How is BMI calculated?

A

Weight (lb) / [heigh (in)]^2 x 703
or
Weight (kg) / [height (m)]^2

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42
Q

What do different BMI values represent?

A

Underweight (

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43
Q

How significant is weight loss for blood pressures?

A

DBP can be lowered by 6 and systolic by 4.6 for every 10kg of weight lost.

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44
Q

HPI

A 
History of Present Illness:
>Tell me more about it 
>8 attributes of a symptom
>Previous treatment and experience
>Current medications
>allergies
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45
Q

What are the 8 attributes of a symptom?

A
  1. Location
  2. Quality (describe the pain)
  3. Severity (Have patient rate the pain on scale)
  4. Modifying factors (what makes pain better or worse)
  5. Associated symptoms
  6. Onset/setting
  7. History (past medications that worked)
  8. Meaning to the patient (what they think is going on)
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46
Q

PH or PMH

A 
Past Medical History:
>Childhood illness
>Adult illnesses 
>Immunizations 
>Are they planning on becoming pregnant in the next year
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47
Q

SH

A 
Social History: 
>Tobacco
>Alcohol 
>Exercise
>Diet
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48
Q

FH

A

Family History:
>Immediate family members
>History of Cardiovascular diseases, diabetes, cancer, arthritis, etc.

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49
Q

Objective information

A

Observations, vital signs, labs and other findings, any medications the patient is currently using

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50
Q

Summary and closure

A

Obtain feedback, verify understanding, written information, documentation (SOAP notes)

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51
Q

What does SOAP stand for?

A

Subjective, Objective, Assessment, Plan

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52
Q

What is the layout of a SOAP note?

A

Heading (Patient name, DOB, chief complaint, allergies)

Subjective (format in full sentences and paragraph form, content should include ID patient, brief description of encounter with patient, 8 attributes of symptom, lastly pertinent histories (PMH, FH, SH))

Objective (List format; content - allergies, medications, physical exam and vital signs, labs and tests)

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53
Q

Define pre- and post-prandial

A

Before and after meals

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54
Q

Define glycation

A

Glucose binding to proteins and lipids

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55
Q

What is the etiology of diabetes?

A

> Metabolic disease
Defects in insulin secretion, action or both
Hyperglycemia

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56
Q

What are the endocrine and exocrine products of the pancreas?

A

Endocrine - glucagon, insulin, somatostatin

Exocrine - Digestive enzymes such as proteases, amylase and pancreatic lipase

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57
Q

Which cells secrete glucagon and which secrete insulin?

A

Alpha cells - glucagon

Beta cells - insulin

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58
Q

Describe GLP-1

A

Secreted by the small intestines causing gastric emptying and an increase in insulin/decrease in glucagon, leading to a decrease in blood glucose

59
Q

What inhibits GLP-1

A

DPP-4 class drugs

60
Q

Describe AGE products

A

Stands for Advanced Glycation End Products.
>formed when glucose binds to proteins and lipids
>Increased glucose leads to an increase in AGE products

61
Q

What are the results of AGE products?

A

> Accumulation of proteins and lipids in the endothelial tissue
Inappropriate release of growth factors
Increased procoagulant activity
Stimulation of inflammatory process
Activation of amino cells

62
Q

Describe the Polyol pathway

A

> Muscles, fat and brain tissues require insulin to absorb glucose
Some tissues do not require insulin to absorb glucose
Glucose converted to fructose and sorbitol which accumulate causing osmolar stress in cells resulting in swelling and damage to the cells

63
Q

Name some tissues that do not require insulin to absorb glucose

A

Kidneys, nerves, blood vessels

64
Q

Describe Type 1 Diabetes

A

> Known as insulin-dependent or juvenile-onset diabetes
5-10 percent of all diagnoses
Caused by autoimmune destruction of beta cells that results in absolute insulin deficiency
Onset typically under 30 years but can occur at any age
Patients appear normal or under weight
Genetics, family history or viral infection are all risk factors

