Health Maintenance and role of screening: chapter 3 Goroll Flashcards

1
Q

Do men or women have a higher prevalence of hypertension?

A

Men. In the 3rd and 4th decades it is more than twice as common among men than women.

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2
Q

Which race has a marked increase in the prevalence of hypertension?

A

African Americans. Compared with whites, asians and nonblack Hispanics the overall prevalence is 2:1. Higher in young black adults and lower in the elderly.

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3
Q

How does a provider confirm the diagnosis of hypertension?

A

Requires at least two separate sets of readings either in the office at least 1 weeks apart or by home/ambulatory monitoring.

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4
Q

True or false: all adults >18 years should be screened for hypertension.

A

True

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5
Q

True or false: screen every 3-5 years those aged 10-39 who are at normal risk.

A

True

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6
Q

True or false: screen annually all adults 40> as well as those with increased risk for developing HTN.

A

True. Those at risk include African American race, overweight/obese, positive family history.

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7
Q

What is considered hypertension stage I? HTN stage II?

A

Stage I: SBP 130-139, DBP 80-89

Stage II: SBP >140, DBP >90

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8
Q

What are the primary determinants of blood pressure? (two of theses)

A

Cardiac output and total peripheral resistance.

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9
Q

How do catecholamines affect blood pressure regulation?

A

Both centrally and peripherally. Centrally: vasomotor centers in the brain, peripherally through the action of the sympathetic nervous system by increasing peripheral resistance and cardiac output

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10
Q

What are causes of secondary hypertension? (9 of these)

A
  1. Coarctation of aorta
  2. Cushings syndrome
  3. Drug-induced syndrome
  4. Increased intracranial pressure
  5. OSA
  6. Pheochromocytoma
  7. Primary aldosteronism
  8. Renal disease
  9. Renovascular disease
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11
Q

What are characteristics of Cushing syndrome?

A

trunacal obesity, facial plethora, violaceous abdominal striae, proximal muscle thinning and weakness, “buffalo hump”, easy bruising or hirsutism.

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12
Q

What labs should be ordered to rule out secondary hypertension?

A

CBC, urinalysis, blood urea nitrogen (BUN), creatinine, potassium, calcium (with albumin), fasting blood sugar, total and high-density lipoprotein (HDL), EKD.

Urinalysis, BUN, creatinine: provide evidence of primary renal disease (i.e. azotemia, proteinuria, active sediment)

Fasting FSG, serum cholesterol and EKG: provide data re: CV risk and present of left atrial enlargement and ventricular hypertrophy

Serum potassium: visual for primary aldosteronism

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13
Q

What is the initial test of choice for Cushing syndrome?

A

24 hour urinary free cortisol. A finding >25o ug/d is diagnostic. a level > 65 ug/d in a person with characteristic clinical features strongly supports the diagnosis.

Persons with clinically suspected disease need an assessment of corticotropin (ACTH) dependence. Best outpatient approach is an overnight 1 mg dexamethasone-suppression test (where 1 mg is taken at midnight and a 0800 plasma cortisol is obtained).

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14
Q

What is treatment for stage I hypertension at Low, intermediate and high CV event risk?

A

Low: lifestyle modification & monitor q6 months. if no improvement start single-drug therapy.

Intermediate: lifestyle modification & monitor q3 moths. if no improvement start 1-drug therapy

High: lifestyle modification & start 1 drug regiment and monitor monthly until at target. then reassess q3-6 months

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15
Q

What is treatment for stage II hypertension at low, intermediate and high CV event risk?

A

Low: lifestyle modification, monitor q3 month and start 1 drug program if no progress

intermediate: lifestyle modification and 1-drug therapy, monitor q3 months

High: lifestyle modification & start 2-drug therapy and monitor monthly until at target, then reassess every 3 months.

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16
Q

What questions are on the ASCVD risk estimator?

A
Age
Sex
Race
SBP, DBP
Total cholesterol, HDL, LDL
Hx diabetes
Smoker (current, former, never)
On HTN therapy? On a statin? On aspirin therapy?
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17
Q

What drug classes are considered first line treatment therapy for hypertension?

