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ScribeAmerica > Course 2: Chronic Illnesses and the Patient Problem List > Flashcards

Course 2: Chronic Illnesses and the Patient Problem List Flashcards

1. Why are chronic illnesses concerning? 2. What is hypertension and how is it managed? 3. What is diabetes mellitus and how is it managed? 4. What is hyperlipidemia and how is it managed? 5. What is coronary artery disease and how is it managed? 6. What is asthma and how is it managed? 7. Project list

1
Q

comorbidity

A

the simultaneous presence of two chronic diseases or conditions in a patient (i.e. asthma, HTN, HLD, DM, CAD)

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2
Q

etiology

A

the cause of a disease

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3
Q

systole (systolic)

A

phase of the heartbeat during which the muscle contracts, pumping blood to the body

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4
Q

diastole (diastolic)

A

phase of the heartbeat during which muscle is relaxed and the heat fills with blood

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5
Q

diuretic

A

a substance that promotes the production of urine

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6
Q

paresthesia

A

sensation of tingling or numbness

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7
Q

polydipsia

A

excessive thirst

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8
Q

ischemia

A

lack of blood supply

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9
Q

anticoagulant

A

a drug that prevents blood clotting

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10
Q

When does an illness become classified as chronic?

A

when it lasts longer than 3 months

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11
Q

Why are patients with comorbidities considered complex?

A

1, the treatment of one Dz may affect or contradict the treatment of a second (i,e, CHF & chronic renal failure – recommended therapy of reduced fluid intake vs. increased fluid intake, respectively)

  1. adverse drug interactions
  2. compounding symptoms may lead to poor compliance with treatment plan
  3. if both illnesses affect a specific organ system, the patient is at increased risk of organ failure
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12
Q

For complex patients, it is important to document what 3 three things?

A
  • symptoms in chronological order
  • the status and progress of each illness
  • level of compliance with treatment plan

**note: complex pt often bill to a higher level, so it is important to document thoroughly and accurately.

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13
Q

HTN: etiology

A

an increase in blood pressure causes excess force against the arterial walls

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14
Q

HTN: risk factors (5)

A

FHx of HTN, obesity, high sodium diet, smoking, ETOH

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15
Q

HTN: CC (chief complaint/s)

A
  • often asymptomatic (a.k.a. silent killer)
  • hypertension (measure at home)
  • headache, chest pain, palpitations, blurred vision, epistaxis (usually present when HTN begins to affect other organ systems)
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16
Q

HTN: PE (specific exam findings that correlate with HTN)

A

lower extremity edema, carotid bruit (heard by auscultation), JVD, abnormal heart sounds

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17
Q

HTN: Dx by…

A

BP check and monitoring with a sphygmomanometer

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18
Q

carotid stenosis

A

also called carotid artery disease; caused by narrowing of the carotid arteries (2 major arteries that carry blood from heart to brain, located in the neck)

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19
Q

HTN: systolic blood pressure

A

measures pressure in the arteries when the heart contracts (beats); top number

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20
Q

HTN: diastolic blood pressure

A

measure pressure in the arteries when the heart is relaxed (between heart beats); bottom number

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21
Q

HTN: hypotensive BP readings

A

sys: less than 90 / dia: less than 60

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22
Q

**HTN: normal range

A

sys/dia : 90/60 to 120/80

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23
Q

HTN: prehypertensive

A

sys/dia : 121/81 to 140/90

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24
Q

**HTN: hypertensive

A

sys/dia: greater than 140/90

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25
Q

Dz caused by HTN: MI/CAD

A

untreated HTN causes arteriosclerosis (thickening of arteries) which increases the risk of CAD or acute MI

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26
Q

Dz caused by HTN: CHF

A

the heart experiences increased effort and decreased efficiency, pumping excess fluid though the body

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27
Q

Dz caused by HTN: CVA

A

consistently increased pressure through the vessels of the brain causes weakening of arteries, leading to potential rupture and hemorrhagic CVA

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28
Q

Dz caused by HTN: Renal Failure

A

increased blood pressure through the kidneys causes weakening, leading to renal failure

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29
Q

Dz caused by HTN: Impaired Vision

A

increased pressure through the delicate vessels of the eyes causes them to rupture or thicken, causing vision loss

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30
Q

Pharmacological management HTN: diuretics

A
  • reduce the volume of fluid in the blood vessels by urinating excess fluid
  • ex: hydrochlorothiazide (HCTZ)
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31
Q

Pharmacological management HTN: beta-blockers

A
  • slow the heart rate and reduce the heart’s workload
  • ex: brand name (generic)
    lopressor (metoprolol)
    toprol (metoprolol)
    tenormin (atenolol)
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32
Q

Pharmacological management HTN: Ca channel blockers

A
  • dilate the arteries and reduce the force of the heart’s contractions
  • ex: norvasc (amlodipine); cardizem (diltiazem)
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33
Q

Pharmacological management HTN: ACE inhibitors

A
  • relax the arteries and block re-absorption of water by the kidneys
  • ex: lotensin (benazepril)
    zestril (lisinopril)
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34
Q

Pharmacological management HTN: ARBs

A
  • dilate the arteries
  • ex: cozaar (losartan)
    benicar (olmesartan)
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35
Q

HTN: treatment with a specific medication depends on…

A
  • severity of HTN
  • effect of medication on comorbidities
  • cost of medication/insurance coverage
  • patient/provider preference
  • effectiveness of medication for specific patient
36
Q

HTN: non-pharmacological management?

