Hypertension & PUD Flashcards

1
Q

Silent Killer

A

Hypertension

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2
Q

Hypertension

A

High blood pressure; when the force of blood pushing against your artery walls is consistently too high

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3
Q

What can HTN damage?

A

Your arteries over time and can lead to serious complications like heart attack, stroke, and kidney failure.

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4
Q

What two organizations guide treatment of hypertension

A

American Heart Association
American College of Cardiology

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5
Q

Primary hypertension

A

Cause is unknown
(90-95% of cases)

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6
Q

Secondary hypertension

A

Cause is known (e.g., tumor)
(5-10% of cases)

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7
Q

What are the Clinical manifestations of primary HTN

A

No symptoms for most
Severe HTN: Painful headaches, confusions, hallucination, vision problems, nose bleeds, N/V (ICP)
Vascular damage
Elevated creatinine, BUN, proteinuria
Target organ diseases (Heard disease, PD, CV disease, nephrosclerosis, Retinal damage)

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8
Q

Elevated BP (SBP & DBP)

A

120 - 129 mmHg SBP
80 mmHg DBP

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9
Q

Complications of HTN

A

Heart attack
Stroke
Kidney disease
Heart failure
Retinopathy

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10
Q

What kind of visit is needed to determine hypertension

A

A wellness visit rather than an emergency visit.

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11
Q

Stage 1 HTN (SBP & DBP)

A

130 - 139 mmHg SBP
80 - 89 mmHg DBP

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12
Q

Stage 2 HTN (SBP & DBP)

A

> 140 mmHg SBP
90 mmHg DBP

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13
Q

White Coat HTN

A

Blood pressure elevated in a healthcare setting but normal at home.

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14
Q

Masked HTN

A

Blood pressure is normal in a healthcare setting but elevated at home.

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15
Q

Malignant HTN

A
  • Blood pressure is greater than 180/120 mmHg
  • Treatment varies on the cause of elevated BP
  • Gradual reduction to normal BP
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16
Q

Fixed RF for HTN

A

Family history
Increased Age
Gender

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17
Q

Modifiable RF for HTN

A

Obesity
Smoking
SES
Sedentary lifestyle
Diabetes
High Cholesterol
Stress
Diet in high sodium
Alcohol use

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18
Q

How do we dx patients with HTN?

A

We take their baseline BP during wellness visits (2x).
Rule out secondary causes
Evaluate end organ damage/disease
Determine cardiovascular risk
ECG
Blood & Urine test
Establish baseline levels (prior to therapy)

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19
Q

How do we manage HTN

A

DASH Diet
Exercise / Weight loss
Decrease stress
Smoking Cessation

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20
Q

End Organ Damage for HTN management

A

Neuro
Heart
Kidneys
Lungs
Peripheral
Vision

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21
Q

Medication Management: Prototypes for HTN

A

ACE inhibitors – relax blood vessels and pressure (esp kidneys).

ARBS (Angiotensin II Receptor Blockers – paired with ACE. Help relax blood vessels and pressure.

Beta Blockers – reduce HR and cardiac workload

Calcium Channel Blockers – relax blood vessels and cardiac workload

Thiazide Diuretics – reduce fluid retention & BP.

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22
Q

Monitor End Organ Damage for HTN

A

Identification
Maintenance
Prevention

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23
Q

What medication relaxes blood vessels and lowers blood pressure (esp kidneys)?

A

ACE Inhibitors

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24
Q

What medication is paired with ACE and helps relax blood vessels and pressure?

A

ARBS (Angiotensin II Receptor Blockers

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25
Q

What medication reduces heart rate and the workload of the heart?

A

Beta Blockers

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26
Q

What medication relaxes blood vessels and cardiac workload?

A

Calcium Channel Blockers

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27
Q

What medication reduces fluid retention and lowers blood pressure?

A

Thiazide Diuretics

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28
Q

Peptic Ulcer Diseases

A

Break in the lining of the mucosa with submucosa involvement. Ulcerations or erosions.

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29
Q

Where do Gastric Ulcers occur?

A

occurs in lesser curvature of the stoma near the pylorus

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30
Q

Where do Duodenal ulcers occur?

A

proximal part of the intestines; exacerbations occur, necessitating surgery in 5-10%

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31
Q

Protective part of the stomach

A

Prostaglandins
Bicarbonate
Blood Flow
Mucous Production

32
Q

Hostile factors of the stomach

A

H Pylori
Gastric Acid
NSAIDs

33
Q

RF for PUD

A

H pylori (releases toxins)
NSAIDS
Excessive smoking
Acid hyper secretion syndrome (Zollinger Ellison Syndrome)
Genetics

34
Q

What does H Pylori do to the stomach

A

Releases toxins that promote inflammation & ulcerations

35
Q

What do NSAIDs do to the stomach

A

Inhibits the production of prostaglandin

36
Q

How doe H Pylori transmit

A

Fecal to Oral (water)

37
Q

What predisposes patients to develop gastric cancer (NSAIDs or H Pylori)?

38
Q

What ulcer type is aggravated by fasting?

A

Duodenal Ulcer

39
Q

What ulcer type is NOT relieved by antacids?

A

Gastric Ulcer

40
Q

What ulcer type IS relieved by antacids?

A

Duodenal Ulcer

41
Q

What diagnostic testing is used for H Pylori?