A

Thiazide diuretics, ACE-i’s, CCBs, ARBs, and beta blockers (if the individual has an additional indication for beta-blockage).

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18
Q

What is the mechanism of action of Thiazide diuretics?

A

MOH: enhance sodium excretion resulting in reduced intravascular volume and reduced peripheral resistance. K excretion is increased and uric acid & calcium excretion are decreased.

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19
Q

What are the most commonly prescribed Thiazide diuretics?

A

Chlorthalidone
HCTZ
Indapamide
Metazolone

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20
Q

What are the adverse effects of Thiazide diuretics?

A

Potassium wasting d/t drug effect on the distal renal tubule. Clinically significant hypercalcemia is rare but possible. Thiazides may cause a rash especially in photosensitive individuals.

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21
Q

What should be monitored in an individual who is initiating Thiazide diuretics therapy?

A

checking the serum potassium regularly as can cause hypokalemia. Serum glucose requires close monitoring when thiazides are used in a diabetic and the uric acid should be watched if the patient has clinical gout.

No need to monitor LDL or serum calcium

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22
Q

True or false: ACE-i’s are the class of choice in patients with type 1 or 2 diabetes because of their protective effect on the kidney and ability to reduce proteinuria

A

True!

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23
Q

What is the MOA of ACE-i’s?

A

Block the conversion of renin-activated angiotensin I to angiotensin II (which is a potent vasoconstrictor that also stimulates the production of aldosterone). Additionally inhibits the breakdown of bradykinin (which is a vasodilator) to stimulate the production of vasodilatory prostaglandins.

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24
Q

What are the most common adverse effects of ACE-i’s?

A

Dry cough. Angioedema. Rash, taste disturbances, agranulocytosis. Hyperkalemia (when used in conjunction with a K-sparing diuretics, K-supplement or NSAIDs).

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25
Q

What is the MOA of ARBs?

A

Blocks the ATII receptor, inhibiting the vasoconstrictive effects of ATII and associated stimulation of aldosterone production.

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26
Q

What is the drug class of choice to treat HTN for African Americas?

A

CCBs

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27
Q

What is the MOA of CCBs?

A

Impede the entry of calcium in heart and vascular smooth muscle cells, resulting in a decreased cellular calcium concentration, which reduces vascular smooth muscle contraction and lower peripheral resistance.

*These drugs also have a mild natriuretic effect which makes them useful in patients with sodium retention.

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28
Q

What are the two classes of CCBs and examples of each?

A

Nondihydropyridines: verapamil, diltiazem

Dihydrophyridines: amlodipine, nifedipine, nicardipine, istardipine, felodipine

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29
Q

What is the most commonly used CCBs? Why? What are the biggest adverse event?

A

Amlodipine. This drug produces less reflex tachycardia and less negative isotropy.

Peripheral edema can occur and can be substantial in persons with preexisting venous insufficiency.

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30
Q

What are the main disadvantages of Verapamil? What are the “do not use” in certain populations?

A

Disadvantages: negative isotropy, conduction system disturbances; this can lead to bradycardia and AV nodal block.

Do NOT USE in patients with heart failure or suspected conduction system disease.

31
Q

What are primary reasons for beta-blocker therapy?

A

CAD, HF, A-fib, Migraines, hyperkinetic states (anxiety, tachycardia, palpitations). They also provide secondary prevention following MI and help to reverse left ventricular remodeling in hypertension.

32
Q

What is the MOA of beta blockers?

A

unclear, but beta blockers reduce cardiac output, renin and catecholamine relate, central sympathetic activity and peripheral resistance.

33
Q

What are adverse effects of beta-blockers?

A

bradycardia, fatigue, decreased exercise tolerance, increased airway resistance.

34
Q

What is an example of an alpha-blocker? What population is this most used for? What are the principal side effects of this drug class?

A

Example: Doxazosin, Prazosin, Terazosin

Population: older hypertensive men with concurrent prostatism

Side effect: postural hypotension- may experience profound postural hypotension leading to syncope 1-3 hours after the initial dose.

35
Q

When would a loop diuretic be indicated?

A

Used in patients with an allergy to thiazides and are reserved for patients with evidence of CKD (creatinine clearance <30% of normal).