A
  • BP log (measure BP at home throughout the day and record the effects of lifestlye changes
  • decreased ETOH intake
  • low sodium diet
  • smoking cessation
  • exercise (consistent exercise for 30 mins, >3x week)
37
Q

Why a low sodium diet for HTN patients?

A
  • sodium increases BP b/c it causes kidneys to hold excess fluid in the body, thereby increasing one’s overall volume
  • decreasing sodium intake lowers BP

**don’t forget to document “low sodium diet encouraged” in the pt chart when directed by provider

38
Q

Diabetes Mellitus (DM): Type I

A
  • insulin insufficiency: pancreas is unable to produce insulin (which moves glucose from the blood into cells)
  • make up only 5% of today’s DM patients
  • treated ONLY with insulin
  • Dx early in life. Strong FHx component
  • **can ONLY be Insulin Dependent DM (IDDM)
39
Q

DM: Type II DM

A
  • insulin resistance: consistently high blood glucose levels cause cells to become resistant to insulin
  • 95% of today’s patients
  • can be treated with diet changes, non-insulin meds, or insulin
  • FHx component, but also SHx factors including diet and exercise
  • ** can be EITHER Insulin Dependent DM (IDDM) OR Non-Insulin Dependent DM (NIDDM)
40
Q

Type II DM: etiology

A

inadequacy of insulin in controlling blood glucose level (insulin resistance)

41
Q

Type II DM: risk factors

A

obesity, high carb diet, lack of exercise, HTN, HLD, FHx

**DM is not caused by HTN, however, comorbidities negatively affect the body and can cause other chronic illnesses. Also, overall health/diet can lead to both. HTN is a risk factor but NOT a direct cause for DM.

42
Q

Type II DM: CC

A
  • unusual weight loss or gain

- polyuria (excessive urination), polydipsia (excessive thirst), blurred vision, fatigue, N/V

43
Q

Type II DM: PE

A
  • distal paresthesia (tingling, prickling, numbness, “pins-and-needles” sensation)
  • pedal edema
  • weight change since last visit
44
Q

Type II DM: Dx by…

A
  • fasting blood glucose (nml < 100mg/dL)

- hemoglobin A1c (3mo avg BG) (nml <5.7%, preDM = 5.7-6.4%)

45
Q

Dz caused by type II DM: cardiac disease

A

diabetes is a risk factor for multiple cardiac conditions including CAD, CHF, and diabetic cardiomyopathy

46
Q

Dz caused by type II DM: PVD

A

damaged blood vessels and decreased blood flow to extremities results in infections, ulcers, and potential amputations

47
Q

Dz caused by type II DM: peripheral neuropathy

A

chronically elevated blood glucose damages the pheripheral nervous system, causing distal paresthesias and extremity pain

48
Q

Dz caused by type II DM: renal failure

A

chronically elevated blood glucose destroys the glomeruli of the kidneys, leading to renal failure

49
Q

Dz caused by type II DM: diabetic retinopathy

A

damage to the small vessels of the eyes can cause them to hemorrhage, leading to blurred vision, nearsightedness, or loss of vision

50
Q

DM: non-pharmacological management

A
  • blood glucose log (measure blood glucose at home throughout the week and record the effects of lifestyle changes
  • weight loss
  • low carb diet
  • exercise (consistent exercise - 30mins, >3x week
51
Q

DM: pharmacological management

A

Injected (insulin) medication (type I & II DM)

  • *Humalog (short acting insulin before or immediately after meals)
  • *Lantus (long acting insulin, injected once daily)
  • Sliding scale treatment: patient determines insulin dosage based on current blood glucose

Oral medication (type II DM only)

  • *Metformin (long acting, taken with meals)
  • *Glyburide (induces pancreas to produce insulin, taken with meals)
52
Q

HLD: etiology

A

an elevated level of lipid in the blood causes plaque to build up along arterial walls

53
Q

HLD: risk factors

A

obesity, high lipid diet, physical inactivity, FHx, ETOH use

54
Q

HLD: CC

A
  • asymptomatic

- typically diagnosed during routine blood work

55
Q

HLD: Dx by…

A

blood work measuring cholesterol and triglyceride levels – elevated LDL

56
Q

HLD: HDL (high density lipoprotein)