65
Q

Describe Type 2 Diabetes

A

> Insulin resistance and accounts for 90-95 percent of all cases
Caused by constantly high glucose levels, leading to a decrease in function of insulin receptors
Onset typically over 40 years of age
Patient appears to be normal or overweight

66
Q

Risk factors of Type 2 Diabetes

A

> BMI over 30 kg/m^2
Physical inactivity
First-degree relative with diabetes
High risk race (AA, Hispanic, Native American, Asian American, Pacific Islander)
Women who deliver a baby weighing over 9 pounds
Constant high blood pressure
Women with polycystic ovary syndrome

67
Q

Name some associated risk factors with Type 2 diabetes

A

Hypertension (>140/90 mmHg), HDL levels under 35 or TG>250, History of Cardiovascular Disease

68
Q

Symptoms of Diabetes

A

> Polyuria, Polydipsia, Polyphagia
Extreme fatigue
Blurry vision
Cuts/bruises heal slowly
Weight loss - even if increased food consumption
Tingling pain and numbness in hands/feet
Nausea, drowsiness, dry skin

69
Q

What are the different types of blood glucose tests?

A

HbA1C, Fasting Plasma Glucose (FPG), Oral Glucose Tolerance Test (OGTT), Random Blood Glucose (RBG)

70
Q

Describe HbA1C

A

Glycated Hemoglobin
>Hemoglobin gets glycated when glucose levels are high
>Remains glycated for duration of red blood cell’s life, which can last 120 days
>Measures average amount of glycated hemoglobin over 120 days are is proportional to blood glucose concentrations

71
Q

How is fasting blood glucose taken?

A

No caloric intake for past 8 hours.

72
Q

Describe OGTT

A 
Oral Glucose Tolerance Test
>Fast beforehand
>Blood sample collected at T=0
>Consume 75 grams of glucose 
>Second blood sample after 2 hours
73
Q

What are the lab values for a normal individual?

A

A1C (

74
Q

What are the lab values for pre-diabetes?

A

A1C (5.7-6.4%); FPG (100-125 mg/dL); OGTT (140-199mg/dL); RBG (140-199 mg/dL)

75
Q

What are the lab values that indicate diabetes?

A

A1C (>6.5%); FPG (>126 mg/dL); OGTT (>200 mg/dL); RBG (>200mg/dL)

76
Q

What lab value indicated hypoglycemia?

A
77
Q

Microvascular Diabetes Complications

A

Retinopathy (damage to blood vessels of retina, increased risk for cataracts and glaucoma)

Nephropathy(caused by damage to glomeruli, results in leakage of proteins into urine causing chronic kidney disease over time)

Neuropathy (damage to nerves)
>Somatic nerve damage causing decrease in pain, tingling, numbness, burning and risk of foot ulcers
>Autonomic nerve damage causing involuntary function of organs, gastroparesis, sexual dysfunction, other GI problems

78
Q

When and how often should screening be performed for microvascular problems?

A

Retinopathy
>Type 1 1st eye exam five years after diagnosis
>Type 2 eye exam ASAP after diagnosis and every 2 years after

Nephropathy - screening annually

Neuropathy
>After first five years in type 1 patients
>As soon as possible after diagnosis in type 2 patients with follow up every 2 years

79
Q

Macrovascular Diabetes Complications

A

(Large blood vessels)

> Atherosclerosis, leading to increased risk of CVD and PVD (CVD is the primary cause of death in diabetics)
Peripheral vascular disease
CVD
Increased risk from stroke, MI and ischemia

80
Q

Define Metabolic Syndrome

A 
A group of risk factors that contribute to risk of CVD
>Waistline
>High triglyceride levels
>Low HDL levels 
>High BP
>High blood glucose
81
Q

What are the key points of Diabetes Management?

