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ILE > Unit 1: Hypertension And Hypersensitivity > Flashcards

Unit 1: Hypertension And Hypersensitivity Flashcards

1
Q

What are sources of patient information?

A

Chief complaint, history of present illness, past medical history,past surgical history, social history, family history, medical history, allergies/intolerances, immunization history

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2
Q

Describe the purpose of a SOAP note.

A

SOAP notes are important because they are a part of the collecting process of the patient care process.

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3
Q

List the sections of a soap note.

A

Subjective, Objective, Assessment, Plan

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4
Q

Define subjective information

A

Subjection information is information provided to you by the patient during an encounter

Examples: chief complaints or reason for the visits, HPI (history of present illness)

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5
Q

Define objective information

A

Objective information is the physical findings and measurable/confirmable data relevant to the encounter

Example: medications, vitals, PE, labs, EHR data

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6
Q

Subjective or objective?

A blood pressure reading of 143/78 taken by the nurse in clinic.

A

Objective

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7
Q

Subjective or objective?

Glucose of 101 reported in the clinic.

A

Objective

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8
Q

Subjective or objective?

Patient medication list in patient handwriting.

A

Subjective

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9
Q

Subjective or objective?
Home BP readings in the patients BP log averaging around 130/80.

What is they bring in the monitor and the nurse can check the history on it?

A

Subjective

Objective

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10
Q

What is the proper technique for blood pressure measurement?

A

First- make sure the patient is in a seated position with their legs uncrossed and their arm is resting on a table or in a comfortable position.

Secondly- palpate the brachial artery and place the correct size cuff on the patient’s arm. (If the cuff is incorrect, replace with the correct size)

Finally- ask the patient what their normal BP is and inflate the cuff to about 20mmHg above their reported BP. Place the diaphragm of the stethoscope over the brachial artery. Listen for the beginning sounds and the ending sounds.

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11
Q

What essential components of a blood pressure measurement should be accurately reported?

A

In addition to the actual BP values and units:

The arm used for the measurement, the position of the patient, the cuff sized used,

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12
Q

What type of hypertension is has a definite cause for elevated BP, but the specific cause is not known?

A

Primary hypertension

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13
Q

What type of hypertension is caused by another medical condition?

A

Secondary hypertension

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14
Q

What is the classification for a BP that is <120mmHg systolic AND <80mmHg diastolic?

A

Normal BP

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15
Q

What is the classification for BP that is 120-129mmHg systolic AND <80mmHg diastolic ?

A

Elevated BP

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16
Q

What is the BP classification for 130-139mmHg systolic OR 80-89mmHg diastolic ?

A

Stage 1 hypertension

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17
Q

What is the BP classification of a BP that is >140mmHg systolic OR >90mmHg diastolic?

A

Stage 2 hypertension

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18
Q

What are some risk factors that can elevate BP?

What are some risk factors that are modifiable?

A

Family history, age, gender, race, chronic kidney disease

Lack of physical activity, an unhealthy diet, especially one high in sodium, being overweight or obese, sleep apnea, high cholesterol, diabetes, smoking and tobacco use, stress

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19
Q

What is masked hypertension?

A

Elevated blood pressure occurs outside of a medical environment (LVMI, smokers, drinkers, diabetics, hypertensive patients)

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20
Q

What is white coat hypertension?

A

Elevated blood pressure only occurs in a medical environment

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21
Q

What is the blood pressure goal for adult patients that are being treated for hypertension?

A

130/80mmHg

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22
Q

What is an adverse drug event?

A

An injury resulting from medical intervention related to a drug including medication errors, adverse drug reactions (ADR), allergic reactions, and overdoses

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23
Q

What is an ADR?

A

Undesirable effect of a medication caused by appropriate use of drug

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24
Q

All AD—s are AD—s but not all AD—s are AD—s

A

All ADRs are ADEs but not all ADEs are ADRs

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25
Q

What are some symptoms associated with hypotension?

A

Dizziness or lightheaded ness, fainting (syncope), blurred vision, nausea, fatigue, lack of concentration

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26
Q

What BP thresholds classify hypotension?

A

<90mmHg systolic OR <60mmHg diastolic

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27
Q

How is hypertension diagnosed?

A

An average of 2 or more BP measurements are above the elevated threshold classification on more than one day.