A

“happy”

  • commonly known as good cholesterol
  • able to move cholesterol from artery plaques and recycle it back to the liver
57
Q

HLD: LDL (low density lipoprotein)

A

“lousy”

- transports cholesterol to arterial walls and aids the formation of plaques

58
Q

Dz caused by HLD: arterial atherosclerosis

A

accumulation of cholesterol in the blood vessels causes thickening and hardening of vessel walls

59
Q

Dz caused by HLD: CAD/MI

A

atherosclerosis of the coronary arteries puts the patient at risk of acute MI

60
Q

Dz caused by HLD: CVA/TIA

A

atherosclerosis of the carotid arteries may lead to carotid stenosis (narrowing of the carotid artery), putting the patient at risk of TIA or CVA (can think of as ischemic CVA)

61
Q

Dz caused by HLD: pancreatitis

A

free fatty acids in the blood can damage pancreatic cells, leading to inflammation of the pancreas

62
Q

HLD: non-pharmacological management

A
  • decrease ETOH
  • lose weight
  • close follow-up
  • consistent exercise (30 mins, >3x week)
  • diet change (high fiber, high omega 3, avoid cholesterol)
63
Q

HLD: pharmacological management

A
  • any medication ending in “statin” is used to treat HLD by inhibiting the production of cholesterol.
  • 3 common drugs:
    lipitor (atorvastatin)
    zocor (simvastatin)
    crestor (rosuvastatin)
64
Q

Coronary Artery Disease (CAD): etiology

A

narrowing of the coronary arteries limits blood supply to the heart muscle, causing ischemia

65
Q

CAD: risk factors

A

HTN, HLD, DM, smoking, FHx <55 y/o

66
Q

CAD: CC

A
  • chest pain or pressure

- worse with exertion, improved with rest or nitroglycerin (NTG)

67
Q

CAD: associated medications

A

ASA, NTG, anticoagulants - blood thinning medications

68
Q

CAD: Dx by…

A

cardiac catheterization by cardiologist and/or stress test

69
Q

CAD: main concern

A
  • coronary artery disease
  • acute coronary syndrome
  • myocardial infarction
  • **CAD is the #1 biggest risk factor for MI
70
Q

CAD: non-pharmacological management

A
  • control risk factors (careful management of HTN, HLD, and DM will minimize the negative impact of CAD)
  • weight loss
  • manage stress and depression
  • smoking cessation
  • consistent exercise (30 mins, >3x week)
71
Q

CAD: pharmacological management

A
  • ASA (aspirin),

- NTG (nitroglycerin)

72
Q

CAD: surgical management (least invasive to most invasive)

A

cardiac cath, angioplasty, stent, CABG

73
Q

cardiac cath

A
  • diagnoses CAD
  • catheter is inserted through groin or wrist and extends up to the heart. IV dye is released to outline areas of bloackage
74
Q

angioplasty

A
  • minimally invasive cardiac procedure

- deflated balloon is inserted then inflated to open area of blockage; balloon is then removed

75
Q

stent

A
  • more invasive cardiac procedure

- similar to angioplasty; however, inserted tubing is left in the artery to keep it open

76
Q

CABG

A
  • invasive surgery

- open heart surgery to bypass area of blockage, usually using a vessel taken from the thigh

77
Q

Asthma: etiology

A

constriction of the airway due to inflammation and muscular contraction of the bronchioles, known as “bronchospasm”

78
Q

Asthma: risk factors

A

FHx of asthma, obesity, allergic rhinitis

79
Q

Asthma: CC

A
  • shortness of breath

- wheezing (improved with nebulizer treatments)

80
Q

Asthma: PE

A

wheezes (inspiratory or expiratory)

81
Q

Asthma: Dx by…

A

peak flow testing

82
Q

Asthma: assessing severity - what questions may the provider ask to assess severity?

A

Do you have a home nebulizer –> Have you been prescribed steroids recently –> Have you previously been hospitalized for asthma? –> Have you previously been intubated (breathing tube)?

83
Q

Asthma: Dx - Peak Flow

A
  • peak expiratory flow (PEF)
  • measured with a peak flow monitor
  • measured in liters/minute
  • baseline PEF must be established at the time of Dx
84
Q

Asthma: inhaler vs. nebulizer

A

Inhaler

  • pressurized device that released a “puff” of medication for inhalation
  • one dose at a time

Nebulizer

  • machine that delivers continuous aerosol mist
  • treatment is delivered over a period of time
85
Q

Asthma: pharmacological management - inhaled

A

bronchodilators (short acting)

  • advair
  • albuterol (ventolin)
  • xopenex (levalbuterol)
  • atrovent (ipratropium)

steriods (full course)

  • pulmicort
  • flovent
  • symbicort
86
Q

Asthma: pharmacological management - oral

A

steroids (full course)

  • prednisone
  • decadron

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