A

> Medication
Healthy diet - low-fat, low carbs, sodium under 2300 mg/day
Physical activity
Monitoring

82
Q

Name two serious hyperglycemic complications

A

Diabetic ketoacidosis and Hyperglycemic hyperosmolar nonketotic syndrome

83
Q

Describe Diabetic Ketoacidosis

A

> Common in type 1 patients
Body breaks down fatty acids into ketones, accumulation of which causes pH imbalance
Distinct fruity breath
Patients exhibit the 3 Ps

84
Q

Describe Hyperglycemic hyperosmolar nonketotic syndrome

A

> Common in type 2 patients
hyperglycemia causes osmolarity differences, drawing fluid into blood vessels
Patients exhibit 3 Ps
UTIs

85
Q

Symptoms of hypoglycemia

A

Sweating, anxiety, dizziness, hunger, shaking, impaired vision, weakness and fatigue, headache, irritability, fast heartbeat (all caused by release of epinephrine by the body in defense of hypoglycemia)

86
Q

Name the drug classes for controlling diabetes

A

Biguanides, Sulfonylureas, Thiazolidinediones, DPP-4 inhibitors, SGLT2

87
Q

Describe Biguanides

A

> decrease hepatic glucose production by decreasing gluconeogenesis and improve insulin function
no weight gain
Some GI intolerance and occasional lactic acidosis, no risk of hypoglycemia

88
Q

Describe sulfonylureas

A

> Increase insulin secretion

>Some GI intolerance, fatigue, dizziness, with some risk of hypoglycemia from increase in insulin

89
Q

Describe Thiazolidinediones

A

> Peroxisome proliferator activated receptor agonist, increase insulin sensitivity in muscle and liver
Possible edema, weight gain and no risk of hypoglycemia

90
Q

Describe DPP-4 Inhibitors

A

> Prolong action of GLP-1

>No major side effects and no hypoglycemia risks

91
Q

CVA definition of a stroke

A

Neurological deficit attributed to acute focal injury of the CNS by a vascular cause

92
Q

Prevalence of Strokes

A

> Fourth leading cause of death and most prevalent cause of morbidity
6.4 million non-institutionalized adults have had a stroke (2.7%)
795,000 people each year
Accounts or 1 out of 19 deaths in the U.S.
Most prevalent in black females, followed by black males and American Indians/natives

93
Q

Define Ischemia

A

Interruption of normal circulatory flow by obstruction of small or large vessels.

Leads to oxygen and glucose deprivation.

Depletion of ATP leading to a loss of membrane potential; increase in cytoplasmic calcium causing enzymatic processes and cellular injury leading to infarction or tissue necrosis.

94
Q

Details of Ischemic Stroke

A

> 15% mortality within 30 days
Embolus (block originated in a different part of the body) or thrombus (formed in a vein)
Treatment includes Tissue Plasminogen Activator (tPA)
Timing goals for Ischemic stroke include imagine within 45 minutes of arrival, tPA within 60 minutes of arrival and within 3 hours of stroke onset

95
Q

How does tPA work?

A

Binds to fibrin in thrombus converting plasminogen to plasmin and causing fibrinolysis

96
Q

Prevention methods for Ischemic Stroke

A

Antiplatelets: Aspirin, Clopidogrel, Dipridamole

Direct Thrombin inhibitor: Dabigatrin

Vitamin K antagonist: Warfarin

Factor Xa inhibitors: Rivaroxiban, Apixiban

97
Q

How is a stroke presented?

A

> Hemiparesis or monoparesis
Visual field deficits such as diplopia (double vision)
Facial droop
Ataxia, or loss of coordination, and vertigo
Aphasia (loss of speech)
Headache
Decrease in level of consciousness

98
Q

Guidelines for Early Management of Stroke

A 
>911 and EMS protocol 
>Non-contrast-enhanced CT or MRI 
>Blood glucose since hypoglycemia may present with similar symptoms (and poorer outcomes for those who are hyperglycemic during stroke)
>Stroke rating scale(NIHSS)
>ECG and other tests

Other measures include control BP and blood glucose, maintaining oxygenation and ensuring patient doesn’t become hypothermic, thrombectomy or other surgery, and 325mg Aspirin within 24-48 of Ischemic stroke

99
Q

Stroke Recovery Includes

A

Physical, occupational and speech therapy.

Management of risk factors (BP, diabetes, atherosclerosis, smoking and alcohol, diet, sleep apnea, metabolic syndrome and cardiac diseases).

100
Q

What is a Hemorrhagic stroke?