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28
Q

Why is out-of-office monitoring of BP important?

A

Because it can rule out white coat hypertension. If the patient’s at home readings are just as high as they are while they are comfortable in their homes, then the doctor has a confirmed diagnosis

29
Q

What are some of the long term complications associated with hypertension?

A
  1. Heart attack/stroke/peripheral arterial disease (atherosclerotic cardiovascular disease (ASCVD))
  2. aneurysm
  3. heart failure
  4. chronic kidney disease
  5. memory problems/dementia
  6. thickened or torn or broken vessels in the eye
30
Q

What drug class works to block the sodium chloride symporter in the distal convoluted tubule?

A

Thiazide diuretics

31
Q

What four classes of drugs are considered first line anti hypertensives?

A

Thiazide diuretics
Calcium channel blockers
Angiotensin converting enzyme inhibitors (ACEI)
Angiotensin (2) receptor blockers (ARBs)

32
Q

Which of the two first line drug classes can you not use together? Why not

A

ACE inhibitors and ARBs. Because they both work to prevent angiotensin 2 from being able to produce aldosterone. They both increase potassium levels and decrease GFR

Angiotensin 2 is important in maintaining normal flow through the glomerulus

33
Q

What are some drugs within the thiazide class?

A

Hydrochlorothiazide and chlorthalidone

34
Q

Describe the mechanism of action for thiazide diuretics

What does this affect short term and long term?

A

They work to block the Na+/Cl- symporter. This reduces blood volume because Na is staying within the lumen to be excreted and is not being reabsorbed. Usually water would osmotically follow Na but since it is not being reabsorbed, neither is water.

Short term: blood volume
Long term: vascular resistance is reduced

Long term vasodilation bc Na normally works as a vasoconstrictor in the vasculature but when it isn’t present, vasodilation occurs

35
Q

Thiazide diuretics work to

Increase excretion of:
Decrease excretion of:

What else?

A

Increase excretion of h20, Na+, K+, Mg+, Cl-

Decrease excretion of Uric acid and Ca+ (may cause a gout attach in someone more prone to gout)

Also may increase glucose levels

36
Q

What are the two sub-classes of CCBs?

What are drug examples of each?

A

Dihydropyridines (DHP) and Non-Dihydropyridines (Non-DHP)

DHP - Amlodipine and other drugs ending in -dipine

Non-DHP - Diltiazem and Verapamil (these are the only two drugs in this class)

37
Q

What is the mechanism of action for bothering DHPs and Non-DHPs?

A

DHPs block the influx of Ca+2 into vascular muscle

Non-DHPs block Ca+2 entry into cardiac muscle

38
Q

What are the adverse effects of CCBs?

What do DHPs additionally effect? Why does this happen?

A

Hypotension, constipation, muscle weakness, flushing, swelling in the lower extremities, gingival hyperplasia, headache

DHPs additionally may cause reflux tachycardia. This happens bc DHPs work only in the muscles of the vasculature so, the stretch receptors in the carotid artery sense the BP drop when a DHP is administered and triggers the brain the have a reflex response. The brain stimulates the sympathetic system to release epi from the CNS to try to “fix” the drop in BP by increasing the heart rate

39
Q

What is the ending for ACE Inhibitors? And some drug examples

A

-pril

Captopril, enalopril maleate

40
Q

Discuss the mode of action of ACE inhibitors

A

They block the conversion of Angiotensin 1 to angiotensin 2 and blocks the breakdown of bradykinin.

Angiotensin 2 is responsible for maintaining normal flow through the glomerulus, causing vasoconstriction, and for producing aldosterone which is important for Na retention (increasing blood volume thus increasing blood pressure) and K+ excretion due to the exchanger

Bradykinin is a vasoconstrictor- ACEI block bradykinin from being broken down so the vasculature dilates
Bradykinin inhibition increases cough and angioedema

41
Q

What are some adverse effects of ACE

Inhibitors?

A

Hypotension, cough, increased K+ levels, angioedema, decreased GFR, rash, taste disturbances

42
Q

What is the ending for ARBs? Drug examples?

A

-artan ending

Valsartan

43
Q

What are ARBs mode of action?

A

Antagonist of angiotensin 2 at angiotensin 1 receptors

44
Q

What are the adverse effects of ARBs?