36
Q

What is a hypertensive emergency? What may be seen on physical assessment?

A

BP > 180/120 in conjunction with new renal, cardiac, near or retinal injury.

Assessment: HF, increased intracranial pressure, acute glomerular injury (hematuria, proteinuria), retinopathy (new hemorrhages).

37
Q

What is preeclampsia? What are complications of this?

A

Defined as onset of HTP (>140/90) or worsening of preexisting HTN in conjunction with proteinuria (>300 mg/24 hrs) after 20 wks gestation.

Complications: stroke, organ failure, eclampsia

38
Q

What are risk factors for HIV?

A

Had sex with someone known to have HIV or AIDS?
Had a hx of sexually transmitted dx?
Had sex with many men or women or had sex with someone who has had sex with many partners?
Had sex with someone who has used needles to take drugs?
Shared needles or works to take drugs?
Received blood products between 1978 and 1985?
Had a hx of occupational exposure?

39
Q

What drugs are utilized to treat tobacco use?

A
Nicotine replacement therapy (patch, gum, lozenge, inhaler)
Bupropion SR (zyban, Wellbutrin)
Varencicline (chantix)
Nortriptyline
Clonidine
40
Q

True or false: Wellbutrin helps with tobacco cessation and depression

A

True

41
Q

When should bupropion SR be started in someone who is quitting smoker? What is the recommended dosage for treatment? Most common side effects?

A

Start 1 week before a smoker’s target quit date. The recommended dose is 150 mg/d for three days THEN 150 mg BID. The recommended duration of treatment is 12 weeks, but is approved for up to 6 months to reduce the risk of relapse to tobacco.

Side effects: insomnia, agitation, dry mouth

42
Q

What is the five-step smoking cessation strategy for office practice?

A
  1. Ask- about smoking q visit
  2. Advise- every smoker to stop smoking
  3. Assess - readiness to quit
  4. Assist- the smoker to stop smoking
  5. Arrange follow-up
43
Q

When should colon cancer screening begin?

A

At age 50 for both men and women

44
Q

For colon cancer screening, what stool-based tests should occur every year? What test should be completed every 3 years?

A

Every year: Guaic based FOBT or FIT (fecal immunochemical test).

Every 1 or 3 years the FIT-DNA

45
Q

For colon cancer screening, how often should a patient have a colonoscopy?

A

10 years

46
Q

When should colon cancer screening be discontinued?

A

After age 85 or when life expectancy is <10 years

47
Q

What is considered Tier 1 screening for colon cancer? What about Tier 2? And tier 3?

A

Tier 1: colonoscopy q 10 years, FIT every year

Tier 2: CT colonography q 5 years, FIT-DNA q 3 years, Flexible sigmoidoscopy every 5 or 10 years

Tier 3: Capsule colonoscopy every 5 years

48
Q

If a patient has a family history of CRC in a first degree relative when should screening begin?

A

40 years of age

49
Q

When should CRC screening for African Americans (even without an established family hx) begin?

A

45 years of age

50
Q

What is the USPSTF guideline for breast cancer screening?

A

Starting at age 50 and biennial mammography.

51
Q

What is the recommended age to initiate HPV screening? How often should normal risk women be screened with Pap testing and with hrHPV DNA testing w/ or w/o pap?

How often should a woman with HIV infection (and others who are immunocompromised) be screened?

A

Start at age 21. Do not start earlier unless patient is immunocompromised and sexually active.

Screen q3 years with pap testing and 5-years with hrHPV DNA testing.

HIV infection/immunocompromised: annual pap smears and hrHPV testing after 2 negative smears 6 moths apart.

52
Q

What are the major risk factors for osteoporosis-related fractures in women?

A

Advanced age, history of low-trauma fracture during adulthood, family hx of osteoporosis in a first-degree relative, low body weight/low BMI, low bone mineral density, current cigarette smoking, excess alcohol consumption, glucocorticoid therapy, secondary osteoporosis (i.e. rheumatoid arthritis, celiac disease)

53
Q

What medical conditions are secondary causes of osteoporosis?