A

Urease breath test
Fasting serum gastrin

42
Q

What do you see in the CBC of someone with gastric ulcers?

A

Decreased (slow drop) of Hematocrit

43
Q

Labs for gastric ulcers?

A

CBC & fecal occult blood tests
LFT/CPK, ekg, abdominal ultrasound, x-rays

44
Q

Complications of gastric ulcers

A

GI hemorrhage
- abdominal pain
- decrease in HCT/HBG
- vomiting blood
Intestinal perforation
- increased WBC
- abdominal pain
- VS changes

45
Q

Medication for management of peptic ulcers

A

H2 receptor antagonist
Proton Pump Inhibitor
Sucralfate

46
Q

What medication for peptic ulcers do patients take on an empty stomach?

A

Proton Pump Inhibitor

47
Q

What are irritants of peptic ulcers?

A

Caffeine
ETOH
Spices
Smoking

48
Q

Peptic ulcer patient education

A

Avoid NSAIDs, spicy foods, ETOH, smoking
Eat small meals
Avoid eating within 2 hrs of bedtime (eating increases gastric acid secretion)

49
Q

What is GERD?

A

A condition that occurs when stomach contents flow back up into the esophagus. Occurs when the muscle at the end of the esophagus does not close properly

50
Q

Symptoms of GERD

A

Worsens after eating, worsens when bending over or lying down, worsens at night

51
Q

Non-modifiable RF for GERD

A

Genetics
Hiatal Hernia
Obesity
Zollinger-Ellison Syndrome (incr gastric secretions)
NSAIDS leads to pyrosis
Scleroderma
Hypercalcemia

52
Q

Pyrosis

A

heart burn

53
Q

Esophageal symptoms for GERD

A

Dysphagia, Pyrosis, Regurgitation, Odynophagia, Nausea

54
Q

Extra esophageal symptoms for GERD

A

Chronic cough, chest pain, laryngitis, Asthma/SOB/pneumonia/bronchitis, pharyngitis, sinusitis, sleep apnea, erosion of dental enamel, otitis media

55
Q

Complications of GERD

A

Reflux esophagitis (erosions of esophagus)
Esophageal strictures (narrowing bc of inflammation and scarring)
Barrett’s Esophagus (precancerous lesions in esophagus)
Esophageal adenocarcinoma

56
Q

Diagnostics of GERD

A

Esophageal pH monitoring
Esophageal manometry or esophageal motility study (EMS)
Barium Swallow
Esophageal-gastroduodenoscopy (EGD)

57
Q

Lifestyle modifications of GERD

A

Improve diet
Avoid trigger food
Eat small meals
Lose weight
Down lay flat (esp after meals)
Avoid alcohol
Stop smoking

58
Q

Medication management of GERD

A

Proton Pump inhibitors
H2 Receptor Antagonist
Sucralfate

59
Q

Surgery for GERD

A

Nissen Fundoplication (tighten up the sphincter)
Linx procedure

60
Q

Notify the provider if you have GERd and esxperience

A

food gets stuck
continued symptoms

61
Q

Sucralfate

A

Binds to ulcer tissue; acts as a barrier

62
Q

Where on the body do people complain of gastric pain (GERD)

A

Epigastric region

63
Q

What is the method of action for ACEIs (Captopril or Lisinopril)

A

Blocks the enzyme ACE, decreases production of angiotensin II and aldosterone release

64
Q

What is the therapeutic use for ACEIs (Captopril or Lisinopril)

A

HTN, HF, MI, Nephropathy, Diabetic Retinopathy

65
Q

MOA for Lorsartan

A

Directly blocks angiotensin II receptor

66
Q

MOA for aldosterone antagonists (Eplerenone (Inspra®) or Spironolactone)

A

Antagonize effects of aldosterone at the collecting tubule – causing renal excretion of NA and H2O

67
Q

MOA for beta blockers (propanolol)

A

Beta1 and Beta2 receptor antagonists – Decrease BP by decreasing CO and decreasing renin release from kidneys – Blocking beta2 receptor causes increased peripheral resistance

68
Q

MOA for Adrenergic Antagonists Alpha Blockers (Prazosin)

A

Blocks alpha1 receptors, decreases peripheral resistance

69
Q

MOA for Alpha 2 Agonists

A

Alpha-2 agonist (central effect), decreases sympathetic outflow (cardiac output and vasodilation)

70
Q

MOA for Calcium Channel Blockers (Verapamil)

A

Blacks calcium channels in the blood vessels AND heart

71
Q

MOA for Calcium Channel Blockers (Nifedipine)

A

Blocks calcium channels in the blood vessels

72
Q

MOA for Thiazide diuretics (Hydrochlorothiazide)

A

Block sodium reabsorption in distal convoluted tubule

73
Q

(SATA) What are some factors that will decrease BP?

increase in job related hours
increase in K+ intake
decrease in sodium containing foods
weight loss
increase in exercise

A

increase in K+ intake
decrease in sodium containing foods
weight loss
increase in exercise

74
Q

(SATA) Thiazide diuretics can:

promote calcium excretion
retain calcium
promote urine excretion
retain potassium

A

retain calcium
promote urine excretion

75
Q

Masked hypertension a person has _______ at home; and whitecoat syndrome the patient has ______ at the doctors office.

A

elevated BP; elevated BP