A

Accounts for 8-18% of all strokes and has a 35-45% mortality rate within 30 days.

Symptoms depend on area but include headache, altered mental status, seizures, nausea and vomiting.

Acute management (Non-contrast CT or MRI, other labs, control BP and oxygenation, surgical and endovascular methods as well as management of any complications)

101
Q

Prevention of Hemorrhagic stroke

A

Management of hypertension, avoid tobacco and alcohol misuse, DASH diet and plenty of exercise.

102
Q

What are intracerebral Hemorrhages?

A

Focal bleeding within the brain parenchyma or ventricular system.

Often occurs in putamen, thalamus, pons or cerebellum.

103
Q

What is a Saccular Aneurysm?

A

Rupture of saccular aneurysm, which is found in about 2 percent of the population, in cerebral artery.

Risk factors include smoking and hypertension

104
Q

Define Arteriovenous malformation

A

Occurs in roughly 1 percent of the population.

No diffusion of blood pressure, causing a high pressure area that can rupture.

25% change of bleed over 15 years, and a rupture leads to hemorrhagic stroke.

105
Q

Define Subarachnoid Hemorrhages

A

20-40% mortality

Causes include aneurysms, AVM, bleeding disorders, intracranial artery dissections, substance abuse, etc.

106
Q

Define transient ischemic attacks

A

An episode of acute neurological dysfunction caused by focal brain, spinal cord, or retinal ischemia without acute infarction.

Symptoms usually last under an hour.

Results in an increased risk for ischemic stroke.

Prevention includes management of risk factors, antiplatelet or anticoagulants as appropriate.

107
Q

What types of headaches can be self-treated?

A

Tension-type, migraine, sinus pressure headaches, medication overuse headaches.

108
Q

OTC Analgesics

A

Acetaminophen (10-15mg/kg in children; no more than 2000mg a day for someone who has 3 or more alcoholic drinks; Warfarin + APAP can increase INRs, decreasing the time it takes blood to clot)

Ibuprofen (dosing typically 5-10mg/kg for children; max 1200mg a day for adults but higher for prescription; Unwanted effects may include GI or stomach upset or GI bleed)

Naproxen

NSAIDS (COX-1 causes mucous production, decrease in stomach acid, vasodilation, platelet aggregation, labour, and regulation of sleep/wake cycle; COX-2 prostaglandin crucial for endothelium)

Salicylates (Aspirin; unwanted effects include tinnitus, GI intolerance and Reye’s syndrome)

Apirin/APAP/Caffeine used for migraines often (2 tab every 24 hours with some formulations 10 times a day; limited quantity for migraine in case head pain is more serious)

109
Q

What is the health belief model?

A

A model developed to explain and predict health-related behaviors.

Consists of perceived threat, perceived benefits, perceived barriers, cues to action, other variables and self-efficacy.

110
Q

What are the stages of change?

A 
Pre-contemplation
Contemplation 
Preparation
Action
Maintenance
111
Q

What are the 5 A’s?

A 
Ask
Advise 
Assess
Assist 
Arrange
112
Q

What are the 5 R’s?

A 
Relevance
Risks
Rewards
Roadblocks
Repetition
113
Q

What are some considerations when making a plan for someone to end a behavior?

A

Plans should be individualized:

Current use, past use, past attempts to quit, reasons, identify triggers or routines, address concerns, methods for quitting, set a quit date, develop coping strategies and ways to deal with withdrawal, and let the patient know you are there for questions.

114
Q

What should be covered in a follow-up behavior change plan?

A

Patient progress checks, address slips/relapses, medication use and tapering, discuss temptations and triggers, encouragement.

115
Q

Define Heart Failure and its statistics

A

Complex clinical syndrome that results from any structural or functional impairment of ventricular filling or ejection of blood

Also called CHF or chronic heart failure

Effects about 5.8 million people in the US and contributes to 1 in 9 deaths.