A

Hypotension, dizziness, headache, nausea and vomiting, cough, increased K+ levels, decreased GFR

45
Q

Why is cough associated with ACE and ARBs but not as much with ARBs?

A

Because ARBs can still break down bradykinin

46
Q

What are the normal lab values for Na+, K+, SCr, and glucose?

A

Na+ 136-145mEq/L
K+ 3.5-5.0mEq/L
Glucose 70-110mg/dL
SCr 0.7-1.5mg/dL

47
Q

What are the six classes of alternative antihypertensives?

A 
Beta blockers
Centrally acting antihypertensives
Loop diuretics
Aldosterone antagonists
Alpha-1 antagonist
Direct vasodilators
48
Q

Which alternative drug is the first choice?

A

Beta blockers

49
Q

What is the ending of beta blockers and drug examples?

A

-prolol

Metoprolol

50
Q

What is the mode of action for beta blockers?

A

Decrease heart rate, decreased central sympathetic outflow, decreased renin release

Decreased HR leads to a decrease in blood pressure bc it is working by blocking the Beta receptors on the heart

Decreased sympathetic outflow by blocking it within the brain so the body will not respond by trying to raise BP

Decreased renin release will slow the conversion of angiotensin 1 to angiotensin 2 preventing vasoconstriction to a certain degree

51
Q

What are adverse effects associated with beta blockers ?

A

Bradycardia, sedation, fatigue, shortness of breath (SOB), headache, sleep disturbances, sexual dysfunction

52
Q

What drug class is clonidine a part of?

A

Centrally acting antihypertensives

53
Q

What is the modes of action for centrally acting antihypertensives?

A

Decreased sympathetic outflow, several are alpha-2 agonists

Alpha-2 agonists work to shut down further release of neurotransmitter…. alpha-2 agonist prevents the release of norepi

A few alpha-2 receptors are in the vasculature and mediate vasoconstriction but are soon overcome bc clonidine gets into the CNS rapidly

54
Q

Sedation, bradycardia, constipation, dry mouth, and dizziness are all adverse effects of which antihypertensive drug class?

A

Centrally acting antihypertensives

55
Q

What kind of antihypertensive is lasix (furosemide)?

A

Loop diuretic

56
Q

What is the mode of action for loop diuretics?

A

They are the most powerful diuretics known due to their site of action. Inhibition of the Na+/K+/2Cl- symporter results in a powerful diuretic effect resulting in the loss of these ions along with Ca+2 (retained with thiazide diuretics) and Mg+2 (used when blood volume is high)

57
Q

Why are thiazide diuretics used over loop diuretics?

A

Because thiazide reduce the overall risk of cardiovascular disease, they are a first line agent, and they are used in patients who don’t have a lot of calcium in their diet.

Loop diuretics result in a loss of Ca too

58
Q

What is the adverse effect of loop diuretics.

A

Electrolyte embalance

59
Q

Spironolactone and eplerenone are examples of what drug class?

A

Aldosterone antagonists

60
Q

Aldosterone antagonists are considering as what type of diuretic ?

A

K+ sparing

61
Q

What are in the mode of action for aldosterone antagonists?

A

Inhibits aldosterone mediated stimulation of ENaC and Na+ATPase synthesis resulting in increased Na+ excretion and decreased K+ excretion

62
Q

What are adverse effects of aldosterone antagonists?

A

N/V, headache, rash and hyperkalemia,

Spironolactone is also a potent anti-androgenic (partial agonist) compound and may produce gynecomastia, impotence, and menstrual disorders

63
Q

What ending is denoted for alpha-1 antagonist drugs? What are some examples?

A

-sin

Terazosin

64
Q

Discuss alpha-1 antagonist mode of action

A

Blocks alpha-1 receptors in the vasculature to promote vasodilation

65
Q

Adverse effects of alpha-1 antagonists are

A

Hypotension, fainting, N/V, runny nose, sexual dysfunction (happens when you inhibit adrenergic function)

66
Q

What are some examples of direct vasodilators?

A

Hydralazine and minoxidil

67
Q

What is the mode of action of direct vasodilators?

A

Open potassium channels resulting in hyper polarization of vascular smooth muscle

68
Q

What are the adverse effects of direct vasodilators?

A

Hypotension, reflex response, hypertrichosis (hair growth)

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