A

Cushing syndrome, exogenous glucocorticoid administration, rheumatoid arthritis, prolonged heparin therapy, thyrotoxicosis, celiac dx, hypogonadism, hyperprolactinemia, anorexia, hyperparathyroidism.

54
Q

When should screening begin for women for osteoporosis? What if they have a major risk factor?

A

Age 65 and older.

*If major risk factor is present being earlier than 65.

55
Q

What is the gold standard for osteoporosis screening? (type of test)

A

DXA bone scanning.

56
Q

What are common differential diagnoses of depression?

A

Chronic fatigue syndrome. Lyme disease, fibromyalgia, rheumatoid arthritis, endocrinopathies

57
Q

What are drug-induced etiologies of depression?

A

alpha-methyldopa, antiarrhythmics, bentos, barbiturates and other CNS depressants, Beta-blockers, cholinergic drugs, digoxin H2 blockers, reserpine

58
Q

What are substance abuse related etiologies of depression?

A

alcohol abuse, sedative-hypnotic abuse, cocaine, other pscyhostimulant withdrawal

59
Q

What are toxic-metabolic disorders related etiologies of depression?

A

hypothyroid or hyperthyroid, Cushing syndrome, hypercalcemia, hyponatremia, diabetes mellitus

60
Q

What are neurologic disorders that are etiologies of depression?

A

Stroke, subdural hematoma, MS, brain tumor, Parkinson’s, Huntingtons disease, epilepsy, dementia

61
Q

What are infection disease disorders that are etiologies of depression?

A

viral infections, HIV w/ or w/o AIDS, syphilis

62
Q

What are nutritional disorders that are etiologies of depression?

A

Vitamin b12 deficiency, pellagra

63
Q

What is the most commonly utilized depression screening tool used in primary care?

A

PHQ-9

64
Q

What drug is considered first-line antidepressant treatment? What drug class is used if patients do not respond to SSRIs?

A

SSRIs= 1st line

Use TCAs and SNRIs next.

65
Q

What are the main side effects of SSRI medications?

A

Exacerbation of agitation, anxiety, insomnia, motor restlessness. Sexual dysfunction, decreased libido and anorgasmia, headache, nausea, diarrhea

66
Q

Which SSRIs inhibit liver cytochrome P450 enzymes?

A

fluoxetine, paroxetine, fluvoxamine.

**Concerning if individuals take other drugs such as warfarin, phenytoin, etc that are hepatic ally metabolized

67
Q

When should someone see clinical improvement when initiating SSRI therapy?

A

3-4 weeks.

68
Q

What are examples of SNRIs?

A

duloxetine (Cymbalta), venlafaxine XR (Effexor XR), desvenlafaxine (Pristiqu), Milnacipran (Savella) [only treatment for fibromyalgia and depression]

69
Q

What is the potentially lethal side effect of TCAs?

A

Can lead to lethal CV toxicity when taken in overdose d/t severe cumulative anticholinergic and alpha-blocking effects.

**postural hypotension can also occur, which is not lethal but for the elderly may lead to falls/fxs/head injuries

70
Q

What is the first choice drug to treat bipolar disorder? What are some symptoms that may come with the onset of therapy and remove with continuation? What symptoms indicate toxicity??

A

Lithium!

onset: fine tremor, mild thirst and nausea, frequent urination, generalized malaise
toxicity: diarrhea, vomiting, drowsiness, muscular weakness, worsening polyuria, poor coordination

71
Q

What is the AUDIT test?

A

A questionnaire to review alcohol use disorder risk. it contains 10 questions with a 0-4 scale

72
Q

What is three pharmacologic treatments for alcohol use disorder?

A

Naltrexone: Also effective for patients with PTSD or depression.

Acamprosate: inhibits GABA activity w/o being a direct agonist at the GABA receptor.

Disulfiram: inhibits the accumulation of acetaldehyde resulting in symptoms such as palpitations, flushing, diaphoresis, tachypnea, tahcycardia, SOB, resolve w/in 90 min.

73
Q

What drugs are FDA approved for the treatment of obesity? (4 of these)

A

Lorcaserin

Orlistat

Phentermine

Phentermine + Topiramate XR (pg 1802)