50% mortality within 5 years of diagnosis

116
Q

Define syndrome

A

A collection of signs and symptoms that characterize a particular condition or abnormality

117
Q

Etiology of HF

A

Chronic work overload (vascular disease or hypertension), ischemic heart disease (post MI with damage), congenital abnormalities, acute hemodynamic stresses, HF is common final stage for many CV diseases

118
Q

Pathophysiology of CHF

A

> Cardiac hypertrophy
Adrenergic activity (increase in HR, contractility and CO)
Abnormal Ca2+ cycling causing increase in myocycte contraction
Renin-angiotoensin-aldosterone system
cell death
genetics
aging (increase in epicardial fat, change in left ventricle size, calcification of valves, atrial arrhythmia’s, aortic stiffening, incrneaesd collagenized connective tissue and a decrease in myocytes, increase in atherosclerosis)

119
Q

What is the classification of CHF by injection?

A

Ejection fraction under 40% is HFrEF (HFpEF greater than or equal to 50%)

Preserved heart failure also called diastolic HF and is classified as improved when EF is greater than 40% and borderline when 41-50%.

120
Q

Define ejection fraction

A

the percent of blood volume ejected from the ventricle during systole (normally between 45 and 65%)

121
Q

Define HFrEF

A

Also called Systolic HF, or HF with reduced ejection fraction as well as forward failure.

LV cavity is dilated, wall is lengthened and thinned, leading to impaired contractility.

Reduced tissue perfusion leading to activation of Renin-angiotensin-aldosterone system

122
Q

Characteristics of Diastolic HF

A

LV is abnormally thick and stiff with impaired relaxation during diastole.

Unable to increase output in response to demands and increase in filling pressure is transferred to the pulmonary circulation/atrium.

More common in women and patients over 65.

Also called backwards failure, typically resulting in pulmonary and peripheral.

123
Q

What is right sided failure?

A

Commonly caused by left-sided failure, or systolic and diastolic HF).

Pulmonary hypertension as blood backs up from failure of left side, ultimately effecting the right side.

Causes an increase in pressure and congestion in systemic veins and capillaries (Jugular vein engorgement easy to spot)

124
Q

How to evaluate HF?

A

Symptoms include dyspnea, fatigue, decrease in exercise tolerance and orthopnea.

Physical exam and diagnostics tests: vitals, volume status, blood work and biomarkers, ECG, chest x-ray, echocardiogram

125
Q

List Risk Factors of HF

A

Hypertension, coronary artery disease, acute coronary syndrome, arrhythmias, impaired renal function, diabetes, viral infections, over 65 years old, male, African American, obese, metabolic syndrome, alcohol use, sometimes chemo drugs, and tobacco

126
Q

ACCF/AHA stages of HF and treatment guidelines

A

A. High risk but no structural heard disease or symptoms of HF (control HTN and lipid disorders; control or avoid obesity, diabetes, tobacco and other cardiotoxic agents)

B. Structural heart disease without signs or symptoms of HF (ACEI or ARB if history of MI and reduced EF; BBs if history of MI and reduced MI - greater mortality than ACEI or ARBs; Statins for history of MI; ICD or implantable cardioverter-defibrillator, especially if patient has arrhythmia)

C. Structural heart disease with prior or current symptoms of HF (diuretics if fluid retention; digoxin in HFrEF to reduce symptoms; anticoagulants in patients with afib and stroke risk; omega-3 polyunsaturated fatty acids; ICD and cardiac resynchronization therapy)

D. Refractory HF requiring specialized interventions (fluid restriction, inotropic support, mechanical circulatory support, cardiac transplantation and end-of-life goals)

127
Q

ACCF/AHA Non-Pharmacologic HF Treatment Guidelines

A

Education for HF self-care, exercise training and regular activity, sodium restriction if symptomatic, continuous positive airway pressure (CPAP) if patient has sleep apnea, cardiac rehab

128
Q

NHYA Functional Classification of HF

A
  1. No limitation of physical activity
  2. Slight limitation of physical activity; normal physical activity results in symptoms of HF
  3. Marked limitation of physical activity due to less-than ordinary activity causing HF symptoms
  4. Unable to carry on any physical activity without symptoms of HF, or symptoms of HF at rest
129
Q

Define insomnia

A

Perception of difficulty falling asleep, staying asleep, or getting restorative sleep despite adequate opportunity and circumstances.

Associated with daytime impairment or distress.

130
Q

Insomnia prevalence.

A

Insomnia symptoms in 33-50% of adults.

Risk factors: increasing age, females, comorbidities, shift work or travel across time zones

131
Q

Types of insomnia

A

Short term (under 3 months)

Chronic (3 times a week for 3 months or more)

132
Q

Etiology of Insomnia

A

Comorbidities: pulmonary disease, HF, pain conditions, neurologic disease, urologic, endocrine, dermatologic, GERD, and psychiatric

Medications: stimulants, antidepressants, BBs, corticosteroids, withdrawal from medications

Sleep related breathing disorders: OSA or central SA

Circadian rhythm sleep-wake disorder: Jet lag, delayed or advanced sleep phase

Parasomnias: disruptive sleep disorders; includes night terrors

133
Q

Assessment tools for insomnia

A

Epworth Sleepiness scale, Pittsburgh Sleep Quality Index, Insomnia Severity Index, Comprehensive Sleep History, Sleep Diary, Polysomnography (overnight sleep study), Multiple Sleep Latency Test (monitored naps) or Sleep Actigraphy (wrist device that detects motion)

134
Q

When should referral be provided for insomnia?

A

For patient less than 12 or older than 65, or pregnant.

For chronic, long-term insomnia, or for awakening early.

If present with other comorbidities or believed to be secondary to another disorder.

135
Q

OTC insomnia treatment options

A

Dipenhydramine (FDA approved): 25-50mg 30-60 minutes before bed; half life approximately 6-13 hours and is generally longer in elderly; may experience anticholinergic side effects

Doxylamine (not FDA approved)

*Beer’s Criteria - a list of medications to avoid using in the elderly

136
Q

List some anticholinergic side effects

A

Blurred vision, constipation, urine retention, dry mouth and drowsiness

137
Q

Complementary or alternatives for Insomnia

A

Alcohol
Melatonin (0.5-5mg) - more than 5 not shows no increased effect
Velerian (usually takes weeks to be beneficial and smells awful)

138
Q

List sleep hygiene considerations

A

Avoid caffeine later in day, exercise, only use bed for sleep and intimacy, engage in relaxing activity before bed, regular schedule, avoid screen time, allow 7-9 hours for sleep, quiet dark room w/o distractions, avoid naps

139
Q

Targets for Insomnia Medications

A

GABA - inhibitor neurotransmitter, GABAA for sleep

Histamine - H1, H2 and H3 receptors in the brain; functions include arousal and wakefullness

Melatonin - secreted by the pineal gland

Orexins - excitatory neurotransmitters for wakefulness and feeding

140
Q

Prescription Insomnia Medications

A

GABA agonists (benzodiazepines for nonspecific effects and non-benzos for specific effects)

Melatonin agonist (remelteon)

Orexin receptor antagonist (suvorexant aka Belsomra)

Sedating low dose antidepressants (doxepin, trazodone, mirtazapine, amitriptyline)

141
Q

Define fatigue

A

Lack of energy and/or mental exhaustion. Men feel tired, women depressed or anxious. Can be secondary, physiologic or chronic. Underlying causes include OSA, insomnia, meds, anemia, depression, CV such as HF, neurological (stroke patients), and endocrine (hypothyroidism)

142
Q

Describe caffeine

A

Effects: Adenosine antagonist, increased arousal and decreased fatigue, anxiety and nausea, rapidly absorbed, 3-6 hour half-life, risks and benefits

Adverse effects/precautions: transient increased heart rate and BP, increased HCl and pepsin in stomach, withdrawal, CYP1A2 metabolizes caffeine for the most part (strongly inhibited by nicotine)

143
Q

Prescription stimulants

A

Modafinil, Methylphenidate, Dextroamphetamine, Atomoxetine

All are often used to treat ADHD

144
Q

List non-pharmacologic stimulants

A

Address physiologic factors (sleep, exercise, napping) and regular moderate aerobic activity

Pharmacy School 2015-16 (34 decks)

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